BOOK OF THE MONTH TERMS OF USE

PsychiatryOnline.com currently offers access in PDF format to a free book each month from the APPI Bookstore. This offering is intended as a promotional tool, to give subscribers a change to review books they might be interested in purchasing separately for continued access. As such, the “Book of the Month” is governed by the following terms of use:
The Book of the Month is supplied as PDF; no other formats will be supplied. Subscribers have access to the Book of the Month for only as long as the “download” link appears on the PsychiatryOnline.com home page (usually one month). This feature may be discontinued at any time without notice or reason to subscribers. The User license does not cover storing the book in any format beyond the one-month period. Users may not copy, modify, reproduce, publish, transmit, display, broadcast, rent, lend, sell, catalog, or otherwise distribute the Book of the Month.

Click here to continue on to the Book of the Month.

Clinical Manual of Geriatric Psychiatry

This page intentionally left blank

Clinical Manual of Geriatric Psychiatry
James E. Spar, M.D.
Professor of Clinical Psychiatry Department of Psychiatry & Biobehavioral Sciences Geffen School of Medicine at UCLA Los Angeles, California

Asenath La Rue, Ph.D.
Senior Scientist Wisconsin Alzheimer’s Institute University of Wisconsin School of Medicine and Public Health Madison, Wisconsin

Washington, DC London, England

Note: The authors have worked to ensure that all information in this book is accurate at the time of publication and consistent with general psychiatric and medical standards, and that information concerning drug dosages, schedules, and routes of administration is accurate at the time of publication and consistent with standards set by the U.S. Food and Drug Administration and the general medical community. As medical research and practice continue to advance, however, therapeutic standards may change. Moreover, specific situations may require a specific therapeutic response not included in this book. For these reasons and because human and mechanical errors sometimes occur, we recommend that readers follow the advice of physicians directly involved in their care or the care of a member of their family. Books published by American Psychiatric Publishing, Inc., represent the views and opinions of the individual authors and do not necessarily represent the policies and opinions of APPI or the American Psychiatric Association. Copyright © 2006 American Psychiatric Publishing, Inc. ALL RIGHTS RESERVED Manufactured in the United States of America on acid-free paper 10 09 08 07 06 5 4 3 2 1 First Edition Typeset in Adobe’s Formata and AGaramond. American Psychiatric Publishing, Inc. 1000 Wilson Boulevard Arlington, VA 22209-3901 www.appi.org 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

4

Mood Disorders—Treatment . . . . . . . . . . . . . . . 127
Psychotherapy for Geriatric Depression . . . . . . . . . . . .127 New Directions in Psychotherapy Research . . . . . . . . .130 Combined Psychotherapy and Pharmacotherapy . . . .132 Psychopharmacotherapy for Geriatric Depression . . .132 Psychopharmacotherapy for Psychotic Depression. . .156 Psychopharmacotherapy for Bipolar Depression. . . . .157 Electroconvulsive Therapy . . . . . . . . . . . . . . . . . . . . . . .157 Experimental Therapies . . . . . . . . . . . . . . . . . . . . . . . . .159 Complementary and Alternative Approaches . . . . . . .161 Hypomania and Mania . . . . . . . . . . . . . . . . . . . . . . . . . .162 Bipolar Disorder . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .162 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .166

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

6

Other Dementias and Delirium . . . . . . . . . . . . 229
Frontotemporal Dementia . . . . . . . . . . . . . . . . . . . . . . .229 Dementia With Lewy Bodies . . . . . . . . . . . . . . . . . . . . .235 Vascular Dementia . . . . . . . . . . . . . . . . . . . . . . . . . . . . .241 Mixed Dementia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .248 Dementia Due to General Medical Conditions . . . . . .249 Substance-Induced Persisting Dementia . . . . . . . . . . .254 Reversible Dementia . . . . . . . . . . . . . . . . . . . . . . . . . . .255 Delirium . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .256 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .265

. . .313 Alcohol Abuse and Dependency . . . . . . . . . . . . . . . . . . . . . . . . 347 Decisional Competency . . . . . . . . . . . . . . . . . . . . . . . . . . . .7 Anxiety Disorders and Late-Onset Psychosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .306 8 Other Common Mental Disorders of the Elderly . . . . . . . . . . . . . . 379 Geriatric Depression Scale . .380 Six-Item Orientation-Memory-Concentration Test. . . . . . . . . . . . . . . . . . . . . . .348 Undue Influence: The Question of Voluntariness . . . . . . . . . . . . . . . . . . . .320 Other Psychoactive Substance Abuse and Dependence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .367 Elder Abuse . . . .366 Competency to Drive . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .341 9 Competency and Related Forensic Issues. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .383 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 313 Insomnia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .371 References . . . . 273 Anxiety Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . .360 Expert Consultation and Testimony on Competency . . . . .273 Late-Onset Psychosis . . . . . . . . . . . .337 Influence of Aging on Disorders of Early Onset . .293 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .339 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .334 Chronic Pain . . . . . . . . . .326 Sexual Dysfunction . . . . . . . . . . .329 Psychiatric Illness Related to a General Medical Condition . .382 Cognistat profile: Example . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .373 Appendix: Clinical Assessment Instruments. . .358 Competency to Care for Oneself and Manage One’s Finances . .

.386 Items Rated on the Neuropsychiatric Inventory. . . . . . . . . . . . . . . 389 . . . . . . . . . . . . . . . . . . . . . . . . . . .Instrumental Activities of Daily Living (IADL) Scale . . . . .384 Revised Memory and Behavior Problems Checklist . . . . . . . . . . . . .388 Index . . . . . . . . . . . . . . . . . . .

In 2003. or nearly 5% of the total population. average life expectancy is more than 16 years. Very old people (85 years and older) constitute one of the fastest-growing subgroups of the elderly population (Figure 1–1). so that by the year 2030. For men at age 65.000 U. most people in societies such as our own can plan on growing old.1 Introduction An Aging World For the first time in history. compared with an estimated 4. residents were 100 years or older. one in three Americans will be age 55 or older. there will be 19 million to 24 million people in this 85 and older age group.000 people were age 85 years or older in the United States. Life expectancy from birth has increased dramatically in the United States.2 million in 2000 (National Center for Health Statistics 2004). an increase of 36% since 1990 (Administration on Aging 2004). population are older than age 55. and one in five will be at least age 65.S.S. and for women at age 65. men can expect to live 6 more years and women 7 years (Federal Interagency Forum on Aging-Related Statistics 2004). In 1900. By 2050. a little more than 100. 1 . More than 20% of the current U. at age 85. and more than 12% are 65 or older (Federal Interagency Forum on Aging-Related Statistics 2004). it is almost 20 years. more than 50. from about 47 years in 1900 to 77. The elderly population is the only age segment of the population that is expected to grow substantially in the next quarter century.3 years in 2002 (Federal Interagency Forum on Aging-Related Statistics 2004). Even those people who are currently “old” can expect to live for many years.

the twentieth century may well be the last in which younger people outnumbered older ones (Cohen 2003). Worldwide. China alone is expected to have 270 million persons age 65 and older—nearly the total current population of the United States—by the middle of this century. Populations of older adults in the United States (in millions). where both fertility and mortality rates are high.5 billion worldwide (20% of the total population) (Olshansky et al. . average life expectancy has increased to about 65 years (Cohen 2003). and by 2050. Europe. and the Caribbean. Asia. Substantial increases in elderly populations are projected in the next quarter century for North America. Source. Latin America. the number of people age 65 years and older is projected at 2. By 2050. Adapted from Federal Interagency Forum on Aging-Related Statistics 2004. with smaller increases expected for areas such as sub-Saharan Africa. 1993). As one demographer recently pointed out. there will be more than three adults age 60 years or older for every child age 4 years or younger.2 Clinical Manual of Geriatric Psychiatry 100 80 Population (millions) 60 40 20 0 1900 1930 1960 1990 65 and older 85 and older 2020 2050 Projected Figure 1–1.

Sensory impairments are also prevalent. and they remained in the hospital about a day longer on average than did middle-aged adults (Administration on Aging 2004).g.to 74-year-olds who were overweight rose from 57% to 73% between 1976 and 2002. Older adults visited their physicians six to seven times per year on average. The most common illnesses affecting elderly people in the United States are arthritis.. cancer. Alzheimer’s disease ranked sixth. medication schedules). rates of cigarette smoking declined by 2002 to 10% among older men and have remained steady in recent years at about 9% among older women. cancer. compared with three to four times for 45. people age 65 and older were hospitalized more than three times as often as those ages 45–64. these rates are approximately twice as high for persons age 85 and older (Federal Interagency Forum on Aging-Related Statistics 2004). transportation. respectively (Federal Interagency Forum on Aging-Related Statistics 2004). hypertension. Of 65. bathing. By contrast. and the obesity rate increased from 18% to 36% (Federal Interagency Forum on Aging-Related Statistics 2004). about 20% of older adults were chronically disabled as a result of health problems. toileting). eating. another 6% were impaired in three to six basic activities. In 2002. and stroke account for two of every three deaths among the elderly and also account for many doctor visits and days of hospitalization. Each of these conditions can limit independent function and detract from quality of life.to 74-year-olds. In 1999. whereas death rates due to diabetes and chronic lower respiratory diseases increased by 43% and 62%. after heart disease. Heart disease. and influenza or pneumonia. financial management. 6% had impairment in one or two basic activities of daily living (e. Death rates due to heart disease and stroke decreased by approximately one-third from 1981 through 2001.g. about 3% had limitations in only higher-order activities of daily living (e. and slightly fewer than 5% were institutionalized (Federal Inter- . respiratory diseases. The percentage of 65. 30% report problems seeing and 18% report problems hearing. Being overweight or obese has increased dramatically among older Americans in recent years. and heart conditions (Figure 1–2).Introduction 3 Health and Functioning of Older Adults Most people age 65 and older have at least one chronic medical illness. cerebrovascular diseases..to 64-year-olds. and many have multiple conditions. among causes of death for Americans age 65 years and older in 2002 (National Center for Health Statistics 2004).

Among persons who reached their 60th birthday in 1990. Those with chronic needs that cannot be met at home generally receive care in nursing homes. 66% received informal care only. Percentage of people age 65 and older with selected chronic conditions. agency Forum on Aging-Related Statistics 2004). Adapted from Federal Interagency Forum on Aging-Related Statistics 2004. Figure 1–3 shows age trends in independent and assisted living within the United States. 26% received a combination of formal and informal services. Although fewer than 5% of elderly Americans are in nursing homes at a given time.4 Clinical Manual of Geriatric Psychiatry 100 80 Americans age ≥65 (%) Men 60 40 20 0 Women Heart disease Hypertension Stroke Emphysema Asthma Chronic Cancer Diabetes Arthritic bronchitis symptoms Figure 1–2. Of disabled older people living in the community. Source. 2001–2002. reflecting improved financial resources of older persons as well as liberalization in coverage rules under Medicare and Medicaid. and 9% had formal care only (Federal Interagency Forum on Aging-Related Statistics 2004). However. the proportion of older persons requiring such care increases quite sharply with age (see Figure 1–3). older black Americans and elders from other minority groups use . The proportion receiving paid care has increased since the early 1980s. generally from relatives. 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.

Health care costs for older Americans increased substantially from 1992 through 2001. after adjustment for inflation. the percentage of older adults residing in nursing homes in the United States declined slightly. Source. by type of residence. the proportion of health care dollars spent on acute hospital care decreased. Between 1985 and 1999. a trend . Long-term-care costs. but the total number of older nursing home residents increased from 1. Percentage of Medicare enrollees age 65 and older. Three-fourths of current nursing home residents are women. paid in-home services and nursing home care less frequently than do white Americans (National Center for Health Statistics 2004). The average cost of providing health care for persons age 65 or older is currently three to five times greater than health care costs for younger persons (Centers for Disease Control and Prevention 2004). 2003.3%. including nursing home and home health expenditures.3 million to 1. from 5. During this time span. while the proportion spent on prescription drugs increased.5 million because of growth in the older population (Federal Interagency Forum on Aging-Related Statistics 2004).Introduction 5 100 Medicare enrollees (%) 80 60 40 20 0 1 5 2 1 5 3 19 7 Long-termcare facility Community housing with services 93 98 92 74 Traditional community ≥65 65–74 75–84 ≥85 Age (years) Figure 1–3.4% to 4. Adapted from Federal Interagency Forum on Aging-Related Statistics 2004. doubled between 1990 and 2001.

Creative approaches are required to stem rising costs while maintaining quality assessment and intervention. Table 1–1 compares rates for several different types of mental disorders in the ECA community-based survey (1-month prevalence data) with a survey of hospitalized geriatric patients conducted at about the same time. Overall. A 1999 consensus conference on geriatric mental health estimated the prevalence of psychiatric disorders in community-residing older adults at 25% or more (Jeste et al. and in long-term-care settings.2 billion in 2002 and is projected to grow to twice that amount by 2012 (Centers for Disease Control and Prevention 2004). 68%–94% of residents have been found to have mental disorders (Hybels and Blazer 2003).810. including dementia (U. In 2001. Mental Disorders in Later Life Older people with mental disorders constitute a significant subgroup of the elderly population.6 Clinical Manual of Geriatric Psychiatry shared by other developed nations. Public Health Service 1999). The ECA findings are believed by many experts in the field to be underestimates because of methodological limitations in the ECA assessment procedures. The multisite Epidemiologic Catchment Area (ECA) Study conducted in the 1980s (Robins and Regier 1991) found that nearly 20% of Americans age 55 and older had diagnosable mental disorders. 1999). Total Medicare spending increased from $33. The need to learn about aging and older people extends throughout the medical and mental health professions. Alliances with families and other natural supports must be formed to ensure continuity of care. Rates of mental disorder are much higher among elderly patients seen in primary care or hospitalized for medical conditions. Rapp et al. These trends present a significant challenge to the health care community. 1988). 30%–50% of whom have psychiatric conditions (Borson and Unützer 2000.466 for community residents of comparable age (Federal Interagency Forum on Aging-Related Statistics 2004).S. . the average annual cost for elderly residents of long-term-care facilities in the United States was $46. compared with $8.9 billion in 1980 to $252. it is reasonable to estimate that 15%–25% of Americans who are currently age 65 or older have significant mental health problems. and the strengths of older patients themselves must be marshaled to cope with illness and to interact effectively within the health care system.

with estimates varying widely depending on the procedures used to assess impairment (see Chapter 2. and in many cases.Introduction 7 Older patients experience the same broad spectrum of mental disorders as do younger adults.S. one-third had moderate to severe memory impairment (Administration on Aging 2004). A larger proportion of older people have mild cognitive problems.” and Chapter 6. Serious depressive symptoms were found in 8%–20% of elderly community residents and in up to 37% of the elderly in primary care settings (U. Rapp et al. psychotherapy. However. treatment of underlying problems can substantially alleviate cognitive symptoms or slow the course of further decline (see Chapter 5. gains in functional ability can be obtained by treating coexisting medical or psychiatric illnesses. at least 5% of people age 65 years or older have prominent cognitive deficits. These small gains can make a great difference to family members caring for these patients. Recent data from the national Health and Retirement Study showed that among Americans age 85 and older residing in the community. “Other Dementias and Delirium”). and respite provided for caregivers. The presence of comorbid depression or anxiety greatly increases health care . certain conditions are particularly notable in later life because of either increased prevalence or high morbidity (see Table 1–1). and nearly 50% of the admissions of older adults to psychiatric hospitals are for depressive conditions. Depression is an equally important condition in older adults. the percentage of older people meeting strict diagnostic criteria for major depression is generally estimated at 5% or less (U. as can support. especially in the oldest age ranges. In the community.. However.S. “Dementia and Alzheimer’s Disease. 1988). Even for individuals with dementia of the Alzheimer’s type. Cognitive deficits in older patients have many different possible causes. The elderly are at much greater risk for cognitive impairment than are younger adults. 1989). 1988). and a widely cited epidemiological survey in the East Boston area reported a prevalence of 47% for Alzheimer’s disease alone among community residents age 85 and older (Evans et al. Public Health Service 1999). The numbers in Table 1–1 may underestimate the extent of problems related to cognitive deficits. compared with fewer than 1% of people ages 18–64 (Regier et al. Public Health Service 1999). In acute-care hospitals. as many as 25% of older patients have diagnosable mood disorders (e. traditional diagnostic criteria may not do justice to the prevalence of depressive symptoms among older people. “Normal Aging”). In the community.g.

Barriers to Geriatric Mental Health Care Improvements have been made since the early 1990s in the detection and treatment of mental disorders in older adults in the United States. Education and interventions directed at these problems may prevent more serious psychiatric or medical problems from developing. their mental health needs may prompt a crisis in geriatric care (Jeste et al. For psychiatrists. Depression. depression is associated with decrements in function and well-being that are similar to. “Other Dementias and Delirium”). and preventive interventions to strengthen older people and their families in managing common stresses of aging. The usefulness of psychotherapeutic interventions for common mental disorders of older . Public Health Service 1999).8% in 1998. to recognize and treat mental disorders in patients in skilled nursing facilities. efforts have been made. and two-thirds of those diagnosed received treatment of some type (Crystal et al.S. “Mood Disorders—Treatment”). surgeon general’s report on mental health (U. The number of effective antidepressant medications has increased (Chapter 4.S. support.8% in 1992 to 5. since passage of the Omnibus Budget Reconciliation Act in 1987. pain syndromes. In an analysis of national Medicare fee-for-service data. Similarly.8 Clinical Manual of Geriatric Psychiatry costs for patients in primary care (Simon et al. The importance of increasing prevention efforts for older adults as well as other age groups was underscored in the U.S. 1995). Public Health Service 1999). “Dementia and Alzheimer’s Disease. and medications to slow the course of common progressive dementias have been introduced (Chapter 5. those associated with chronic medical disease (Hays et al. Many older people without major mental disorders experience adjustment reactions to personal stresses. 2003). Geriatric depression can be treated effectively with standard therapies in 60%–80% of cases (U. it is important not only to identify and treat specific psychiatric disorders but also to provide education. anxiety. 1999). but it is unlikely to resolve spontaneously. and sleep disturbance. with varying degrees of success. 1995). and as the 55 million baby boomers grow old. or greater than. rates of diagnosed depression in older adults increased from 2. and alcohol and drug abuse in the elderly today are only about one-quarter to one-third as common as among middle-aged persons. bereavement. for example. therefore. and over time.” and Chapter 6.

” “Other Dementias and Delirium. 2003). Moak and Borson 2000).3 7.9 2. In nursing homes. Despite these improvements.” “Anxiety Disorders and Late-Onset Psychosis. 2003. Mental disorders among older adults Distribution of psychiatric diagnoses (%) Category of illness Cognitive impairment Affective disorders Anxiety disorders Alcohol abuse or dependence Schizophrenic disorders Somatization Personality disorder Other psychiatric disorder aAdapted b Community residentsa 4.1 0 0 Medical-surgical inpatientsb 30. adults has been more thoroughly confirmed (Chapters 4 through 8. psychiatric services are generally restricted to a consultative. 1988. Adapted from Rapp et al. 2004. and in the burgeoning numbers of assisted- . as have the complex relationships between mental disorders and medical illness. Adults older than 75.1 0.” “Dementia and Alzheimer’s Disease.Introduction 9 Table 1–1.2 18.9 0. Ganguli et al. white.5 5. and better-insured patients to have received treatment for depression in recent years (Crystal et al.6 0 0 8. “Mood Disorders—Treatment. and persons with Medicare only were less likely than younger. Charney et al.2 2. and even the most recent studies continue to show that most cases of cognitive impairment without obvious dementia go undetected and untreated in primary care (Chodosh et al.5 0. 1988.” and “Other Common Mental Disorders of the Elderly. minority group members.5 5. 2004).” respectively). significant inequities remain in identification and treatment of mental health conditions in older people and in accessibility and use of geriatric mental health services (Areán and Unützer 2003. as-requested mode instead of being a consistent and integrated part of care management teams.9 from Regier et al. Less common or less widely publicized conditions are even more likely to remain unrecognized and inadequately treated.

2003. transportation. Contemporary older Americans report less past use of mental health services than do younger adults. than did those referred to mental health clinics or specialists. is likely to continue for several reasons: • Multiple medical illnesses in elderly patients may divert physicians’ attention away from psychiatric signs and symptoms. elderly primary care patients who screened positive for depression. As the baby boom generation edges into the geriatric age range. even with enhanced assistance aimed at increasing the odds of compliance with the referral. scheduling. especially within the time-pressured context of the standard brief office visit. and older Americans are less likely to express a need for such services (Klap et al. or memory problems may be viewed as normal for older people with serious medical illness. only one-half or fewer follow through with referrals to specialty mental health providers. 2004). Depression. or increased risk of alcohol use problems were offered collaborative mental health services within primary care or enhanced referral assistance (e. and typically. Older adults most often turn to primary care providers for help with mental health problems (Kaplan et al.10 Clinical Manual of Geriatric Psychiatry living and community-based programs for senior care. A significantly higher percentage of the patients followed through on pursuing mental health treatment when it was available within primary care (71% vs. mental health services are patchy and largely unregulated (Moak and Borson 2000).g. 2004). but the desire for proximal. In a recent multisite randomized trial. anxiety. especially among older patients (Young et al. integrated medical and mental health services is likely to continue. 2001). and payment assistance to outside mental health specialists) (Bartels et al. and they completed more mental health visits overall. Physicians with neither psychiatric nor geriatric training may have difficulty distinguishing normal aging changes from signs of mental disorder or may be reluctant to “open the can of worms” that treatment of emotional or cognitive problems may entail. 49%). 1999). underrecognition of mental health problems. anxiety. • • A probability survey of primary care providers found that only 6% of general internal medicine physicians and 22% of family practice physicians used . the “stiff upper lip” approach to managing emotional distress (Wetherell et al. 2004) may change. Wetherell et al. Without more effective collaborative care..

as well as the patient and family members. “Fallacy for good reasons” is a phrase coined to refer to the common situation in which a provider.. Primary care physicians report that the subtlety of mild dementia makes it difficult to recognize during brief interviews. under Medicare. the psychotherapy fees allowed for an experienced psy- . and who are less likely to die in the course of treatment. age bias seems to take more specific forms (Gatz and Pearson 1988). attitudes about aging and age-related conditions and limited training in geriatric psychiatry may further restrict the availability and quality of mental health care for older patients. and some of these professionals. who remind them less of their own mortality. especially the very old (Cole et al.g. Inadequate insurance coverage for patients and limited reimbursement for providers are ongoing barriers to geriatric mental health care. Because prescription drugs have not been covered under Medicare until very recently. 1997). Nonetheless. Instead. multiple losses. Many psychiatrists and other mental health professionals find it difficult to work with elderly patients. attributes the depression or anxiety experienced by the older patient to medical illness. or financial difficulties that many older persons face. American psychiatrists and other mental health professionals tend to refer older patients less often for psychotherapy than comparably ill younger patients. in an attempt to avoid discrimination against the elderly. relying instead on very brief informal interviews (Kaplan et al. The 50% copayment rule for psychotherapy services under most insurance policies makes the decision to engage in therapy costly to the patient. although this attitude may delay arrangements for community support services and increase family strain (see Chapter 5. “Dementia and Alzheimer’s Disease”).Introduction 11 questionnaires or other structured procedures to screen for depression in their older patients. 1999). Among psychiatrists. may exaggerate the competencies and excuse the deficits of elderly patients. 1999). there is little purpose to diagnosing mild dementia. recent research has not found mental health professionals to be strongly or pervasively negative in their attitudes about older patients. Understandably. many also believe that in the absence of effective treatment. they may prefer to work with patients who have less daunting problems with physical illness and personal loss. but many physicians remain reluctant to use formal cognitive screening tests (Boise et al. and allowable fees are often inadequate (e. elders who could not afford a coinsurance policy with drug benefits were unable to afford psychiatric medications.

in key areas such as life expectancy. the oldest old. persons of minority descent. In 2000–2001. Methodological difficulties encountered in the processes of sampling. designing valid interview protocols. significant differences have been documented across groups. and Asian populations in the United States. but this approach needs to be extended beyond clinical research. Effective models for collaborative medical and mental health services recently have been developed for primary care (see Chapter 4. residential patterns.5 years longer for white persons than for black Americans (Federal Interagency Forum on Aging-Related Statistics 2004). However. “Mood Disorders—Treatment”). and by age 85. and education. who generally have many health care needs. but by 2050. and controlling interviewer and subject bias have hampered attempts to generalize about the health and other characteristics of black. Diversity in Patterns of Health and Aging In 2003. and these trends are projected to continue (Figure 1–4). At age 65. including Hispanic whites.6% of the U. however. often have trouble coordinating their own care.S. The elderly. Hispanic. but there is usually no reimbursement for mental health providers to help with coordination. life expectancy was slightly longer for older black persons compared with white persons. American Indian. The need for psychiatrists who are capable and willing to work with elderly patients. In the United States in 2001. among people age 65 and older. this percentage is projected to rise to 36%. Hispanic and Asian American groups as a whole are the most rapidly growing minority populations. the life expectancy gap narrowed to about 2 years. achieving subject cooperation. 2001). is clear. prevalence of chronic health conditions. older Hispanics were . 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. both in primary care and in specialty roles. average life expectancy from birth was 5. accounted for 17.12 Clinical Manual of Geriatric Psychiatry chiatrist are half or less of the typical fee expected for this service). and those with significant chronic mental illness present particular challenges to existing service models (Borson et al. hypertension and diabetes were more common among black than among non-Hispanic white persons. population age 65 and older.

Adapted from Federal Interagency Forum on Aging-Related Statistics 2004. and other psychiatric disorders.S. Black and Hispanic elders are less well educated than non-Hispanic white and Asian elders (see Figure 2–1 in Chapter 2. by race and Hispanic origin. “Normal Aging”). Reports of prevalence of mental disorders for minority groups must be viewed with caution because language and cultural differences can affect results on tests and interviews assessing depression. Percentage of population age 65 and older. comparable to non-Hispanic white Americans in rates of hypertension but were more likely to have diabetes. and older black and non-Hispanic white persons 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).Introduction 13 100 80 Americans age ≥65 (%) 2003 2050–projected 60 40 20 0 Non-Hispanic white alone Black alone Asian alone All other races alone Hispanic or in combination of any race Figure 1–4. 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). Public Health Service . A recent supplement (U. Source. However. By contrast. data are emerging on the relative prevalence of mental health–related problems in various groups and on availability and use of mental health services. dementia.

low-income or homeless persons) Delivering effective. Important gender differences have been reported for longevity.14 Clinical Manual of Geriatric Psychiatry 2005) to Mental Health: A Report of the Surgeon General (U. and protection from. and rates of alcohol abuse and dependence are higher among elderly black men and women compared with elderly white and Hispanic persons (U. ethnicity.g. prevalence of specific . the suicide rate is much higher among non-Hispanic white men than in any other elderly subgroup (National Center for Health Statistics 2004). gender. Public Health Service 1999). high-need subgroups in which racial and ethnic minorities are overrepresented (e. disparities in availability of and access to mental health services among Americans from minority backgrounds.S. evidence-based treatments that are individualized according to age. the recommendations for reducing barriers are as important for diverse geriatric populations as they are for younger groups. however. some important differences in prevalence of mental health–related conditions have been documented for racial/ethnic and gender subgroups. often striking.S.. outnumbering men by a ratio of nearly 3 to 1 by age 85 and older. The recommendations include the following: • Continuing research to establish the efficacy of evidence-based treatments for racial and ethnic minorities and to better characterize how factors such as acculturation and ethnic identity affect risk for. and policy makers • • • Women constitute the majority of older persons in the United States. increasing availability of services in preferred languages. For example. and Asian Americans and Pacific Islanders) is similar to that of white Americans. mental illness Improving access to treatment by improving geographic distribution of services. race. Hispanics. and coordinating care for the most vulnerable. 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. Although not specific to older adults. Among older adults. and culture Working toward equitable racial and ethnic representation among mental health providers. The surgeon general’s recent supplement underscored the pivotal role of culture in maintaining mental health and the continuing. administrators.

and social changes Mental disorders predominantly observed in later life. Knowledge needed to work effectively with elderly patients Normal aging: biological. limited options for home care. format and pace of psychotherapy Managing social and physical problems of later life: bereavement. pain. . In addition to mastering the content areas covered in this Clinical Manual. many more lack the energy. sophistication. Recent research. Working Effectively With Older Adults Psychiatric care of older patients requires a blending of specialized knowledge with a broadly based.g. flexible approach to the patient (Table 1–2). drug-drug interactions. including mood and anxiety disorders Adjusting psychiatric treatments for aging changes: dose and schedule of psychoactive medications.Introduction 15 Table 1–2. role loss. and an increased likelihood of spending their last years in a nursing home.. heart disease. or funds to negotiate a specialty-oriented system successfully. prompted by the Women’s Health Initiative. sleep disturbance Interactions of psychiatric and medical-surgical illnesses and their treatments medical or mental conditions (e. and rates of disability. can reduce the functional limitations now experienced disproportionately by women in later years. related dementias. a psychiatrist treating older patients needs certain personal qualities and professional approaches that are important for effective work in geriatric psychiatry (Table 1–3). the price that women pay for longer lives appears to be a greater proportion of the late life span compromised by functional disability. late-onset psychoses Effects of age on other psychiatric disorders. Alzheimer’s disease). or more prompt and appropriate diagnosis and treatment of medical conditions. As a result. At present. Although some older people can manage today’s complex health care system. cognitive ability. is helping to elucidate whether preventive health care. including Alzheimer’s disease. combining routine medical management with psychiatric interventions or helping with specific social or situational problems. psychiatrists working with older people must be willing to play a generalist role. psychological.

References Administration on Aging: A Profile of Older Americans: 2004. 2004. Finally. DC. Elderly patients often defer to physicians without truly comprehending benefits and risks. minority. Elderly patients may be inclined to view younger therapists as similar to their children. it is helpful to have a willingness to explore one’s own feelings about aging. 2006. Unützer J: Inequities in depression management in low-income.aoa. Administration on Aging. as well as to be open to discussing older patients’ reservations about the wisdom of youth.. Washington. but it may place the older person at risk for iatrogenic illness (e.gov/prof/Statistics/ profile/2004/profiles2004. 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). This deference may increase efficiency of care in the short run. and old-old adults: a matter of access to preferred treatments? J Am Geriatr Soc 51:1808–1809.g.16 Clinical Manual of Geriatric Psychiatry Table 1–3. Personal qualities and professional approaches needed to work effectively with elderly patients Willingness to provide broadly based. Available at: http://www. and the therapist. Accessed March 9. 2003 . flexible management Comfort in working closely with other health care professionals Patience and skill in providing medical information and assisting in medical decision making Willingness to explore one’s own feelings about aging Openness to discuss patients’ concerns about being treated by younger professionals Acceptance of and comfort with limited treatment goals Ability to maintain therapeutic optimism in the context of an ultimately poor prognosis The psychiatrist also must have patience and skill in explaining diagnoses and treatments and in assisting older people in medical decision making. in response.asp. Areán PA. delirium secondary to drug interactions).

Christensen JF. in Behavioral Medicine in Primary Care: A Practical Guide.pdf or http:// www. et al: Depression. Charney DS. U.org/press/content/11.04_SOA_Report. 1988 . Raju M. Accessed March 9. Bartels SJ. Coakley EH. 2004. 1989 Federal Interagency Forum on Aging-Related Statistics: Older Americans 2004: Key Indicators of Well-Being. Sadock BJ.aoa. Colenda CC. et al: Physician recognition of cognitive impairment: evaluating the need for improvement. et al: Diagnosing dementia: perspectives of primary care physicians. J Am Geriatr Soc 52:1051–1059. 2003 Evans DA. Edited by Feldman MD. J Am Geriatr Soc 51:1718–1728. Government Printing Office. 2004 Gatz M. Stamford. Appleton & Lange.miahonline. Am J Geriatr Psychiatry 9:191–204.pdf. 2003 Cole SA. 2001 Centers for Disease Control and Prevention and Merck Institute of Aging and Health: The State of Aging and Health in America 2004. 1999 Borson S. Unützer J: Psychiatric problems in the medically ill. Am Psychol 43:184–194. Walkup JT. Sambamoorthi U. Philadelphia.gov/prof/Statistics/profile/2004/ profiles2004. pp 177–192 Crystal S.Introduction 17 Bartels SJ. Washington. Am J Psychiatry 161:1455–1462. Accessed August 26. Rodriguez E. disparities. Arch Gen Psychiatry 60:664–672.S. et al: Depression and bipolar support alliance consensus statement on the unmet needs in diagnosis and treatment of mood disorders in late life.22.cdc. Zubritsky C. anxiety. et al: Geriatric mental health services research: strategic plan for an aging population. et al: Detection and management of cognitive impairment in primary care: the Steel Valley Seniors Survey. pp 3045–3053 Borson S. J Am Geriatr Soc 52:1668–1675. and at-risk alcohol use.gov/ aging/pdf/State_of_Aging_and_Health_in_America_2004. Elliott M. and trends. CT. Science 302:1172–1175. Mulsant B. JAMA 262:2551–2556. Reynolds CF III. Edited by Kaplan HI. Petitti DB. DC. Lippincott Williams & Wilkins. et al: Diagnosis and treatment of depression in the elderly Medicare population: predictors. 2006. 2005. et al: Improving access to geriatric mental health services: a randomized trial comparing treatment engagement with integrated versus enhanced referral care for depression. Available at: http://www. Camicioli R. Ganguli M. Morgan DL. Lewis L. 2004 Boise L. Available at: http://www.asp. 1997. 2000. 2003 Chodosh J. Christensen JF. Pearson CG: Ageism revisited and the provision of psychological services. Gerontologist 39:457–464. Albert MS. in Comprehensive Textbook of Psychiatry/VII. PA. 2004 Cohen JE: Human population: the next half century. et al: Prevalence of Alzheimer’s disease in a community population of older persons. Funkenstein HH.

Cassel CK: The aging of the human species. pp 395–412 Moak G. 2nd Edition. 2003 Jeste DV. 1988 Robins LN. et al: Consensus statement on the upcoming crisis in geriatric mental health: research agenda for the next two decades. Accessed January 27. Yudofsky SC. 2006. American Psychiatric Press. With Chartbook on Trends in the Health of Americans.surgeongeneral. Rockville. 1999 Klap R. National Center for Health Statistics. Burke JD. United States.gov/library/ mentalhealth. Carnes BA. 1999. et al: One-month prevalence of mental disorders in the United States. Free Press. Rockville. in The American Psychiatric Press Textbook of Psychiatry. Boyd JH. 1993 Rapp SR.18 Clinical Manual of Geriatric Psychiatry Hays RD. MD. Am J Psychiatry 152:352–357. Wells KB. Unroe KT. Washington. Bartels SJ. Parisi SA. Gerontologist 39:417–425. Office of the Surgeon General. Accessed March 9. Von Korff M. 2006. J Consult Clin Psychol 56:851–855. 2004. and Ethnicity: A Supplement to Mental Health: A Report of the Surgeon General. Adamek ME. MD. Race. 2000 National Center for Health Statistics: Health. . Regier DA: Psychiatric Disorders in America: The Epidemiologic Catchment Area Study.surgeongeneral. Talbott JA. Alexopoulos GS. et al: Health care costs associated with depressive and anxiety disorders in primary care. Sci Am 268:46– 52. Ormel J. Hyattsville. 1995 U. Sherbourne CD. Walsh DA: Psychological dysfunction and physical health among elderly medical inpatients. Public Health Service: Mental Health: Culture. 2005. 1995 Hybels CF. 1999 Kaplan MS. New York. Available at: http://www. Blazer DG: Epidemiology of late-life mental disorders. David CD: Psychotherapy. Unützer J: Caring for mental illness in the United States: a focus on older adults. 1991 Simon G. MD. 1988 Regier DA. Office of the Surgeon General. Public Health Service: Mental Health: A Report of the Surgeon General. Edited by Hales RE.S. U. Available at: http:// www. 2003 Meador KB. DC. Am J Geriatr Psychiatry 11:517–524. 2004 Olshansky SJ. Calderon A: Managing depressed and suicidal geriatric patients: differences among primary care physicians.S. Arch Gen Psychiatry 56:848–853. Am J Geriatr Psychiatry 8:96–100. Borson W: Mental health services in long-term care: still an unmet need. 1994. Arch Gen Psychiatry 52:11–19.gov/library/mentalhealth. Arch Gen Psychiatry 45:977–986. et al: Functioning and well-being outcomes of patients with depression compared with chronic general medical illness. Clin Geriatr Med 19:663–696.

Sherbourne CD. Kaplan RM. Int J Psychiatry Med 34:219–233. Kallenberg G. 2004 Young AS. Klap R. et al: Mental health treatment preferences of older and younger primary care patients. et al: The quality of care for depressive and anxiety disorders in the United States. Arch Gen Psychiatry 58:55–61.Introduction 19 Wetherell JL. 2001 .

This page intentionally left blank .

It is also important to keep in 21 . they can be useful in identifying important differences in levels of functioning and can help to limit overgeneralization about characteristics of older adults. The common practice of designating people older than 65 as “old” began in Germany in the 1880s. but there was much variation in perceptions (Abramson and Silverstein 2004). the upward shift is also indicative of the increasing vitality and productivity of the aging population. Although this change is primarily a response to fiscal concerns. Although these distinctions are also arbitrary. whereas another one-fourth cited ages less than 60 years. and as a result. respectively) or between these groups and the oldest old (generally 85 years and older).2 Normal Aging Conceptual Issues Who Is Old? Biological and psychological aging changes usually occur gradually. More than one-third of the sample named an age greater than 70 as the start of old age. when Otto von Bismarck selected 65 as the starting age for certain social welfare benefits. those younger than and older than age 75. 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. 63 years is the average age at which Americans perceive individuals as becoming old. According to a recent national survey. Gerontologists often draw finer chronological demarcations within the general group of aging persons. Comparisons may be made between the youngold and the old-old (generally. over years or decades. there is no single age at which people in general can be said to be old.

and a burgeoning number of cross-sectional studies are being done. A longitudinal study of 426 elderly community dwellers by Christensen and associates (1999) found increases in interindividual variability with age in memory.g. Heterogeneity in Patterns of Aging On many psychological and biological measures. diet. so longitudinal investigations may provide an overly optimistic estimate of the extent of decline with age.22 Clinical Manual of Geriatric Psychiatry mind that individuals may age faster in some dimensions than others (e. health practices. and having weaker muscle strength were associated with greater variability. variability is greater in oldage samples than among younger adults. and speed but not in crystallized intelligence. Cross-Sectional and Longitudinal Views The most common way to study the effects of aging is to compare a group of older people with a separate group of younger adults. The best picture of normative aging trends is obtained from studies in which multiple cohorts are assessed longitudinally or by combining the results of separate cross-sectional and longitudinal studies. outcomes of which have helped to shape understanding of cognitive processes that remain stable or reliably decline with age. and other important factors are confounded with age differences when young and old subjects are compared. At least 25 other longitudinal investigations of behavioral aspects of aging are ongoing at this time. The least healthy and able subjects are often the first to drop out from these samples. being more depressed. cross-sectional investigations often provide an inflated estimate of the magnitude of aging changes that will occur in individuals.. whereas having a higher level of education was associated with reduced variability. Many different normal ag- . Being female. Because generational differences in education. The Seattle Longitudinal Study conducted by Werner Schaie (2005) and colleagues provides one of the best examples of a multiple-cohort longitudinal aging study. Longitudinal designs also have been used to study normal aging. being “old” physically but more youthful psychologically or socially). Pronounced variability decreases the sensitivity in upper age ranges of many measures that are used to infer pathological changes and casts doubt on the search for singular normative aging trends. spatial functioning. These investigations track the same individuals over years. being more ill. or even decades.

especially when active manipulation of information is required (e. so to keep details “alive” for a longer time requires active rehearsal or continuing refocusing of attention. Cognitive Abilities in Later Life: A Processing Resource Model Cognitive changes with aging are well documented and affect a broad range of functions (see the subsection “General Aging Trends” later in this section). and mentally traversing a route that one intends to walk or drive.g. 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.. Aging is associated with a decline in working memory skills. 2003). Intraindividual variability (i. repeating numbers . memory. fluctuating performance within and across assessments) is also increased in old age. with varying trends for different genetic and sociocultural subgroups. Information fades from working memory within about 2 seconds. a type of “online” cognitive processing (Baddeley 1986). many of the differences in specific abilities can be traced to declines in three fundamental cognitive-processing resources: the speed at which information can be processed. However. Working Memory Working memory refers to short-term retention and manipulation of information held in conscious memory. and decision making and can influence performance even on tasks that have no obvious speed requirements (Salthouse 1996). and sensory and perceptual skill (Park 1999).Normal Aging 23 ing trajectories may exist..e. especially for cognitive and physical performance measures. mentally calculating the sale price of an item that is reduced by 15%. Processing Speed Perhaps the most predictable of all cognitive changes is the reduced speed of information processing and response. Examples include consciously recalling a telephone number long enough to write it down. Slowed execution of component perceptual and mental operations can affect attention. working memory.

and although hearing aids help with detection of low-frequency tones. In advanced old age. In effect.24 Clinical Manual of Geriatric Psychiatry backward as opposed to forward). and learning and recall of new information. Recent studies suggest a strong correlative link between sensory and perceptual changes and cognitive performance in old age.. Data are more conflicting regard- . and sensory and perceptual changes limit the processing resources that older persons can bring to bear in particular situations. including reasoning and other executive processes. Reductions in working memory. in turn. especially with competing background noise and poor lighting conditions. Within the cortex. of the age-related visual changes can be corrected by glasses. Neuropsychological Explanations of Cognitive Aging Changes Neuropathological and neuroimaging studies have documented widespread changes in the human brain with aging (Raz 2000. reduced working memory. with the result that older persons must devote more conscious cognitive resources to these activities. Victoroff 2000). Subcortical monoaminergic cell populations.g. The extra time and effort required to process information necessitated by sensory and perceptual problems tax working memory. Sensory and Perceptual Changes Most older adults experience decrements in visual and auditory acuity and other perceptual changes. effectively overloading the system. even basic activities such as walking or maintaining postural control become less automatic. but not all. many older adults find it hard to hear or see well. the prefrontal lobes are disproportionately affected by aging changes. they often amplify background noise. by background noise or reduced visual contrast) perform much like older adults on measures of learning. These changes increase the likelihood of processing overload in circumstances that may have once presented little challenge. There are generalized atrophic and white matter changes as well as region-specific variations in the extent of cell loss. whereas temporoparietal association areas are less affected. memory. which connect to the frontal lobes by a complex network of projections. are also subject to prominent decline in aging. and language (Schneider and Pichora-Fuller 2000). The combined effects of central nervous system slowing. Some. place limits on other complex cognitive skills. Younger adults tested with degraded perception (e.

mild decline refers to changes that are generally within a standard deviation of the mean for young adults. The “frontal lobe hypothesis” is perhaps the most popular neuropsychological model of normal aging at this time. This interpretation coincides in a general way with the behavioral model of reduced processing resources and increased susceptibility to overload on complex tasks. and changes in efficiency of executive functions are some of the findings that suggest a mild degree of frontal or subcortical brain dysfunction in normal aging (Prull et al. Hippocampal volume. the sensory cortices. What remains to be resolved. correlates with memory performance in older adults. as measured by magnetic resonance imaging. the paleocerebellum. 2000. Other changes appear to mirror the selective pattern of differential change in prefrontal cortical structures and striatal dopaminergic nuclei. In this table. whereas moderate decline refers to differences on the order of one to two standard deviations below the average for young adults. As the table indicates. General Aging Trends Table 2–1 summarizes general aging trends for intelligence and specific areas of cognitive function. Some of the behavioral changes in aging. however. and those with smaller hippocampal volumes are at greater risk for developing dementia. may be related to generalized changes such as decreased brain volume and white matter density. and the pons (Raz 2000). However. 2000). is whether reduced hippocampal volume is truly within the normal aging spectrum or instead is a preclinical phase of dementia. One interpretation of this finding has been that older persons must recruit more neural systems to perform even relatively simple mental operations. problems with effortful learning and recall. Decreased working memory.Normal Aging 25 ing changes in the hippocampus and entorhinal cortex. cognitive changes associated with normal aging generally fall within the mild to moderate range. hippocampal changes also may play a role in normal aging memory. 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. such as slowed information processing and response. Raz 2000). with some studies noting minimal cell loss with normal aging in these regions and others showing decremental changes. The differential pattern . and there are some areas in which performance remains stable or improves. Areas in which there is relative sparing with age include the globus pallidus.

shifting attention In absence of sensory impairment Varies with education Occasional word-finding lapses Some erosion in processing complex messages May be more imprecise. but easily disrupted by interference Reduced ability to manipulate information in short-term memory Encoding and retrieval deficits.Table 2–1. filtering out noise. naming Comprehension Discourse Memory Short-term (immediate) Working Secondary (recent) Direction of aging change Comment 26 Clinical Manual of Geriatric Psychiatry Stable or increasing Declining Stable to mild decline Mild decline May decline slightly in very old age. storage intact Stable Stable Mild decline Stable to mild decline Variable Stable to mild decline Mild to moderate decline Moderate decline . repetitive Forward digit span intact (7±2 items). fund of knowledge Perceptual-motor skills Attention Attention span Complex attention Language Communication Syntax. most pronounced on novel tasks Decline begins by ages 50–60 Problems with dividing attention. Aging effects on cognitive performance Ability Intelligence Vocabulary. word knowledge Fluency.

Aging effects on cognitive performance (continued) Ability Memory (continued) Implicit Remote Prospective Direction of aging change Comment Stable to mild decline Variable Variable May recall incidental features more easily than consciously processed information Intact for major aspects of personal history Mild to moderate decline on laboratory tasks.Table 2–1. but older adults often outperform younger people on naturalistic prospective memory tasks Intact for simple but not complex figures Most noticeable in unfamiliar terrain Slower and less accurate in shifting from one thought or action to another Some redundancy and disorganization Qualitatively intact. but reduced efficiency on complex or novel tasks Slowing of thought and action is the most reliable aging change Visuospatial Design copying Topographic orientation Executive functions Cognitive flexibility Logical problem solving Practical reasoning Speed Variable Declining Mild to moderate decline Declining Mild to moderate decline Declining Normal Aging 27 .

. Short-term or immediate memory remains stable or declines to a modest degree in later life. they usually mention problems with memory. For example. for example. indicates that physical and mental exercise. compared with seven items for persons in their 30s (Wechsler 1997). Factors That Influence Cognitive Aging Table 2–2 summarizes characteristics and experiences that influence the degree of cognitive change individuals show as they age. the median forward digit span for healthy persons in their 80s is six items. in addition to early life advantages such as adequate education. 85 or older). Higher absolute levels of intellectual ability may benefit contemporary older adults in learning new information and acquiring new skills (see the subsection “Effect of Cognitive Change on Everyday Function” later in this section).to 74year-olds.g. but as shown in Table 2–1. some aspects of memory decline more with age than do others (La Rue 1992. adults. Prull et al.g. as opposed to younger. such as recalling information after an interfering message. Fratiglioni et al. vocabulary scores on the commonly used Wechsler Adult Intelligence Scale (Wechsler 1997) have increased nearly 5 IQ points per decade for 65. The cumulative effect of these factors.5 points for 18.to 24-year-olds (Uttl and Van Alstine 2003).. 2004). On more demanding tests of short-term memory. and strong social supports may serve as protective factors against the development of dementia (e. 2000). Learning and Memory When older people complain about their cognitive abilities. compared with 1. age differences favoring the young are likely to be observed.. Research substantiates these complaints. which coincides with the declines in working memory discussed earlier. may be responsible for increasing variability in cognitive performance at older ages. For example. for whom some studies report a generalized pattern of gradual decline. Increasing evidence. Healthy and stimulating lifestyles. operating over months or years. Another important qualification concerns secular trends in levels of performance.28 Clinical Manual of Geriatric Psychiatry of abilities shown in Table 2–1 is less apparent among the oldest-old (e. are hypothesized to strengthen the “cognitive reserve” that individuals have available to cope with neurobiological changes resulting from aging or illness (Scarmeas and Stern 2003). and the rate of increase is higher among older. a healthy diet. Intellectual performance scores have been increasing over the past few decades.

Mentally stimulating activities correlate with higher cognitive performance and reduced longitudinal decline. Aerobic fitness is associated with better cognitive performance in old age. Optimally healthy elderly persons outperform those with medical illnesses on many cognitive tests. Cognitively unimpaired older persons benefit from practice and training in specific cognitive skills. but when education is equated across groups. Recently born cohorts are outperforming those born near the turn of the century on many cognitive skills. Depression correlates with self-perceived memory failure and with performance impairments if symptoms are severe. Cognitive aging trends are similar for the two sexes. Everyday memory lapses may be judged more critically when experienced by older people than by young adults. but women may show decrements on spatial tasks at an earlier age than men. and men may show decrements on verbal tasks at an earlier age than women.Table 2–2. Cognition in normal aging: moderating variables Genetic factors Health Education Mental activity Physical activity Expertise Personality and mood Social and cultural milieu Cognitive training Cohort effects Sex differences About 50% of cognitive variability in old age can be traced to genetic factors. Education accounts for up to 30% of cognitive variability in old age. these differences are reduced or eliminated. Aging experts may develop compensatory strategies to maintain a high level of performance despite some erosion in underlying cognitive skills. Performance differences favoring elderly white persons have been reported on some cognitive tests. Normal Aging Racial and ethnic differences 29 .

for example. depending on how and where it is measured (Henry et al. Many older people take a more passive approach to learning and remembering than do .g. On the average. Prull et al. episodic memory (La Rue 1992. on naturalistic tasks (e.g. 2000). older adults typically do less well than younger persons. older persons recall less information initially compared with young adults. such as remembering items on shopping lists. such as 5-minute delayed recall of three or four simple words. healthy older individuals make more mistakes than young adults on memory items from mental status examinations. and remembering content of stories and conversations. Incidental facts or features (e. older adults often show superior follow-through. memory for actions intended in the future) shows divergent age trends. Prospective memory (i. Research results are not so clear. but their performance improves with repetition. Prull et al. However. and they retain most of what they learn after delays and distractions. learning to associate pairs of words. Overall. older adults’ absolute levels of performance on remote-memory tests are often impressively high. remembering to call to make an appointment). mainly because of more reliable use of external aids such as reminder notes.e. Some of the problems that older people have with initial learning may be related to strategies used for processing new information (La Rue 1992). “Dementia and Alzheimer’s Disease”). the color of someone’s dress) can be recalled with about equal accuracy by young and old. is one of the best ways to distinguish normally aging memory from that of patients with amnestic conditions or Alzheimer’s disease (see Chapter 5..g. copying designs from memory.. Age differences favoring the young have been found on many explicit tests of recent memory. whereas the old are more prone to forget information that they had explicitly hoped to retain (e. Another type of memory that shows minimal or modest age change is implicit or incidental recall. partly because remote memory is difficult to measure because initial or intervening exposure to the material cannot be precisely controlled (La Rue 1992. 2004). the person’s name). The largest age decrements are observed in recent.. On demanding explicit memory tasks.. once it is acquired. remote or long-term memory is well maintained in old age. 2000).30 Clinical Manual of Geriatric Psychiatry Anecdotally. This ability to retain information. however. In laboratory settings. one study found that people recognized names or photographs of more than 70% of high school classmates after an interval of almost 50 years.

locations of objects. Older adults (and younger persons. this may simply mean that the training served its intended purpose (i..Normal Aging 31 younger 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. Training also works best in an individual or a small-group format and with relatively short (e. Education and counseling about memory improvement is best approached from a broad perspective. Also. Learning Throughout Life (National Retired Teachers Association et al. 2004) is another good guide for the general reader. In some cases. to prove that one can remember more if need be). Follow-up studies often show that people discontinue memory techniques they have learned within a few weeks. Alternatively. and lists of things to be purchased or done. breadth.g. their learning and recall often improve dramatically. For example. in which improving memory is seen as part of an overall wellness plan. 2002). If older individuals are explicitly instructed to use mnemonics or organizational strategies. Small (2004) out- . too) often ask about ways to improve their recall of everyday information. for old as well as young adults. and linkage to research. A greater drawback of mnemonic training approaches is that benefits often fail to generalize to everyday tasks not specifically included in training (Ball et al. elderly people report less spontaneous use of mnemonic 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. Active encoding and retrieval may require greater expenditure of effort and energy than most older people can afford. Mnemonic training can produce notable gains in troublesome areas. In The Memory Prescription. such processing changes may be seen as an adaptive response to the diminished demands of older adults’ everyday lifestyles. Of the many self-help books providing advice on how to maintain memory function into old age. such as recall of names. Declines in effortful processing may be caused by altered neurotransmitter functions (especially catecholamines).e. but it is also likely that the use of mnemonics may be too effortdemanding in the long run. especially without the aid of reminders or cues. at least in the short term. 1992). 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. half-hour) sessions as opposed to longer workshops or lectures. Keep Your Brain Young (McKhann and Albert 2002) is among the best in terms of readability.

However. monitoring one’s own behavior. but independent studies are needed to assess benefits of this approach. planning. not all studies show this trend.32 Clinical Manual of Geriatric Psychiatry lines a 2-week program of diet. most older adults are not impaired in everyday activities. 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). Performance of such skills requires the coordinated activity of multiple regions of the brain and can be affected by injury to several different areas. Executive Function The term executive function refers to cognitive abilities necessary for complex goaldirected behavior and adaptation to change. stress reduction. Performance on executive function 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 determining which older people come to clinical attention for mild cognitive changes (Royall et al. As noted earlier. For example. and mental exercise designed to boost brain function. even when relatively complex cognitive processing is required. normal aging has a greater decremental effect on these brain regions than on many other areas. one recent investigation found that cognitively healthy 65. anticipating outcomes of behavior. Effect of Cognitive Change on Everyday Function Although normal aging is accompanied by a variety of cognitive changes. directing attentional resources in a flexible manner. age differences are relatively large on executive function tasks (see Table 5–5 in Chapter 5. 2003). and selfawareness.to 74-year-olds provided more relevant solutions to problem situations—such as trying to improve the acrimonious tone of a meeting. In general. or having blood drawn by a physician who is having difficulty with the procedure—than did a comparison group of 20.” for examples of neuropsychological tests of executive function). exercise. . dealing with excessive demands by one’s sons to babysit their children. The program is derived from an ongoing program of research.to 29-year-olds (Artistico et al. Some of the skills included in this category are reasoning. interpersonal problem solving is an area of strength for older people (Thompson and Dumke 2005). the prefrontal cortex and frontal-subcortical brain circuits have been shown to play a central role in executive functions. and predictably. “Dementia and Alzheimer’s Disease.

for example. that older age proved to be an advantage in learning new information about cardiovascular disease. an overabundance of new information and rapidly changing technologies place a heavy demand on learning skills. younger adults were more adept at learning about a new technology. The fact that general 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. When they are taking multiple medications that require dosing several times a day. pose particular risks (Park 1999). In industrialized nations. 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. The very gradual nature of age-related change allows time to adjust to diminished speed and efficiency in cognitive function. Older adults bring to this situation a wealth of accumulated knowledge and experience. it is important to note that some studies show better compliance with medication regimens among older adults than among younger or middleaged persons. presumably because of older adults’ greater baseline knowledge of health-related subjects (Beier and Ackerman 2005). Regarding medications.g. many older adults make frequent and effective use of external cognitive aids such as writing reminder notes. the risk of errors is increased.” for additional information on driving). left turns in intersections). particularly if the older adults are taking only a single medication for a long-standing condition (e. Also.g. One recent study found.. many tasks become automatic and require little cognitive processing or effort to perform. With practice. Older adults are more likely to be involved in accidents while driving than are younger persons. “Competency and Related Forensic Issues. which can facilitate learning of new information in areas of prior knowledge. such as driving and monitoring medications. particularly in certain situations (e. and it has been estimated that about 1% of acute hospital admissions for older persons are precipitated by medical errors or medication reactions. Research on training methods has shown that older adults learn best with self-paced training or other training environments that allow ample time to . 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 maintaining a familiar environment and routine further reduces cognitive load. Some areas..Normal Aging 33 Several factors help to maintain daily function in the face of mild cognitive decline (Park 1999). hypertension or arthritis). By contrast.

34 Clinical Manual of Geriatric Psychiatry assimilate the information presented (Callahan et al. Extra care may be required in explaining medical procedures to ensure informed decision making. 2003). Asking the patient to repeat the main points and providing written summaries or illustrations may help to make details of procedures clear. These modes of educating most effectively remediate. Often. the reduced pace of new learning and changes in reasoning processes may result in a slower rate of clinical improvement. as many as one in three older patients with mild Alzheimer’s disease who are otherwise healthy and have at least a high school education can be expected to score in the normal range on very brief tests for cognitive screening. Chapter 5 (“Dementia and Alzheimer’s Disease”) provides more specific guidelines for screening for dementia through the use of cognitive mental status examinations. Outcomes of cognitive mental status examinations in older people must be interpreted cautiously. or compensate for. . reduced speed of processing and working memory or sensory limitations. brief cognitive screening may fail to detect focal brain impairment or dementia in early stages. Among healthy. In psychotherapy. most old persons without dementia who had less than 5 years of education were rated with standard mental status examinations as impaired (Wilder et al. although very complicated medication organizers or instructional charts may be counterproductive. Clinical Implications of Cognitive Change Cognitive declines that accompany normal aging complicate detection and diagnosis of organic mental disorders. and the clinician should follow up with a more thorough diagnostic assessment for those who score in the impaired range or whose adequate performance on a screening examination is inconsistent with lapses in everyday behavior. and the following subsection discusses more specific diagnostic issues concerning age-associated cognitive syndromes. this can be dealt with effectively by increasing the number of therapy sessions. Paying attention to the pattern and types of errors may also help to distinguish normal from abnormal cognitive changes. particularly in persons with limited education. For example. One common error is overdiagnosis of dementia. In one large multicultural study. 1995). well-educated old persons. Age-related cognitive changes also have implications for the doctor-patient relationship and for selection and monitoring of treatment.

have subjective complaints of memory loss affecting routine activities. diagnostic criteria have been proposed for a related. it is presumed to reflect normal aging. but narrower. 2004). Clinicians are also likely to see older adults whose cognitive skills are somewhat worse than expected for their age but who are still coping well overall and do not appear to have dementia. Diagnostic criteria for this condition are still evolving. psychiatric. may be an early warning of occult illness (so-called terminal decline) and should be carefully monitored. generally referred to as mild cognitive impairment. AAMI has been shown to be stable over intervals of at least 4 years. However. category of age-associated memory impairment (AAMI). Thus. According to one recent study. the category of age-related cognitive decline (780. No guidelines have been developed for identifying age-related cognitive decline. and several definitions have been proposed (see Winblad et al. Persons with a diagnosis of AAMI must be 50 years or older. but in some cases. thus. five of every six very old.Normal Aging 35 Abrupt changes in cognitive function always warrant medical attention. problems are noted in . The prevalence of AAMI based on objective assessment has been estimated to range from 40% for persons in their 50s to 85% for those 80 and older (Larrabee and Crook 1994). exclusionary criteria include any neurological. healthy persons can be expected to perform somewhat lower than young or middle-aged adults do on memory tests and possibly to have mild memory lapses in everyday activities. as opposed to beginning dementia or other brain disorder. The skill most commonly affected in mild cognitive impairment is learning and recall of new information. Diagnosing Age-Related Cognitive Change and Mild Cognitive Impairment In DSM-IV-TR (American Psychiatric Association 2000) nomenclature. emerging over a year or two. subclinical cognitive decline increases the risk of mortality in older men as much as a history of cancer does.9) may be coded to denote functioning of an older person with mild cognitive changes that are within normal limits for age and not attributable to a medical disorder. Much research has been devoted to this gray area of performance. or medical disorders that could reasonably be assumed to be producing the memory change. Even more gradual declines. and perform below the average level of young adults on a standardized memory test.

metabolic or medical disorders. or other major organic mental disorders. delirium. depression or other psychiatric disorders. memory) or in multiple domains (e. “Dementia and Alzheimer’s Disease”). and a high pro- . To improve screening accuracy for amnestic mild cognitive impairment. or reasoning..36 Clinical Manual of Geriatric Psychiatry other cognitive areas. visuospatial skills. substance abuse or medication reactions. trauma. However. there may be subtle difficulty with higher-order activities of daily living such as financial management. As shown in Table 2–3. neurodegeneration of an Alzheimer’s type is believed to be the most common etiology (Petersen and Morris 2005). and other conditions also may cause mild cognitive impairment of the various types. such as language.g. Additional subcategorization has been proposed to distinguish between cases in which a mild deficit is observed in a single domain (e..” for examples of memory tests). a substantial proportion of persons with amnestic mild cognitive impairment eventually develop dementia.9) may be appropriate for some cases of mild cognitive impairment (i. it may be helpful to review the full range of potential causes and contributing factors that have been established for dementia (see Chapter 5.g. In evaluating an individual who presents with mild cognitive impairment. and when deficits do not meet criteria for dementia. referral for neuropsychological testing is recommended. The term amnestic mild cognitive impairment is used when memory is impaired.. Table 2–3 compares diagnostic criteria for amnestic mild cognitive impairment with those for AAMI. American Psychiatric Association 2000). 294. The very short tests included in mental status examinations are generally not sensitive to mild cognitive impairment. when there is mild cognitive dysfunction in two or more areas. memory and reasoning). a more challenging test of learning and memory should be incorporated into the psychiatric examination (see Table 5–5 in Chapter 5. and if this condition is suspected.e. and the term nonamnestic mild cognitive impairment is used for other types of mild cognitive deficits. DSM-IV-TR research criteria for mild neurocognitive disorder (coded as cognitive disorder not otherwise specified. In amnestic mild cognitive impairment. but this difficulty is often intermittent and can be dealt with by extra effort or compensatory approaches such as note taking or double-checking one’s work. The syndrome of mild cognitive impairment can have several different underlying causes. “Dementia and Alzheimer’s Disease. In all forms of mild cognitive impairment.

Older adults with mild cognitive impairment who received donepezil or vitamin E did not differ from control subjects in cognitive course over a 3-year follow-up.. Clinical course is not as well established for nonamnestic mild cognitive impairments. portion have Alzheimer-type brain changes on autopsy (Morris et al. Some persons with mild cognitive impairment have a stable mild level of cognitive difficulty over intervals of several years. For further information on AAMI. although participants with an apolipoprotein ε4 allele did show some benefit from donepezil (Petersen et al. Clinical presentations of memory loss in old age Feature Clinical presentation Age-associated memory impairment (AAMI) Memory complaint Normal mental status Normal activities of daily living Mild cognitive impairment— memory type (amnestic MCI) Memory complaint or memory problems noted by an informant Normal mental status Normal activities of daily living or very subtle changes ≥1. These particular interventions may not have been optimal for treating prodromal demen- ..g. Early interventions (e.Normal Aging 37 Table 2–3. but the first large-scale clinical trial of this type yielded disappointing results.5 SDs below the average level for age peers on a standardized memory test Progresses to dementia at the rate of 10%–12% per year. see Larrabee and Crook 1994. 2001). clinic-based populations) are more likely to show a progressive course than are patients with mild cognitive impairment identified through population-based surveys. individuals who seek help from a physician because of memory concerns (i.e. but some remain free of dementia for at least 10 years Memory test results Clinical course ≥1 SD below the average level for young adults on a standardized memory test Generally stable for periods of at least 4 years Note. For MCI diagnosis and course. In general. SD= standard deviation. 2004. others (as many as 40% in some studies) revert to normal performance. and it is important to recognize that mild cognitive impairment in any form is not invariably progressive. see Petersen and Morris 2005 or Winblad et al. 2005). with medications to enhance cholinergic system function) could potentially be of benefit in slowing clinical progression of mild cognitive impairment.

before mild cognitive impairment becomes apparent).. psychological tempo. desirable traits are perceived as outweighing undesirable traits to an increasing degree through middle age and early old age. increased use of note taking and organization. When a clinical diagnosis of mild cognitive impairment is combined with other markers of Alzheimer’s disease (see Chapter 5. descriptive research suggests that basic personality traits such as introversion-extroversion. in most cases. In clinical situations. Also. 1999). A difficulty for clinicians is that it is not yet possible to separate the individuals with mild cognitive impairment who will progress to dementia within a few years from those who will not. and only follow-up will determine whether the patient has a progressive course. this additional information is not available. it is most useful to explain the category of mild cognitive impairment to the patient. The trends summarized in this section are most applicable to currently old persons in Western urban societies. that is. Coexisting Stability and Change When older adults compare their current and past selves. and hostility are stable throughout adult life (McCrae et al. the likelihood of dementia is increased.e. effective prevention of Alzheimer’s disease and other dementias may require intervention earlier in the life course (i. These personality disposi- . “Dementia and Alzheimer’s Disease”). assertiveness. discuss the need to track performance over time (as in other chronic medical conditions). Personality and Emotional Changes Personality and emotions have not been studied as thoroughly as cognition in old age. In contrast. Developmental optimism is a term that has been coined to describe this subjective growth in personality (Krueger and Heckhausen 1993). they usually perceive more growth than decline in personality. However. it is unknown whether observations about personality made within the confines of a particular generation and culture can be generalized to other places and times. Moreover. and encourage active compensation for functional effect in the form of simplification of schedules.38 Clinical Manual of Geriatric Psychiatry tia symptoms or preventing their progression. and sharing of responsibility for mentally demanding tasks with others.

The social clock sets the pace for psychosocial development within a given generation and provides a standard that individuals may internalize as a normal. expectable life cycle. certain causal processes appear to be consistently important. 1992). each person is faced with making sense of his or her actions over a lifetime and with judging the purpose and effect of these actions. or retirement). which occurs at all ages. In late adulthood. the primary tasks concern integrity versus despair. One influential developmental force is the “social clock” (Neugarten 1970). but most are informally imposed. Morale in old age may depend on success in resolving this issue. However. for marriage. Most societies have rather firm beliefs about age appropriateness of various actions.Normal Aging 39 tions are formed early in life and remain fairly constant in their relative prominence in an individual’s makeup. Positive affect showed some resemblance across family members. that is. Continuity has been described as “a grand adaptive strategy” promoted by individual preference and reinforced by social approval (Atchley 1989). Each stage is associated with primary developmental tasks. A study of elderly twins and multigenerational families found a genetic contribution to negative affect but not to positive affect. A second important force is the individual’s desire for continuity in personal past and present. despite variations in life experiences over the years (Roberts and DelVecchio 2000). in addition to those of earlier life phases.g. . A third but poorly understood set of influences is genetic factors. and accomplishment of each task has a bearing on subsequent stages. but the resemblance appeared to be attributable to shared environments rather than genetic similarity (Baker et al. and of the process of life review that is so common among elderly adults. Influences on Adult Personality Precise patterns of ebb and flow in personality probably vary with generations. Individual and social influences may combine to produce ordered transitions or stages in adult personality. voting. The search for continuity may be at the heart of reminiscence.. Erikson’s (1950) widely cited theory depicts development as progressing through eight age-correlated phases. Some of these beliefs are formalized through minimum-age laws or standards (e. because each cohort encounters a unique set of pressures and opportunities at successive life phases.

Depression affects subjective health concerns. Emotions. combined with declining dependency. Personality and Perceptions of Health Older adults’ perceptions of their health have been linked to a variety of objective health outcomes. they may differ for women and men. an increase in interpersonal orientation and nurturance in later years is seen. 2000).” Some studies have noted that older people tend to cope with stressful events in different ways than do younger adults. relative to more neutral knowledge and skills. 2003). the priority given to emotion among older people has been interpreted by some as a reaction to shortened time left. and the salience of emotion. Neuroticism is inversely associated with self-perceptions of good health. increases in later years (Carstensen 1992). these associations were stronger among persons age 75 and older than among persons in their 60s and early 70s (Duberstein et al. including mortality. increasing assertiveness and feelings of efficacy are evident. Mentally normal older people have better control over emotions than do younger adults. as do certain personality traits. parenting (Gutmann 1987)— or the dynamic interplay of cognitive processing resources and particular social contexts in shaping expressed personality (Staudinger and Pasupathi 2000). in a recent study. older people rely more often . Coping. Among middle-class women in the United States. whereas extraversion is positively associated. This richness of emotional processing in older persons runs counter to the generally declining patterns seen in many cognitive and physical skills. Most contemporary developmental theorists do not propose stage theories but instead emphasize the creative effect on personality of assuming and relinquishing adult roles—most importantly. as they approach their 50s. Instead of necessarily being linked to aging. they reason more flexibly about emotion-laden dilemmas. This same study found that openness to experience correlated with higher functional status throughout the late-life age range. or “endings.40 Clinical Manual of Geriatric Psychiatry To the extent that ordered transitions exist. and Well-Being Research suggests that old age is an emotionally rich and complex phase of life. Among men of similar socioeconomic background. and they remember emotionally charged information better than neutral facts (Isaacowitz et al.

Older adults maintain a sense of contentment in the face of functional declines through a combination of mobilizing additional resources. Throughout the adult life span. other research has pointed out that the problem situations that older people face are often less changeable than those of younger adults.Normal Aging 41 on emotion-focused forms of coping. However. Examples of emotion-focused coping include distancing from the problem. studies of longterm care show that sense of well-being tends to increase when residents are given greater opportunities to regulate their own environment. In the community. as opposed to active. 2003). and reappraising the problem positively. poor morale has been found to be the exception rather than the rule among older adults. and is oriented toward control of distressing feelings rather than toward alteration of stressful situations. belief in an external locus of control is associated with increased visits to physicians during times of very high stress. individuals compare their own performances and experiences with those of others and often come to positive conclusions. Specific stressful events have less of an effect on subjective well-being in old age than does attainment of personal goals or the onset of physical disability. . older adults with the highest morale tend to have better education and socioeconomic status when compared to those older adults who did not have such advantages. and they do not show lowered self-esteem as a general rule. older people who believe that their health is controlled by powerful others adjust better to acute-care hospitals and high-constraint long-term care than do those who consider their physical well-being to be under their own control. This self-enhancing appraisal serves to sustain self-esteem through difficult transitions and is a support for mental health (Kwan et al. Emotion-focused coping is more passive than confrontational. Not surprisingly. regardless of preexisting control orientation. “downsizing” performance standards. and reducing the value placed on particular skills or attributes (Rothermund and Brandtstadter 2003). problem-solving approaches. and when the type of problem is equated across ages. Although old age presents many personal and social obstacles. However. accepting responsibility. Current cohorts of older adults are not more prone to depression or anxiety disorders than are young or middle-aged persons. differences in coping styles are reduced or eliminated (Staudinger and Pasupathi 2000). For example. is more individual than interpersonal. Locus of control is another dimension that affects response to stressful situations.

g.. the clinician must accurately appraise an individual’s beliefs about locus of control. and resources are spared for personally important activities that sustain self-esteem (Baltes 1997). In acute-care situations. By contrast. and any marked change in mood or social behavior may indicate a disorder. by participating in health-oriented support groups). Elderly persons with the strongest sense of personal efficacy are flexible in prioritizing goals and accommodating to role changes and resource limitations. Those individuals with an internal locus of control adjust best if given an opportunity to participate in medical decision making. particularly if the problem being faced (e. The increased vulnerabilities that accompany old age may amplify neurotic traits. socially extroverted persons may respond well to encouragement to share their experiences with others (e.. However. whereas those individuals with an external locus of control may benefit more from knowing that they are attended by recognized experts.42 Clinical Manual of Geriatric Psychiatry An influential model of adult development that has emerged in recent years relates resilience in old age (i. increasing susceptible individuals’ worries about health and making it more difficult to provide reassurance based on objective results. more subtle reordering of personal priorities and shifts in coping styles are common with normal aging. in which goals are reshaped to fit current limitations and environments. . Those individuals who suspect that their fate depends on chance may adjust best if the care environment is consistent and predictable. Emotion-focused coping may be a sign of personality development rather than regression. Those with several self-domains in which they hold themselves in high esteem seem best able to cope with transitions imposed by role losses or poor health (Staudinger and Pasupathi 2000). maintaining adaptive behavior in the face of stress and recovering from adversity) to a process of selective optimization.g. It is particularly important not to measure older people’s coping by youthful standards. bereavement or serious illness) is difficult to resolve through action. Clinical Implications of Personality and Emotional Changes Core features of personality remain stable throughout adulthood. Other aspects of personality need to be considered as well..e.

especially of cognitive skills. often. and in general.g. Education. The leveling off of work rates in recent decades has been attributed to elimination of mandatory retirement laws and . and community roles. Most people can expect transformations in occupational. in 2003. situational interventions. In industrialized countries. For many others. role loss. from 21% to 12% (Federal Interagency Forum on Aging-Related Statistics 2004). and among those 70 and older. goal setting for the future should be part of the psychotherapy agenda. older black and Hispanic Americans remained disadvantaged in terms of education (Figure 2–1). the percentage of men ages 62–64 years in the workforce declined from 76% to 50%. problemfocused therapies in recent years. aimed at modifying real-life problems. participation of older men in the labor force has declined in recent decades. Work.. Older patients may not see the relevance of being asked to learn a list of words or may editorialize about emotional themes in stories they have been asked to remember.Normal Aging 43 Increasing salience of emotional matters can influence assessment. and for many. Varying the instructions of the task (e. may be most appropriate. Older people can benefit from the full range of psychotherapies used with younger people (see Chapter 4. By contrast. Older Asian Americans had the highest percentage of persons (29%) with at least a bachelor’s degree. nearly three-fourths of persons age 65 and older had a high school diploma. there has been a trend toward short-term. Most of the decline took place before the 1980s. the number of different roles declines in later life. “Mood Disorders—Treatment”). Some highly educated and thoughtful elderly people are well suited for long-term therapy addressing intrapsychic tasks of later life. and Financial Status The average education level of older Americans has increased in recent decades. In either case. as the youngest age for Social Security eligibility dropped to 62 and older people began to enjoy better incomes. Social Context of Aging Old age is accompanied by role change and. In the United States between 1963 and 2003. encouraging the person to try to remember the story as if he or she were going to relate it to a friend or grandchild) can sometimes help to direct attention and effort toward the task requirements to permit a valid assessment. family.

Employment trends for women have moved in the opposite direction. Although people who retire report that they miss the money and opportunities for social contact provided by their everyday work. as new cohorts with a history of working outside the home have begun to age. a strong psychological commitment to work. This type of adjustment is particularly likely when retirement is predictable or self-imposed and when postretirement income is adequate. 2003. were employed. Labor force participation rates have increased for older women since the early 1960s. Source. Good health.44 Clinical Manual of Geriatric Psychiatry 100 80 Americans age ≥65 (%) High school graduate or higher Bachelor’s degree or higher 60 40 20 0 Total Non-Hispanic white alone Black alone Asian alone Hispanic of any race Figure 2–1. Educational attainment of Americans age 65 and older. and 23% of those ages 65–69. . most take retirement in stride. changes in Social Security policies regarding delayed retirement credits and earned income. Adapted from Federal Interagency Forum on Aging-Related Statistics 2004. Health problems. 64% of women ages 55–61 years. adopting new routines and activities to take the place of their work. In 2003. and an active distaste for retirement are among the strongest predictors of continuing to work past traditional retirement ages.

Social Security provided 39% of the total income for Americans age 65 and older. The poorest older adults are heavily dependent on Social Security. 71% of men and 41% of women age 65 and older were married. compared with 8% of older men. In 2003. usually do not increase in the weeks or months after retirement. However. In 2002. compared with 35% in 1959 (Federal Interagency Forum on Aging-Related Statistics 2004). 59% of men. Social Security provided more than 80% of the funds of older Americans in the lowest two-fifths of the income distribution. 12% of older women lived in poverty. and some studies show that retirees have lower stress levels and engage in more healthful behaviors than do similar-age peers who are still employed (Midanik et al. and there may be greater agreement between the partners on important topics such as money management and relationships with children. Because of Social Security and other pension programs. Marriage and Widowhood The availability of marital relationships in old age differs sharply for women and men. a majority of older people in the United States are financially independent.Normal Aging 45 either physical or mental. rates of widowhood are . for example. Twenty-four percent of older black Americans and 21% of older Hispanics had incomes below the poverty line. Many older women live alone in their final years because their husbands have died or because separations are imposed by a spouse’s failing health (Figure 2–2). but only 14% of women. satisfaction may increase in later life compared with earlier marital phases. with an additional 25% provided by personal earnings. and 14% by asset income. In 2003. Persons with medium income now constitute the largest group of older Americans (35%). elderly women and members of minority groups have more severe financial strain than do older white men. For those with long-term marriages that continue into old age. In 2003. compared with 8% of older non-Hispanic white Americans. 1995). Because of increased life expectancy. among those age 85 and older. 19% by pensions. About 10% of Americans age 65 and older were considered poor by federal guidelines in 2002. were married (Federal Interagency Forum on Aging-Related Statistics 2004). and 26% have been rated as having high income (Federal Interagency Forum on Aging-Related Statistics 2004).

Rates of widowhood are similar for Hispanic and non-Hispanic white women but are higher for black women.. a marked increase in distress following the loss.46 Clinical Manual of Geriatric Psychiatry gradually declining. 2003. 2004). According to a recent prospective study. Adapted from Federal Interagency Forum on Aging-Related Statistics 2004. With other relatives With spouse Alone With nonrelatives 100 80 60 40 20 0 M W M W M W M W M W Americans age ≥65 (%) Total Non-Hispanic white alone Black alone Asian alone Hispanic of any race Figure 2–2. Normal bereavement generally . approximately one-half of new widows or widowers cope with the loss of their spouse with relatively low levels of distress.e. Source. Older adults respond to bereavement in many different ways. and what was once considered a typical response to bereavement (i. but this trend is being offset by increasing numbers of divorced and single older persons. Living arrangements (percentage of population) for men (M) and women (W) age 65 and older. with abatement over time) is much less common (Bonanno et al.

one in Japan and one in the United States. However. “Mood Disorders—Diagnosis”).S. more than 50% of the persons at this age reported one or more close friends. Elderly people are also actively involved with their siblings. and Group Involvement Compared with younger people. Illinois. sibling relationships appear to increase in importance. Extended Families. Fulfilling multiple social roles (e. Friends. and siblings. spouses are most likely to be listed as confidants. among currently old Americans. However. Among persons age 85 years and older. most older persons are socially active within this smaller arena. men and women with few friends tend to have a harder time adjusting to widowhood. followed by friends.g. 2004). About four of five elderly persons report having confidants. declining functional ability is the biggest obstacle to continuing old friendships or making new friends. worker. When available. spouse. caregiver. Being socially involved and depended on by others is important for successful aging. Two recent studies. elderly individuals tend to have smaller social networks and less frequent interpersonal contacts. and at least two-thirds report that they have seen their children within the past week (U. and 75% had weekly contact with persons they identified as friends (Johnson and Troll 1994). Nearly 80% of older adults have at least one living child.. women are less likely than men to view their spouse as the main source of social support (Gurung et al. However. in one study. Older people rely more heavily than younger adults on family members and long-term friendships for input on important matters. persisting beyond 1–2 years. A recent population-based study in Chicago. Nonetheless. 2003). Having a sense of social worth is also important for health and survival. found smaller social networks and lower levels of social engagement among elderly black persons compared with elderly white persons (Barnes et al. Intimate. is relatively rare. As individuals realize that they are aging. confiding relationships may be most valuable to a person’s wellbeing and mental health in old age. and grandparent) has been linked to higher life satisfaction and feelings of self-efficacy for both white and black older Americans.Normal Aging 47 does not produce a loss of self-esteem or inappropriate guilt (see Chapter 3. and chronic grief. found reduced rates of death among . Senate Special Committee on Aging 1987–1988). with sisters playing a particularly active role in maintaining kinship networks. children.

Increasing numbers of grandparents are now providing custodial care for grandchildren or extensive noncustodial caregiving. and promote reciprocity in assistance when possible. especially in black and Hispanic families. Intergenerational family therapy can be useful. and about one in six are active in volunteering. which over time lowers the probability of survival and reduces the physiological capacity for self-regulation. despite changes in physical or mental abilities. facilitate meaningful contacts for those without social networks.48 Clinical Manual of Geriatric Psychiatry older adults who perceived themselves as useful to others or were involved in giving social support (Brown et al. can be as important as providing opportunities to mourn the loss of past abilities or social roles. Clinical Implications of Social Context Psychiatrists must identify sources of social support for older people. they are especially likely to find themselves alone in advanced old age. Because older women are frequently widowed and may outlive other kin. repair and adaptation to environmental demands” (p. Biological Aging What Is Aging? A useful definition of aging was proposed by Birren and Zarit (1985): “Biological aging. particularly if it reinforces older patients’ ability to give as well as to receive. 9). is the process of change in the organism. About one-half of older Americans attend church regularly. Helping older patients to identify meaningful ways to stay involved. senescing. Being needed by others and making contributions to one’s family or society as a whole are important for maintaining a sense of self-worth. 2004). Okamato and Tanaka 2004). 2005. but this possible strength may be counteracted by physical or sensory disability. which is postulated to re- . therapists must sometimes be willing to provide periodic support on a long-term basis. Religious beliefs may play an especially important role in adaptation for older Americans of African descent. whereas elderly white persons may rely more often on nonreligious social connectedness (Consedine et al. Women may be more adept than men at forming friendships in later life. For those with very restricted social resources. Modern gerontologists distinguish primary aging.

many functional capacities are lost. and when a certain limit is reached. including those with little or no reproductive capacity. such as neurons. Primary aging seems to account for the relatively constant maximum life span observed in almost all animal species studies. such as progeria (Hutchinson-Gilford syndrome) and Werner’s syndrome. Evidence that the observed telomeric shortening is a key determi- . doublings in vivo appear to “count” as well as those that occur in vitro. As cultured cells approach this limit. That primary aging is “built into” the cell was first appreciated by Hayflick and associates (Hayflick 1965.e. Hayflick and Moorhead 1961) in a series of experiments that established the maximum number of cell divisions (doublings) that would occur in carefully cultured normal human cells at about 50±10. that is. presumably genetically preprogrammed limit on cellular longevity. Multiple studies have shown that telomeres shorten with each cell division. but several lines of evidence point to telomeric shortening as at least one likely “clock” mechanism.. from secondary aging. it is composed of repeated stretches of six nucleotides (TTAGGG in vertebrates) that seem to perform a stabilizing or protective function for the end of the chromosome (Hodes 1999). Telomeres are unique protein-DNA structures that make up the terminal region of chromosomes in eukaryotic cells. which is due to the accumulated effects of environmental insult.Normal Aging 49 flect an intrinsic. whereas secondary aging explains much of the variability among individual members of a species. The precise mechanism underlying the observed limits on normal cellular division is not completely known. rather. Similar losses of functional capacity (i. The observation that cells in culture retain their preprogrammed doubling limit even after being frozen for years suggests that the doubling limit is not related only to total time elapsed. Evidence that the “Hayflick phenomenon” is under genetic control includes 1) a fair correlation between the doubling limit and the maximum species-specific life span of the cell donor and 2) a reduced doubling limit in cells cultured from patients with genetic diseases of accelerated aging. cellular division no longer occurs and cellular “senescence” has been reached. The observed inverse relation between doubling capacity and the age of the cell donor indicates that the limit is not just an in vitro phenomenon. and trauma. with the final cessation of cellular reproduction apparently reflecting accumulated functional losses. disease. cellular aging) have since been observed in all cell types. The telomere section of the chromosome does not contain genetic information.

random samples are rarely used in this type of research) and by the uncontrollable effects of secondary aging. and behavioral signs and symptoms do not fit cleanly into well- . senescence is determined by whichever clock mechanism reaches its critical threshold first. is found in high concentration in germ cells and malignant cells. Primary Aging: Structural and Functional Changes The major structural changes in humans that have been attributed to primary aging are listed. Note that cross-sectional studies produced most of the tabulated findings.. or on multiple clock mechanisms. environmental and intracellular factors operate either on a single clock mechanism. emotional. a large proportion of elderly patients who present with cognitive. such as telomeric shortening. both of which are “immortal” and do not senesce. In his models. in Table 2–4. DNA demethylation. In the latter model. also have been proposed to play a role in normal cellular senescence.e. Aging and the Clinical Process Although psychiatry textbooks and manuals (including this one) are traditionally divided into chapters and sections that cover specific diagnostic entities. and accumulation of DNA cross-links. and “environmental” factors such as oxidative stress. Regardless of which model turns out to be best supported by the evidence. However. Reddel (1998). a ribonucleoprotein enzyme that mediates RNA-dependent synthesis of telomeric repeats and prevents telomeric shortening. senescence is delayed significantly. summarizing this literature. it is not at all clear that the failure of cells to continue reproducing can account for all aging changes in the organism per se. which can induce “premature senescence” (i. data on the anatomical and physiological effects of age are usually confounded by selection biases (i.e. In addition to the general shortcomings of such studies described earlier. telomeric shortening has not been observed in all senescent cell cultures. proposed two models of senescence induction that take these and other potential inducers of premature senescence into account. failure of cells to divide before the Hayflick limit has been reached). along with the major functional consequences of these changes.50 Clinical Manual of Geriatric Psychiatry nant of cellular senescence includes 1) the observation that telomerase. by organ system. and 2) the observation that when the expression of telomerase is induced in normal cells..

By the end of the interaction. and occasional constipation. 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. a few general principles of diagnosis and treatment are important to keep in mind. a proton pump inhibitor. I don’t need a psychiatrist. an 85-year-old married. Mr. Mental status examination finds mildly depressed mood. ginkgo biloba. tells the clinician. anxiety.” Gentle probing induces Mr. but was “invited” to stop coming to the office about 6 months ago and has not been back since. shortterm memory impairment that is partially ameliorated by cues. you wouldn’t be so chipper. and social withdrawal and an increasing tendency to stay in bed. two antihypertensive medications (including a βblocker). in addition to stool softeners. intermittent urinary retention. chronic worrying. low-dose aspirin. including dry mouth. A discounts the importance of both of these events. and multiple somatic symptoms. and inconsistent results on assessment of frontal executive functions. and I don’t need treatment for any ‘mental illness. and the older the patient. A to admit to mild memory impairment. retired businessman presenting for an outpatient assessment. A is suffering and that his physical and social functioning have declined. “There’s nothing wrong with me. Mr. and intermittent hydrocodone bitartrate– acetaminophen preparations. A’s spouse adds that she has noticed his irritability. A. which is now being run by their son. or his other illnesses and their treatments. A has chronic moderate hypertension and coronary artery and peptic ulcer disease. The patient has no history of mental or emotional problems and does not qualify for any DSM-IV-TR diagnosis (outside the not-otherwise-specified categories). she mentions that Mr. to continue to gather information and modify the treatment plan as a clearer picture emerges.Normal Aging 51 defined (DSM-IV-TR) diagnostic categories. and he says. The following case report is typical: Mr.’” With this “typical” patient in mind. some loss of appetite and energy. Late in the session. other social stressors. A’s brother died a month prior to the clinic visit. occasional episodes of dizziness. She goes on to say that he had been working part-time at a company that he started 40 years ago. then. . he takes daily doses of a statin. and vitamin E. and I don’t need to be here. the more this tends to be the case. The ability to initiate treatment on the basis of only provisional diagnostic impressions. either. if you’d been through what I’ve been through. Mr. chronic pain in several body parts. if you had my medical problems. and to take agerelated changes in clinical circumstances into account throughout the process is the hallmark of the well-adapted and successful geriatrician. it is clear that Mr. “Doc.

flexibility of collagen matrix. increased kyphosis. some loss of hepatocytes. reduced metabolism of drugs atrophy of gastric mucosa. reduced β-adrenergic (i. Primary aging: changes in anatomy and function of major organ systems System Cardiovascular Heart Anatomical changes with age Functional changes with age 52 Clinical Manual of Geriatric Psychiatry Arteries Decreased size. leading to decreased peak myocardium. increase in gastric pH. fatty infiltration and exercise cardiac index and ejection fraction (Schulman calcification of aortic and mitral valves 1999) Redistribution and molecular rearrangement Increased systolic blood pressure (cross-linking) of elastin and collagen in arterial walls. Reduced eliminatory efficiency: constipation.. Impaired left ventricular diastolic filling. especially during exercise elasticity Same as above Increased chest wall and joint rigidity.Table 2–4. chronotropic and inotropic) lipofuscin and fat deposition in response to catecholamines. degeneration and calcification of cartilage Some loss of smooth muscle cells of intestine. loss of Reduced ventilatory capacity. calcification Enlarged alveolar ducts and alveoli.e. reduction in hepatic blood flow Respiratory Lungs Musculoskeletal Gastrointestinal .

but resting hormone changes may be very minimal blood levels may remain constant as clearance also declines Inconsistent evidence of reduced blood flow. loss of neurons. reduced Loss of brain weight and volume in most metabolism of glucose and oxygen. amygdala. obliteration of arterioles in cortical glomeruli (Davison 1998). intimal thickening of arteries. especially in women. Primary aging: changes in anatomy and function of major organ systems (continued) System Genitourinary Anatomical changes with age Functional changes with age Endocrinological Nervous Reduced glomerular filtration rate and renal plasma Loss of renal mass. loss of dendritic arbor. in Later Life: A Processing Resource Model”) with reduced interneuronal connectivity. development of tubular diverticula. reduced bladder elasticity.Table 2–4. neurofibrillary degeneration of neurons. prostate enlargement in men Atrophy and fibrosis. loss of vascularity. accumulation of senile plaques. intellectual studies. General decline in secretory rate. flow. interneuronal accumulation of lipofuscin and loss of organelles. depending on changes as described in text (see “Cognitive Abilities brain area studied. loss of bladder-emptying capacity thickening of basement membrane of glomeruli and tubules. and frontal cortex Normal Aging 53 . development of afferent-efferent shunts in juxtamedullary glomeruli. loss of glomeruli. especially in hippocampus.

especially night vision . increased fat in muscles and calcium in cartilage. increased proportion of activated/memory T cells. decreased cellular proliferative response to T-cell receptor stimulation (Ginaldi et al. loss of elasticity in joints Involution of thymus. demineralization of bone. reduced proportion of naïve T cells. 1999) Yellowing of lens in eye Functional changes with age Loss of muscular strength and stamina 54 Clinical Manual of Geriatric Psychiatry Immunological Increased susceptibility to cancer Special senses Loss of auditory and visual acuity. degeneration of cartilage.Table 2–4. decreased expression of interleukin-2 receptors. Primary aging: changes in anatomy and function of major organ systems (continued) System Musculoskeletal Anatomical changes with age Reduced muscle and bone mass.

may render specific psychopharmacological treatment unnecessary. If the history does not fit the current clinical picture. or exacerbate depressive or anxiety symptoms. mimic.Normal Aging 55 Diagnostic Process • Identify “secondary syndromes” first. • • • Therapeutic Process • First. See Table 2–5 for a list of common offenders. Seek information from ancillary sources when possible. only to “remember” when the patient switches into one: “Oh yes. undo harm. Some elderly patients who vehemently deny being depressed will admit to “the dwindles” or will acknowledge loss of interest in usual activities or irritability. Do not hesitate to treat just because a full syndrome is not present. board and care home or nursing home sponsor or head nurse. Replacement with an alternative agent. with terms that the patient can understand and is comfortable with. Do not accept bland denial of symptoms. Some bipolar patients and their family members “forget” hypomanic episodes. Sometimes the clinician must use several different approaches. and other physicians. appropriate treatment of the general medical condition and/or modification of the medication regimen may be sufficient to ameliorate depressive symptoms. the clinician should probe more deeply. Lack of insight exacerbated by a widespread cultural bias against acknowledging emotional or mental infirmity may render the patient the least reliable informant. There is growing recognition of the clinical significance of subsyndromal condi- • . caregiver. Maintain a healthy index of skepticism. Ancillary sources include the spouse. before the true picture emerges. Some presenting signs and symptoms may be due to side effects and adverse reactions to over-the-counter and prescription medications used for physical conditions. 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 response to a relatively minor change in living circumstances. A growing list of general medical conditions and medications appear to be risk factors for clinically significant depression. and in some cases. or dosage adjustment of medications that can provoke.

the psychiatrist must evaluate hepatic and renal function and the function of any organ or organ system .56 Clinical Manual of Geriatric Psychiatry Table 2–5. mild neurocognitive disorder (see Appendix B. memory impairment Sedation. and age-associated memory impairment (listed in DSMIV-TR as “780. Musculoskeletal aging may impair mobility and interfere with older patients’ ability to come to appointments.” in DSM-IV-TR). For example. Sensory losses may require that the therapist sit closer and speak more loudly and slowly than would be appropriate for middle-aged patients. so sessions may need to be shorter than with younger patients. older patients may be more prone to forget appointments and may need reminder calls. psychomotor retardation. Sensory losses and reduced short-term memory also may contribute to a generalized reduction in attention span and decreased capacity for therapeutic work. agitation Sedation. desktop systems offer much greater clarity and resolution than standard hearing aids. “Criteria Sets and Axes Provided for Further Study. Usually. Modify psychotherapeutic technique as necessary. anxiety • • tions in elderly patients. reduced energy Hallucinations. emotional lability Sleep disturbance. Medication-induced signs and symptoms of mental disorder Medication Antihistamines β-Blockers Antiparkinsonian agents Narcotic analgesics Steroids Decongestants. generally. Amplification devices may be of value. as shown by the emergence of new diagnostic categories such as minor depressive disorder. Impaired short-term memory may require that the therapist reiterate key points several times and may contribute to learning difficulties that are indistinguishable from resistance and denial. Determine the patient’s baseline physiological and pharmacological status before initiating pharmacotherapy.9 Age-Related Cognitive Decline” in the “Other Conditions That May Be a Focus of Clinical Attention” chapter). and the role of telephone contact in their care may be expanded. bronchodilators Signs and symptoms Sedation. impaired attention and concentration Anxiety.

and few generalizations are possible. such as diazepam. such as lithium carbonate. sulfate. Both of these changes result in relatively increased plasma concentrations of drugs that are distributed in body water. such as digoxin (Cusack et al. examination of the actual rate of metabolism of drugs in elderly subjects has produced contradictory results. Respect age-related pharmacokinetic and pharmacodynamic changes. and excretion—all but absorption are significantly affected by normal aging changes (Desai 2003). reactions catalyzed by enzymes in the microsomal fraction of homogenated liver tissue. Conversely. more than 95%). are distributed in a larger “apparent volume” (Greenblatt et al. A careful review of the list of other medications the patient is taking. Aging is also associated with reduced amounts (in the range of a 20% reduction) of serum albumin. with resultant greater drug effect.Normal Aging 57 • that may be adversely affected by medications (e.. metabolism. most drugs undergo two-phase metabolism in the liver. This effect can cause significant changes in the blood levels of nonpsychotropic and psychotropic medications. The distribution of drugs in the body is reliably altered by the aging process. or conjugation with glucuronide. drugs that deposit in lean body mass and adipose tissue. reduction.g.. or likely to begin taking. Of the four major determinants of pharmacokinetics—absorption. and in hepatic enzyme activity have been seen in elderly individuals. such as furosemide or warfarin. 1980) and will attain somewhat lower plasma concentrations than in a younger patient. or hydrolysis. the serum protein most highly “bound” to drugs in plasma. After distribution. an electrocardiogram should be obtained before initiating therapy with tricyclic antidepressants). primarily as a result of relative loss of body water and lean body mass. in relative hepatic mass (about one-third). distribution. Although reductions in hepatic blood flow (about 45% between ages 25 and 65). The first phase is oxidation. or glycine. One . or in lean body mass. The second phase of metabolism is acetylation. is also important because psychotropic medications affect the function of several hepatic microsomal cytochrome P450 enzymes. the reduction may free a significantly higher proportion of drug for distribution to its site of action. second-phase metabolism usually produces active or inactive water-soluble compounds that are then excreted by the kidney.e. 1979). For drugs that are highly albumin bound (i.

so an approach that reaches that dosage as rapidly as is safe is most appropriate in the inpatient setting. is likely to produce clinically applicable findings in the near future (Malhotra et al. the principle of start low. 1976). such as desipramine (i. such as lithium salts. including absorption and secretion (Rowe et al. In the outpatient setting. Age effects on renal excretion of drugs have been much more clearly delineated. which attempts to understand and predict genetically determined interindividual differences in pharmacokinetic and pharmacodynamic responses to drugs. The emerging field of pharmacogenetics. increased or decreased effectiveness of drugs can be assumed to reflect pharmacodynamic changes (the actual physiological response produced by a drug at its site of action). this change is less important. For drugs that are excreted by the kidney unchanged. increased sensitivity to the effects of warfarin. go slow is more appropriate. 1977). 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. Psychopharmacotherapy in the inpatient setting should be conducted much more aggressively than in the outpatient setting. Only a few such pharmacodynamic changes have been documented in healthy elderly persons: increased sensitivity to the depressant effects of benzodiazepine anxiolytics and hypnotics on the central nervous system (Greenblatt et al.58 Clinical Manual of Geriatric Psychiatry such generalization is that hepatic conjugation of drugs is relatively spared by age effects. The age-related changes in pharmacokinetics and pharmacodynamics cited above are reflected in the following bullet points: • Respect the treatment setting.. and decreased sensitivity to the chronotropic effects of isoproterenol. the significance of this sparing with respect to benzodiazepine therapy is shown clearly in Table 7–8 in Chapter 7 (“Anxiety Disorders and Late-Onset Psychosis”). For other agents with inactive water-soluble metabolites. 2-OHdesipramine). where side effects and adverse reactions can be monitored and managed. as has comparable reduction in renal plasma flow and renal tubular function. 2004). this reduction may have great clinical significance. The clinician should begin with relatively small . Almost every psychopharmacological agent on the market is most effective at the highest dosage the patient can tolerate. When pharmacokinetic factors are constant. or that have active water-soluble metabolites.e.

the latter are appropriate early indicators of adequate treatment. Failure to identify appropriate target symptoms is a common cause of unsuccessful treatment.Normal Aging 59 • • • doses—for example. adjusting antipsychotic therapy to eliminate delusional content while failing to appreciate improved behavior and reduced agitation. subjective improvement in mood usually appears later in the course of therapy. and changes are made one at a time is it possible to determine which treatments are ineffective or unnecessary and need no further exploration. Similarly. is subject to more interrater variability. appetite.g. change one thing at a time. social withdrawal in a depressed patient who is characterologically antisocial. helplessness.. The clinician should proceed slowly when dosage increase is indicated and remain alert for the development of adverse reactions. such polypharmacy renders the clinical picture unnecessarily complex. and anticonvulsants to achieve just the “right balance” of neurotransmitter activation and inhibition is inadvisable on several counts. typical early indicators of response to antidepressants are improvement in sleep. and specific psychological states such as hopelessness. One goal of psychopharmacotherapy is to identify ineffective approaches. and anhedonia. one-third to one-half of the usual adult dose. and anxiety. adequate dosages are prescribed. Choose appropriate target symptoms. Target symptoms may be absolutely inappropriate (e. When possible. Only if treatment is conducted systematically. global improvement is a suboptimal target of therapy because it is relatively more sensitive to the vicissitudes of daily life. and second. Keep it simple. and drug interactions. because these combinations have had essentially no systematic study. For example. making the task of sorting out which symptoms are “primary” and which are side effects or adverse reactions a matter of guesswork. First. sleep. side effects. antipsychotics.g. The apparently widespread practice of “mixing and matching” antidepressants. every instance of their use is an “n of 1” clinical trial in which the patient is an unwitting subject. or unhappiness and dissatisfaction in a patient who feels stuck in a bad marriage) or temporally inappropriate (e. and is more influenced by the mood and expectations of a single rater than are more concrete targets such as appetite. In general. in a patient whose symptoms are unre- . whereas the former may require months of therapy).. adequate amounts of time are allowed.

. the dose is increased and lithium is added.g. prescribing antihistamines for their hypnotic or anticholinergic side effects. Common violations of this principle include prescribing increasing amounts of neuroleptic medications when sedation is desired.) Failure to follow this principle with elderly patients increases the risk of adverse reactions caused by overtreatment (e. this approach requires particularly close monitoring of clinical response and determination of serum drug levels when available. such as the use of a sedating antidepressant for a depressed patient with sleep disturbance. Trazodone is difficult to use as an antidepressant in the elderly because of its sedative effects and its tendency to provoke orthostatic hypotension in antidepressant dosages. the clinician can be reasonably confident that the most effective (i.60 Clinical Manual of Geriatric Psychiatry • • sponsive to a tricyclic antidepressant. if response diminishes or plateaus before complete remission. Such is not the case with undertreatment. dosages should be increased again. (A possible exception is the use of trazodone in subantidepressant dosages as a hypnotic. so a clear signal usually alerts the clinician when the dosage is reaching its ceiling. 50–100 mg] dosages.. In this way. when partial response can “freeze” therapeutic response at a suboptimal level.. Which maneuver is responsible? Is the lithium necessary? Would a higher dose alone have sufficed? Do not use medications only for their side effects. it is safe and effective as a hypnotic. The geriatric literature appropriately emphasizes the side effects and adverse reactions that all psychotropic medications can cause. with agents for which a true therapeutic window exists (possibly including nortriptyline)..e. At this point. the highest) dosage possible for that patient has been reached. However. but in low [i. or prescribing antidepressants as hypnotics for nondepressed patients. Of course. A good rule of thumb is to increase dosages until clinical response is clear. with the ceiling defined as the development of minor side effects that do not remit over several days. rapid response follows.e. most elderly patients are quite sensitive to medication side effects. minor dosage reduction may be appropriate. This principle does not discourage selection of an agent when its therapeutic effects and its side effects are both desirable. Beware of undertreatment. Diagnostic uncertainty or therapeutic timidity on the part of the clinician may lead to these outcomes. neuroleptic malignant syndrome or anticholinergic delirium).

This stance is particularly important during the first few days and weeks of therapy. Mendes de Leon CF. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. 2002 Baltes PB: On the incomplete architecture of human ontogeny: selection. 2003 Atchley RC: A continuity theory of normal aging. 4th Edition. Cesa IL. 2000 Artistico D. 2006. Optimism does not entail or justify unrealistic expectations but helps to maximize the placebo effect. Berch DB. 1997 Barnes LL. Clarendon Press/Oxford University Press. DC. Psychol Aging 7:158–163. American Association of Retired Persons and the University of Southern California. Washington. Available at: http://www.html. and compensation as foundation of developmental theory. When a patient is hospitalized and his or her “regular dosage” of medication is continued in the hospital. when the ratio of side effects to clinical gain is particularly high. 1986 Baker LA. Oxford. et al: Genetic and environmental influences on positive and negative affect: support for a two-factor theory. J Gerontol B Psychol Sci Soc Sci 59:S146–S153. Gerontologist 29:183–190. 1992 Ball K. Text Revision. Am Psychol 52:366– 380. Washington. 2004 . which has been shown to account for about one-half of the efficacy of psychopharmacological agents. Psychol Aging 18:68–79. Accessed March 9. problems may occur. References Abramson A. DC. Maintain an optimistic and supportive attitude. Helmers KR.aarp. Pezzuti L: Perceived self-efficacy and everyday problem solving among young and older adults. Bienes JL. 1989 Baddeley AD: Working Memory.Normal Aging 61 • • Beware of inducing withdrawal or overdose. optimization. et al: Effects of cognitive training interventions with older adults: a randomized controlled trial. Cervone D. Gatz M. et al: Longitudinal study of black-white differences in social resources. JAMA 288:2271–2281. Silverstein M: Images of Aging in America 2004.org/research/reference/agingtrends/ aresearch-import-926. Unreported undermedication or overmedication before admission can render the prescribed dosage much too low or too high. 2004. American Psychiatric Association. UK.

1992 Christensen H. et al: Digoxin in the elderly: pharmacokinetic consequences of old age. Government Printing Office. O’Malley K.S.gov/prof/Statistics/profile/2004/ profiles2004. behavior. 1998 Desai AK: Use of psychopharmacologic agents in the elderly. NJ. 2004. D’Ostilio A. Psychol Aging 19:260–271.aoa. Washington. 2005 Birren JE. Consedine NS. Journal of Management 29:663–680. Sorensen S. 2004 Cusack B. Available at: http://www. New York. 1999 Consedine HS. Psychol Aging 7:331–338. Accessed March 9.asp. 1999 . 2004 Ginaldi L. J Cross Cult Gerontology 19:97–131. Fratiglioni L. et al: An analysis of diversity in the cognitive performance of elderly community dwellers: individual differences in change scores as a function of age. Psychol Aging 18:25– 37. Kiker DS. Paillard-Borg S. Zarit JM: Concepts of health. et al: Personality is associated with perceived health and functional status in older primary care patients. 2003 Erikson EH: Childhood and Society.62 Clinical Manual of Geriatric Psychiatry Beier ME. et al: The immune system in the elderly. Winblad B: An active and socially integrated lifestyle in late life might protect against dementia. Edited by Birren JE. Psychol Aging 20:341–355. Magai C. 1985. 2006. 2004 Brown WM. 1950 Federal Interagency Forum on Aging-Related Statistics: Older Americans 2004: Key Indicators of Well-Being. Lancet Neurol 3:343–353. Immunol Res 20:109–115. Kelly J. Nephron 80:6–16. ability. Prentice-Hall. Mackinnon AJ. Cross T: Does method matter? a meta-analysis of the effects of training method on older learner training performance. WW Norton. Livingston J. Englewood Cliffs. 2005 Callahan JS. 1979 Davison AM: Renal disease in the elderly. Conway F: Predicting ethnic variation in adaptation to later life: styles of socioemotional functioning and constrained heterotypy. Clin Geriatr Med 19:697– 719. U. Ackerman PL: Age. De Martinis M. and aging. in Cognition. J Gerontol B Psychol Sci Soc Sci 60:P143–P152. 2003 Duberstein PR. Clin Pharmacol Ther 25:772–776. DC. II: specific cellular immunity. Jorm AF. and the role of prior knowledge on the acquisition of new domain knowledge: promising results in a real-world learning environment. Lyness MJ. Nesse RM: Prospective patterns of maladjustment during widowhood. 2003 Carstensen LL: Social and emotional patterns in adulthood: support for socioemotional selectivity theory. Psychol Aging 14:365–379. Magai C: Altruism relates to health in an ethnically diverse sample of older adults. Stress and Aging. Wortman CB. pp 1–18 Bonanno GA.

2002 . Moorhead P: The serial cultivation of human diploid cell strains. 1980 Gurung RAR. Phillips LH. et al: Age differences in personality across the adult life span: parallels in five cultures. Kennedy JL: Pharmacogenetics of psychotropic drug response. Dixon RA: Performance variability is related to change in cognition: evidence from the Victoria Longitudinal Study. Allen MD. Troll LE: Constraints and facilitators to friendships in late life. J Gerontol 48:100–108. 1993 Kwan CML. and somatic cell turnover. Plenum. Basic Books. Am J Psychiatry 161:780–796. 1999 McKhann G.Normal Aging 63 Greenblatt DJ. et al: A meta-analytic review of prospective memory and aging. NJ. Shader RI: Toxicity of high-dose flurazepam in the elderly. 2004 Hodes RJ: Telomere length. 1961 Henry JD. Psychol Aging 19:27–39. Edited by Craik FIM. MacLeod MS. 1999 Isaacowitz DM. 1992 Larrabee GJ. 2000. Hultsch DF. 1965 Hayflick L. 1977 Greenblatt DJ. Dev Psychol 35:466–477. in Handbook of Aging and Cognition. 2003 La Rue A: Aging and Neuropsychological Assessment. J Exp Med 190:153– 156. Psychol Aging 18:510–523. Mahwah. Clin Pharmacol Ther 21:355–361. et al: Diazepam disposition determinants. Albert M: Keep Your Brain Young. de Lima MP. aging. Lawrence Erlbaum. Carstensen LL: Emotion and cognition. Clin Pharmacol Ther 27:301–312. Wiley. Int Psychogeriatr 6:95–104. New York. 2003 Gutmann D: Reclaimed Powers: Toward a New Psychology of Men and Women in Later Life. Ryff CD. New York. Crook TH: Estimated prevalence of age-associated memory impairment derived from standardized tests of memory function. 2003 Malhotra AK. Exp Cell Res 37:614–636. Heckhausen J: Personality development across the adult life span: subjective conceptions vs cross-sectional contrasts. 1994 MacDonald SWS. Allen MD. Murphy GM Jr. et al: The role of self-enhancing evaluations in a successful life transition. Exp Cell Res 25:585–621. 2nd Edition. Charles ST. Love GD. Harmatz JS. 1987 Hayflick L: The limited in vitro lifetime of human diploid cell strains. Salthouse TA. New York. Psychol Aging 18:487–496. 2004 McCrae RR. Costa PT Jr. Taylor SE. Gerontologist 34:79–87. Seeman TE: Accounting for changes in social support among married older adults: insights from the MacArthur studies of successful aging. 1994 Krueger J. Psychol Aging 18:3–12. pp 593–631 Johnson CL.

J Gerontol B Psychol Sci Soc Sci 50:S59–S61. et al: Mild cognitive impairment represents early stage Alzheimer disease. Edited by Craik FIM. Salthouse TA. Gabrieli JDE. New York. Dana Alliance for Brain Initiatives. pp 1–90 Reddel RR: A reassessment of the telomere hypothesis of senescence. in Cognitive Aging: A Primer. 2005 Prull MW. in Handbook of Aging and Cognition. Mahwah. 2nd Edition.64 Clinical Manual of Geriatric Psychiatry Midanik LT. Soghikian K. DelVecchio WP: The rank-order consistency of personality traits from childhood to old age: a review of longitudinal studies. N Engl J Med 352:2379–2388. Morris JC: Mild cognitive impairment as a clinical entity and treatment target. Edited by Craik FIM. 2004 Park DC: The basic mechanisms accounting for age-related decline in cognitive function. Arch Neurol 58:397–405. Salthouse TA. Edited by Park DC. Bioessays 20:977– 984. Grundman M. in Handbook of Aging and Cognition. NJ.org_/articles/NRTA/LearningThroughoutLife. J Gerontol B Psychol Sci Soc Sci 58:P246–P249. Thomas RG. Psychol Bull 126:3–25. Philadelphia. Andres R. Tobin JD. 1976 . Storandt M. et al: The effect of age on creatinine clearance in men: a cross-sectional and longitudinal study. et al: Vitamin E and donepezil for the treatment of mild cognitive impairment. Bunge SA: Age-related changes in memory: a cognitive neuroscience perspective. 1995 Morris JC. 2006. 1998 Roberts BW. Psychol Aging 18:896–905. 2001 National Retired Teachers Association. Ransom LJ.aarp. Neugarten BL: Dynamics of transition of middle age to old age: adaptation and the life cycle. Tanaka Y: Subjective usefulness and 6-year mortality risks among elderly persons in Japan. Accessed February 23. 2004. Lawrence Erlbaum.aarp. Arch Neurol 62:1160–1163. American Association for Retired Persons: Staying Sharp: Learning Throughout Life. 2000 Rothermund K. Brandtstadter J: Coping with deficits and losses in later life: from compensatory action to accommodation. NJ. 1999.pdf. 2003 Rowe JW. 2005 Petersen RC. et al: The effect of retirement on mental health and health behaviors: the Kaiser Permanente Retirement Study. PA. 1970 Okamato K. Available at: http://assets. 2000. Dana Alliance for Brain Initiatives. J Gerontol 31:155–163. Miller JP. 2nd Edition. pp 3–22 Petersen RC. Lawrence Erlbaum. Psychology Press. J Geriatr Psychiatry 4:71–100.org/ www. Mahwah. Schwarz H. 2000. pp 91–153 Raz N: Aging of the brain and its impact on cognitive performance: integration of structural and functional findings.

pp 155–219 Schulman SP: Cardiovascular consequences of the aging process. towards a consensus: report of the International Working Group on Mild Cognitive Impairment. Edited by Craik FIM. 2000. Department of Health and Human Services. Palmer K. pp 633–688 Thompson WJL. Pichora-Fuller MK: Implications of perceptual deterioration for cognitive aging research. Sadock VA. Psychological Corporation. Psychol Rev 103:403–428. J Clin Exp Neuropsychol 25:625– 633. Palmer R. Stern Y: Cognitive reserve and lifestyle. Cardiol Clin 17:35– 49. Washington. J Am Geriatr Soc 53:11–17. in Handbook of Aging and Cognition. et al: Mild cognitive impairment—beyond controversies. 1995 Winblad R. viii. Edited by Sadock BJ. NJ. Goossens L: Improving memory performance in the aged through mnemonic training: a meta-analytic study [published erratum appears in Psychol Aging 8:338. New York. J Intern Med 256:240–246. 1987–1988 Uttl B. Lippincott Williams & Wilkins. 2003 Verhaeghen P. 1993]. Salthouse TA. Lawrence Erlbaum. 1997 Wilder D. Marcoen A. Am J Geriatr Psychiatry 3:96–107. 2003 Schaie KW: Developmental Influences on Adult Intelligence: the Seattle Longitudinal Study. 1999 Small GW: The Memory Prescription. 2004 . Chen J. Edited by Craik FIM. Psychol Aging 18:616–621. Chiodo LK. Van Alstine CL: Rising verbal intelligence scores: implications for research and clinical practice. Dumke HA: Age differences in everyday problem-solving and decision-making effectiveness: a meta-analytic review. personality. DC. 2005 U.Normal Aging 65 Royall DR. Mahwah. Hyperion. 1992 Victoroff J: Central nervous system changes in normal aging. 2005 Salthouse TA: The processing-speed theory of adult age differences in cognition. Psychol Aging 7:242–251. in Kaplan & Sadock’s Comprehensive Textbook of Psychiatry. Mahwah. Salthouse TA. 7th Edition. Pasupathi M: Life-span perspectives on self. and social cognition. 2nd Edition. New York. U. et al: Operating characteristics of brief screens for dementia in a multicultural population. in Handbook of Aging and Cognition. pp 3010–3021 Wechsler D: Wechsler Adult Intelligence Scale—III. Oxford University Press. 2005 Schneider BA. San Antonio. Psychol Aging 20:85–99. 2nd Edition. PA.S. Senate Special Committee on Aging: Aging America—Trends and Projections. NJ. et al: Executive control mediates memory’s association with change in instrumental activities of daily living: the Freedom House Study. 2004 Staudinger UM. 2000. 1996 Scarmeas N. TX.S. Philadelphia. Lawrence Erlbaum. Kivipelto M. 2000. Cross P.

This page intentionally left blank .

geriatric depression has been identified as a major public health problem. poor appetite. p.3 Mood Disorders—Diagnosis Depression is the most common mood disorder in later life. mortality from comorbid medical conditions or suicide. and medical condition. demands on caregivers. It can have serious consequences. it is likely that a substantial minority were less than optimally compliant with treatment (Katon et al. Because of the seriousness of these consequences. social circumstances (including recent losses). functional decline. 664). Several factors contribute to this suboptimal response by the medical profession. diminished quality of life.7% of elderly patients with major depression were taking an antidepressant. Even when it is recognized. including “disability. and increased service utilization” (Charney et al. 1999). 2003. 3) the reluctance of many older patients to acknowledge “mental” problems. 67 . depression in the elderly tends to be undertreated: Steffens and colleagues (2000) found that only 35. and disturbed sleep) to concomitant medical problems. the belief that symptoms of depression are “normal” or “expectable” given the patient’s age. yet it is undiagnosed in about 50% of cases (Mulsant and Ganguli 1999). including 1) the “normative fallacy”—that is. 2) the tendency of clinicians to attribute neurovegetative symptoms and signs (such as loss of energy. of these.

The chapter sections comprise a differential diagnosis of depressive features. anhedonia. Appetite and sleep disturbance. and finally attending to the proposed primary syndromes of minor depression and depressive personality disorder.” sadness. multiple somatic complaints. and occur as features of diagnostic entities that remain under study.68 Clinical Manual of Geriatric Psychiatry which. especially when exacerbated by memory impairment. “Normal” Grief (Bereavement) Studies generally concur that uncomplicated grief or bereavement may include any or all of the features of major depression except suicidality. Clinically significant depression takes many forms in the elderly. then discussing the primary syndromes of major depression (including some common variations in clinical presentation) and dysthymia. such as minor depressive disorder and depressive personality disorder. mild feelings of self-deprecation. discuss suicidality in the elderly. It assumes that the clinician has identified clinically significant symptoms and signs of depression and is attempting to make a definitive diagnosis. anxiety. and psychomotor retardation. . the passive wish to “join the loved one. The first part of this chapter is organized accordingly. Subsequent sections tackle laboratory and psychological tests and depression rating scales useful in the diagnostic process. Depressive signs and symptoms are commonly seen in normal and complicated grief. and sometimes risky diagnostic searches for nonexistent physical conditions. and provide a brief review of theories of the pathogenesis of depression. may force the clinician into an uncomfortable reliance on third parties for historical information. present as welldefined “primary” syndromes (including major depression and dysthymia). beginning with “normal” grief and complicated grief. are associated with several medical illnesses and medications. severe loss of self-esteem and/or functionality. and 4) the complementary tendency of many older patients to express psychic distress in physical terms (Gallo and Rabins 1999). and the well-defined diagnostic categories recognized in DSM-IV-TR (American Psychiatric Association 2000) may not cover every clinical presentation. expensive. next focusing on substance-induced depression. leading to unnecessary. then addressing depression secondary to a general medical condition. psychosis. both listed in Appendix B (“Criteria Sets and Axes Provided for Further Study”) of DSM-IV-TR.

numbness.Mood Disorders—Diagnosis 69 and other dysphoric moods are common but generally less severe than in major depression. the best predictor was depression itself: 75% of those depressed at 13 months were depressed at 1 month (Bornstein et al. 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. 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. (1974) and Parkes (1965. 2. sleep disturbance. A study of 217 caregivers of family members with dementia (Schulz et al. 3. baseline status by the end of the first year. fantasy. who tend to think more of the lost object (Gallagher et al. The first year after the death of a loved one: This is a period of adjustment. 1972) discerned the following approximate stages of normal bereavement: 1. they do suggest that the time course of normal grief in the individual patient is fairly variable and that most patients should be at. Clayton et al. but only 17% remained depressed after 13 months. 1982). 1973. and somatic complaints. Although the studies cited earlier did not address the specific circumstances surrounding the onset and course of bereavement. and emptiness are often accompanied by intense anxiety. In a sample of 133 widows and widowers (average age=70. But specific circumstances also appear to be important. shock. are more likely to feel guilt and reduced selfesteem than are nondepressed mourners. The first few weeks after the death of a loved one: During this initial period. consequently. 2003) found that 72% of the caregivers reported feeling relief after the death of their loved one. In this study. but 14% had symptoms that met criteria at 25 months. the authors also observed “clinically significant” depressive symptoms in the 86% whose conditions did not meet formal diagnostic criteria (Zisook et al. Moreover. Glick et al. or clearly moving toward.6 years). Depressed patients are more prone to focus on themselves and their role in the loss and. during which cognitive and affective “working through” occurs via a process of recollection. Their scores on the Center for Epidemiologic Stud- . disbelief. In another series of studies. This phase is completed when acceptance occurs. during which “redefinition” of self without the lost loved one occurs. After the first year postloss: A recovery phase ensues. and rationalization. 1994). 1972).

. 1370) Depression Due to a General Medical Condition DSM-IV-TR specifies that mood disorder due to a general medical condition must be judged to be the “direct physiological consequence of a general medical condition. Proposed diagnostic criteria for this syndrome are shown in Table 3–1. has been differentiated from both normal grief (bereavement) and clinical depression or anxiety. These findings revealed a need to identify and treat complicated grief as a psychiatric disorder distinct from major depressive disorder (MDD). cancer. is recorded separately on Axis I. if any.70 Clinical Manual of Geriatric Psychiatry ies Depression Scale increased about 50% over prebereavement scores immediately after the death but returned to prebereavement levels within 15 weeks.g. the general medical condition may be regarded as a “risk factor.” but in the former.. Complicated Grief A syndrome of complicated grief. which occurs in 10%–20% of bereaved individuals. cardiac events. and tobacco intake. In the latter situation. are not effectively reduced by interpersonal psychotherapy and/or tricyclic antidepressants. ulcerative colitis. (Prigerson and Jacobs 2001. however. but is judged not to be a direct physiological consequence of it. suicidality. p. within 1 year. Complicated grief symptoms are clearly distinct from normal bereavement–related depressive and anxiety symptoms and may endure for several years in some cases. it is considered a “causal factor”. high blood pressure. in this section. scores were below the levels reported when these persons had been active caregivers. regardless of the direction. and the general medical condition is recorded on Axis III. anergia. clear guidelines for making the distinction are lacking. of causality. These symptoms predict substantial morbidity and adverse health behaviors over and above depressive symptoms (e.” whereas depression that co-occurs with a general medical condition. Accordingly. we ignore the distinction and consider the conditions most closely associated with depression. changes in food. and global dysfunction) and. unlike depressive symptoms. alcohol. social dysfunction.

experienced at least daily or to a marked degree: 1. American Medical Association.Mood Disorders—Diagnosis 71 Table 3–1. occupational. 8. trust. Source. detachment. Intrusive thoughts about the deceased Yearning for the deceased Searching for the deceased Excessive loneliness since the death Criterion B In response to the death. Criterion D The disturbance causes clinically significant impairment in social. disbelief ) Feeling that life is empty or meaningless Feeling that part of oneself has died Shattered worldview (e.825 subjects ages 54–65 in a national probability sample and found a strong association between chronic . Chronic Illness Major depression is a common accompaniment of many chronic medical illnesses. or other important areas of functioning. 3. Dunlop and colleagues (2004) studied 7. or absence of emotional responsiveness Difficulty acknowledging the death (e. or related to. bitterness. 2. the deceased person Excessive irritability. or anger related to the death Criterion C Disturbance must endure for at least 6 months. and response involves 3 of the 4 following symptoms. Jacobs SC: “Caring for Bereaved Patients: ‘All the doctors just suddenly go. 4. at least 4 of the following 8 symptoms are experienced at least daily or to a marked degree: 1. Prigerson HG. 3.’” Journal of the American Medical Association 286:1369–1376. 6. control) Assumes symptoms. lost sense of security.. 7.. 2. Copyright © 2001. 2001. or harmful behaviors of. Purposelessness or feelings of futility about the future Subjective sense of numbness. All rights reserved. Proposed criteria for complicated grief Criterion A Person has experienced the death of a significant other. 5.g.g. 4.

(2004) examined 155 patients of average age (64 [±12]) who had a mean left ventricular ejection fraction of 24. Of the conditions studied. diabetes. cancer. Bisschop et al. but the two studies disagreed on the role of functional disability. heart disease and arthritis were most often associated with major depression. the depressed patients were slightly .6% of the subjects without chronic illness had major depression. 46% had ischemic heart disease. Gottlieb et al. lung disease. This protective effect is robust enough that some authors have proposed that selective serotonin reuptake inhibitors be prescribed for all patients with ischemic heart disease (Jiang and Krishnan 2004). 1995).5% of the subjects with chronic illness had major depression. patients with ischemic heart disease who are taking serotonin reuptake inhibitors (but not other classes of antidepressants) have a reduced risk of myocardial infarction (Sauer et al. 48% met study criteria for depression (Beck Depression Inventory [BDI.and 18-month mortality (Frasure-Smith et al. which tends to be abnormally increased in patients with ischemic heart disease or depression and even higher in patients with both diseases.288). Congestive heart failure is also associated with a high prevalence of depression. Beck et al. (2004) also found heart disease and arthritis to be most frequently associated with major depression.72 Clinical Manual of Geriatric Psychiatry illness and depression: only 3. Interestingly. which included arthritis. 2001). Depression is a risk factor for myocardial infarction (Ariyo et al. whereas the latter 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. and major depression occurring in the weeks after a myocardial infarction significantly increases 6.9%–18. 2000). hypertension. Moreover. In the former study. stroke. but 9. 1961] score of 10 or higher). The mechanism of this protective effect has been hypothesized to be related to the inhibiting effects of selective serotonin reuptake inhibitors on platelet aggregation. Of these patients. and the combination of heart disease and arthritis had the strongest association of any combination of two conditions. and obesity. and 38% were diabetic. In the Longitudinal Aging Study Amsterdam (N= 2. the risk of major depression in both conditions (as well as in all the other conditions studied) was strongly mediated by functional disability. heart disease.

Poststroke depression is mediated by functional impairment (Bisschop et al. The authors concluded that “pharmacologic or non-pharmacologic treatment of depression could conceivably reduce morbidity and. but the presence of depressive symptoms was associated. Despite the well-documented clear association between stroke and depression. Alzheimer’s Disease and Vascular Dementia Although depressive symptoms are commonly seen in patients at various stages of Alzheimer’s disease. with women about twice as likely to be affected as men (Paradiso and Robinson 1998). perhaps. Interestingly. The effect of poststroke depression on long-term prognosis is also negative. Of stroke patients have poststroke depression.000 stroke patients and found that those who received a diagnosis of depression 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. this study found a comparable risk of death if mental conditions other than depression. 1548) from congestive heart failure.S. anxiety disorders.Mood Disorders—Diagnosis 73 younger than the nondepressed patients (average age= 62 vs. 65). major depression per se is relatively uncommon. Ballard et al. and patients with major depression following dominant-hemisphere stroke have more severe cognitive impairment (Robinson et al. 1986) than is seen in stroke without depression. including substance abuse. 1). (2004) analyzed a Veterans Affairs database of more than 50. about half have a major depression–like syndrome that is clinically indistinguishable from primary major depression. 2004). House and colleagues (2001) found that major depression within 1 month poststroke was not statistically associated with mortality at 12 and 24 months poststroke. schizophrenia. and personality disorder. were diagnosed within 3 years of the stroke. mortality” (p. 2004) found “no evidence to support the routine use of pharmacotherapeutic or psychotherapeutic treatment for depression after stroke” (p. Williams et al. and the other half meet criteria for dysthymia (if the duration requirement is waived). (2000) found a 1-month prevalence of 8% (on the basis of . Stroke Between 20% and 50% of stroke patients have poststroke depression. L. a systematic literature review (Hackett et al. even after adjusting for other confounding variables such as age and cognitive impairment.

“Vascular Depression” Alexopoulos and colleagues (1997) have argued for the recognition of a distinct category of depression due to a general medical condition called vascular depression. the high rate of depression in patients who have had a stroke. compared with 19% in patients with vascular dementia. (2004) also published supportive data. they have cited the high rate of depression in patients with hypertension. (1997) compared 33 elderly patients with late-onset vascular depression with a control group of elderly depressed patients without features of vascular disease. diabetes. and less likely to have experienced a major stroke event than were those without major depression. depression was more frequent in patients with Mini-Mental State Examination (MMSE) scores lower than 20. The authors found that those patients with vascular depression were more cognitively . compared with 32% of the participants with vascular dementia. and the infrequent family history of mood disorders in depression occurring in the context of silent stroke. more likely to have a history of depression. 2004). 562) The validity of this syndrome remains controversial. Mast et al. Lyketsos and colleagues (2000) reported a similar prevalence when the Neuropsychiatric Inventory was used.74 Clinical Manual of Geriatric Psychiatry DSM-III-R criteria). the frequent occurrence of silent stroke and white matter hyperintensities in lateonset depression. When data for the two groups were combined. whereas in vascular dementia. depression was equally common at all severities. In the Alzheimer’s disease group. who found that elderly subjects with severe white matter lesions (as detected by magnetic resonance imaging of the brain) were three to five times more likely to have depressive symptoms than were those with only mild or no white matter lesions. Vascular dementia patients with major depression in the month prior to assessment were significantly older. They found depression in 20% of the subjects with a diagnosis of Alzheimer’s disease. Alexopoulos et al. the prevalence of depression was not related to stage of progression of dementia. (p. Validity was supported by de Groot and colleagues (2000). They found that geriatric rehabilitation patients with two or three cardiovascular risk factors had greater depressive symptoms at 6and 18-month follow-up assessments than did patients with only one or no cardiovascular risk factors (Mast et al. and coronary disease.

and higher diastolic blood pressure” (p. depression (diagnosed 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. Depression was found to be independently associated with smoking. female gender. and had less depressed mood than those with nonvascular depression. and depression in a community-based Caribbean-born population ages 55–75 years living in the United Kingdom. and they suggested that further research may define a distinctive pharmacological approach to the prevention and treatment of this syndrome. and other vascular disease risk factors.Mood Disorders—Diagnosis 75 impaired and more disabled. encoding for apolipoprotein E. 202). They found a significant increase 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. encoding for the very low-density lipoprotein cholesterol receptor. VLDLR. (2001). This pathogenetic hypothesis was only partially supported by Thomas et al. had more psychomotor retardation and less insight. vascular risk factors. determined late-life depression. who studied postmortem tissue from 20 elderly patients with a history of depression and 20 with no such history. Stewart and colleagues (2001) examined the association between stroke. In the 287 subjects who were studied. The . Other studies have cast doubt on the strength of association between vascular disease and late-onset depression. These authors found “no association between late-life depression and three polymorphisms related to vascular disease. These findings did not change when the small number of subjects who reported onset of depressive 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. They hypothesized that disruption by vascular lesions of striato-pallidothalamo-cortical pathways may constitute the pathogenesis of depression in such patients. encoding for angiotensin-converting enzyme) that are related to vascular disease. and DCP1. poorer cognitive functioning. Kim and colleagues (2004) found a similar association between depression (diagnosed with a community version of the Geriatric Mental State Schedule) and previous stroke but not other vascular risk factors (except an atherogenic lipid profile) in 732 Korean subjects whose average age was 72.8.

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. 2000). Substance Intoxication or Withdrawal” or that “medication use is etiologically related to the disturbance [in mood]. or almost all. “vascular depression” remains a hypothetical entity at present. or irritable mood” along with “evidence from the history. 409) as “a prominent and persistent disturbance in mood” that is characterized by “depressed mood or markedly diminished interest or pleasure in all. 202). in a similar 50:50 ratio of major depression to dysthymia (Nuti et al. expansive. Diagnostic criteria further require that the depression not be better accounted for by a non-substance-induced mood disorder and that “the symptoms cause clinically significant distress or impairment in social. As in stroke. Finally.” . p. 2004). In light of these conflicting data.” Substance-induced mood disorder may not be diagnosed if depressive symptoms occur exclusively during the course of a delirium. about 40%) has been observed in patients with Parkinson’s disease. occupational. and so is an important focus of diagnostic and therapeutic attention for geriatric psychiatrists (Tröster et al. but they did not limit their sample to subjects with late-onset depression. or laboratory findings” that the symptoms “developed during. or within a month of. physical examination. Substance-Induced Mood Disorder Substance-induced mood disorder is defined in DSM-IV-TR (American Psychiatric Association 2000. Parkinson’s Disease A similar prevalence of depression (i. depression in Parkinson’s disease patients increases the risk for and severity of dementia and exacerbates disability.e.. activities” and/or “elevated. or other important areas of functioning. Treatment generally follows guidelines for primary mood disorder as detailed in Chapter 4 (“Mood Disorders— Treatment”). 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).

The first comprises substances with primarily psychoactive properties that are prone to abuse and can become addictive. Bakken and colleagues (2003) found that 48% of 241 substance abusers (age unspecified) studied at some time in their lives had experienced a substance-induced major depression. “Ecstasy”). Comparable estimates for nonpsychoactive substances have not been published. With regard to psychoactive substance–induced depression. both feelings she had never experienced before. barbiturates. Ko and colleagues (2002) conducted a meta-analysis of 42 selected articles and found no association between β-blocker therapy and . phencyclidine (PCP). A depressive syndrome that begins within a month of commencing regular ingestion of any of the medications listed in Table 3–2 is adequate presumptive evidence to justify dosage adjustment or discontinuation. including amphetamines. opiates and related compounds such as ketamine. The second category comprises substances whose psychoactive properties are incidental to their main therapeutic effects. along with detailed assessment of mood symptoms. hallucinogens such as lysergic acid diethylamide (LSD) and mescaline. cocaine and related compounds such as methylenedioxymethamphetamine (MDMA.Mood Disorders—Diagnosis 77 Two broad categories of substances can be distinguished in this context.” Careful questioning determined that the β-blocker nadolol had been prescribed for a minor cardiac dysrhythmia about 3 weeks before the onset of symptoms. when medically feasible. inhalants. This category includes alcohol. All symptoms disappeared with no specific treatment within 1 week of discontinuing the medication. of the suspected agent. This category includes numerous medications used for acute and chronic nonpsychiatric conditions. stimulants. A 75-year-old woman with no history of mood disorder denied symptoms of depression but admitted to experiencing “waves of doom” coming over her and fearfully described “crazy” thoughts of suicide. and 41% had experienced at least one episode of dysthymia. The critical diagnostic procedure is a careful drug ingestion history. benzodiazepines and other central nervous system depressants. and miscellaneous substances such as γ-hydroxybutyrate (GHB). She had lost almost 20 pounds in the preceding 4– 6 weeks and came to psychiatric attention when her dermatologist found her “weeping in his waiting room. marijuana and hashish. the great majority of subjects had also had non-substance-induced mental disorders. Interestingly. but case histories have implicated all of the substances listed in Table 3–2.

nimodipine.g. including Alcohol Benzodiazepines Cancer chemotherapeutic agents L-Asparaginase Dactinomycin Cisplatin Cycloserine Mitotane Dacarbazine ..g. Medications that can cause symptoms of depression Analgesics Narcotics. chlorpromazine. thioridazine. verapamil) Clonidine Guanethidine Methyldopa Propranolol and related β-blockersa Reserpine Thiazide diuretics Antipsychotic agents. fluphenazine. flunarizine. nifedipine. diltiazem.. including synthetics Codeine Meperidine Nonsteroidal anti-inflammatory agents (ibuprofen. naproxen) Antiepileptic agents Antihypertensive agents Acetazolamide Calcium channel blockers (e.78 Clinical Manual of Geriatric Psychiatry Table 3–2. including Phenothiazines (e. thiothixene) Haloperidol Molindone Anxiolytic agents. indomethacin. nicardipine.

including Barbiturates Ethchlorvynol Glutethimide Methyprylon Miscellaneous Asparaginase Baclofen Cimetidine Dexamethasone Digoxin Disulfiram Isotretinoin Levodopa Levonorgestrel implant Mefloquine Methysergide Metoclopramide Metronidazole Oral contraceptives Prednisone Ranitidine hydrochloride Steroids aRelatively common offenders in the authors’ experience. . Medications that can cause symptoms of depression (continued) Cancer chemotherapeutic agents (continued) Nitrogen mustard Procarbazine Tamoxifen Vinblastine Vincristine Sedative-hypnotics.Mood Disorders—Diagnosis 79 Table 3–2.

respondent-initiated separation. 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. 2000). as defined in DSM-IV-TR. humiliation. a few specific illnesses. (2003) studied 98. only loss and humiliation events were statistically significantly associated with onset of major depression in the month of occurrence. and exposure to certain substances are clear risk factors for the onset of major depression in the elderly. although none has focused on elderly patients per se. 1999). Major Depression Epidemiology Major depression. However. Kendler et al. less so of other-initiated separation.592 person-months in 7. chronic illness in general.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. and the prevalence appears to increase with age. whereas humiliation included only other-initiated separation. 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. Risk Factors As discussed in earlier sections. entrapment. Loss included death. loss events likely play an increasingly significant role in the provocation of major depression in the elderly.80 Clinical Manual of Geriatric Psychiatry depressive symptoms. and in almost every study the method of assessing depressive symptoms was not specified.7% (Steffens et al. As the preceding case illustrates. The role of stressful life events as precipitants of major depression has been studied by several groups. and danger). 1982) and in about 15% of nursing home residents (Falck et al. one study of subjects (average age=85) found a community prevalence of 4% (Forsell and Winblad 1999).6%. and other key losses. Because old age is a time of loss. merely asking elderly patients about “depression” may elicit misleading responses. the studies analyzed had few elderly subjects. . Of the stressful life events studied (which were categorized as loss.

outpatient. For example.e.. middle and late insomnia. 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 affects young adults. (1997) reported that diminished self-esteem and guilt were less common in older depressed patients (i. Table 3–4 lists the most troublesome of these normal aging changes. focusing on relatively abrupt changes in one or more neurovegetative functions. guilt. loss of interest in work and activities. . Finally.Mood Disorders—Diagnosis 81 Diagnostic Criteria The diagnosis of major depression in an elderly person begins with a detailed history of the present illness. lack of energy. and higher rates of psychotic and melancholic depression. 60 or older). (1994) reviewed the literature and concluded that “medical illness emerges consistently as the most common clinical feature associated with depressive symptoms and diagnoses in community. Informants such as a spouse or a child. 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. 38). 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. recognition and diagnosis of major depression may be complicated by variable presentation of illness. somatic anxiety. but these patients had more severe depression (higher Hamilton Rating Scale for Depression [HamD] scores). accurate detection of major depression in old age can be challenging because several features of normal aging overlap with complaints of depression. or the family physician can be invaluable in establishing the timing of these changes (Wiener et al. a board and care home operator. as discussed in the following subsection. 1997). Still. Caine et al. Brodaty et al. and inpatient samples” (p. more appetite loss and weight loss. Nelson et al. Similarly. psychic anxiety. Signs and symptoms associated with normal and complicated bereavement can also complicate diagnosis. 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. (2005) analyzed data from 728 elderly subjects with nonpsychotic major depression and found that depressed mood.

Washington. D. at least one is either (1) depressed mood or (2) loss of interest or pleasure. after the loss of a loved one. 356. E. Used with permission. DC. (1) depressed mood most of the day. The symptoms cause clinically significant distress or impairment in social. activities most of the day. or indecisiveness. The symptoms are not better accounted for by bereavement. Source. the symptoms persist for longer than 2 months or are characterized by marked functional impairment. psychotic symptoms.82 Clinical Manual of Geriatric Psychiatry Table 3–3. The symptoms are not due to the direct physiological effects of a substance or a general medical condition. 2000.e. nearly every day (3) significant weight loss when not dieting or weight gain. or other important areas of functioning. morbid preoccupation with worthlessness. not merely subjective feelings of restlessness or being slowed down) (6) fatigue or loss of energy nearly every day (7) feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day (not merely self-reproach or guilt about being sick) (8) diminished ability to think or concentrate. i. Text Revision. American Psychiatric Association. . American Psychiatric Association. Copyright © 2000. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. recurrent suicidal ideation without a specific plan. p. or almost all. C. The symptoms do not meet criteria for a mixed episode.. Five (or more) of the following symptoms have been present during the same 2-week period and represent a change from previous functioning. nearly every day (2) markedly diminished interest or pleasure in all. or decrease or increase in appetite nearly every day (4) insomnia or hypersomnia nearly every day (5) psychomotor agitation or retardation nearly every day (observable by others. Summary of DSM-IV-TR criteria for major depressive episode A. or a suicide attempt or a specific plan for committing suicide B. occupational. nearly every day (9) recurrent thoughts of death (not just fear of dying). suicidal ideation. or psychomotor retardation. 4th Edition.

especially obstructive lung disease and heart failure Also exacerbated by β-blockers. Psychotic Depression Psychotic features (delusions or hallucinations or both) occur in about 25% of elderly patients with major depression. especially diminished vision and hearing Exacerbated by medications with central anticholinergic effects Reduced appetite Reduced energy. fatigue Impaired concentration and memory Variations in Clinical Presentation Late Versus Early Onset Devanand et al. poor dentition. and in one large epidemiological survey .from the late-onset cases. they found that late-onset major depressive disorder was less severe (based on the 24-item Ham-D scores) and less frequently associated with melancholia (31% vs.Mood Disorders—Diagnosis 83 Table 3–4. clonidine. α-methyldopa. or unappealing diet Exacerbated by chronic illness. (2004) studied 211 patients (average age=70) who had received diagnoses of major depression. anticonvulsants. and benzodiazepines Normal forgetfulness may be experienced as a symptom Exacerbated by sensory losses. When they used a cutoff of first episode of major depressive disorder after age 60. 50%) than was early-onset major depressive disorder and that fewer than half as many late-onset patients as early-onset patients reported a family history of mood disorder. burden of medical illness (according to the Cumulative Illness Rating Scale). Age. Functional complaints common to elderly persons Complaint Sleep disturbance Comment Reduced total sleep time Increased sleep latency More frequent awakenings More time spent in bed Reduced sleep efficiency Reduced energy expenditure Reduced activity Exacerbated by diminished taste and olfactory sensation. and presence of cardiovascular illness did not differentiate the early.

The following cases are illustrative: A 76-year-old woman changed apartments because she believed that her neighbors were aware of her responsibility for the president’s “losing his veto power. Although neuroleptics partially controlled her fear and her bizarre behavior. her symptoms were not completely ameliorated until antidepressant treatment was initiated. lacking proper parts.84 Clinical Manual of Geriatric Psychiatry (N=18. delusions. that is. Identification of psychotic depression as a mood disorder is relatively straightforward when symptoms occur in the classic sequence. at which time her mood also greatly improved.” which was going to lead to a “communist takeover. A 72-year-old woman was an ongoing problem for neighbors and police because 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. Accurate diagnosis is also impeded when patients cannot or will not report 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. subjects who reported feelings of worthlessness or guilt were the most likely to have psychotic features (Ohayon and Schatzberg 2002). moodcongruent delusions) are present or when the patient has a history of mood disorder. More challenging are patients in whom the presenting complaint.. By the time she was hospitalized. she attributed her failure to grasp its meaning as being directly responsible for the president’s downfall. is of a persecutory delusion accompanied by prominent behavior disturbance. and bizarre behavior. when mood and neurovegetative changes occur before the development of hallucinations. and anhedonia that accompanied and. preceded the onset of her delusion.” The delusion had emerged in the course of a series of unsatisfactory transactions with an air conditioner repairman who had told the patient that. loss of appetite and weight. 2002). her thinking was extremely disorganized. The clinician’s task is rendered easier still when typical depressive delusions (i. often registered by family members. and the term jerry-rigged had acquired magical significance. he would attempt to jerry-rig something for her. Near-catatonic behavioral withdrawal is one such particu- .e.980). but suicide attempts are probably not more frequent (Lykouras et al. Most studies find that depressive symptoms are more severe in patients with psychotic features than in those without psychosis. to some extent. She responded very well to treatment for depression. Several days of treatment with high-potency neuroleptics were required before the patient was able to give the history of change in mood.

. or the occurrence of physical symptoms that are illogical or that are temporally linked to social stressors (e.. A relatively sharp increase in the number and severity of physical complaints at or around the time of onset of neurovegetative signs. In the course of medical diagnosis and treatment. and it is likely that this proportion is higher in elderly patients. A perhaps more common version of this syndrome presents with a similar acute exacerbation of physical complaints accompanied by significant psychological distress (e. the depressive syndrome is only partially masked by the patient’s insistence that the psychological distress is “because of ” the physical complaints (Simon and VonKorff 1991). In the absence of a history of psychosis. One study (Posse and Hallstrom 1998) found that major depression presented as somatic complaints in 13 (14%) of 93 mixed-age primary care patients. can alert the clinician to the possibility of “underlying” major depression. these complaints are found to be either unaccompanied by anatomical or physiological abnormalities or out of proportion to the severity of these abnormalities. Identification of this syndrome is particularly difficult when it occurs in patients with somatic complaints that are associated with clear physical causes. abdomen. complaints of depression and anxiety). to maintain personal grooming.g. In this presentation. arms. losses) typically associated with mood changes. The prevalence of this syndrome in the elderly is not known.g. She insisted that the symptoms reflected a “heart . Masked Depression The literature has long reflected awareness by clinicians that depression in the elderly can be masked by physical complaints (Kielholz 1973). but the clinician must be particularly sensitive to objective indicators of depressed mood and must investigate carefully to discern associated neurovegetative features of major depression. and hands. subjective complaints of mood changes per se are replaced or masked by multiple somatic complaints. or to take medications. In the classic version of this presentation.Mood Disorders—Diagnosis 85 larly common type of bizarre behavior and is often accompanied by refusal to eat. A 90-year-old woman complained of her “arms and legs twisting. DSM-IV-TR criteria are usually adequate to diagnose such presentations. late-life presentation of this syndrome should be regarded as psychotic depression until proven otherwise.” along with a feeling of “buzzing” from the top of her head radiating into her chest.

modifying criterion A as follows: . they may be simultaneously disabled by but relatively indifferent to their symptoms. He cites the expansion of that diagnosis onto a vast number of disorders. along with appropriate levels of psychic distress. She eventually gained a modest degree of insight into the functional nature of her complaints. conversion disorder. neurasthenia or hypochondriasis” (p. Unfortunately. 2) the history. which is typically as high as 20 or more in somatization disorder. Careful interviewing found that the onset of these symptoms was associated with marital conflict. which are typically not present in somatization disorder. Over the long run. Indeed. available data do not support precise criteria for establishing the diagnosis of masked depression. The variant of major depression depicted in this case differs from somatization disorder with depressed mood in 1) the number of physical symptoms. the positive proof of psychic symptoms as an exclusion criterion for that diagnosis)…and the introduction of DSM-III and ICD-10 as operationalized. and exacerbation tended to occur when marital tensions escalated. the continuing lack of clarity of the concept (disorder of recognition vs. We believe that a reasonable diagnostic approach is to use DSM-IV-TR criteria (American Psychiatric Association 2000) for major depressive episode. At one extreme. 207). disorder of communication. Elderly patients with masked depression may vary considerably in their hypochondriacal preoccupation with physical symptoms. she responded well to psychotherapy but refused antidepressants. which is typically much more chronic and unremitting in somatization disorder. 207) as reasons for its disappearance. psychosomatic disorder. they may have a near-delusional conviction that symptoms reflect life-threatening illness. the positive proof of psychic symptoms as a prerequisite vs. and may make a lifestyle of doctor and diagnostic procedure shopping. Bschor (2002) has argued that the concept of masked depression has been “abandoned” and replaced with “somatization disorder. whereas at the other extreme. Unfortunately. purely descriptive and rather theory-free systems of diagnostic classification (p. somatoform disorder. some patients still present with multiple somatic complaints that do not meet criteria for any of the disorders listed by Bschor and that dramatically melt away with appropriate antidepressant treatment. and 3) the presence of neurovegetative features of depression.86 Clinical Manual of Geriatric Psychiatry attack” and made frequent unproductive visits to her local emergency department.

at least one of the symptoms is either (1) depressed mood. suggesting functionally significant cognitive impairment. and poor eye contact and may appear to exaggerate or dramatize their cognitive deficits on mental status examination. One study of hospitalized depressed elderly patients (La Rue et al. (italicized text added by authors) Depression With Cognitive Impairment A substantial proportion of elderly individuals with depression have concurrent cognitive impairment. clinically silent cognitive impairment associated with depression that may be detected by neuropsychological testing. climbing into other patients’ beds. or picking at their clothing. executive deficits in particular may be strongly associated with late-onset depression and vegetative symptoms (Butters et al. or (3) persistent physical symptoms that do not meet DSM-IV-TR criteria for any somatoform or other disorder. Minor functional deficits. such as forgetting staff names or repetitive asking of questions. 15– 22 on the MMSE) and may perform poorly on more detailed intellectual and memory testing. is distinguished from the milder. Patients with DSD may show poor grooming. slumped posture. When severely disturbed behavior of this type is seen in a patient who otherwise meets criteria for a mood . However. sometimes known as depressive pseudodementia or the dementia syndrome of depression (DSD). they typically do not have grossly disordered behavior.Mood Disorders—Diagnosis 87 Five (or more) of the following symptoms have been present during the same 2-week period and represent a change from previous functioning. cannot be explained by structural or functional pathology. Patients with DSD often score in the moderately impaired range on cognitive mental status examinations (e. such as attempting to eat pencils. (2) loss of interest or pleasure (p. or have a distinctly bizarre or unusual quality that is not consistent with any known medical diagnosis. 1986) found that 12 of 55 scored below 23 on the MMSE. Milder cognitive impairment is much more common and tends to be positively correlated with the severity of depressive symptoms. Depression with functionally significant cognitive impairment.g. 2000). Differentiating DSD from early dementia of the Alzheimer’s or vascular type can be quite difficult. and executive functioning. Moreover.. placing underwear over outerwear. also may be observed. particularly in visuospatial ability. 356). The prevalence of the former syndrome is not well established and depends on where one draws the line defining functional impairment. psychomotor speed.

88 Clinical Manual of Geriatric Psychiatry disorder. we found that elderly depressed patients with functionally significant cognitive impairment responded as well to antidepressant therapy as did those without cognitive impairment. but only in subjects with more than 8 years of education. was associated with relapse and recurrence of geriatric depression. Two studies conducted in the Netherlands found that depression in older patients that was not accompanied by significant cognitive impairment at baseline predicted cognitive decline (defined as a decline of 3 or more points on the MMSE) and the development of Alzheimer’s disease at follow-up an average of 3. 10-item . The authors interpreted the findings to support the notion that depression is “a subclinical expression or an early symptom of an underlying dementia process. but not memory impairment.2 years later. However. it may be necessary to observe response to treatment before forming a firm opinion about the presence of DSD. and several other studies have reported that depression per se is a risk factor for the development of dementia. (2002). (2000) found that executive dysfunction (including abnormal initiation and perseveration scores). However. One study found that a substantial proportion of patients with DSD progressed to a more profound dementia within a few years (Kral and Emery 1989). the presence of underlying organic brain disease or superimposed delirium must be ruled out. a lengthier and more aggressive course of treatment was required to achieve equivalent improvement (La Rue et al. 1986). and Alexopoulos et al. and the subsequent development of dementia and Alzheimer’s disease remains unclear. Kalayam and Alexopoulos (1999) found that psychomotor retardation and deficits in initiation-perseveration predicted poorer response to treatment in elderly depressed patients. they should be applied cautiously. Support for this hypothesis was provided by Wilson et al. Often. p. 2000. The relation between late-life depression. which may become apparent in a subgroup of more highly educated older people in whom commonly used mental status tests do not yet detect a decline from a previous level of cognitive functioning” (Geerlings et al. Table 3–5 lists features that can help differentiate DSD from organic dementia in troublesome cases. who studied Catholic clergymen over a 7-year period and found that scores on a modified. Because these guidelines have not been validated by prospective investigation. In our own work in this area. with or without DSD. Butters and colleagues (2004) failed to replicate the latter finding in a later study with a larger series of subjects. 574).

there may be false-positive errors Source.Mood Disorders—Diagnosis 89 Table 3–5. Kaszniak and Christenson 1994. Differences between depression with cognitive impairment and dementia Depression with cognitive impairment Dementia Clinical course and history Onset fairly well demarcated History short Course rapidly progressive History of psychiatric difficulty or recent life crisis Onset indistinct History quite long before consultation Early deficits often go unnoticed History of psychiatric problem or emotional crisis uncommon Clinical behavior Detailed complaints of cognitive loss Distress caused by cognitive problems Behavior does not reflect cognitive loss Persistent mood disorder Nocturnal exacerbation rare Mood-congruent delusions Few complaints of cognitive loss Varied reaction to cognitive loss Behavior compatible with cognitive loss Mood apathetic or environmentally responsive Nocturnal exacerbation common Mood-incongruent delusions Examination findings Patients expend little effort during examination Patients commonly struggle to perform cognitive tasks Patients frequently answer. . Adapted from Strub and Black 1988. “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 Inconsistent performance across similar types of tasks Prompting and semantic organization are helpful in improving recall Recognition memory is relatively intact Patients do not have specific memory gaps Consistently impaired performance on tasks of a particular ability Prompting and semantic organization have limited benefit Recognition memory is impaired.

and the rendering of treatment aimed at restoring appetite is regarded as an insult to the elderly patient. The patient gradually becomes less physically and socially active. a reasonable proportion of patients in this category respond to antidepressant treatment with restoration of normal appetite. neglects personal hygiene and necessary medical treatment. deteriorated. and discontinues shopping and begins living off canned or other- . Anorexia A less common presentation of depression in the elderly is profound anorexia. and the emergence of a new will to live. and annual decline on a global cognitive measure increased by an average of 24%. which may occur in the absence of any other neurovegetative features of depression and in the presence of what otherwise appear to be normal mood and affect. this clinical picture is interpreted by friends and family as an indication of the patient’s wish to die. allows the home environment to become disordered and filthy.” medical illnesses. weight gain. severely exacerbated by concomitant mood disorder. Behavioral Regression Major depression in the elderly occasionally presents with a picture of behavioral regression. This form of depression seems to occur mainly in the old-old and is often accompanied by multiple chronic. These and similar considerations notwithstanding. In some patients. particularly those from non-Western cultures.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. the quality of life required to warrant aggressive treatment. by refusing to eat. the risk of developing Alzheimer’s disease increased by an average of 19%. dysphoric patient who has “given up” and. appears to be committing passive suicide. loses contact with friends and family. The typical clinical picture is of a visibly aged. For each depressive symptom. Hospitalization of such patients may be complicated by passive refusal of treatment and family discord around the issue of the patient’s “right to quit”. who may be prone to engage in prolonged discussion of the appropriateness of hospitalization. and is classified here as a form of major depression mainly because of its severity. and so forth. It can be thought of as the “anorexia of aging” (Morley 2001). similar ambivalence is not uncommon among treatment staff. often “end-stage.

subjective change in mood and anhedonia may be denied. Kirby and colleagues (1999) studied 40 dysthymic individuals (average age= 74.5% felt that life was not worth living. and 7. appears to decline with age (Beekman et al.Mood Disorders—Diagnosis 91 wise easily obtained food. and mental status examination may indicate some of the features described in patients with DSD. On mental status examination. 2004). The average age of onset of dysthymic disorder in 68 subjects over age 55 was 31. poor concentration or difficulty making decisions. sleep disturbance. relative lack of social and emotional support.5% had suicidal ideation.. 2004). low self-esteem. like major depressive disorder. and feelings of hopelessness.. Overall.4) and found a relatively low rate (15%) of comorbid Axis I disorder (3 with generalized anxiety. female sex. Dysthymic disorder is similar to but less severe and more chronic than major depression and has a somewhat earlier onset in elderly individuals. 17. Dementia is commonly suspected in such individuals. .g. low energy or fatigue.g. history of traumatic events) and personal vulnerability factors (e.5% expressed a death wish. and objective signs of depression may be minimal. may occur as an isolated syndrome (“primary dysthymia”). It occurs in about 1. the prevalence of dysthymic disorder. with major depressive disorder superimposed on dysthymic disorder).. This figure increases to 80% if the presenting illness is “double depression.8% of elderly individuals during any given month.” The risk of developing dysthymic disorder appears to be related to environmental factors (e. Dysthymic Disorder Dysthymic disorder in adults as described in DSM-IV-TR is a chronic depression of mood (for at least 2 years) that is variably accompanied by associated symptoms of appetite disturbance. while the average age of onset of major depression in 61 subjects over age 55 was 53 (Beekman et al. 3 with agoraphobia without panic) and a high prevalence of hopelessness: 47. Dysthymic disorder may be preceded by an Axis I (nonmood) or Axis III disorder (“secondary dysthymia”).e. and almost half of elderly patients with dysthymic disorder have a history of major depressive disorder. response to antidepressant medications may be dramatic. although the difference declines with age. it is more common in women. or may present as “double depression” (i. As with anorexia.

e. 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 dysthymia 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.7% of a community sample of subjects age 65 or older had “substantial depressive symptoms” but only 3. after age 60) dysthymic disorder were more likely to have cardiovascular disease and less likely to have comorbid anxiety disorder than were those with early-onset dysthymia. Minor Depression The importance of minor or “subthreshold” depression (i. These criteria are presented in Table 3–6. 1988). in partial remission (American Psychiatric Association 2000). based on criteria presented in Appendix B to DSM-IV-TR (“Criteria Sets and Axes Provided for Further Study”). but the two groups were similar otherwise. Age at onset also may be important. (2004) found that elderly patients with late-onset (i. unlike major depression.. Beekman and colleagues (1997) found that minor depression. seems to resolve this apparent contradiction. One potential cause of a dysthymia-like syndrome is partial treatment of major depression. Devanand et al.92 Clinical Manual of Geriatric Psychiatry family history). Interest in subthreshold depression was further stimulated by the Epidemiologic Catchment Area studies (Regier et al. This condition is properly termed major depressive disorder. was closely associated with physical illness in elderly subjects.7% met DSM-III (American Psychiatric Association 1980) criteria for major depression (Blazer and Williams 1980).e.. . which confirmed Blazer and Williams’s findings of low prevalence of major depression in this age group. depression that causes clinically significant distress or impairment in social. either with anxiolytics alone or with inadequate doses of antidepressants. occupational. or other functioning but does not meet criteria for major depression or dysthymia) has been recognized at least since 1980. resulting in amelioration of enough signs and symptoms as to no longer qualify as major depression. when Blazer and Williams found that 14. and is usually identifiable with an accurate treatment history.

This study (Heikkinen and Kauppinen 2004) also found that people who had difficulties in the use of public transport had three times the risk of minor depression compared with those with no such difficulties. We also found the same impact from deteriorating health. and exercising) as major depression was. The authors concluded that “minor depression among the elderly is most typically a dynamic and episodic phenomenon. socializing.g. Other studies have generally confirmed these findings.Mood Disorders—Diagnosis 93 However.. Ohayon and Schatzberg (2002) investigated the associations between depressive symptoms and psychotic features in a sample of 18. 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. 1999). Minor depression also was associated with a significant (but less than in major depression) reduction in the subjective sense of well-being. Adverse life-events such as the loss of a spouse or some other close person had predictive value for depressive symptoms in our study. it also was associated with as much disability (e. in a later study. 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 diseases doubled the risk for minor depression. deteriorating financial situation and increased loneliness” (p. which was independent of general health status and. even after controlling for the effects of chronic physical illness. when compared with persons with no diseases or just one chronic disease. Psychotic features also have been reported in subsyndromal depression. 248). and in a review of this topic.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 episode) had psychotic features. was associated with an increased risk of dying (1. Functional decline also appeared as a highly significant risk factor. affecting general functioning as well as specific functions such as housekeeping.” .80 times the risk to nondepressed control subjects) (Penninx et al. 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.

g. a normal reaction to the death of a loved one). a drug of abuse.g. feels sad or empty) or observation made by others (e. not merely subjective feelings of restlessness or being slowed down) (f ) fatigue or loss of energy nearly every day (g) feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day (not merely self-reproach or guilt about being sick) (h) diminished ability to think or concentrate... or indecisiveness. recurrent suicidal ideation without a specific plan. occupational. (3) The symptoms are not due to the direct physiological effects of a substance (e.. There has never been a major depressive episode and criteria are not met for dysthymic disorder.g. nearly every day. defined as follows: (1) At least two (but less than five) of the following symptoms have been present during the same 2-week period and represent a change from previous functioning. appears tearful) (b) markedly diminished interest or pleasure in all. (4) The symptoms are not better accounted for by bereavement (i. Summary of DSM-IV-TR research criteria for minor depressive disorder A. or almost all. a change of more than 5% of body weight in a month).e. at least one of the symptoms is either (a) or (b): (a) depressed mood most of the day.g. B. a medication) or a general medical condition (e. . A mood disturbance. nearly every day (as indicated by either subjective account or observation made by others) (c) significant weight loss when not dieting or weight gain (e.. hypothyroidism).94 Clinical Manual of Geriatric Psychiatry Table 3–6. nearly every day (either by subjective account or as observed by others) (i) recurrent thoughts of death (not just fear of dying). or a suicide attempt or a specific plan for committing suicide (2) The symptoms cause clinically significant distress or impairment in social. or decrease or increase in appetite nearly every day (d) insomnia or hypersomnia nearly every day (e) psychomotor agitation or retardation nearly every day (observable by others..g. activities most of the day.. as indicated by either subjective report (e. or other important areas of functioning.

The difficulty that patients with these personality disorders typically have in establishing and maintaining interpersonal relationships seems to catch up with them late in life. the essential feature of depressive personality disorder is “a pervasive pattern of depressive cognitions and behaviors that begins by early adulthood and that occurs in a variety of contexts” (American Psychiatric Association 2000. American Psychiatric Association. American Psychiatric Association. There has never been a manic episode. The mood disturbance does not occur exclusively during schizophrenia. borderline. Summary of DSM-IV-TR research criteria for minor depressive disorder (continued) C. such as dysthymic disorder or major or minor depression. when they are forced to confront the loneliness and isolation that their personality problems have caused. Copyright © 2000. or a hypomanic episode and criteria are not met for cyclothymic disorder. or psychotic disorder not otherwise specified. Elderly patients with depressive personality disorder also may have episodes meeting criteria for more specific mood disorders. Depressive Personality Disorder As defined in DSM-IV-TR. a mixed episode. Laboratory Evaluation of Depression Laboratory evaluation of the elderly patient with clinically significant depression is aimed at ruling out endogenous etiological or contributing factors. Text Revision. including narcissistic. and hopeless. 2000. schizophreniform disorder. A perhaps less stable but persistent variant of this condition is commonly seen as a complication of other personality disorders. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. D. delusional disorder. Note: This exclusion does not apply if all of the manic-. discouraged. Washington. 788). such as hypothyroidism and adrenal insufficiency. and dependent personality disorder. schizoaffective disorder. and establishing the pretreatment baseline status of physiological systems likely to be affected by psychoactive med- . but even between such episodes. DC. Used with permission. Source. 4th Edition. mixed-. avoidant.Mood Disorders—Diagnosis 95 Table 3–6. or hypomanic-like episodes are substance or treatment induced. p. these patients are dejected.

Psychodiagnostic tests document current mood. Several laboratory procedures have been reported to be useful in establishing or ruling out a diagnosis of major depression. If an individual’s scores closely . and the sleep electroencephalogram. so neither test is recommended for routine clinical purposes. and social tendencies and can suggest personality features that may affect the presentation of major depression or response to treatment. personality disorders amplify the effect of depression and have been associated with long-term reductions in function and quality of life. Such testing provides a detailed survey of cognitive functions. 1988)—it has not been shown to increase diagnostic accuracy beyond that of the clinical evaluation alone and is too expensive to be of widespread clinical use. which is compared with normative values for healthy older people and patient populations with depression or dementia (see Chapter 5.96 Clinical Manual of Geriatric Psychiatry ications. the thyrotropin-releasing hormone (TRH) test. which is typically quite variable. although the sleep electroencephalogram is acceptably reliable—typically indicating an increased proportion of rapid eye movement (REM) sleep (Beck et al. a referral for neuropsychological testing may be appropriate. prevalence) of major depression in the population being studied. 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. a Minnesota Multiphasic Personality Inventory–2 profile in which elevated scores on the hysteria or hypochondriasis scales are combined with depressive symptoms is often observed in individuals with masked depression. Moreover. thought patterns. and an increased density of phasic eye movements in elderly depressed patients compared with nondepressed age-matched control subjects (Reynolds et al. More generally.. 1974). A recommended battery of tests with their potential uses is listed in Table 3–7. Unfortunately. For example. the diagnostic confidence associated with these tests depends on the underlying base rate (i. These include the dexamethasone suppression test (DST). In older patients with a combination of depressive and cognitive symptoms. “Dementia and Alzheimer’s Disease”). Similarly. a shorter REM sleep latency (period of non-REM sleep before the first REM episode). the rates of false-positive and false-negative results for both the DST and the TRH test are quite high in elderly patients. a longer first REM sleep period.e.

hypokalemia. stroke approximate those of other depressed patients. hyperglycemia Uremia Brain tumor. to take medications as prescribed or attend therapy sessions regularly). and their ability to complete complex work assignments or self-care tasks may be undermined. serum cortisol (A. viral infection Hypothyroidism and hyperthyroidism. Information on a depressed individual’s cognitive strengths and weaknesses also can be helpful for treatment planning and psychosocial management. executive skills.M. Symptom Rating Scales and Depression Screening Although depression rating scales were originally designed for research purposes.Mood Disorders—Diagnosis 97 Table 3–7. neuropsychological findings might serve to strengthen a clinical impression of DSD. or memory that exceed mild levels may require the support of another person to participate fully in therapies (e. Screening laboratory tests for evaluation of depression in the elderly Test Complete blood count with differential white blood cell count Serum thyroid-stimulating hormone. Symptom rating scales are not sufficient to establish a diagnosis of depression. but they can help to identify individuals whose depressive symptoms exceed the norm and they can provide a means of tracking treat- . serum urea nitrogen Computed tomography or magnetic resonance imaging of head (as indicated by results of above tests. thyroxine.. and P. Because full response to antidepressant therapies may take weeks or months.M. physical examination) Potential diagnosis Folate deficiency anemia. hypoadrenocorticism and hyperadrenocorticism Hypercalcemia. patients whose depression-related deficits in attention. use of such scales in clinical practice can enhance the uniformity and reliability of assessment.) Sequential multiple analysis of 18 chemical constituents of blood (SMA-18) Urinalysis.g.

severity of bias. uncooperative or confused patient Same as for MMPI-2 Same as for MMPI-2 Anchored to DSM Axis II categoriesb.. fewer data available for older adults than with MMPI-2 Millon Clinical Multiaxial Inventory–III (MCMI-III)c Revised NEO Personality Inventory (NEO-PI-R) and NEO Five-Factor Inventory (NEO-FFI)d Self-rated questionnaire Self-rated questionnaire Five-dimension taxonomy Ratings on dimensions Traits (e. depression presence of suicidality.g. may detect masked depression.Table 3–8. neuroticism) may of personality of personality relevant predict use of to everyday coping medical services. diagnosis. categoriesb estimate of response diagnosis. adjustment to stresses . Psychological tests useful in assessing geriatric depression Type of test Objective personality Name of test Minnesota Multiphasic Personality Inventory–2 (MMPI-2)a Description Self-rated questionnaire Indications Outcomes Comment 98 Clinical Manual of Geriatric Psychiatry Anchored to DSM Helps establish differential Personality profile.

Psychological Assessment Resources. National Computer Systems. University of Minnesota Press. McCrae RR: Revised NEO Personality Inventory (NEO-PI-R) and NEO Five-Factor Inventory (NEO-FFI): Professional Manual. also Description of reluctant to prominent concerns. Berne. 1971. Huber. Kronenburg B. Harvard University Press. bComputerized scoring and interpretation available. Minneapolis. d Costa PT. MN. et al: Manual for the Restandardized Minnesota Multiphasic Personality Inventory: MMPI-2. Cambridge. New York. 1983. Odessa. 99 . and thought disorder and in too ambiguous. useful for assessment of respond. f Murray HA: The Thematic Apperception Test. cMillon T: Millon Clinical Multiaxial Inventory Manual. 1943. Dahlstrom WB. Psychological tests useful in assessing geriatric depression (continued) Type of test Projective personality Name of test Rorschach Inkblot Teste Description Patient describes complex unfamiliar patterns Indications Outcomes Comment Many older adults Same as for MMPI-2. Translated by Lemkau P. Graham JR. but also identifies interpersonal concerns and habits Geriatric version also availableg Thematic Apperception Test (TAT)f Patient creates stories about pictures of people in different situations Mood Disorders—Diagnosis a Butcher JN. FL. 3rd Edition. see test as thought patterns. Switzerland. eRorschach H: Psychodiagnostics: A Diagnostic Test Based on Perception. gWolk RL. 1989. 1942. pathological patients unaware of or may give too few tendencies unwilling to admit answers to score b psychiatric problems Same as for MMPI-2 and Same as for Rorschach test Rorschach test. 1992. Minneapolis. Wolk RB: The Gerontological Apperception Test.Table 3–8. Behavioral Publications. MA.

the BDI-II (Beck et al. Most items are still rated on a 4-point scale. The most recent version of the BDI. including dysphoric mood. A simple yes-no answer format is another attractive feature. This instrument is recommended for tracking symptom severity in older persons with relatively clear-cut depression that is not complicated by psychosis or prominent somatization. Items on the initial version that pertained to body image. most somatic items have been omitted from the GDS to prevent inflation of scores due to normal aging changes. The GDS has been shown to be reliable and valid in clinical research with elderly medical and psychiatric patients.100 Clinical Manual of Geriatric Psychiatry ment-related change. it includes only a single cognitive item that does not correlate strongly with the other cognitive items on the full GDS (Adams et al. A 15-item short form of this scale has been developed that includes most of the key items for assessing dysphoria and hopelessness. weight loss. self-criticism. but rating options on the sleep and appetite items have been expanded to allow for both increases and decreases in those areas. It also may help to distinguish normal or complicated bereavement from major depression because bereaved individuals would not be expected to obtain high scores on items evaluating guilt. The BDI is particularly useful for assessing psychological features of depression. self-criticism. in contrast. however. Mood is extensively examined in this 30-item scale. 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. and guilt. The full form typically takes 10 minutes or less to complete. and the questions assess cognitive complaints and social behavior. the full 30-item GDS is recommended. and most older adults can complete it independently or with only brief task orientation. or risk of suicide. 1961) is another self-rated scale that has been widely used with older adults. The GDS (Yesavage et al. pessimism. 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. 1982) is a self-rated measure developed specifically for older adults (see the Appendix for GDS items and scoring instructions). . The BDI (Beck et al. 1996). 2004). is a 21-item questionnaire that has been modified from the original to coincide more closely with DSM-IV-TR diagnostic criteria for depression. For most mental health assessment settings. and it is often the standard against which other rating scales are compared in clinical research with older patients.

by trained professional.Table 3–9. Depression rating scales and screening procedures for older adults Approximate time to complete (min) 5–10 Scale or procedure Geriatric Depression Scale (GDS) Type Self-rated Number of items 30 or 15 Recommended uses Screening in mental health or medical settings. based on interview of patient Observer-rated. both patient and caregiver interviewed 17–28 17. tracking symptom changes with treatment Screening in mental health or medical settings.and 21-item versions most commonly used 20–25 Cornell Scale for Depression in Dementia 19 30 101 . tracking symptom changes with treatment Beck Depression Inventory (BDI and BDI-II) Self-rated 21 5–10 Mood Disorders—Diagnosis Hamilton Rating Scale for Depression (Ham-D) Observer-rated. tracking symptom changes with treatment Screening in mental health or medical settings. by trained professional. tracking symptom changes with treatment Screening cognitively impaired patients.

Table 3–9. Depression rating scales and screening procedures for older adults (continued)
Approximate time to complete (min) ≤5

102 Clinical Manual of Geriatric Psychiatry

Scale or procedure Beck Depression Inventory for Primary Care (BDI-PC) Depression items from the Patient Health Questionnaire (PHQ-9)

Type Self-rated

Number of items 7

Recommended uses Screening in medical settings Screening in medical settings

Self-rated

9

≤5

Mood Disorders—Diagnosis

103

and somatic preoccupation were replaced in the BDI-II with questions pertaining 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 acceptably 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 applicable 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 encouraged to contact persons responsible for translations before using translated instruments. One small-scale study found comparable GDS scores for Englishand 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 comparing 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, especially those who have visual deficits, limited education, poor language proficiency, psychosis, or masked depression. An observer-rated instrument, such as the Ham-D (Hamilton 1980), is recommended for these situations. Observer 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 measure 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 depression 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 expression, posture, voice and tendency to weep 4=Patient reports VIRTUALLY ONLY these feeling states in his spontaneous 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 compared with the original Ham-D, with intraclass correlations ranging from 0.78 to 1.0 for individual items (Moberg et al. 2001). Nonetheless, considerable 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 assessing 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 interviews with both the person with dementia and his or her caregiver. Although intended as a severity rating instrument once a diagnosis of depression has been established, the Cornell scale has been shown to be effective in identifying depression in nursing home patients with dementia. Internal consistency and interrater reliability are acceptable when the scale is used by trained examiners. Procedures for identifying depression in medically ill populations have received 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 situations. 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 psychiatric 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 individuals in busy medical settings where time is at a premium.

Assessing Suicidality in the Elderly
One of every five suicides in the United States involves an adult age 65 years or older (Edelstein et al. 1999). This high rate of suicide has prompted a re-

106 Clinical Manual of Geriatric Psychiatry

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 individual 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 substance abuse; and past suicide attempts. If answers to these questions raise concern about suicidality, direct questions should be asked to assess the severity of suicidal thoughts and any possible plan that may involve injury to self or others. Whenever possible, family members should be interviewed for suicide 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 provided could be useful to a wide range of health professionals. Other thorough discussions of geriatric suicide can be found in Gallagher-Thompson and Osgood (1997) and McIntosh and colleagues (1994).

Mood Disorders—Diagnosis

107

Table 3–10.
Increased risk

Risk and protective factors for geriatric suicide

Age ≥75 years Male White Widowed or divorced Living alone, isolated, or recently moved Retired or unemployed Poor physical health, terminal illness, multiple or debilitating illnesses, or pain Depression, substance abuse or dependence, hopelessness History of suicide, depression, or other mental illness in close family members Compensatory or protective Able to learn from experience and accept help; sense of meaning in life; sense of humor and capacity for loving; able to reminisce about positive life experiences History of successful transitions and coping with life challenges Caring and available family member or supportive community network; accessible and caring health care provider Membership in a religious community, especially Catholic or Jewish
Source. Adapted from Holkup 2003.

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 depression in the families (particularly first-degree relatives) of affected individuals 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 etiology and pathogenesis of depression, and they are summarized in the following subsections.

Psychodynamic Theories
Psychodynamic theories of depression were among the earliest published, beginning with Freud’s elaborations on the theories of Karl Abraham regarding psychopathological developments in the process of mourning. In Freud’s conception, 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 disappointments—thereby becomes directed at the self. The resultant guilt, loss of selfesteem, and need for punishment form the core of the symptom complex of pathological grief (not to be confused with complicated grief, a clinically defined condition discussed earlier in this chapter). More recently, Blatt and Zuroff (1992) proposed that certain personality configurations are predisposed 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 geriatric 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 inevitably associated with the functional declines of aging. Loss or threatened loss during childhood also has been a focus of psychodynamic 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).

Cognitive and Behavioral Theories
Seligman’s concept of “learned helplessness” offers a theoretical connection between certain unavoidable losses of later life (such as declines in physical vigor, sexual function, and general health) and the sensation of passive helplessness

Mood Disorders—Diagnosis

109

often expressed by elderly depressed patients (Seligman and Maier 1967). Similarly, cognitive theorists point to the interaction between these losses and subsequent 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). Contemporary research on cognitive-behavioral therapy in late-life depression (e.g., Thompson et al. 2001) accepts (with little critical analysis) “negative cognitions” as the proper focus of therapeutic attention, and the reported effectiveness 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 disorders, 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 indirect 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 colleagues (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

flight of ideas. with emphasis on the role of age-related reductions in brain concentrations of norepinephrine. distractibility. fits neatly into Chaisson-Stewart’s model in the place of what she calls “defenses.. increased body temperature.” which include both learned psychological and genetically determined psychobiological mechanisms that have been variably weakened by age and age-related infirmity. hyperactivity. as such. Other investigators have studied endogenous rhythms.g. This trait is a definer of the personality factor known as neuroticism and.g. irritability. . cognitive. serotonin. changes in sleep architecture) and those seen in normal aging (Sack et al.” Hypomania and Mania With or without hallucinations and delusions. 155). signs and symptoms of elevated mood—including reduced need for sleep. grandiosity. cultural. and acetylcholine and agerelated increases in brain concentrations of monoamine oxidase (Lipton 1976).110 Clinical Manual of Geriatric Psychiatry depression. In summary. dopamine. abnormalities in brain concentrations of monoamine neurotransmitters and their metabolites and in platelet α2-adrenoreceptor and 3H-imipramine binding also have been reported (Alexopoulos 1994). They conceptualized this tendency as an enduring personality trait that can be measured by appropriate assessment instruments and that predisposes its owner to episodes of clinical depression. Costa and McCrae (1994) supported this model by arguing that “there are individual differences in the tendency to experience dysphoric affect” (p.. circumstantiality and tangentiality. her view is that depression in the elderly represents the final result of an interaction between biological (e.g. cerebrovascular lesions and cortical atrophy) and/or psychosocial stressors (e. Chaisson-Stewart (1985) attempted to synthesize behavioral. 1987). In adult and elderly depressed patients. pressured speech.. decreased nocturnal secretion of melatonin and thyroid-stimulating hormone. but to date no single neurobiological theory of depression in the elderly is widely accepted. The often observed temporal association between ingestion of certain medications (see Table 3–2) known to affect particular neurotransmitters and their presynaptic and postsynaptic receptors and the onset of depressive symptoms has provided support for several of these theories. losses) and “defenses. noting the similarity between certain abnormalities found in depression (e. advances in the phase of circadian cortisol secretion. and biological factors into a comprehensive model of geriatric depression based on the work of Adolf Meyer and Sir Aubrey Lewis.

and if psychotic features are not present. monoamine oxidase inhibitors. tricyclic antidepressants. hypomania or mania that begins during or within 1 month of treatment with one or more of the medications listed here should be considered substance induced. Substance-Induced Mania Substances known to induce mania include sympathomimetic agents (iproniazid. procarbazine). Hypomania is diagnosed if the disturbance does not cause marked impairment in occupational functioning or in usual social activities or relationships with others. Several investigators have suggested that mania due to a general medical condition is more likely than primary mania to be of late onset and to occur in patients with a negative family history. or when psychotic features are present. but a review of the literature by Chen and colleagues (1998) fails to support this claim. bromide.g. and many other substances (Table 3–11). corticosteroids. if the disturbance does not necessitate hospitalization. levodopa. psychostimulants (e. amphetamines. Endogenous illnesses that have been associated with the manic syndrome are listed in Table 3–11. Mania is diagnosed when signs and symptoms are severe enough to cause marked impairment in occupational functioning or in usual social activities or relationships with others.. phencyclidine). In light of the 1%–2% prevalence of major depression. when signs and symptoms are severe enough to necessitate hospitalization to prevent harm to self or others. and excessive involvement in pleasurable activities that have a high potential for painful consequence—may occur in the context of certain medical illnesses. this finding suggests that about . methylphenidate. Bipolar Disorder Epidemiology The Epidemiologic Catchment Area study found a 1-year prevalence of 0. In this regard. yohimbine. and as one phase (or “pole”) of bipolar disorder. alprazolam. as an adverse reaction to certain medications or electroconvulsive therapy.Mood Disorders—Diagnosis 111 impulsivity. Mania Due to a General Medical Condition Mania or hypomania due to a general medical condition may be clinically indistinguishable from the functional variety.1% of bipolar disorder among adults older than 65 living in the community. cocaine.

corticosteroids. propafenone. iproniazid. bromide. dopamine agonists (bromocriptine. yohimbine Hemodialysis Postoperative state Uremia. right basotemporal cortex. bilateral orbitofrontal meningioma Medial frontal tumor. baclofen. selegiline. phencyclidine. antidepressants. carcinoid syndrome. metrizamide. cocaine. ranitidine). metoclopramide. cyanocobalamin deficiency Influenza. amantadine). suprasellar diencephalic tumor. antiepileptics. isoniazid. inferior temporal lobe Temporal basal polar lesions Right orbitofrontal white matter Right temporal focus Metabolic disturbances Infectious diseases Neoplasms Vascular lesions Closed head injury Seizure disorder . chloroquine. Q fever Encephalitis Human immunodeficiency virus Cryptococcal meningitis Diencephalic glioma Parasagittal meningioma. hydralazine. Medical and neurological conditions and drugs associated with secondary mania Category Drugs Specific agent or condition Amphetamines. histamine H2 blockers (cimetidine. hyperthyroidism. cyclobenzaprine. hyperbaric chamber use. pellagra. benzodiazepines. right dorsolateral frontal cortex. anabolic steroids. levodopa. clarithromycin. hypothalamic tumor Right head of caudate nucleus.112 Clinical Manual of Geriatric Psychiatry Table 3–11. thyroxine. procyclidine. thalamus. spheno-occipital tumor Right inferior temporal lobe glioma. angiotensin-converting enzyme inhibitors.

Clinical Presentation Bipolar disorder typically is first diagnosed in young adulthood. Relatively little research has been published on bipolar disorder in the elderly. and the average age at onset of mania was 56. Chen ST. etiology.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 reported. These ages are significantly later than the reported age at onset of mixed-age patients with bipolar disorder. “To date. there have been no published large-scale multi-center studies of prevalence. Inc. Spar JE: “Bipolar Disorder in Late Life: A Review. nor have there been any double-blind randomized controlled trials of pharmacologic treatments in this population” (p. 343). general paresis.Mood Disorders—Diagnosis 113 Table 3–11. The average age at onset of any mood disorder was 48. Medical and neurological conditions and drugs associated with secondary mania (continued) Category Other neurological conditions Specific agent or condition Multiple sclerosis. . 5%–10% of elderly patients with major mood disorder have bipolar disorder. Wilson’s disease Source. 1998. which tends to be in the 20s. Pick’s disease.” Journal of Geriatric Psychiatry and Neurology 11:29–35. stated. Reprinted by permission of Sage Publications. Huntington’s disease. Depp and Jeste (2004). 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 (sampleweighted mean age=68. in a review. 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). Altshuler LL. Klinefelter’s syndrome. or clinical features of bipolar disorder in late life. Kleine-Levin syndrome. Few other consistent findings distinguish bipolar disorder in the elderly from bipolar disorder in young and middle-aged adults. thalamotomy. but Depp and Jeste did conclude that older bipolar patients are less likely to have comorbid substance abuse than are younger patients and that late-onset mania is associated with more neurological impairment.

electroconvulsive therapy. and the mood must be clearly different from the usual nondepressed mood. The episode is associated with an unequivocal change in functioning that is uncharacteristic of the person when not symptomatic. expansive. C. A distinct period of abnormally and persistently elevated. or irritable mood.g. The disturbance in mood and the change in functioning are observable by others. lasting at least 1 week (or any duration if hospitalization is necessary). or there are psychotic features.. B. Note: Manic-like episodes that are clearly caused by somatic antidepressant treatment (e. The mood disturbance is sufficiently severe to cause marked impairment in occupational functioning or in usual social activities or relationships with others. or to necessitate hospitalization to prevent harm to self or others. D. medication. but only 4 days’ duration is required. B. During the period of mood disturbance. . Summary of DSM-IV-TR criteria for manic episode and hypomanic episode Manic episode A. The same as criterion B for manic episode above. light therapy) should not count toward a diagnosis of bipolar I disorder. The symptoms are not due to the direct physiological effects of a substance or a general medical condition.114 Clinical Manual of Geriatric Psychiatry Table 3–12. D. The same as criterion A for manic episode above. E. The symptoms do not meet criteria for a mixed episode. three (or more) of the following symptoms have persisted (four if the mood is only irritable) and have been present to a significant degree: (1) inflated self-esteem or grandiosity (2) decreased need for sleep (3) more talkative than usual or pressure to keep talking (4) flight of ideas or subjective experience that thoughts are racing (5) distractibility (6) increase in goal-directed activity or psychomotor agitation (7) excessive involvement in pleasurable activities that have a high potential for painful consequences C. Hypomanic episode A.

4th Edition. Generally. Although the question remains open. Source. Early psychodynamic considerations about mania compared the relative importance of predisposing personality characteristics with that of precipitating events. or to necessitate hospitalization. Copyright © 2000. egocentric. The episode is not severe enough to cause marked impairment in social or occupational functioning. chronically depressed. Used with permission. Washington. DC. psychodynamic theories of mania have come to be seen as more relevant to shifts in mood in nonmanic individuals and have largely been supplanted by neurobiological theories in attempts to understand frank hypomania and mania. Text Revision. Pathogenesis—Psychodynamic Theories Relatively little has been written about the psychodynamics of hypomania and mania in elderly patients per se. .Mood Disorders—Diagnosis 115 Table 3–12. reflected in behavior by primitive impulsiveness. Abraham saw mania as a psychic regression to a state of intense ambivalence directed toward love objects. and there are no psychotic features. Later theorists conceptualized mania as a defense and tended to see the manic personality as immature. Summary of DSM-IV-TR criteria for manic episode and hypomanic episode (continued) Hypomanic episode (continued) E. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. 2000. Analytical theorists beginning with Abraham attempted to understand these constitutional factors in terms of predisposing personality characteristics and the interplay of classic psychodynamic mechanisms. Investigators such as Emil Kraepelin were influenced by what seemed to be an inconsistent relationship between manic episodes and external life events. American Psychiatric Association. dependent on others for self-esteem. The symptoms are not due to the direct physiological effects of a substance or a general medical condition. and dominated by feelings of interpersonal competitiveness and envy. F. In this regard. the psychodynamic literature from that point has generally agreed on the primary importance of constitutional factors in the development of the illness. American Psychiatric Association.

Similarly.M. A recommended battery of tests with their potential uses is listed in Table 3–13. .) Sedimentation rate Lumbar puncture Computed tomography or magnetic resonance imaging of head Hyperthyroidism Hyperadrenocorticism Collagen vascular disease. inositol) also have been described in subjects with bipolar disorder (Dean 2004). some evidence indicates that the configuration of γ-aminobutyric acid (GABA)A receptors in the frontal cortex of subjects with bipolar disorder is altered (Dean et al. but the significance of this finding remains unclear.M. and temporal cortices from subjects with bipolar disorder. 1994) found decreases in serotonin turnover in the frontal. Also.116 Clinical Manual of Geriatric Psychiatry Table 3–13. and P. especially lupus Encephalitis Brain tumor. parietal. Laboratory tests for evaluation of hypomania and mania in the elderly Test Blood studies Thyroid-stimulating hormone. and occipital cortices. 2001) compared with nonbipolar subjects. multiple sclerosis Potential diagnosis Pathogenesis—Neurobiological Theories A postmortem study of brain tissue (Young et al. changes in various neurotransmitter receptor–G-protein interactions (which modulate neurotransmission at the intracellular level) and certain “downstream” signal transduction components (e.g. temporal. stroke. as well as decreased dopamine turnover in the parietal and occipital cortices and increased norepinephrine turnover in the thalamus and frontal. thyroxine Cortisol (A. but no coherent theory has yet emerged from these findings. Laboratory Evaluation of Hypomania and Mania Laboratory evaluation of the elderly patient with mania or hypomania is aimed at ruling out general medical causes such as hyperthyroidism and at establishing the pretreatment baseline status of physiological systems likely to be affected by antimanic medications..

Note. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. Washington. C. irritability. Copyright 2000 American Psychiatric Association.g. American Psychiatric Association. 2000. The mood disturbance is sufficiently severe to cause marked impairment in occupational functioning or in usual social activities or relationships with others. 1994. The criteria are met both for a manic episode [Table 3–12] and for a major depressive episode [Table 3–3] (except for duration) nearly every day during at least a 1-week period. pp 101–116 Alexopoulos GS. Source.. References Adams KB. Used with permission. Summary of DSM-IV-TR criteria for mixed episode B. a drug of abuse. Abrams RC. DC. or there are psychotic features. Fourth Edition. medication.g. in Diagnosis and Treatment of Depression in Late Life: Results of the NIH Consensus Development Conference. a medication. Text Revision. or to necessitate hospitalization to prevent harm to self or others. et al. or other treatment) or a general medical condition (e. hyperthyroidism). light therapy) should not count towards a diagnosis of bipolar I disorder. Sanders S: Confirmatory factor analysis of the Geriatric Depression Scale. American Psychiatric Press. Mixed-like episodes that are clearly caused by somatic antidepressant treatment (e. Edited by Schneider LS. Young RC. Mixed Mood Disorder Elderly patients with major mood disorder commonly present with a syndrome of mixed manic and depressive features. et al: Cornell Scale for Depression in Dementia.. The symptoms are not due to the direct physiological effects of a substance (e. anorexia. 1988 . Lebowitz BD. Gerontologist 44:818–826.g. The question of whether agitated depression or mixed manic-depressive syndrome is the correct diagnosis usually can be resolved by applying DSM-IV-TR criteria for “mixed episode” (Table 3–14). Washington.Mood Disorders—Diagnosis 117 Table 3–14. A typical picture might include severe psychomotor agitation accompanied by intrusive and demanding behavior. 2004 Alexopoulos GS: Biological correlates of late-life depression. Biol Psychiatry 23:271–284. Matto HC. and insomnia. DC. electroconvulsive therapy. Reynolds CF III. flight of ideas and circumstantiality.. A.

J Consult Clin Psychol 42:861–865.118 Clinical Manual of Geriatric Psychiatry Alexopoulos GS. Arch Gen Psychiatry 4:561–571. Washington. Deeg DJ. Mendelson M. Circulation 102:1773–1779. Am J Geriatr Psychiatry 3:43–51. Smit JH. 1987 American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. Weissman A. Neill D. Braam AW. J Affect Disord 81:191–199. in Depression and Mania. Clin Psychol Rev 12:527–562. Deeg DJ. 1995 Bakken K. TX. et al: An inventory for measuring depression. O’Brien J. Brown G. Tangen C. 1974 Beck AT. Ward C. Psychological Corporation. et al: Anxiety. Edited by Georgotas A. et al: The longitudinal relation between chronic diseases and depression in older persons in the community: the Longitudinal Aging Study Amsterdam. Washington. 2000 American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. Meyers BS. Cancro R. et al: The measurement of pessimism: the hopelessness scale. 3rd Edition. Young RC. 2003 Ballard C. 1988. 2004 Blatt SJ. 1997 Alexopoulos GS. Meyers BS. 1992 . J Clin Epidemiol 57:187–194. DC. 1961 Beck AT. Lester D. et al: Consequences of major and minor depression in later life: a study of disability. Landheim AS. 2004 Bemporad JR: Psychodynamic models of depression and mania. Velli SA. 1980 American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. Deeg DJH. Text Revision. 3rd Edition. Zuroff DC: Interpersonal relatedness and self-definition: two prototypes for depression. Revised. DC. American Psychiatric Association. et al: Depressive symptoms and risks of coronary heart disease and mortality in elderly Americans. depression and psychosis in vascular dementia: prevalence and associations. et al: Clinically defined vascular depression. Washington. et al: Executive dysfunction and long-term outcomes of geriatric depression. Am J Psychiatry 154:562–565. J Affect Disord 59:97–106. American Psychiatric Association. Elsevier. pp 167–180 Bisschop MI. 2000 Ariyo A. American Psychiatric Association. et al: Dysthymia in later life: a study in the community. New York. 1996 Beekman ATF. San Antonio. Steer RA: Beck Depression Inventory II Manual. Vaglum P: Primary and secondary substance misusers: do they differ in substance-induced and substance-independent mental disorders? Alcohol Alcohol 38:54–59. 1997 Beekman AT. DC. 2000 Beck AT. 4th Edition. Kriegsman DM. et al: Screening tests for depression in older black vs. Psychol Med 27:1397–1409. Young RC. well-being and service utilization. Arch Gen Psychiatry 57:285–290. 2000 Baker FM. Friedman J. Haan M. white patients.

et al: Executive functioning. 2000 Butters MA. 1980 Bornstein PE. Prince M. Edited by Schneider LS. New York. Br J Psychiatry 122:561–566. Luscombe G. Reynolds CF III. DCP-1) and other vascular factors in late-life depression. McCrae RR: Depression as an enduring disposition. Altshuler LL. J Geriatr Psychiatry Neurol 11:29–35. Psychiatr Prax 29:207–210. Edited by Breslau LD. Williams CD: Epidemiology of dysphoria and depression in an elderly population. Joels S. 1998 Clayton PJ. 1973 Brodaty H. Bhalla RK. Psychol Med 27:1205–1213. Haug MR. pp 23–53 Cervilla J. Washington. Edited by Schneider LS. in Diagnosis and Treatment of Depression in Late Life: Results of the NIH Consensus Development Conference. Springer. DC. 2004 Caine ED. 2004 . Aust N Z J Psychiatry 38:135–140. Nebes RD. 2002 Butters MA. Lebowitz BD. 1994. Reynolds CF III. Am J Psychiatry 137:439–444. et al: Genes related to vascular disease (APOE. et al: Increased rate of psychosis and psychomotor change in depression with age. Lyness JM. et al: Changes in cognitive functioning following treatment of late life depression. Halikas JA. and relapse/recurrence in continuation and maintenance treatment of late-life depression: is there a relationship? Am J Geriatr Psychiatry 12:387–394. Edited by Chaisson-Stewart GM. in Depression in the Elderly. DC. Lebowitz BD. Maurice WL: The depression of widowhood. Br J Psychiatry 120:71–77. VLDL-R. Reynolds CF 3rd. pp 75–93 Blazer D. et al. et al: Depression and Bipolar Support Alliance consensus statement on the unmet needs in diagnosis and treatment of mood disorders in late life. Mulsant BH. King DA. et al: Clinical and etiological heterogeneity of mood disorders in elderly patients. pp 155–167 Dean B: The neurobiology of bipolar disorder: findings using human postmortem central nervous system tissue. Washington.Mood Disorders—Diagnosis 119 Blau D: Depression and the elderly: a psychoanalytic perspective. Am J Geriatr Psychiatry 12:202–210. in Depression and Aging. illness course. American Psychiatric Press. Becker JT. Parker G. 2003 Chen ST. Am J Psychiatry 157:1949–1954. New York. Lewis L. 1997 Bschor T: Masked depression: the rise and fall of a diagnosis [in German]. Wiley. in Diagnosis and Treatment of Depression in Late Life: Results of the NIH Consensus Development Conference. 1972 Costa PTJ. 1985. 1994. pp 56–104 Charney DS. et al: The depression of widowhood after thirteen months. 2004 Chaisson-Stewart GM: An integrated theory of depression. American Psychiatric Press. Spar JE: Bipolar disorder in late life: a review. Arch Gen Psychiatry 60:664–672. 1983. Clayton PJ. et al. Halikas JA.

1982 Gallagher-Thompson D. 2000 Depp CA. Jeste DV: Bipolar disorder in older adults: a critical review. et al: Cerebral white matter lesions and depressive symptoms in elderly adults. Essence 5:127–140. Int J Geriatr Psychiatry 14:368–372. Bipolar Disord 6:343–367. Drozdick LW. in Handbook of Assessment in Clinical Gerontology. Lyons JS. 2004 Devanand DP. Ames MH: Reliability and validity of the Beck Depression Inventory for a white and Mexican-American gerontic population. McLeod M. Edited by Lichtenberg PA. 1999. Breckenridge JN. 1974 . et al: Prevalence and diagnosis of depression in frail nursing home patients. pp 11–58 Falck RP. Schoevers RA. in Brodmann’s area 9 from subjects with bipolar disorder. Pavey G. Arch Gen Psychiatry 57:1071–1076. J Affect Disord 78:259–267. Manheim LM. 1999 Frasure-Smith N. et al: A change in the density of [3H]flumazenil. New York. Cheng J. Tijdschr Gerontol Geriatr 30:193–199. Med Care 42:502–511. 1999 Forsell Y. J Affect Disord 66:147–158. Psychol Rep 65:1163–1165. et al: Arthritis and heart disease as risk factors for major depression: the role of functional limitation. et al: Assessment of depression and bereavement in older adults.120 Clinical Manual of Geriatric Psychiatry Dean B. et al: Late onset dysthymic disorder and major depression differ from early onset dysthymic disorder and major depression in elderly outpatients. Kalish KD. Kaczmarek M. 2004 Duman RS: Depression: a case of neuronal life and death? Biol Psychiatry 56:140– 145. de Leeuw FE. Rabins PV: Depression without sadness: alternative presentations of depression in late life. 1999 Gatewood-Colwell G. Osgood NJ: Suicide in later life. Wiley. Lespérance F. Pot AM. Thompson LW. 2000 Glick ID. Braam AW. Circulation 91:999–1005. Beekman AT. 1995 Gallagher D. 1997 Gallo JJ. Br J Psychiatry 176:568–575. Parkes CM: The First Year of Bereavement. Behav Ther 28:23–41. Oudkerk M. Adorno E. 2004 Dunlop DD. New York. Weiss RS. but not [3H]muscimol binding. Talajic M: Depression and 18-month prognosis after myocardial infarction. Winblad B: Incidence of major depression in a very elderly population. Am Fam Physician 60:820–826. et al: Depression and risk of cognitive decline and Alzheimer’s disease: results of two prospective community-based studies in the Netherlands. Wiley. 2004 Edelstein B. 1989 Geerlings MI. et al: Similarities and differences between normal grief and depression in older adults. 2001 de Groot JC. a pilot study [in Dutch].

Gatz M.Mood Disorders—Diagnosis 121 Gottlieb SS. 1999 Kendler KS. et al: Stepped collaborative care for primary care patients with persistent symptoms of depression: a randomized trial. 2003 House A. 2004 Heithoff K: Does the ECA underestimate the prevalence of late-life depression? J Am Geriatr Soc 43:2–6. Berg S. 2000 Jansson M. J Am Coll Cardiol 43:1542– 1549. Krishnan RR: Should selective serotonin reuptake inhibitors be prescribed to all patients with ischemic heart disease? Curr Psychiatry Rep 6:202–209. Friedmann E. Arch Gen Psychiatry 56:1109–1115. Cochrane Database Syst Rev (3):CD003437. 2003 Kielholz P (ed): Masked Depression. et al: The influence of age. Edited by Storandt M. Bruce I. 1973 Kim JM. 2004 Hackett ML. entrapment. Knapp P. Butera F. Anderson CS. Bern. Huber. Von Korff M. et al: Life event dimensions of loss. et al: Dysthymia among the community-dwelling elderly. Arch Gen Psychiatry 60:789–796. Int J Geriatr Psychiatry 14:440–445. 1999 Kaszniak AW. Bamford J. Vollmayr B: Neurogenesis and depression: etiology or epiphenomenon? Biol Psychiatry 56:146–150. Stewart R. 2004 Jiang W. 2001 Jacobs BL. et al: Gender differences in heritability of depressive symptoms in the elderly. Switzerland. and race on the prevalence of depression in heart failure patients. gender. Alexopoulos GS: Prefrontal dysfunction and treatment response in geriatric depression. Arch Gen Psychiatry 56:713–718. Shin IS. Gage FH: Adult brain neurogenesis and psychiatry: a novel theory of depression. Coakley D. House AO: Interventions for treating depression after stroke. DC. 1980 Heikkinen RL. J Gerontol Nurs 29:6–17. 2004 Kirby M. Lin E. Khatta M. Mol Psychiatry 5:262–269. Br J Psychiatry 185:102–107. and danger in the prediction of onsets of major depression and generalized anxiety. Kauppinen M: Depressive symptoms in late life: a 10-year follow-up. 1999 . J Clin Psychiatry 41:21–24. 1995 Henn FA. Hettema JM. 2004 Kalayam B. VandenBos GR. American Psychological Association. in Neuropsychological Assessment of Dementia and Depression in Older Adults: A Clinician’s Guide. et al: Mortality at 12 and 24 months after stroke may be associated with depressive symptoms at 1 month. Stroke 32:696–701. 2004 Hamilton M: Rating depressive patients. 1994 Katon W. Psychol Med 34:471–479. Christenson GD: Differential diagnosis of dementia and depression. Praag H. humiliation. 2004 Holkup PA: Evidence based protocol: elderly suicide—secondary prevention. et al: Vascular disease/risk and late-life depression in a Korean community population. Washington. Arch Gerontol Geriatr 38:239–250.

1994 Mast BT. Am J Geriatr Psychiatry 9:35–40. et al: Monitoring depression treatment outcomes with the Patient Health Questionnaire–9. American Psychological Association. Leon AC. J Affect Disord 69:225–229. 1989 Kroenke K. Clary CM. and ageing. 2000 Lykouras L. et al: Comparison of the standard and structured interview guide for the Hamilton Depression Rating Scale in depressed geriatric inpatients. et al: Autonomous pathways to late-life major depressive disorder identified using a path analytic approach (abstract). DC. J Affect Disord 11:179–184. Bilker W. Curr Opin Clin Nutr Metab Care 4:9–13. Mesholam RI. 2001 Morley JE: Anorexia. J Am Geriatr Soc 42:1006–1008. 2000 La Rue A. et al: Screening for depression: single question versus GDS. 1976 Löwe B. Can J Psychiatry 34:445–446. J Gerontol A Biol Sci Med Sci. et al: Mental and behavioral disturbances in dementia: findings from the Cache County Study on Memory in Aging. Santos JF.122 Clinical Manual of Geriatric Psychiatry Ko DT. J Gerontol 31:293– 299. et al: Elder Suicide: Research. Mintz J. 2004 McIntosh JL. 59:1290–1294. MacNeill SE. Hill CD: Cognitive impairment in late-life depression: clinical correlates and treatment implications. 2002 Kral VA. and sexual dysfunction. Fortos A. J Clin Psychiatry 60 (suppl 20):9–15. Hebert PR. 1992 Nelson JC. 1994 Moberg PJ. Ganguli M: Epidemiology and diagnosis of depression in late life. 2001 Kumar A. Emery OB: Long-term follow-up of depressive pseudodementia of the aged. body composition. Hubbard RW. JAMA 268:1018–1024. Abler R. Tschanz JT. 2002 Mahoney J. Spitzer RL. JAMA 288:351–357. et al: Symptoms of late-life depression: frequency and change during treatment. Steinberg M. Theory and Treatment. Abstr Soc Neurosci 26:495. Coffey CS. Unützer J. 1986 Lipton MA: Age differentiation in depression: biochemical aspects. fatigue. Williams JB: The PHQ-9: validity of a brief depression severity measure. et al: β-Blocker therapy and symptoms of depression. Callahan CM. Lazarus LW. Gournellis R. 1999 National Institutes of Health Consensus Conference: Diagnosis and treatment of depression in late life. Med Care 42:1194–1201. et al: Psychotic (delusional) major depression in the elderly and suicidal behaviour. Am J Geriatr Psychiatry 13:520–526. Washington. Spar J. 2004 Lyketsos CG. 2005 . J Gen Intern Med 16:606–613. Am J Psychiatry 157:708–714. Drinka TJ. et al: Risk factors for geriatric depression: the importance of executive functioning within the vascular depression hypothesis. 2001 Mulsant BH. Yochim B.

1965 Parkes CM: Bereavement: Studies of Grief in Adult Life. 1999 Pincus HA. International Universities Press. Hallstrom T: Depressive disorders among somatizing patients in primary health care. Can J Psychiatry 39:S19–S26. N Engl J Med 349:1936– 1942. Kupfer DJ. Schatzberg AF: Prevalence of depressive episodes with psychotic features in the general population. Am J Psychiatry 139:799–802. Haley WE. Boyd JH. Robinson RG: Gender differences in poststroke depression. Ceravolo R. Barnes RF. 1998 Parkes CM: Bereavement and mental illness. Caring for bereaved patients: “all the doctors just suddenly go. Jacobs SC: Perspectives on care at the close of life.” Br J Psychiatry 174:288–296. 2003 Seligman ME. Parry BL. et al: Reliable discrimination of elderly depressed and demented patients by electroencephalographic sleep data. Circulation 104:1894–1898. Veith RC. et al: Psychiatric comorbidity in a population of Parkinson’s disease patients. Eur J Neurol 11:315–320. Br J Med Psychol 38:13–26. 1994 Sauer WH. 1967 . Rosenthal NE. New York.” JAMA 286:1369–1376. Burke JJ. Maier SF: Failure to escape traumatic shock. Am J Psychiatry 159:1855–1861. Mendelsohn AB. Deeg DJH. New York. 1999 Posse M. Edited by Meltzer HY. J Exp Psychol 74:1–9. in Psychopharmacology: The Third Generation of Progress. Kimmel SE: Selective serotonin reuptake inhibitors and myocardial infarction. Arch Gen Psychiatry 45:977–986. Berlin JA. J Neuropsychiatry Clin Neurosci 10:41–47. et al: Depression influences intellectual impairment in stroke patients. et al: Biological rhythms in psychiatry. 1998 Prigerson HG. Arch Gen Psychiatry 56:889–895. Br J Psychiatry 148:541–547. pp 669–686 Sadavoy J: Integrated psychotherapy for the elderly. 2002 Okimoto JT. 2004 Ohayon MM. 1982 Paradiso S. part 2: classification of bereavement reactions. 1987. Arch Gen Psychiatry 45:258–264. 1972 Penninx BWJH. Bolla-Wilson K. et al: End-of-life care and the effects of bereavement on family caregivers of persons with dementia. Davis WW.Mood Disorders—Diagnosis 123 Nuti A. et al: Minor and major depression and the risk of death in older persons. Kaplan E. 1986 Sack DA. 2001 Regier DA. et al: Screening for depression in geriatric medical patients. 2001 Schulz R. Houck PR. 1988 Reynolds CF. 1988 Robinson RG. Raven. McQueen LE: “Subthreshold” mental disorders: a review and synthesis of studies on minor depression and other “brand names. Geerlings SW. Piccinni A. Acta Psychiatr Scand 98:187–192. et al: One-month prevalence of mental disorders in the United States: based on five Epidemiologic Catchment Area sites.

Black FW: Neurobehavioral Disorders: A Clinical Approach. Arch Gen Psychiatry 57:601– 607. Gallagher-Thompson D. Kalaria RN. DC. 1999 Steer RA. Beck AT: Use of the Beck Depression Inventory-II with depressed geriatric inpatients. 1997 Wiener P. JAMA 282:1737–1744. et al: Comparison of desipramine and cognitive/behavioral therapy in the treatment of elderly outpatients with mildto-moderate depression. et al: Prevalence of depression and its treatment in an elderly population: the Cache County study. et al: Case-finding instruments for depression: two questions are as good as many. J Gen Intern Med 12:439–445. p. Fields JA.S. et al: Stroke.S. 2000 Steffens DC. vascular risk factors and depression: cross-sectional study in a UK Caribbean-born population. Public Health Service. Avins AL. FA Davis. Norton MC. 1991 Spitzer RL. Office of the Surgeon General: The Surgeon General’s Call to Action to Prevent Suicide. et al: Validation and utility of a self-report version of PRIME-MD: the PHQ primary care study. Edited by Coffey CE. 2001 Tröster AI. Am J Geriatr Psychiatry 5:116–125. pp 559–600 U. Arch Gen Psychiatry 45:742–747. in The American Psychiatric Press Textbook of Geriatric Neuropsychiatry. Washington. 2000 Stewart R. 2001 Thompson LW. 1988 . Skoog I. Cummings JL. 2nd Edition. Kroenke K. Williams JB. Ann Intern Med 136:760–764. Coon DW. Br J Psychiatry 178:23– 28. Am J Geriatr Psychiatry 9:225–240. Koller WC: Parkinson’s disease and parkinsonism. 1988. J Neurol Neurosurg Psychiatry 70:83–87. Philadelphia. 2001 Strub RL. Henderson VW. Prince M. Washington. 171 Taussig IM. Behav Res Ther 38:311–318. 1997 Williams JB: A structured interview guide for the Hamilton Depression Rating Scale. PA. Ferrier IN. Rissmiller DJ. Alexopoulos GS. 1992 Thomas AJ. Richards M. Miranda J. VonKorff M: Somatization and psychiatric disorder in the NIMH Epidemiologic Catchment Area study. Department of Health and Human Services. Mack W: Spanish translation and validation of a neuropsychology battery: performance of Spanish. DC. Am J Psychiatry 148:1494–1500. U. American Psychiatric Press. Kakuma T.S. Preventive Services Task Force: Screening for depression: recommendations and rationale. et al: The limits of history-taking in geriatric depression. 1999 Whooley MA.124 Clinical Manual of Geriatric Psychiatry Simon GE. Clin Gerontol 11:95–108. et al: A neuropathological study of vascular factors in late-life depression. Public Health Service. 2002 U. 2000.and English-speaking Alzheimer’s disease patients and normal comparison subjects.

Warsh JJ. Shuchter SR. J Psychiatr Res 17:37–49. Sledge P: Diagnostic and treatment considerations in depression associated with late-life bereavement. 1994 Zisook S. 2002 Yesavage JA. Kish SJ. Barnes LL.Mood Disorders—Diagnosis 125 Williams LS. et al: Reduced brain 5-HT and elevated NE turnover and metabolites in bipolar affective disorder. Reynolds CF III. Biol Psychiatry 35:121–127. Lebowitz BD. Edited by Schneider LS. 1994. et al: Depressive symptoms. Brink TL. Washington. Mendes de Leon CF. American Psychiatric Press. cognitive decline. Rose TL. et al. 2004 Wilson RS. Neurology 59:364–370. Swindle RW: Depression and other mental health diagnoses increase mortality risk after ischemic stroke. in Diagnosis and Treatment of Depression in Late Life: Results of the NIH Consensus Development Conference. Ghose SS. et al: Development and validation of a geriatric depression screening scale: a preliminary report. and risk of AD in older persons. 1982 Young LT. pp 419–435 . DC. Am J Psychiatry 161:1090–1095.

This page intentionally left blank .

to all of the depressive variants discussed in Chapter 3 (“Mood Disorders—Diagnosis”). Older adults frequently face chronic illness and disability. Factors that are important to consider in selecting an approach include the nature of the problems involved. the clinical goals. To avoid repetition and redundancy. in the first part of this chapter. and place on the continuum of care (American Psychological Association 2004). but the treatment principles apply.4 Mood Disorders—Treatment reatment of mood disorders in the elderly generally follows the same principles 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. preferences. treatment trials should be conducted in a systematic and logical sequence. T Psychotherapy for Geriatric Depression A variety of psychotherapeutic approaches can be effective with depressed older adults. the immediate situation. Treatment of bipolar depression is discussed at the end of the chapter in the “Bipolar Disorder” section. For purposes of discussion. we focus mainly on nonpsychotic major depression. and the individual patient’s characteristics. grief for the loss of loved ones or cherished 127 . with modifications as indicated.

appropriate clinical goals may be to manage. All share a common theoretical framework that emphasizes the importance of learning adaptive responses. Gatz et al. 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). Higher-functioning older adults often do well with the usual forms of individual. or family therapies that are provided in outpatient settings. Adjustments for sensory losses (e. These interventions have been examined in well-controlled studies in relatively diverse populations by several independent investigators. benefits for those who respond to such therapies have been shown to persist for at least 1–2 years. “Other Dementias and Delirium”). In major depression. and these problems often form the content of psychotherapy.g. amplification for hearing-impaired patients and large-print homework or educational materials) may be required. Home visits may be needed for older patients with limited mobility. and clear benefits have been shown relative to no-intervention and wait-list control subjects. Most studies have found little difference in efficacy between these procedures. 1998). “Other Dementias and Delirium”). The best-studied psychotherapeutic interventions with older adults are behavior therapy. techniques for addressing specific medical comorbidities (e. Cognitive-behavioral therapy has been . For patients with memory impairment. Depressed elders with cognitive impairment may benefit more from systematic adjustments in the social or physical environment to maximize functional skills.128 Clinical Manual of Geriatric Psychiatry assets or roles. or specialized cognitive training techniques (see Chapter 6. to increase participation in pleasurable activities). group. pain or insomnia) can be especially beneficial. and demands of caregiving. cognitive-behavioral therapy. For persons with high levels of disability or recurrent mental and physical problems. and as discussed in Chapter 1 (“Introduction”). Helping with a specific. rather than eliminate. tangible problem can strengthen the provider-patient relationship and increase the likelihood that other issues can be successfully addressed.. a simple written summary of topics covered in a session can help to support continuity from one session to the next (see Chapter 6. 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.g.. behavior modification (e. For individuals with chronic health problems or significant physical disabilities.g.. and problem-solving therapy (Areán and Cook 2002. symptoms and to sustain as high a level of independence as possible.

personality disorder) Worsen prognosis of the depression (e.” in Diagnosis and Treatment of Depression in Late Life. Used with permission. also has been shown to be effective in alleviating geriatric depression. et al.. with homebound elderly) through use of written materials and periodic telephone contacts (Landreville 1998)... 1994. early Alzheimer’s disease) Necessitate different medications Impair participation in psychotherapy Reduce response to antidepressant medications (e. Confounds in the diagnosis and treatment of depression in elderly patients Concurrent nonpsychotropic medications may Cause depression Change blood antidepressant levels Increase antidepressant side effects Biochemically block antidepressant effects Require modifying the oral dose Concurrent medical illnesses may Cause depression biologically Reduce the efficacy of antidepressant medication or psychotherapy Create disability.g. adapted for use over distance (e. Copyright © 1994. Interpersonal psychotherapy. Edited by Schneider LS. contributing to both chronicity and reduced treatment efficacy Increase the need for simplified medication dosing schedules (e. American Psychiatric Press. Lebowitz BD. Washington... Reynolds CF. Adapted from Rush AJ: “Overview of Treatment Options in Depressed Elderly.Mood Disorders—Treatment 129 Table 4–1. American Psychiatric Press. which combines elements of psychodynamic therapy with cognitive-behavioral approaches. but it has been studied less often than . once daily) Concurrent nonmood psychiatric conditions may Cause depression (e. DC.g. alcoholism) Other issues are that Slower metabolism with age often requires lower doses Transportation difficulties may restrict access to care Increased interview time may be needed Fixed income may limit availability of therapy and nongeneric antidepressant medications because of cost Source.g.g. 171–180. pp.g.

or dyspnea are relatively poor candidates for group therapy. A recent study that compared reminiscence therapy with a social services support control condition found improvement in the level of depressive symptoms and increased life satisfaction in the reminiscence therapy group (Serrano et al. Although individual psychotherapy has been studied most extensively. the lives of two or three generations of the family often have been considerably disrupted. psychosis. severe pain. particularly if diagnosis and administration of treatment are significantly delayed and significant deterioration of function is allowed to develop. New Directions in Psychotherapy Research Although studies of older adults’ preferences for mental health treatments have shown an openness to talk therapy.. By the time adequate medical attention is obtained. significant involuntary movements.g. the family therapy format is the preferred approach in many cases (Tisher and Dean 2000). encouraging compliance with treatment). Because family members are often required to provide details of medical and psychiatric history and are frequently involved in patient management (e. depressed older persons are rarely referred for psychotherapy. Exercising care in selecting patients for group treatment is particularly important for older patients because cognitive impairment. and physical illness may limit an individual’s capacity to tolerate and benefit from group therapy and may negatively influence group process. also appears to have some promise for reducing depressive symptoms. assisting with transportation. sensory deficits. but research on this approach has been less methodologically rigorous than for some other psychotherapy approaches. 2004).130 Clinical Manual of Geriatric Psychiatry the learning-based therapies and typically has been assessed in combination with medication rather than as an independent therapy. group and family therapies are also appropriate for many older adults. based on Eriksonian developmental theory and developed specifically for use with older adults. Major depression commonly presents a crisis for families. Reminiscence therapy (Haight and Webster 1995). Patients with moderate to severe cognitive impairment. but in one investigation. it was less effective than cognitive-behavioral therapy for older adults with major depression. Brief dynamic therapy has been found to be effective in a few studies. and advancements in learning how best to tailor psychotherapy techniques to serve their needs are hampered by the paucity of new studies .

and in clinical practice. the primary care provider. compared with 700 medication trials). and Haverkamp et al. Studies of interventions aimed at helping older people adhere to medication regimens have tended to be small scale and of poor methodological quality (Higgins and Regan 2004). 2002). followed by less frequent maintenance sessions as needed. The multisite IMPACT (Improving Mood: Promoting Access to Collaborative Treatment) project has been providing either medication. Choice of treatment is determined jointly by the patient. a depression care manager (either a nurse or a psychologist). Individuals participating in the IMPACT intervention program have experienced significantly lower depression for at least 12 months compared with patients in usual care. one problem is addressed per session for a total of four to eight sessions. structured psychotherapeutic interventions for treating depression within primary care. or combined therapies to depressed older adults identified in primary care (Unützer et al. but most suggest that one-time. and a seven-stage approach to problem solving is introduced and practiced for each problem. Specific problems are identified. (2004) present a case example of its application with a chronically depressed older person. generally a nurse clinical specialist or psychiatric nurse practitioner. Dropout rates in therapeutic studies of antidepressant medications run as high as 33%. Additional studies of psychotherapy and combined medication and psychosocial approaches are clearly needed. for black and Latino elderly as well as white patients (Areán et al. Such collaborative models for intervention offer the hope of access to effective treatments for depression to a broader range of older adults and offer opportunities for psychiatrists with geriatric expertise to educate about depression and other mental health conditions within a general medical context. 2003). One promising line of research is examining the effectiveness of brief. Areán and colleagues (2001) provide a more detailed description of PST-PC procedures suitable for older adults. Other studies have been examining methods for countering older adults’ negative attitudes toward depression and its treatment and for increasing adherence to recommended therapies. and it is provided by a nurse. 2005).. psychotherapy. only 9 psychotherapy trials had been published. and a consulting psychiatrist. in the 5 years preceding the 2002 review by Areán and Cook. education-only . discontinuation rates of psychoactive medications are even higher (Pampallona et al. Problem-Solving Treatment in Primary Care (PST-PC) is the principal psychotherapeutic intervention being studied.Mood Disorders—Treatment 131 (e. Typically. 2005).g. and despite the presence of multiple medical comorbidities (Harpole et al.

in various combinations with standard pharmacotherapy. 718). and not yet investigated for some other psychotherapeutic approaches (Areán and Cook 2002). 1997). and found that psychotherapy alone was as effective as pharmacotherapy or the combination of psychotherapy with pharmacotherapy in patients with “mild” depression (defined as a pretreatment Hamilton Rating Scale for Depression [Ham-D] score of 19 or less). cognitive-behavioral therapy. This effect has been most clearly documented for interpersonal psychotherapy. The authors speculated that it may be possible to develop briefer and less expensive “compliance-enhancing” interventions than psychotherapy per se. and outcomes have been mixed. Combined Psychotherapy and Pharmacotherapy Only a few studies have compared the efficacy of psychotherapy with that of antidepressant medication in treating depression in older adults. A recent meta-analysis that focused on adherence as an outcome in clinical trials found no difference in dropout rates between pharmacotherapy only and combined psychotherapy and pharmacotherapy in the short term (less than 12 weeks). However. but over longer periods. and “clinical management” to elderly patients with major depression. Psychopharmacotherapy for Geriatric Depression Taylor and Doraiswamy (2004) reviewed the randomized. less often examined for cognitive-behavioral therapy. combination treatment was clearly superior in reducing dropout rates (Pampallona et al. placebo-controlled trials of antidepressants in populations older than 55 and found only 18 trials . but they also noted that “psychological treatment may have a stronger effect than pharmacotherapy on patient satisfaction and social functioning or other dimensions of well being” (p. However. patients with “severe” depression (Ham-D score of 20 or higher) did significantly better with combination therapy (Thase et al. They administered interpersonal therapy. Thase and colleagues (1997) conducted a “mega-analysis” (a meta-analysis of their own original data) of five studies. the combination of antidepressant medication with psychotherapy has shown effectiveness for treatment of major depression.132 Clinical Manual of Geriatric Psychiatry approaches are ineffective. 2004).

The controlledresearch literature indicates that these medications are about twice as effective as placebo in elderly depressed patients and that remission rates of 65%–75% may be expected in nonpsychotic patients. severe thought disorder. and minor depression. Because the presence of psychosis (hallucinations. at least indirectly. and mirtazapine)—all of which act. or behavioral regression) appears to significantly reduce the rate of response to antidepressant therapy. Because little evidence of superior efficacy of one agent over another exists. Because they have a relatively low side-effect profile. by blocking central presynaptic reuptake of norepinephrine. in the following section. psychotic depression is discussed under a separate heading later in this chapter (“Psychopharmacotherapy for Psychotic Depression”). Some also agonize or antagonize various presynaptic and postsynaptic receptors. Large placebo response rates. and the side effects they . (p. the SSRIs. the choice of first treatment is usually based on side-effect profiles. delusions. serotonin. 2285) With this limited “evidence base” in mind. which are related to each agent’s affinity for central muscarinic receptors (anticholinergic effects). 2002). including major depression. They concluded that there is a paucity of published controlled antidepressant trials in the elderly. bupropion. lack of controlled head to head comparisons. or both. we review the advantages and disadvantages of currently available antidepressants in the treatment of nonpsychotic depression. Efficacy studies examining relapse prevention are lacking. and 1 studied mirtazapine. venlafaxine. given an adequate trial of medication. even when concomitant antipsychotic medications are prescribed. dysthymia. and other methodological design differences make cross-trial comparisons difficult. and several nonselective reuptake-inhibiting antidepressants (trazodone. 5 studied selective serotonin reuptake inhibitors (SSRIs). Most published studies examine small sample sizes and do not include common comorbid conditions.Mood Disorders—Treatment 133 that met their criteria: 12 trials studied tricyclics. and noradrenergic receptors (orthostatic hypotension) (Table 4–2). histaminic (H1) receptors (drowsiness and appetite stimulation). The most well-studied and widely used psychopharmacotherapy for nonpsychotic depression in the elderly is the reuptake-inhibiting antidepressants— which include the tricyclic antidepressants (TCAs). 2 studied bupropion. including those age 76 and older (Gildengers et al.

Cyclic antidepressant receptor affinities Agent Amitriptyline Imipramine Doxepin Nortriptyline Desipramine Sertraline Fluoxetine Paroxetine Citalopram Bupropion Trazodone Venlafaxine Mirtazapine Duloxetine Daily dosage (mg) 75–150 75–150 75–200 25–100 75–200 50–150 5–20 10–20 20–40 150–300 150–300 37.Table 4–2.5–75 15–45 40–120 H1 affinitya +++ ++ ++++ ++ + 0 0 0 + 0 +d 0 +++ e 0 α1-Adrenergic affinityb ++++ +++ +++ +++ ++ + 0 0 0 0 ++++ 0 ++(?) 0 Muscarinic affinityc ++++ +++ +++ ++ ++ + 0 ++ 0 0 0 0 + 0 134 Clinical Manual of Geriatric Psychiatry .

2000. tend to be overcome by noradrenergic effects at higher doses. Based on data from Richelson E: “The Pharmacology of Antidepressants at the Synapse: Focus on Newer Compounds. 1 eSedative effects predominant at low doses. Tran PV. c Approximately correlates with potential for anticholinergic symptoms. a Dual Reuptake Inhibitor of Serotonin and Norepinephrine. and NaRIs: New Agents for the Treatment of Depression. Safety and Tolerability of Mirtazapine for the Treatment of Patients With Major Depression. Mood Disorders—Treatment 135 . 0= no effect.” Journal of Clinical Psychopharmacology 25:132–140. ++= moderate effect.” Journal of Clinical Psychiatry 55 (suppl A):34–39. 2005. ++++ =very strong effect. Kent JM: “SnaRIs. dDespite relatively low H affinity. += weak effect.Table 4–2. NaSSAs. Source. Wiltse C.” Lancet 355:911–918. and Thase ME. +++= strong effect. 1994. bApproximately correlates with potential for orthostatic hypotension. et al: “Cardiovascular Profile of Duloxetine. trazodone is very sedating. aApproximately correlates with potential for appetite stimulation and sedation. Cyclic antidepressant receptor affinities (continued) Note. Barkin RL: “Review of the Results From Clinical Studies on the Efficacy. Fawcett J.” Journal of Affective Disorders 51:267–285. 1998.

eating disorder Sexual side effects Weight gain may be a problem in the long run. although rare .Table 4–3. Sexual side effects Trazodone Dangerous side effects: May be more effective than Orthostatic hypotension nontricyclics in severe depression Delayed cardiac conduction Inexpensive Once-daily dosing Inexpensive Dangerous side effects: Orthostatic hypotension Can cause priapism. Advantages and disadvantages of major categories of antidepressants Category First-line agents SSRIs Bupropion Advantages Disadvantages 136 Clinical Manual of Geriatric Psychiatry Venlafaxine Mirtazapine Duloxetine Second-line agents Tricyclics Benign side effects Once-daily dosing Benign side effects Relatively unlikely to cause rapid cycling Benign side effects Stimulates appetite Benign side effects Benign side effects Sexual side effects Interact with many medications prescribed for elderly patients Three-times-daily dosing required Contraindicated in patients with seizures.

Dietary and medication restrictions required Potentially fatal interaction with meperidine.Table 4–3. Advantages and disadvantages of major categories of antidepressants (continued) Category Third-line agents MAOIs Advantages Disadvantages Inexpensive Effective in atypical depression Inexpensive Immediately effective Benign side effects Lithium Psychostimulants (methylphenidate. SSRIs =selective serotonin reuptake inhibitors. amphetamines) Note. SSRIs Only two-thirds as effective as above agents No controlled studies Development of tolerance common MAOIs= monoamine oxidase inhibitors. sympathomimetics. Mood Disorders—Treatment 137 .

such as sexual dysfunction (including inhibited desire. increased QRS). All TCAs have type 1 antiarrhythmic effects and are relatively contraindicated in patients with ischemic heart disease or preexisting cardiac conduction disturbance (increased P-R interval. bundle-branch block. others.g. paroxetine. Some side effects. typically diminish within the first few days to weeks of initiation of therapy. First-Line Agents—Selective Serotonin Reuptake Inhibitors SSRIs have been studied in elderly depressed patients and have been shown to be effective and generally well tolerated and to have few side effects (Newhouse 1996). Because the tetracyclic agent maprotiline has a relatively strong association with seizures and has no advantages that are not matched by other less risky agents. and escitalopram) and the nonselective amine inhibitors bupropion.. citalopram. amitriptyline. nausea. venlafaxine. trimipramine) because of their greater sedating. the dibenzoxazepine amoxapine has mixed neuroleptic-antidepressant properties and attendant risks of extrapyramidal symptoms and tardive dyskinesia and is not recommended. even these experts avoid the tertiary tricyclics (e. 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 summary presented in Table 4–3. Similarly. may not diminish at all. the SSRIs (including fluoxetine. fluvoxamine. protriptyline). It must be noted that some authorities still prefer TCAs in patients with severe. The SSRIs all competitively inhibit several cytochrome P450 (CYP) isoenzymes that are responsible for the hepatic metabolism of several pharma- . nortriptyline. melancholic depression. anticholinergic.. imipramine. the secondary tricyclics (e. and cardiac side effects and their relatively greater tendency to cause orthostatic hypotension than their demethylated counterparts. sertraline. it is not recommended for elderly patients. and anorgasmia) and later-onset weight gain. jitteriness.g. gastrointestinal upset. delayed ejaculation. doxepin. desipramine. however. and mirtazapine are generally preferable to the TCAs and are therefore regarded here as first-line agents. and headache. Trazodone is an effective and safe antidepressant in the elderly.138 Clinical Manual of Geriatric Psychiatry do cause tend to be less dangerous than those caused by tricyclics. such as mild anorexia.

the SSRIs can therefore cause clinically significant increases in serum levels of other medications if administered concurrently. paroxetine is the most potent.S. Although there is no practical way to determine any given patient’s 2C19 phenotype. Fluoxetine. paroxetine. Citalopram is metabolized predominantly by the CYP isoenzymes 2C19 and 3A4. and fluvoxamine. to a lesser extent. the final dosage of 20 mg/day (for the vast majority of patients) is only twice the recommended starting dosage of 10 mg/day. and.Mood Disorders—Treatment 139 ceutical agents (Table 4–4). 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. Fluoxetine has a long elimi- . As is true of the other SSRIs. SSRIs all have an elimination half-life of about 1 day. and at least six polymorphisms of 2C19 that result in slowed metabolism of citalopram have been identified. producing nonlinear increases in plasma concentrations with dosage increases. or sertraline) inhibit their own metabolism. Fluoxetine has mild psychostimulant-like effects and is very weakly anticholinergic. 2003) to reduce the risk of myocardial infarction. Fluoxetine Advantages. In this regard. potentially fatal interactions with monoamine oxidase inhibitors (MAOIs) and should not be administered within 2 weeks of discontinuation of an MAOI. escitalopram. fluvoxamine (but not citalopram. followed by fluoxetine. Stimulant-like properties may interfere with sleep and appetite. escitalopram. 2003). particularly in the first few weeks of therapy. Patients with these phenotypes will have higher blood levels of citalopram at any given dose than will patients with the wild-type allele. citalopram. which has a significantly longer half-life (discussed in the following subsection). which vastly simplifies the process of dosage adjustment in the induction phase of therapy. sertraline. except fluoxetine. similarly fatal interactions have been reported with the antihistamines terfenadine and astemizole. All of the SSRIs can produce serious. although the effect is modest. market but are still available in other countries. both of which have been withdrawn from the U. and dosages must be adjusted accordingly. SSRIs also attenuate platelet activation by depleting serotonin storage and have been shown in at least one study (Sauer et al. Disadvantages.

aripiprazole. alprazolam. propafenone. terfenadine. felodipine. risperidone. desipramine. paroxetine Antipsychotics: Haloperidol.b erythromycin. perphenazine. ondansetron. chlorpromazine. nifedipine. hydrocodone Others: Dextromethorphan.b carbamazepine. timolol Opioids: Codeine. corticosteroids. trazodone Benzodiazepines: Diazepam. cisapride. metoprolol. nortriptyline. verapamil Others: Amiodarone. imipramine. quetiapine 140 Clinical Manual of Geriatric Psychiatry 3A4 . fluphenazine ACE inhibitors: Captopril Antihistamines: Chlorpheniramine β-Blockers: Propranolol. midazolam Hypnotics: Zolpidem Antihistamines: Loratadine. imipramine. tramadol.Table 4–4. astemizoleb Calcium channel blockers: Diltiazem.b quinidine. thioridazine. citalopram. sertraline. lovastatin. clozapine. clomipramine. inducers will lower levels of Antidepressants: Amitriptyline. Psychotropic medications that inhibit or induce cytochrome P450 (CYP) isoenzymes Psychotropic agent Inhibitors Antidepressants Fluoxetinea Paroxetinea Clomipramine Sertraline Citalopram Antipsychotics Haloperidol Inhibitors Antidepressants Fluoxetinea Fluvoxaminea Sertraline Inducers Anticonvulsants Carbamazepine Phenobarbital CYP isoenzyme affected 2D6 Effect May increase levels of Antidepressants: Amitriptyline. astemizole. tamoxifen Inhibitors will raise. venlafaxine.b propafenone. pimozide. triazolam. clarithromycin.

imipramine. fluvoxamine Antipsychotics: Phenothiazines. theophylline. haloperidol. caffeine. ciprofloxacin.Table 4–4. 141 . bAdministration of nefazodone (or other nonpsychotropic inhibitors of CYP isoenzyme 3A4) with these agents may lead to potentially fatal torsades de pointes ventricular arrhythmia. Psychotropic medications that inhibit or induce cytochrome P450 (CYP) isoenzymes (continued) Psychotropic agent Inducers (continued) Antidepressants Citalopram Fluvoxaminea Antidepressants Fluoxetinea Fluvoxaminea Sertraline Antidepressants Fluoxetine Fluvoxaminea CYP isoenzyme affected 1A2 Effect May lower levels of Antidepressants: Amitriptyline. ACE =angiotensin-converting enzyme. warfarin Mood Disorders—Treatment 2C9 2C19 May lower levels of Antidepressants: Amitriptyline. phenytoin. lansoprazole. clomipramine Proton pump inhibitors: Omeprazole. progesterone Note. naproxen. clozapine Others: Acetaminophen. a Relatively more potent inhibitor. phenytoin. pantoprazole Others: Diazepam. warfarin May lower levels of Diclofenac. ibuprofen. estradiol.

Paroxetine causes relatively potent inhibition of CYP2D6 and therefore may pose a problem for patients taking multidrug regimens. It has been studied relatively little in geriatric depression. at least 5 weeks must elapse after discontinuing fluoxetine therapy before an MAOI can be safely administered. Disadvantages. as well as citalopram and venlafaxine. sertraline is somewhat stimulating and may interfere with sleep if administered late in the day. Sertraline has a relatively low potential for competitive inhibition of any of the CYP isoenzymes and is therefore a good choice for patients taking complex multidrug regimens. Disadvantages.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. . 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. Paroxetine has no active metabolites and is less activating than either fluoxetine or sertraline and therefore may be given at bedtime. It is also a relatively potent reuptake inhibitor of dopamine. CYP3A3/4) and therefore may elevate serum levels of propranolol and omeprazole. Paroxetine Advantages. Sertraline Advantages. at least in vitro. Therefore. although several authorities recommend against the use of SSRIs in such patients because of the risk of confusion. Disadvantages. 26). Fluvoxamine causes potentially clinically significant inhibition of CYP1A2 and CYP2C19 (and probably a third. Sertraline has the most linear dose–plasma level relation of the SSRIs. and may have theoretical advantages in patients with Parkinson’s disease. Fluvoxamine is the most sedating of the SSRIs and may be administered at bedtime. It also has mild anticholinergic effects. Fluvoxamine Advantages. Possibly because of its dopaminergic properties.

It does not cause sexual side effects or orthostatic hypotension. Escitalopram Advantages. a review (Settle et al. Escitalopram. The dopaminergic properties of bupropion may be beneficial for patients with Parkinson’s disease. Disadvantages. with consequent risk of serious arrhythmia. An incompletely understood interaction results in significant increases in the QTc interval. is similar to citalopram but more selective and may cause side effects less frequently than does citalopram. and no single dose may be greater than 150 mg. even if only by history. Citalopram is a very weak inhibitor of all the CYP isoenzymes and therefore is the SSRI of choice for patients with complex multidrug regimens. Citalopram is contraindicated in patients receiving pimozide. Disadvantages. which appear to be less frequent in elderly than in middleaged patients. the extended-action form (Wellbutrin SR) may be given twice a day. Bupropion must be given in divided doses at least 4 hours apart (usually three times a day). Significant . and it is very safe in overdose. and the Wellbutrin extended-release version is given once daily. Disadvantages. derly patients. diarrhea). or in patients with a history or current diagnosis of anorexia or bulimia. It has mild gastrointestinal side effects associated with all of the SSRIs (nausea. a weak tendency to cause bradycardia (in about 2%–3% of patients) appears to increase with age. Few studies on escitalopram have been done to date in el- First-Line Agents—Non–Selective Serotonin Reuptake Inhibitors Bupropion Advantages. It does not cause weight gain.Mood Disorders—Treatment 143 Citalopram Advantages. 1999) of three clinical trials found that the sustained-release form of bupropion produced dose-related weight loss in all three studies. the S-enantiomer of citalopram. Bupropion is contraindicated in patients with seizure disorder.

The advantages notwithstanding. . reduced the critical flicker fusion threshold. β-blockers. sexual dysfunction. Weight gain may be intolerable for many patients. Disadvantages. 2004) found that venlafaxine actually increased the “critical flicker fusion” threshold in 88 depressed patients (average age=71). so monitoring is advisable in the early phases of treatment. Disadvantages. its side-effect profile is generally benign and very similar to that of the SSRIs. Only one double-blind. Although venlafaxine blocks reuptake of serotonin and norepinephrine. 2002). The authors concluded that venlafaxine does not cause cognitive impairment in elderly patients. and resulted in significantly more weight gain than did paroxetine (Schatzberg et al. One study (Trick et al. and type 1C antiarrhythmic agents. had fewer side effects in general. whereas the comparator medication. placebo-controlled study in elderly patients has been published to date. Mirtazapine Advantages. The latter effect is consistent with clinical experience suggesting that mirtazapine is particularly effective as an appetite stimulant in elderly depressed patients with poor appetite and weight loss. which tends to diminish as the dosage is increased and noradrenergic effects overcome antihistaminic effects. Downward adjustment of dosage is recommended in patients with liver or kidney disease. making it one of the preferred therapeutic agents in the elderly. weight gain. dothiepin (a TCA not available in the United States). Mirtazapine is an atypical antidepressant with α 2-adrenergic antagonist and serotonin type 2 and type 3 receptor–blocking activity. It is well tolerated and has few side effects other than sedation. One controlled study comparing mirtazapine with paroxetine in elderly patients found that mirtazapine produced an earlier therapeutic response. Venlafaxine also causes supine blood pressure elevations in 3%–5% of patients. and gastrointestinal upset are seen fairly commonly.144 Clinical Manual of Geriatric Psychiatry inhibition of CYP2D6 may result in increased blood levels of certain antipsychotic medications. Venlafaxine Advantages.

liver function tests (e. Thase et al. Other potentially important findings include sinus node dysfunction (sick sinus syndrome). caution is also recommended in patients with first-degree block (i.Mood Disorders—Treatment 145 Duloxetine Advantages. 1999. and alkaline phosphatase) also are obtained because significant hepatic disease is a relative contraindication to use of TCAs and may lead to very high serum levels and possible toxicity. The physical examination is specifically oriented toward detection of signs of narrow-angle glaucoma.. and supraventricular arrhythmia. alanine transaminase [ALT]. Although bundlebranch block presents the greatest risk for development of complete heart block. aspartate transaminase [AST]. bilirubin. prostatism. and congestive heart failure. prolonged P-R interval) and prolonged QRS interval. Data on duloxetine in elderly depressed subjects are lacking Second-Line Agents—Tricyclic Antidepressants TCAs produce side effects that warrant a pretreatment evaluation whenever possible. Reynolds and colleagues (Reynolds et al.. Finally. to date. which could be aggravated by anticholinergic effects of TCAs. which precludes augmentation with lithium salts (see “Pretreatment Evaluation— Lithium Therapy” subsection later in this chapter). Disadvantages. and xerostomia.e. these drugs may increase the risk of sudden death in patients with arrhythmia of any type or who have had myocardial infarction. A 12-lead electrocardiogram is obtained to determine the presence of cardiac conduction disturbance and ischemic heart disease. 1997) published results of a series of very-well-designed treatment studies with elderly subjects that clearly showed the safety and efficacy of nortrip- . Roose and Glassman (1994) originally raised the possibility that because TCAs have type 1A antiarrhythmic properties. Duloxetine is an inhibitor of norepinephrine and serotonin reuptake and has been shown to be effective for depression. and stress urinary incontinence in women. neuropathic pain. which may predispose to the development of significant orthostatic hypotension. all of which may be aggravated by anticholinergic effects of TCAs.g. Nortriptyline Advantages.

is relatively activating. Second-Line Agents—Nontricyclics Trazodone Advantages. so it may have a role in the treatment of patients with significant sleep disturbance. In nonelderly adults. Trazodone has no anticholinergic effects and is extremely sedating. especially in patients with cardiac conduction disturbance and congestive heart failure.146 Clinical Manual of Geriatric Psychiatry tyline. . Disadvantages. was more effective than either desipramine alone or cognitive-behavioral therapy alone in subjects with an average age of approximately 67. Thompson et al. Desipramine is not as well studied as nortriptyline. no therapeutic window). desipramine appears to have a roughly linear serum level response relation (i.. lower desipramine dosages did not appear to be effective. Desipramine has a low side-effect profile. found that desipramine in dosages at or greater than 100 mg/day (when combined with cognitive-behavioral therapy). 1982). Its sedative properties limit its usefulness in many patients. Disadvantages. administered in dosages adjusted to achieve plasma levels between 80 and 120 ng/mL. Desipramine Advantages. and it may not be as safe as nortriptyline. Nortriptyline has the side effects and cardiac risks described earlier for TCAs as a group. desipramine may be less effective in patients whose depression responds better to a mixed noradrenergic-serotonergic agent such as nortriptyline. and is generally well tolerated. As a purely noradrenergic agent. in the absence of desipramine levels for all subjects. Disadvantages. for treatment of major depression. (2001). Trazodone may cause mild gastrointestinal upset and orthostatic hypotension. Response to desipramine may be predicted by a methylphenidate challenge (see “Predictors of Response to Cyclic Antidepressants” later in this chapter). with the likelihood of response increasing as serum level rises above 115 ng/mL (Nelson et al.e.

1993. later age at onset was the strongest predictor of slow recovery (Alexopoulos et al. 2003). In one study. pretreatment measures of orthostatic hypotension (Diehl et al. pretreatment folate blood levels (Alpert et al. Age at onset of illness has produced conflicting results. whereas hospitalization for the index episode of depression and attempted suicide predicted shorter time to response. 1983). pretreatment red blood cell counts (Mentre et al. Cognitive dysfunction also may affect treatment response. and dopaminergic supersensitivity as measured by the apomorphine challenge test (Healy and McKeon 2000). The researchers concluded that prefrontal dysfunction was associated with poor or delayed antidepressant response in depressed elderly patients. Jarvik et al. subacute reduction in prefrontal cortical activity per quantitative electroencephalography (Cook and Leuchter 2001). in another study. However. 1996). 2000) have been reported to have predictive power with respect to subsequent antidepressant response. . Specific laboratory measures and the interaction between specific life events and personality–cognitive characteristics (Mazure et al. specific polymorphisms of the norepinephrine transporter gene (Yoshida et al. high baseline anxiety level was associated with delayed response (median of 5 weeks vs. response to a test dose of methylphenidate (Spar and La Rue 1985). 2004). These laboratory measures include serum cortisol response to administration of oral dexamethasone (Spar and La Rue 1983). In the latter study. patients with earlyonset depressive disorder who received treatment with nortriptyline and interpersonal therapy achieved remission of the index episode more slowly (Reynolds et al. Kalayam and Alexopoulos (1999) found that depressed patients who remained symptomatic after treatment had more abnormal initiation and perseveration scores and longer P300 latency (elapsed time between a stimulus and the occurrence of one voltage peak in a cortical evoked potential) compared with control subjects and depressed patients who achieved remission. 1998). 4 weeks for patients with low anxiety scores). age and chronicity of episode were also significantly associated with time to recovery. none of these laboratory measures has yet gained widespread clinical utility.Mood Disorders—Treatment 147 Predictors of Response to Cyclic Antidepressants Several clinical and demographic factors have been studied as possible predictors of response to treatment of acute depression in the elderly. In a study conducted by Flint and Rifat (1997). 1998).

has been reported for SSRIinduced weight gain. which have been reported in up to 50% of adults. but controlled studies are lacking (Ashton and Rosen 1998. The likelihood of obtaining improved response by increasing the dosage beyond the recommended level is generally low. In this regard. Sertraline. fluvoxamine. to the full adult dosage within the first week or two of therapy. preferably in the morning for the activating agents such as fluoxetine or at bedtime for the sedating agents such as trazodone. as limited by side effects. Initiation of TCA therapy follows the same guidelines but typically calls for a gradual increase of dosage. No effective treatment. bedtime doses of venlafaxine are generally well tolerated. starting dosages for SSRIs and other non-TCA agents are half the usual adult dosage and are increased. but bupropion is quite activating. antacids for nausea and analgesics for headache are often effective. as side effects allow.M.148 Clinical Manual of Geriatric Psychiatry Initiation and Dosage Adjustment of Cyclic Antidepressant Therapy In general. Sexual side effects of SSRIs. paroxetine. mirtazapine. Compliance is usually enhanced by minimizing the number of doses administered during any 24-hour period. and escitalopram activate some patients and sedate others. and the TCAs. Venlafaxine and bupropion must be administered in divided doses. and the last daily dose should not be given after 4:00 or 5:00 P. or central nervous system stimulants such as methylphenidate. Woodrum and Brown 1998). so the timing of dosage is by trial and error. amantadine. to produce a plasma level of 80–120 ng/mL for nortriptyline. bupropion. may respond to treatment with cyproheptadine. Management of Cyclic Antidepressant Side Effects Most side effects caused by non-TCA agents are managed symptomatically. but an increase is worth trying because the side effects of these agents are so benign. citalopram. . other than dosage reduction or switching to another class of antidepressant. or the highest dosage that is safely tolerated for the other TCAs. for example. most of the antidepressants discussed in this chapter have an elimination half-life of about 24 hours and can be administered in a single dose. yohimbine. This dosage is maintained for 6 weeks before dosage increase is considered.

called MAO A and MAO B. dopamine. and serotonin.g. In milder cases. bulk laxatives. serotonin. blurry vision. and dopamine. Dry mouth is relieved by sucking on hard. Urinary hesitancy is often responsive to oral bethanechol. A 1% solution of pilocarpine used as a mouthwash every 3 or 4 hours also has been reported to be helpful (Bernstein 1983). 0. the enzyme responsible for synaptic degradation of the monoamine neurotransmitters norepinephrine. constipation. one drop every 4–6 hours as needed. are instructed to be aware of the possibility of complete urinary obstruction and to have appropriate plans should complete obstruction occur (e.025–0. repeated patient instruction in arising slowly and holding on to something stable for support. particularly men. In the extreme case. preferably sugarless candies or by chewing gum. Orthostatic hypotension is a more difficult problem. 1–2 mg of physostigmine administered by slow intravenous push is effective. Constipation can be managed with stool softeners. Most of the anticholinergic effects can be managed with dosage adjustment and adjunctive agents. artificial tears usually suffice. Because it is worsened by dehydration and by pooling of blood in the lower extremities. MAOIs have not been as well studied .Mood Disorders—Treatment 149 Side effects of TCAs include anticholinergic effects (dry mouth. 10– 30 mg three times a day.. MAO occurs in two forms. Blurry vision may respond to 1% pilocarpine eyedrops.g. Patients.05 mg of fluorohydrocortisone).. urinary hesitancy. and MAO B is found in both brain and gut and oxidizes norepinephrine. Delirium can be life threatening and is usually responsive to discontinuation of the offending agent and supportive treatment. and delirium) and orthostatic hypotension. Support hose can be helpful. MAOIs irreversibly inhibit monoamine oxidase (MAO). and adequate fluid intake. as can careful. orthostatic hypotension may be ameliorated by increasing salt in the patient’s diet or by administering small doses of salt-retaining steroids (e.and second-line treatments or who have a history of good response to agents in this class. to report to the nearest emergency department). MAO A is found in brain only and primarily oxidizes dopamine. Third-Line Agents—Monoamine Oxidase Inhibitors Third-line agents are usually reserved for patients who have not responded to first. This symptom tends to occur early in treatment and appears to be a “threshold” phenomenon that occurs at a certain dosage but does not necessarily worsen if the dosage is increased.

e. phenelzine and tranylcypromine are available for treatment of depression.. and selegiline. and in the presence of sympathomimetic drugs. is available in Canada but not in the United States at the time of this writing. Phenelzine is administered at an initial dosage of 15 mg twice a day. It is more reversibly bound to . Phenelzine is nonstimulating and may be mildly sedating. however. 40 mg/day). increasing to a maximum of 50 mg/day. but it probably does interact at antidepressant dosages. Phenelzine Advantages. patients taking these MAOIs need to be on restricted diets and need to be strongly cautioned against ingesting certain drugs. Disadvantages. gradually increasing to a maximum of 60–75 mg/day. Phenelzine causes irreversible degradation of MAO and therefore may continue to exert effects for 2 weeks or longer after discontinuation of administration. Tranylcypromine Advantages. it loses this selectivity. 1986). which selectively inhibits MAO B. These agents do cause orthostatic hypotension. and tranylcypromine can cause severe hypertensive reactions that can be life threatening. Selegiline does not interact with dietary amines at low dosages. is marketed primarily for adjunctive treatment of Parkinson’s disease but also has been studied in depression. Because of these properties. Orthostatic hypotension from MAOIs is somewhat different from that produced by TCAs in that it tends to be dose related. But at antidepressant dosages (i. at this dosage.150 Clinical Manual of Geriatric Psychiatry as cyclic antidepressants in elderly patients. occurs later in therapy. it is selective for MAO B and enhances dopaminergic transmission. as total body MAO is gradually replaced. tranylcypromine is administered at an initial dosage of 10 mg twice a day. Tranylcypromine is mildly stimulating and may be preferable for patients with psychomotor retardation. one of the first reversible inhibitors of MAO A. dietary monoamine precursors such as tryptophan or naturally occurring pressor substances such as tyramine. Selegiline is administered at dosages of 5–15 mg/day (with levodopa) for Parkinson’s disease. but they appear to be as effective (Georgotas et al. Each of these agents is relatively free of sedative and anticholinergic effects and does not appear to affect cardiac conduction. Moclobemide. phenelzine. and may gradually subside at a fixed dosage. In the United States.

As mentioned. it is probably not. patients who have dementia and who are monitoring their own diet and medications are poor candidates for MAOI therapy. moclobemide is prone to potentially dangerous interactions with other drugs. assessment of the patient’s likelihood of requiring sympathomimetic agents. It has been well studied as an antidepressant. Moclobemide Advantages. Selegiline Advantages. Reversibility of MAO inhibition makes it less likely to pose a problem interacting with other agents. including in elderly subjects. Disadvantages. 1997). Like all MAOIs. Because of its psychostimulant effects. Selegiline is poorly studied at antidepressant dosages and. is prone to potentially dangerous interactions with other drugs. Moclobemide is selective for MAO A and does not require dietary restriction. 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 candidates for MAOI therapy. and has been shown to be comparable to TCAs and SSRIs in efficacy (Amrein et al. Disadvantages. Disadvantages.Mood Disorders—Treatment 151 MAO and therefore requires only a 1-week washout period before sympathomimetic agents or diet ad libitum can be administered safely. The patient’s reliability vis-à-vis dietary and medication restrictions must be assessed carefully. by itself. an antidepressant at these dosages. . like all MAOIs. tranylcypromine may have greater abuse potential than phenelzine. selegiline is selective for MAO B and will not interact with dietary tyramine in low dosages. including determination of pretreatment orthostatic changes in blood pressure and. General Principles of Treatment With MAOIs Pretreatment physical and laboratory examinations should be conducted as described earlier for cyclic antidepressants. However. Specifically. based on the medical history and physical examination.

phenylephrine [NeoSynephrine]. ephedrine. phenylpropanolamine). 10 mg twice a day for tranylcypromine. and maximum tolerable dosage or clear clinical response remains the end point of dosage titration. Antidepressant effects of selegiline tend to appear at 60 mg/day. and palpitations and may progress to frank hypertensive encephalopathy and neurological dysfunction. Meperidine.. Management of MAOI Side Effects Orthostatic hypotension may be managed via the approaches described earlier in this chapter for cyclic antidepressants.or 100-mg tablet of chlorpromazine to carry with them for ingestion in an emergency has been criticized on the grounds that after ingestion. The common practice of giving patients a 50. which may not be regarded as “real medicine” by older patients.152 Clinical Manual of Geriatric Psychiatry Initiation of MAOI Therapy and Determination of Final Dosage Typical starting dosages are 15 mg twice a day for phenelzine. for reasons that are not yet clear. Although it has been shown in nongeriatric subjects that platelet MAO inhibition must reach 80% or more to maximize response. Other synthetic narcotics such as dextromethorphan also have been implicated in causing this syndrome. Special Considerations Regarding MAOIs A particular hazard is the use of sympathomimetic drug–containing cold tablets and nasal sprays (e. most elderly patients experience dosage-limiting orthostatic hypotension at or before 60 mg/day of phenelzine or 40 mg/day of tranylcypromine. α-Adrenergic blocking agents such as phentolamine (2–5 mg intravenously) or chlorpromazine (50–100 mg intramuscularly) followed by smaller doses titrated against blood pressure may be lifesaving. patients may . flushing. and coma that has been fatal in several reported instances. which apparently does not occur with natural narcotics such as morphine or codeine. Patients must be most strenuously cautioned against taking these medications. diaphoresis. interacts with MAOIs to produce an extremely serious syndrome of hyperpyrexia. and 400 mg/day for moclobemide. in clinical practice this laboratory test is rarely available. pseudoephedrine. muscular rigidity.g. many older patients may be so incapacitated as to be unable to reach the nearest emergency department or may experience life-threatening loss of alertness while driving for help. Hypertensive crisis is usually signaled by headache. Practically speaking. For added safety.

augmenting. and insomnia requiring discontinuation of treatment may occur rarely. generally immediately before breakfast and lunch so as not to interfere with appetite or sleep. or combining antidepressants. Cardiovascular side effects are typically limited to very minor increases in blood pressure and heart rate.4 days compared with 27 days for nortriptyline (Lazarus et al.Mood Disorders—Treatment 153 wear MedicAlert bracelets indicating that they are taking MAOIs and specifying that they should not receive meperidine. a more recently developed wake-promoting agent with psychostimulant properties. 1998). Ninan et al. a relatively large body of clinical literature supports the use of psychostimulants in elderly depressed patients. 2004. A double-blind. and results from several open-label studies in nongeriatric subjects are encouraging (DeBattista et al. 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. although methylphenidate is generally preferred because of its relatively lower cardiovascular side-effect profile. Modafinil. dental procedures should be performed with local anesthetics that do not contain epinephrine. 2004). appetite disturbance. Both amphetamines and methylphenidate have been administered. The most common side effect is mild jitteriness. Similarly. Third-Line Agents—Psychostimulants Although controlled studies in elderly patients are lacking. Dosages range from 5 to 20 mg administered orally twice a day. particularly those in whom medical illness precludes the use of cyclic antidepressants or MAOIs (Emptage and Semla 1996). has been proposed as an adjunct to antidepressant therapy. which may be managed with small doses of benzodiazepine anxiolytics. Strategies for Antidepressant Treatment Resistance Depressed patients whose symptoms have not responded to an adequate trial of a single antidepressant are candidates for one or more alternative treatment strategies: switching. 1994). For pur- . 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. but severe dysphoria and agitation.

the published database for lithium augmentation of a cyclic antidepressant or an MAOI and thyroid hormone augmentation of a TCA is most substantial and warrants review (Nelson 2000). The switch 1) from a TCA to an MAOI or venlafaxine or 2) from an MAOI to a TCA or venlafaxine also has been reported to be effective in some cases. random-assignment studies of any of these approaches have been done in elderly patients. methylphenidate. This literature generally focuses on nonelderly adults. For the SSRIs. pindolol. but in one study by Flint and Rifat (1996). for other TCAs and MAOIs. For nortriptyline. or a TCA)— or if the first agent is a combined reuptake blocker. to switch to a different class of medication (i. bupropion. risperidone. Medications used as augmenters include lithium. a small percentage of patients may become responders if the adult dosage is doubled. Augmenting Ongoing Antidepressant Treatment Augmentation involves adding to an ongoing antidepressant regimen a medication that in amount or kind would not be expected to have antidepressant effects. nonresponse means that significant residual symptoms persist despite 6 weeks of treatment at adequate dosages of medication. Although no double-blind. which achieved a 61% response rate. or other reuptake inhibitor) that is likely to be safely tolerated given the patient’s overall medical status (Hirschfeld et al. MAOI. buspirone. the dosage is adequate if it produces a plasma level between 80 and 120 ng/mL. patients who did not respond to nortriptyline were then switched to phenelzine. and for trazodone. thyroid hormone (levothyroxine or triiodothyronine). Of course.. the cumulative response rate was 85% in 101 elderly patients receiving nortriptyline. and duloxetine. TCA. duloxetine. venlafaxine. the meaning of “adequate dosage” depends on the medication used. adequate means the highest dosage tolerated. which achieved a 64% response rate. Switching to Another Antidepressant The literature suggests that the preferred strategy is to switch from a single neurotransmitter–reuptake blocker (e. 2002). The following procedure for lithium augmentation is recommended: after an adequate trial .. SSRI. mirtazapine.g. bupropion. placebocontrolled. and olanzapine. it means the full recommended adult dosage.e.154 Clinical Manual of Geriatric Psychiatry poses of this section. an SSRI) to a combined serotonin and norepinephrine–reuptake blocker (venlafaxine.

Side effects (orthostatic hypotension. bupropion plus an SSRI. 2004). bupropion plus venlafaxine. to be safe and to provide some enhanced effectiveness over either agent administered alone include a TCA plus an MAOI. Rapid response (i. One double-blind. augmentation would appear to be the optimal strategy for older patients with treatment-resistant depression.e.g. moclobemide (a reversible MAOI) plus an SSRI.Mood Disorders—Treatment 155 of cyclic antidepressant or MAOI. mirtazapine plus an SSRI. and combination therapy exposes patients to at least additive side effects and risks of adverse reactions. Thyroid augmentation involves the addition of 25–50 µg/day of triiodothyronine to an ongoing regimen of a TCA. a TCA plus an SSRI. an SSRI plus another SSRI. Generally. within 3–5 days) is common. venlafaxine plus an SSRI. . tachycardia) were those typical for desipramine (Nelson et al. lithium is added in low doses (e. Which Strategy Is Best? Because switching antidepressants requires tapering the first agent. side effects are additive. random-assignment study of middle-aged adults with nonpsychotic major depression found that desipramine (norepinephrine reuptake blocker) and fluoxetine (SSRI) together were significantly more effective than either drug alone in inducing remission after 6 weeks of treatment.4 mEq/mL. small studies. on the basis of largely uncontrolled. Combinations that appear. and reboxetine plus an SSRI (Lam et al. 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.. 2002). followed by administration of the second agent (with its own latency of onset of action). Given the increased sensitivity of older patients to side effects and adverse reactions. Combinations chosen to produce reuptake inhibition of both serotonin and norepinephrine may be most effective. but some patients require up to 2 weeks of augmentation before peak response occurs. 300 mg twice daily) and titrated to at least 0. combination therapy must be regarded as the least advisable of the three approaches to treatment resistance discussed in this section.. an SSRI plus trazodone. then a washout period.

perphenazine. fear. Psychopharmacotherapy for Psychotic Depression The proportion of depressed patients who present with delusions and/or hallucinations appears to increase with age but does not seem to be related to age at onset of depression (Brodaty et al.. risperidone. 1997). social withdrawal.. and hallucinations (if present). Their algorithm specified that partial responders were switched from a TCA plus an antipsychotic to a non-TCA plus an antipsychotic or from a non-TCA plus an antipsychotic to a TCA plus an antipsychotic. . or other antidepressant. and lithium augmentation. insomnia.. or olanzapine in combination with a TCA. within weeks to months) by fading of the delusional beliefs per se. 2004). Flint and Rifat (1998a) reported a 50% response rate in elderly persons with psychotic depression who received treatment for 7 weeks with nortriptyline.e. Treatment entails the simultaneous administration of high-potency. followed by gradual improvement (i.e. and partial responders to ECT were treated with a previously untried antidepressant with lithium augmentation (Trivedi et al. The Texas Medication Algorithm Project used this combination successfully to treat psychotic depression in nonelderly adults. within days) reduction of anxiety. Remission rates are usually much lower than is typical for nonpsychotic depression. SSRI. within a few weeks) in mood. The typical pattern of response is marked by rapid (i. low-dose antipsychotic medications such as haloperidol. Maintenance treatment requires full dosages of both categories of medication because evidence indicates that the prognosis for successful long-term remission is relatively poor when antidepressant monotherapy is administered (Flint and Rifat 1998b). patients who still did not respond were switched to electroconvulsive therapy (ECT). Reynolds (1994) used this approach with nortriptyline (titrating blood levels between 80 and 120 ng/mL) and reported that 80% of remissions were sustained for a year or more.156 Clinical Manual of Geriatric Psychiatry 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.e. neurovegetative symptoms. and disordered behavior related to the delusional beliefs. hypervigilance. followed finally (i.

1999). but the most cautious approach calls for simultaneous treatment with a mood stabilizer. and side effects are usually limited to transient memory impairment (Tew et al. with an important modification. antidepressants may be added. and mirtazapine) or 2) MAOIs. Although switch rates for elderly patients per se have not been published. in this context. Antidepressant treatment alone may be prescribed. those who have not tried and failed other treatments).e. Other indications for ECT as the treatment of first choice include .Mood Disorders—Treatment 157 Psychopharmacotherapy for Bipolar Depression For patients with bipolar depression. Dosing of lithium is as per guidelines in the section “Psychopharmacotherapy for Bipolar Disorder” later in this chapter. Gijsman et al. treatment may be initiated with mood stabilizers alone. TCAs are the third-line treatment option in bipolar depression because TCAs may be more prone to induce a switch into mania or hypomania than either 1) the SSRIs or other first-line agents (including venlafaxine. lithium. response rates (defined as a decline of 50% or more in pretreatment depression ratings) are in the 80%–90% range.2% for all other antidepressants combined (although the difference was not statistically significant). valproate. this condition is the strongest indication for ECT as a first-line therapy. because psychopharmacological therapy has relatively limited effectiveness in psychotic depression. however. lamotrigine. If monotherapy is ineffective. but in the more typical elderly patient who has had an inadequate response to other treatments. the second-line treatment. (2004) reviewed six clinical trials in middle-aged adults and found a 10% switch rate for TCAs and only 3. older than 75). even in the “old-old” (i.e.. and dosing of lamotrigine follows the same guidelines as for young and middle-aged adults. following the principles spelled out earlier. Electroconvulsive Therapy ECT remains the single most effective treatment for major depression with or without psychosis in elderly patients. and carbamazepine are all appropriate. duloxetine.. and both lithium and lamotrigine have been shown to be effective antidepressants (Young et al. ECT is about equally effective in psychotic and nonpsychotic depression. 2004). Remission rates in the range of 75%– 90% or greater can be obtained in “naïve” patients (i.

Treatments are administered until symptom reduction has reached a plateau. 2004). or an atypical antipsychotic medication (e. bilateral electrode placement at levels just above seizure threshold (typically between 60 and 140 millicoulombs).158 Clinical Manual of Geriatric Psychiatry • • • • Active suicidality Severe anorexia High likelihood of inability to tolerate antidepressant side effects High likelihood of medication noncompliance ECT is more commonly used. Theophylline has been linked to status epilepticus during ECT and also should be discontinued if possible (Fink and Sackeim 1998). ziprasidone. risperidone. quetiapine) as needed for control of anxiety. Unilateral. or psychosis—are discontinued during the course of ECT. A naturalistic study of ECT as administered in the community found that outcomes were significantly worse (i. and the investigators concluded that the most likely explanation for the unexpectedly low remission rate was that community practitioners often discontinued treatment before full remission was reached (Prudic et al. and stimuli producing a seizure that lasts for less than 25 seconds are repeated. Our approach produces outcomes similar to (or better than) those achieved in clinical trials and typically requires about 9 treatments to produce full remission (although the range can be from 6 to 20). haloperidol. olanzapine.” This approach is more aggressive than that used by either the typical community-based program or most clinical trials. nondominant electrode placement minimizes memory impairment. after psychopharmacological treatment failure. Seizure generalization and duration are monitored via the cuff-isolation technique. 1999).5 times seizure threshold or more) are required to match the therapeutic efficacy of bilateral treatment in elderly patients (Tew et al. but suprathreshold dosages of current (2. Our approach also . One effective approach is to use brief-pulse. remission achieved in only 30%–47%) than those reported in clinical trials.. sleep.e.g. The switch to high-dose unilateral electrode placement is made only if memory impairment threatens to endanger the patient or causes sufficient subjective distress to threaten continued compliance with treatment. defined retrospectively as “no further improvement over the past three treatments. agitation.. administering three treatments per week. however. Psychopharmacological treatments— other than low-dose benzodiazepines.

Results from open studies have been mixed. controlled study found “a modest. and the extremely low mortality rate of ECT (less than 1 death per 10. Experimental Therapies Repetitive Transcranial Magnetic Stimulation Repetitive transcranial magnetic stimulation (rTMS) uses a rapidly changing magnetic field (produced by electrical coils placed near the scalp) to induce electrical current in brain tissue. (2003) concluded that “current trials are of low quality and provide insufficient evidence to support the use of rTMS in the treatment of depression” (p. clinically nonrelevant decrease in HAM-D scores in both rTMS and sham patients over 2 weeks of treatment” (p. 480). p. at least in the first several weeks after treatment. A doubleblind. the rTMS group continued to improve significantly compared with the placebo group. Given this information. but in some cases. which is cumulative over the course of treatment. may persist much longer. Retrograde memory loss.000 patients). 1323). All of these symptoms usually clear rapidly and are clinically undetectable a week or so after the last treatment. the great majority of patients are willing to accept this degree of memory loss as part of the cost of treatment. 2004. they may persist for as long as 3 or 4 weeks. It has been studied as an adjunct to antidepressants and as a solo treatment for depressive disorders and is regarded by some investigators as a potential alternative to ECT. Studies published since that review offer little to challenge that assessment. but over the subsequent 12-week follow-up. along with the recovery statistics mentioned earlier. and a meta-analysis by Martin et al. The associated anterograde memory impairment.Mood Disorders—Treatment 159 seems to produce a more enduring response. especially for events occurring during the course of treatment. typically reaches the level of mild disorientation to time and mild to moderate anterograde and retrograde memory loss. The authors concluded that “decrease of depressive symptoms may continue after the cessation of rTMS stimulation” (Koerselman et al. 1323). Prophylactic antidepressant treatment is initiated immediately after the last ECT treatment. and memory for some intrahospitalization events may be permanently lost. than that reported by most investigators. An .

a large-scale. The procedure requires surgical implantation of a device that applies small doses (typically less than 1. neck pain.160 Clinical Manual of Geriatric Psychiatry open study supported this conclusion. multicenter. 2002). sham-controlled study is under way at 21 academic sites in North America. as measured by Ham-D and Clinical Global Impression Scale scores. 2002) found that the response rate was sustained and that the remission rate actually increased (from 17% [5 of 30] to 29% [8 of 28]). Side effects are usually minimal and include voice alteration. The dose is externally controllable and is typically set to cycle continuously. . 2004). but there was a trend toward greater reduction in Ham-D scores in the subjects who received 22 weeks of active treatment (Carpenter et al. Vagus Nerve Stimulation Brain stimulation via application of pulsed electrical current to the left cervical vagus nerve has established efficacy as adjunctive therapy in treatmentresistant epilepsy and also has been studied in treatment-resistant depression. although the device was turned off during ECT (Marangell et al. Preliminary results from a subset of 21 subjects (11 who received active treatment for 22 weeks and 10 who received active treatment for 10 weeks and sham treatment for 12 weeks) in this study indicated no statistically significant difference in outcome. randomized. None of the studies of vagus nerve stimulation has focused on elderly patients. and dyspnea. On the basis of these and other results. with a typical schedule being 30 seconds every 5 minutes. 2005).5 mA) of electrical current to the vagus nerve multiple times per second (a typical frequency is 20 Hz) for varying periods. double-blind. and even ECT has been administered to patients with an implanted stimulator. 24 hours per day. (2000) reported 40% improvement in 30 patients receiving treatment for 10 weeks. and a more definitive conclusion regarding the role of vagus nerve stimulation in geriatric depression must await the results of the larger study. open studies have been promising: Rush et al. parallel-group. and a 1-year follow-up study of the same subjects (Marangell et al. Results of several small. finding persistent antidepressant effects of rTMS over a 4-month follow-up period (Benadhira et al. Psychotropic medications are commonly administered concomitantly.

group. and inform patients of any potential known risks. become familiar with current data on efficacy.. by a psychiatrist. 2001). 2005).g. it was more effective among relatively young (55. However. Clinicians need to inquire about the use of complementary and alternative approaches. Educational materials that explain geriatric depression and its effect on family systems (e. 50% or more of patients who report severe depression have used complementary and alternative therapies in an attempt to alleviate symptoms (Kessler et al.to 75-year-old) white women than among minority women and individuals older than 75 (Husaini et al. which provides an opportunity to assess for possible adverse effects of combining alternative therapies with pharmacotherapies (e. physical treatments such as massage and chiropractic. Miller and Reynolds 2003) are a potentially beneficial adjunct to family. or general physician). psychologist.Mood Disorders—Treatment 161 Complementary and Alternative Approaches According to a recent national survey. 2004). A recent meta-analytic review (Anderson et al.g. however. A recent meta-analysis on adverse effects of St.g. mild serotonin syndrome from mixing St. especially in combination with other therapies. John’s wort and SSRIs). few controlled studies of the effectiveness of such self-help materials in treating depression have been done. and other approaches such as spiritual healing and dietary modification. but use of this supplement appears to have declined among adults in the United States from a peak in the 1990s (Kelly et al. Group therapy that used an eclectic approach that combined exercise and preventive health behaviors with psychotherapies (including cognitive and reminiscence therapies) and social skills training was effective in reducing depressive symptoms among a large group of older women living in subsidized housing. John’s wort concluded that it is safe and well tolerated if taken under control of a physician (Knuppel and Linde 2004). oral medications such as herbal medicine and homeopathy. Most persons using these approaches also seek treatment professionally (e. These approaches include cognitive techniques such as relaxation and biofeedback.. or individual therapy.. Encouraging lifestyle modifications such as regular exercise may be useful in reducing depressive symptoms. 2005) not limited to studies of geriatric patients found beneficial effects compared with a delayed-treatment control condition for bibliotherapies that use the popular .

when patients may find themselves alien- . Hypomania and Mania The treatment of signs and symptoms of elevated mood (including reduced need for sleep. Similarly. whereas outpatient management is often sufficient for hypomania or bipolar depression without suicidality. pressured speech.162 Clinical Manual of Geriatric Psychiatry book Feeling Good (Burns 1999). when possible. In the acute manic phase. distractibility. many other self-help depression books on the market have not been systematically studied. safety considerations may warrant initiating psychosocial and psychopharmacological management of signs and symptoms while waiting for the substance effects to wear off and euthymia to return. In hypomania or mania due to a general medical condition. irritability. inpatient treatment is indicated. circumstantiality and tangentiality. grandiosity. impulsivity. and excessive involvement in pleasurable activities that have a high potential for painful consequences). with or without hallucinations and delusions. in elderly patients generally follows the same principles as for young and middleaged adults. Psychosocial Therapy for Bipolar Disorder Psychosocial treatment of mania and hypomania is typically aimed at optimizing compliance with somatic therapies and assisting patients and families with the often daunting task of establishing and maintaining appropriate behavioral boundaries. Bipolar Disorder The site of treatment of bipolar disorder depends on the urgency of the clinical situation. however. Counseling and support are also useful in the aftermath of a hypomanic or manic episode. flight of ideas. substance-induced hypomania or mania is treated by discontinuing or adjusting the dosage of offending substances. hyperactivity. Although this discontinuation or adjustment may be adequate to bring signs and symptoms under control. the underlying medical condition is typically treated in parallel with psychosocial and psychopharmacological management of signs and symptoms of hypomania.

which can occur spontaneously or be provoked by antidepressant therapy. and then dosages are adjusted to achieve serum levels in the 0. low-dose neuroleptic medications such as oral or intramuscular haloperidol. Phase One—Acute Stabilization and Phase Two—Acute Treatment A widely used approach to phase one entails administration of high-potency. insight-oriented therapies are avoided during the acute phase of illness but may be quite effective when the most severe symptoms are under control. 1–4 mg/day of risperidone. or another mood-stabilizing agent. It is important to remember that elderly patients typically have reduced . the appropriate pretreatment evaluation is conducted (see subsection “Pretreatment Evaluation—Lithium Therapy” later in this chapter). or ziprasidone. recent myocardial infarction. and 10–20 mg/day of ziprasidone (which is contraindicated in patients who have a prolonged QTc interval. Psychopharmacotherapy for Bipolar Disorder Depending on the acuity of illness. whereas group settings may not provide enough structure to allow the elderly bipolar patient to benefit.5–2. psychopharmacological management of hypomania or mania in elderly patients may occur in an inpatient or an outpatient setting. In phase one. divalproex. phase two entails oral administration of lithium carbonate. olanzapine. Once symptoms are controlled. family. Both individual and family therapy approaches can be used. Inpatients are typically more impaired and may require a twophase approach to treatment.Mood Disorders—Treatment 163 ated from friends. and other caregivers. Psychosocial treatment of bipolar depression is similar to the treatment of unipolar depression but calls for more psychoeducation of the patient and family regarding the early signs of a switch into mania. the most dangerous or crippling symptoms are rapidly brought under control. remission is sought. Initial doses are in the range of 0. Generally.0 mg for each and are gradually raised until side effects supervene or symptoms are controlled. 5–10 mg/day of olanzapine. If lithium is selected. and in phase two. or uncompensated congestive heart failure or who are taking other medications that can prolong the QTc interval). treating physicians. Typical effective dosages are 1–2 mg/day of haloperidol. or comparable oral doses of risperidone.8 mEq/mL range.4–0.

After 6–7 days at a steady daily dosage. 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. particularly in those who develop deterioration of cognitive performance during lithium treatment (Young et al. oxcarbazepine. Carbamazepine may be most effective in manic patients who cycle rapidly and who have predominantly irritable rather than euphoric mood.000 mg/day (in divided doses) and are adjusted to produce serum levels between 50 and 120 µg/mL. and ataxia. Side effects of and adverse reactions to carbamazepine include sedation. with depressive symptoms and manic symptoms). Divalproex may be of particular value in rapid-cycling patients and those with mixed mania (i. 2004).164 Clinical Manual of Geriatric Psychiatry glomerular filtration rates (by 30%–50%) compared with young adults. Therefore. Side effects are usually minimal and include sedation. lamotrigine. The increased half-life allows once-a-day dosing. serum for determination of lithium level is drawn. 2000. 1987). Other agents that have been proposed for acute and maintenance treatment of geriatric bipolar disorder include the anticonvulsants carbamazepine. Dosages of divalproex range from 400 to 1. topiramate. features that have been reported to occur relatively commonly in elderly manic patients. and an approximately linear dose–serum level relation is assumed within therapeutic dosage ranges. and hypotension. Rare cases of aplastic anemia and agranulocytosis also . phase two) antimanic effects and also may be effective for prophylaxis of mania and hypomania (Ichim et al. and gabapentin. ataxia. Divalproex is an acceptable alternative to lithium in manic elderly patients. dosage increase is commonly required after 4–6 weeks of therapy to maintain therapeutic blood levels. nausea. mild anticholinergic effects... dizziness. Sachs et al. a typical starting dosage may be as low as 150 mg/ day. and antimanic effects appear after 4–7 days. skin rash (rarely including Stevens-Johnson syndrome and toxic epidermal necrolysis).e. elderly patients generally require smaller dosages of lithium to reach therapeutic serum levels. nausea and vomiting. but none has been studied in elderly bipolar patients per se. Because carbamazepine induces its own metabolism. which is also believed to reduce side effects compared with divided doses (Hardy et al. and worsening of congestive heart failure.e. 2000). and the elimination half-life of lithium may be increased up to 36 hours. hypertension. Studies in middle-aged subjects suggest that carbamazepine and lamotrigine both have acute (i.

principles of management are essentially the same as for younger patients. evidence of renal dysfunction. Divalproex and carbamazepine are also effective for longterm management. or bipolar depression is achieved. and elderly patients are somewhat more prone to develop toxicity at any given plasma level of lithium. Carbamazepine undergoes hepatic microsomal metabolism. it is 25 mg once daily for 1 week. the next goal of treatment is long-term prevention of recurrence. carbamazepine.3–0. The physical and neurological examination should be specifically oriented toward detecting thyroid enlargement. Elderly patients may require even smaller dosages at each step. laboratory studies. Phase Three—Long-Term Management of Bipolar Disorder Once remission of mania. Plasma levels of lithium in the elderly are generally lower than those required for reduction of acute symptoms. As is the case for young adults. a rigid schedule of dosage increases is required: for nonelderly adults. Pretreatment Evaluation—Lithium Therapy Physical and neurological examination. all of which may be exacerbated by lithium therapy. and one study in elderly patients found that lamotrigine added to lithium or divalproex led to remission (Robillard and Conn 2002).8 mEq/mL. Evidence of congestive heart failure. hypomania. other anticonvulsants. and a 12-lead electrocardiogram are recommended. 50 mg once daily for the second week. Dosages required to sustain these levels are typically lower than those needed for middle-aged adults.Mood Disorders—Treatment 165 have been reported. is particularly important because diuretics can significantly increase lithium blood levels. baseline blood studies and periodic reevaluations are necessary for patients taking this drug. Lamotrigine in nonelderly manic patients is as effective as lithium for phase two management. thus. so the general pharmacokinetic and pharmacodynamic considerations discussed in Chapter 2 (“Normal Aging”) apply. which may require initiation of diuretic therapy. divalproex. To reduce the risk of rash. and 100 mg once daily for the last 2 weeks. and lithium are the primary agents in widespread use. typically in the range of 0. and dosages are adjusted to minimize side effects while maintaining blood levels in the therapeutic range described earlier. otherwise. and tremor. In patients with musculoskeletal disease who may require treatment with nonsteroidal anti-inflammatory agents or patients with hypertension who may require angiotensin-converting .

total triiodothyronine). mild polydipsia and polyuria. and carbamazepine can cause neutropenia. periodic (e. References Alexopoulos GS. which is a strong relative contraindication to lithium therapy because significant bradycardia or dysrhythmia may be precipitated. rarely. every 6 months) physical examination of the thyroid and reevaluation of serum thyrotropin and triiodothyronine levels are recommended. A complete blood count is recommended prior to initiating treatment with either agent. and the question of renal tubular damage remains controversial.e. Arch Gen Psychiatry 53:305–312. Tremor is not usually of clinical significance and rarely requires dosage manipulation. Side effects of long-term lithium therapy may include hypothyroidism and goiter.g. The laboratory evaluation is oriented toward detection of renal dysfunction (i. et al: Recovery in geriatric depression. Diarrhea is usually mild and intermittent and rarely requires concomitant antidiarrheal therapy. Pretreatment Evaluation—Other Mood Stabilizers Divalproex can cause thrombocytopenia. Delirium. Because lithium therapy can affect thyroid function. 1996 . sedation. >1.e.. and. hepatic toxicity. Young RC. The electrocardiogram is aimed at ruling out sick sinus syndrome. and “cognitive dulling” can occur but are typically seen at higher serum levels (i. serum urea nitrogen. Meyers BS. and liver function studies should be done prior to initiating carbamazepine therapy. agranulocytosis. Management of Lithium Side Effects Acute side effects include nausea. diarrhea.166 Clinical Manual of Geriatric Psychiatry enzyme inhibitors.. serum creatinine.. Nausea can be minimized by administering doses after meals and by preceding doses with prophylactic antacids. Benign nonspecific T-wave abnormalities and U waves that reverse with cessation of treatment are common in patients taking lithium and do not require discontinuation of treatment. and generalized fine tremor.0 mEq/mL). electrolytes) and establishment of pretreatment thyroid function (thyrotropin. caution is necessary because both categories of medication can cause clinically significant increases in serum lithium levels.

Ann Pharmacother 30:151–157. et al: Increased rate of psychosis and psychomotor change in depression with age. Lembke A. Solvason HB. 2004 Cook IA. et al: Transcranial magnetic stimulation for refractory depression (letter). 2003 American Psychological Association: Guidelines for psychological practice with older adults. and gammaaminobutyric acid concentrations in depressed patients. Am Psychol 59:236–260. Med Care 43:381–390. New York. and selective serotonin reuptake inhibitors in elderly depressed patients: a clinical overview. Boston. Paradis C. Stabl M. 1998 Benadhira R. Wright. Lewis G. Moreno FA. Araya R. Silva RR. Psychol Med 27:1205–1213. et al: Improving depression care for older. Semin Clin Neuropsychiatry 6:113–120. et al: Pretreatment systolic orthostatic blood pressure and treatment response in geriatric depression: a revisit. Journal of Clinical Geropsychology 7:93–104. et al: Self-help books for depression: how can practitioners and patients make the right choice? Br J Gen Pract 55:387–392. 2005 Bernstein JG: Drug Therapy in Psychiatry. Reynolds CF: Treating depression in older medical patients with psychotherapy. Can J Psychiatry 42:1043–1050.Mood Disorders—Treatment 167 Alpert M. Biol Psychiatry 52:293–303. et al: A prospective trial of modafinil as an adjunctive treatment of major depression. 2004 Amrein R. Parker G. J Clin Psychopharmacol 24:87–90. Saba G. 2005 Ashton AK. Hegel MT. 1993 Emptage RE. Samaan A. Hunkeler E. et al: Effect of vagus nerve stimulation on cerebrospinal fluid monoamine metabolites. Pouget ER: Prediction of treatment response in geriatric depression from baseline folate level: interaction with an SSRI or tricyclic antidepressant. Semla TP: Depression in the medically ill elderly: a focus on methylphenidate. Am J Psychiatry 162:193. MA. 2004 Diehl DJ. J Clin Psychopharmacol 13:189–193. 2001 Areán PA. Avon Books. J Clin Psychopharmacol 23:309–313. Leuchter AF: Prefrontal changes and treatment response prediction in depression. 1997 Anderson L. 1996 . 1997 Burns DD: Feeling Good: The New Mood Therapy. 2001 DeBattista C. Ayalon L. 2005 Areán PA. minority patients in primary care. Biol Psychiatry 56:418– 426. et al: Efficacy and tolerability of moclobemide in comparison with placebo. Henauer S. tricyclic antidepressants. 1983 Brodaty H. Houck PR. norepinephrine. 2002 Areán PA. Rosen RC: Bupropion as an antidote for serotonin reuptake inhibitor– induced sexual dysfunction. Kling MA. J Clin Psychiatry 59:112–115. Luscombe G. Cook BL: Psychotherapy and combined psychotherapy/pharmacotherapy for late life depression. 1999 Carpenter LL.

pp 61–92 Gatz M. 2000 . et al: Course and rate of antidepressant response in the very old. Perspect Psychiatr Care 40:45– 52. Fox LS. Taylor & Francis. Gen Hosp Psychiatry 27:4–12. and Applications. 1997 Flint AJ. et al: Methylphenidate in early poststroke recovery: a double-blind. McKeon P: Dopaminergic sensitivity and prediction of antidepressant response.168 Clinical Manual of Geriatric Psychiatry Fink M. Shulman KI. PA. Arch Phys Med Rehabil 79:1047– 1050. et al: Comparative efficacy and safety of MAOIs versus TCAs in treating depression in the elderly. et al: Pharmacokinetics of lithium in the elderly. Knight BG. J Clin Psychopharmacol 7:153–158. J Affect Disord 69:177–184. et al: Empirically validated psychological treatments for older adults. Houck PR. Rifat SL: The effect of sequential antidepressant treatment on geriatric depression. Chrostowski J. J Psychopharmacol 14:152–156. Olsen MK. Thompson LW: Applying cognitive-behavioral therapy to the psychological problems of later life. 1995 Hardy BG. Geddes JR. Webster JD (eds): The Art and Science of Reminiscing: Theory. et al: Problem-solving treatment for complicated depression in late life: a case study in primary care. Journal of Mental Health and Aging 4:9–46. Areán P. Int J Geriatr Psychiatry 13:23–28. 1998 Haight BK. Hapworth W. 1996. 1986 Gijsman HJ. Rendell JM. 1996 Flint AJ. 1998 Flint AJ. 2004 Gildengers AG. Mackenzie SE. et al: Improving depression outcomes in older adults with comorbid medical illness. Edited by Zarit SH. 2004 Healy E. in A Guide to Psychotherapy and Aging: Effective Clinical Interventions in a Life-Stage Context. Mulsant BH. Hegel MT. Biol Psychiatry 21:1155–1166. Depress Anxiety 5:103–107. 2005 Haverkamp R. J Affect Disord 36:95–105. 1998a Flint AJ. Williams JW Jr. Washington. placebo-controlled study. McCue RE. Rifat SL: Two-year outcome of psychotic depression in late life. Sackeim HA: Theophylline increases the risk of status epilepticus in ECT. et al: Antidepressants for bipolar depression: a systematic review of randomized. 1987 Harpole LH. 1998b Gallagher-Thompson D. 1998 Georgotas A. controlled trials. 2002 Grade C. Methods. American Psychological Association. J ECT 14:286–290. Research. Rifat SL: The treatment of psychotic depression in later life: a comparison of pharmacotherapy and ECT. Redford B. Rifat SL: Effect of demographic and clinical variables on time to antidepressant response in geriatric depression. DC. Am J Psychiatry 161:1537– 1547. Bristol. Fiske A. Am J Psychiatry 155:178–183.

Kelley K. Regan C: A systematic review of the effectiveness of interventions to help older people adhere to medication regimes. et al: Pretreatment orthostatic hypotension in geriatric depression: predictor of response to imipramine and doxepin. 2001 Knuppel L. 2004 Lam RW. et al: Methylphenidate and nortriptyline in the treatment of poststroke depression: a retrospective comparison. Cummings S. Ann Clin Psychiatry 12:5–10. Read SL. Arch Phys Med Rehabil 75:403–406. J Clin Psychiatry 65:1470–1479. placebo-controlled study of repetitive transcranial magnetic stimulation in depression. Alexopoulos GS: Prefrontal dysfunction and treatment response in geriatric depression. van Duijn H. Am J Psychiatry 157:896–903. 2002 Landreville P: Cognitive bibliotherapy for depression in older adults with a disability. Arch Gen Psychiatry 56:713–718. Barbanoj MJ. Systematic review and meta-analysis. Int J Group Psychother 54:295–319. 2002 Martin JL. Arch Intern Med 165:281–286. 2005 Kessler RC. Bruce ML. 1998 Lazarus LW. 2004 Koerselman F. et al: Combining antidepressants for treatment-resistant depression: a review. Davis RB. 2000 . Montgomery SA. Age Ageing 33:224–229. Cohen NL. Linde K: Adverse effects of St. Maciejewski PK. 2003 Mazure CM. et al: Partial response and nonresponse to antidepressant therapy: current approaches and treatment options. Berk M. follow-up. Langsley PR. Kilbourne B. Wan DD. et al: Recent trends in use of herbal and other products. Rush AJ. 2004 Hirschfeld RM. et al: Group therapy for depressed elderly women. 1983 Kalayam B. J Clin Psychiatry 63:826–837. Moberg PJ.Mood Disorders—Treatment 169 Higgins N. J Clin Psychiatry 63:685–693. John’s wort: a systematic review. Br J Psychiatry 182:480–491. 2002 Husaini BA. 1999 Kelly JP. George MS. Am J Psychiatry 158:289–294. 1994 Marangell LB. et al: Vagus nerve stimulation (VNS) for major depressive episodes: one year outcomes. 2004 Ichim L. randomized. Laman DM. J Clin Psychopharmacol 3:368–372. Brook S: Lamotrigine compared with lithium in mania: a doubleblind randomized controlled trial. Schlaepfer TE. et al: Repetitive transcranial magnetic stimulation for the treatment of depression. Mintz J. 2000 Jarvik LF. Biol Psychiatry 51:280–287. J Clin Psychiatry 65:1323–1328. Soukup J. et al: The use of complementary and alternative therapies to treat anxiety and depression in the United States. et al: A 3-month. Clin Gerontol 19:69–75. Aguglia E. Kaufman DW. et al: Adverse life events and cognitivepersonality characteristics in the prediction of major depression and antidepressant response.

Am J Geriatr Psychiatry 7:64–69. randomized study. and Preventing Depression in Later Life. Bollini P. Dew MA. Reynolds CF: Living Longer Depression Free: A Family Guide to Recognizing. MD. Quinlan DM. et al: Desipramine plasma concentration and antidepressant response. Arch Gen Psychiatry 39:1419–1422. Frank E. Tibaldi G. Olfson M. 2004 Newhouse PA: Use of serotonin selective reuptake inhibitors in geriatric depression. 2000 Nelson JC. Jatlow PI. 1999 Nelson JC: Augmentation strategies in depression 2000. 1996 Ninan PT. et al: Patient adherence in the treatment of depression. Am J Psychiatry 155:795–799. 1998 Miller MD. Johns Hopkins University Press. et al: Treatment of 70(+)-year-olds with recurrent major depression: excellent short-term but brittle long-term response. 2003 Nebes RD. Bollini P. Hassman HA. Baltimore. 2004 Reynolds CF III: Treatment of depression in late life. 1994 Reynolds CF III. Golmard JL. Am J Med 97:39S–46S. Glass SJ. J Clin Psychiatry 61 (suppl 2):13–19. 1999 Robillard M. Br J Psychiatry 180:104–110. Dew MA. et al: Combined pharmacotherapy and psychological treatment for depression: a systematic review. Biol Psychiatry 55:301–312. Arch Gen Psychiatry 61:714– 719. J Clin Psychiatry 60:26–29. Mazure CM. 1998 Reynolds CF III. Pollock BG. et al: Combining norepinephrine and serotonin reuptake inhibition mechanisms for treatment of depression: a double-blind. Can J Psychiatry 47:767–770. Psychiatry Res 81:403–405.170 Clinical Manual of Geriatric Psychiatry Mentre F. Biol Psychiatry 55:296–300. et al: Effectiveness of electroconvulsive therapy in community settings. J Clin Psychiatry 57:12–22. 2004 Prudic J. et al: Relationships between low red blood cell count and clinical response to fluoxetine in depressed elderly patients. Launay JM. 2004 Pampallona S. Conn DK: Lamotrigine use in geriatric patients with bipolar depression. Treating. 1982 Nelson JC. et al: Effects of age at onset of first lifetime episode of recurrent major depression on treatment response and illness course in elderly patients. Frank E. Mulsant BH. Marcus SC. J Clin Psychiatry 65:414–420. Kupelnick B. et al: Adjunctive modafinil at initiation of treatment with a selective serotonin reuptake inhibitor enhances the degree and onset of therapeutic effects in patients with major depressive disorder and fatigue. et al: Cognitive effects of paroxetine in older depressed patients. Jatlow P. 2002 . 2002 Pampallona S.

Am J Psychiatry 156:1865–1870. Rodrigues HE. Coon DW. Dean S: Family therapy with the elderly. Greenhouse JB. Circulation 1:32–36. Kremer C. Psychol Aging 19:270–277. Am J Geriatr Psychiatry 9:225–240. George MS. 2002 Serrano JP. Am J Geriatr Psychiatry 10:541–550. Haskett RF. 2000 Sauer WH. Neuropsychopharmacology 29:2285–2299. Biol Psychiatry 47:276–286. 2004 Settle EC.Mood Disorders—Treatment 171 Roose SP. Australian and New Zealand Journal of Family Therapy 21:94–101. Glassman AH: Antidepressant choice in the patient with cardiac disease: lessons from the Cardiac Arrhythmia Suppression Trial (CAST) studies. Kimmel SE: Effect of antidepressants and their relative affinity for the serotonin transporter on the risk of myocardial infarction. Clin Ther 21:454–463. Latorre JM. Kahn DA. et al: Treatment of major depression with psychotherapy or psychotherapy-pharmacotherapy combinations. 1985 Taylor WD. Batey SR. et al: Vagus nerve stimulation (VNS) for treatmentresistant depressions: a multicenter study. Berlin JA. La Rue A: Major depression in the elderly: DSM-III criteria and the dexamethasone suppression test as predictors of treatment response. et al: Mirtazapine vs. 2000 Sachs GS. 2000 . 2001 Tisher M. Paroxetine Study Group: double-blind. Doraiswamy PM: A systematic review of antidepressant placebo-controlled trials for geriatric depression: limitations of current data and directions for the future. randomized comparison of mirtazapine and paroxetine in elderly depressed patients. Printz DJ. La Rue A: Acute response to methylphenidate as a predictor of outcome of treatment with TCAs in the elderly. 1994 Rush AJ. Arch Gen Psychiatry 54:1009–1015. 1997 Thompson LW. 2003 Schatzberg AF. J Clin Psychiatry 55 (suppl A):83–87. Postgrad Med (Spec No):1–104. et al: Comparison of desipramine and cognitive/behavioral therapy in the treatment of elderly outpatients with mildto-moderate depression. Gatz M. et al: Safety profile of sustained-release bupropion in depression: results of three clinical trials. 2004 Tew JD. Am J Psychiatry 140:844–847. et al: The Expert Consensus Guideline Series: medication treatment of bipolar disorder 2000. Stahl SM. 1999 Thase ME. Sackeim HA. et al: Acute efficacy of ECT in the treatment of major depression in the old-old. et al: Life review therapy using autobiographical retrieval practice for older adults with depressive symptomatology. J Clin Psychiatry 46:466–469. Gallagher-Thompson D. 1999 Spar JE. Mulsant BH. Frank E. 1983 Spar JE.

Ann Pharmacother 32:1209–1215. J Am Geriatr Soc 51:505–514. Arch Gen Psychiatry 61:669–680. et al: Pharmacotherapy of bipolar disorder in old age: review and recommendations. Gyulai L.801 depressed older adults in primary care. et al: Pharmacokinetics of citalopram in relation to genetic polymorphism of CYP2C19. 2004 Unützer J. Brown CS: Management of SSRI-induced sexual dysfunction. Katon W. Am J Geriatr Psychiatry 12:342–357.5 mg b.172 Clinical Manual of Geriatric Psychiatry Trick L. randomized. 1998 Yoshida K. Mulsant BH. Takahashi H. Am J Psychiatry 161:1575–1580. et al: Clinical results for patients with major depressive disorder in the Texas Medication Algorithm Project.) venlafaxine and 75 mg (25 mg mane. Chen GL. et al: A double-blind. Callahan CM. Higuchi H. 2003 Woodrum ST. 26-week study comparing the cognitive and psychomotor effects and efficacy of 75 mg (37. 50 mg nocte) dothiepin in elderly patients with moderate major depression being treated in general practice. et al: Prediction of antidepressant response to milnacipran by norepinephrine transporter gene polymorphisms. He N. Rush AJ. 2003 . Drug Metab Dispos 31:1255–1259. Crismon ML. J Psychopharmacol 18:205–214. 2004 Trivedi MH. Stanley N. Rigney U. et al: Depression treatment in a sample of 1. 2004 Yu BN.d.i. 2004 Young RC.

past and present exposure to potential toxins. The family history should include inquiry about Down syndrome. signs or symptoms of neurological or psychiatric illness. in order to 1) establish the temporal relationship between possible etiological factors and the onset of cognitive decline. and past and present psychosocial stressors. Accordingly. level of alertness. form. Mental Status Examination A comprehensive clinical mental status examination remains the cornerstone of the diagnosis of dementia. including the patient’s medical records. past surgeries. which can help to identify the underlying pathophysiological process causing dementia. affect (direction and degree). substance use. should be used to supplement information provided by the patient and the patient’s primary caregiver. General categories of appearance.and late-onset Alzheimer’s disease. 173 . and an attempt should be made to establish detailed timelines. including alcohol and medications. mood. and neurological or mental illness. and 2) permit the potentially important distinction between early. flow. degree of cooperation.5 Dementia and Alzheimer’s Disease Identifying the Dementia Syndrome History An accurate history of the current illness is particularly important in the diagnostic evaluation of dementia. It is particularly important to focus on trauma. multiple sources of information. dementia.

Items are hierarchically ar- . psychomotor activity. Table 5–1 lists several cognitive mental status examinations appropriate for geriatric patients. 1994). The Dementia Rating Scale (DRS. Some tests. Results of these procedures can provide a valuable baseline for assessing treatment-related cognitive changes and also can be used to determine whether a referral for neuropsychological assessment is desirable or feasible. Folstein et al. where the base rate of serious cognitive problems is lower. Mattis 1976). it is generally not appropriate to extrapolate from initial studies of new instruments that rely on well-characterized. All cognitive screens perform better in practice settings where dementia is commonly observed and less well in community-based settings or primary care. Clinical assessment of mental status may be supplemented by administration of a structured examination of the type described in the next section. 1987) are of intermediate length and may be useful in a wide range of psychiatric and medical settings. should have acceptably high diagnostic accuracy. As additional validation studies accumulate for a particular instrument.g.. and should meet the practical needs of the situation (e. The selected screen should tap the core cognitive processes of the disorders most commonly represented in the practice setting. are very brief and are intended only for gross screening. delusions. the Mini-Cog. clinically distinct samples of dementia patients and control subjects in estimating how the instrument will perform in a more heterogeneous practice setting. is the most comprehensive of the mental status instruments developed for older adults. Jurica et al. it becomes easier to determine whether a particular screening scale is right for a given situation. such as Animal Naming. and judgment and insight are assessed along with cognitive function. now available in an updated form (DRS-2. Teng et al. and the short form of the Orientation-Memory-Concentration Test. presence or absence of hallucinations. the Cognitive Abilities Screening Instrument (CASI. and the Neurobehavioral Cognitive Status Examination (Kiernan et al.174 Clinical Manual of Geriatric Psychiatry and content of thought. and other morbid thought content. 1975). The Mini-Mental State Examination (MMSE. and the Appendix provides test forms or additional information on several of these scales. 2001). Standardized Measures for Rating Cognition The choice of a cognitive screening tool should be based on several considerations. As a result. available time and personnel).

attention. screen and metric allow quick testing of intact persons Limited data on validity of separate scales or applicability to diverse samples Dementia and Alzheimer’s Disease 20–30 175 . wide application. 30-point scale assesses orientation. good norms positive rate with poorly educated patients 20 items from modified Cognitive Abilities form of the MMSE and Screening Instrument (CASI. memory. 1975) Description 11-item. 1987) Separate scales assess attention. orientation. Teng et al. most populations different versions developed in different locales and languages Profile format assists in giving feedback. language. Folstein et al.Table 5–1. registration and delayed recall. high falsefunctions. calculation. plus judgment question Cognistat (Neurobehavioral Cognitive Status Examination [NCSE]. examines several deficit. reasoning 10–15 May not be more sensitive 100-point scoring range to dementia than the may make it sensitive to standard MMSE for mild impairment. Kiernan et al. visuoconstruction Administration time (min) 5–10 Advantages and applications Limitations Insensitive to mild or focal Brief. 1994) Hasegawa Dementia Screening Scale. language. Cognitive mental status examinations and brief screening tools Measure Mini-Mental State Examination (MMSE. visuoconstruction.

2001) memory. sensitive to wider range of situations. Mattis 1976) DRS-2 (Jurica et al. initiation and perseveration. no generally accepted patients. Duff Canning et al. (DRS. sensitive to method of parietal function and administration and some aspects of frontal or scoring. well accepted by Insensitive to mild deficit. will detect moderate to severe memory processes most directly affected by dementia Alzheimer’s disease 1 Clock Drawing Test (e.g. may be useful cutoff scores likely to as an initial screen when vary by education level time is very limited and ethnicity Very brief. Shulman 2000) Drawing the face of a clock and setting hands to a specified time 2–5 . Cognitive mental status examinations and brief screening tools (continued) Measure Description Administration time (min) 30–45 Advantages and applications Limitations 176 Clinical Manual of Geriatric Psychiatry Scales assess attention.. dementia. limited data on use with diverse dementia than are briefer samples scales Extremely brief. will detect Insensitive to mild deficit or conditions affecting moderate to severe nonlanguage skills. does not assess executive function.Table 5–1. as possible for 60 seconds 2004) May detect subcortical or Take too much time to administer in some frontal brain deficit..g. visuoconstruction Naming animals as quickly Animal Naming task (e. Dementia Rating Scale conceptualization.

designed to tap Limited data available on applicability to diverse memory processes most samples. 1983) Six items assess temporal orientation. 1999) 3–5 Very brief. 2000) Description Three-word learning and recall task plus clock drawing Administration time (min) 2–4 Advantages and applications Limitations Insensitive to mild deficit. and moderate to severe independent validation dementia. will detect relatively new test. mental control 3–5 Free and cued recall of four Memory Impairment words Screen (MIS. Katzman et al. Buschke et al. assesses only impaired in early one cognitive domain dementia 177 . Very brief. Cognitive mental status examinations and brief screening tools (continued) Measure Mini-Cog (Borson et al. will detect moderate to severe dementia Insensitive to mild deficit and visuospatial impairment Dementia and Alzheimer’s Disease Orientation-MemoryConcentration Test (OMCT.Table 5–1. recall of an address. developed for studies are needed use with ethnically and linguistically diverse populations Very brief.

delayed recall and copying of pentagons—are likely to be failed by patients with Alzheimer’s disease. subsequent studies have shown that this cutoff score is likely to overidentify poorly educated persons as impaired and fail to detect true decline in well-educated individuals.178 Clinical Manual of Geriatric Psychiatry ranged within sections. memory. Recalling of only two of three words. Scores at the twenty-fifth percentile are above typical cutoffs for impairment. The MMSE.000 persons from several areas within the United States. has been translated into several languages. but if the history or other observations raise a question of decline. a score at this level may warrant further assessment or monitoring. A Closer Look at the MMSE Table 5–2 presents sample items from the popular MMSE. and praxis than do most mental status examinations and includes items that may be sensitive to frontal-lobe impairment (initiation and perseveration sections). as with all screening instruments. despite some recognized limitations. Although the MMSE was not specifically designed to screen for Alzheimer’s disease. 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 score of 23 or fewer correct items was recommended as a cutoff to screen for cognitive impairment. initially validated with elderly psychiatric groups and nonpsychiatric community control subjects. Folstein and colleagues (1975) have emphasized that the MMSE does not establish a diagnosis of dementia. or even one word. instead. Table 5–3 presents median values and scores at the twenty-fifth percentile for several age and educational groups. The MMSE has high interrater reliability and adequate retest reliability in stable conditions. Initially. may fall within normal limits for . so that the first item serves as a screen for intact ability in each domain. This scale provides more extensive assessment of language. The widespread use of this test with diverse populations is likely to ensure its continued popularity. it identifies individuals with possible cognitive impairment that may warrant further assessment. certain items—most notably. based on an epidemiological survey of more than 18. However. 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. and a modified form suitable for hearingimpaired patients is also available.

) Naming Written command 0–1 0–1 aComponent of the MMSE that is particularly sensitive to mild Alzheimer’s disease (Galasko et al. it is less useful in screening for frontotemporal dementia or subcortical dementia (see Chapter 6.” (Repeat up to five times. and as a result. This scale is not sensitive to executive or psychomotor changes. 16204 North Florida Avenue. particularly when prompts are provided. I am going to say three words. 1987). CAR (pause). 1990. Published 2001 by Psychological Assessment Resources. Lutz. Sample items from the Mini-Mental State Examination (MMSE) Cognitive skill Task(s) Score 0–1 0–3 Orientation for timea “What is the date?” Registration “Listen carefully. “Other Dementias and Delirium”). Further reproduction is prohibited without permission of PAR. Inc. Reproduced by special permission of the Publisher. Inc. Inc. Psychological Assessment Resources. Despite careful attempts at translation. You say them back after I stop. LAKE (pause). Many patients with Alzheimer’s disease will have forgotten that they were asked to remember some words when delayed recall is requested. 1998 by Mini Mental LLC. some older persons.) “What is this?” (Point to a pencil or pen.” (Show examinee the words on the stimulus form: CLOSE YOUR EYES. FL 33549. Teng et al. which are largely white and middle class. Inc. research suggests that some MMSE items may be biased for use with populations whose primary language is not English or whose cultural identification differs from that of normative samples.) “Please read this and do what it says. but score only the first trial. Source. by Marshal Folstein and Susan Folstein. Inc. by calling (813) 968–3003. strongly suggests a problem with retention characteristic of Alzheimer’s disease or other disorders producing amnesia. from the Mini Mental State Examination.. Now repeat those words back to me.Dementia and Alzheimer’s Disease 179 Table 5–2. but inability to recall any words. Several items showed significant ethnicity or language differences in a comparison of white . The MMSE can be purchased from PAR. Copyright 1975.. Ready? Here they are… HOUSE (pause). Other items on the MMSE that are sensitive to early or mild Alzheimer’s disease are design copying and temporal orientation.

: “Population-Based Norms for the Mini-Mental State Examination by Age and Educational Level.Table 5–3. et al. Mini-Mental State Examination scores by age and educational level Age (years) Education 0–4 years Median 25th percentile 5–8 years Median 25th percentile 9–12 years Median 25th percentile Some college or higher Median 25th percentile 30 28 29 28 29 28 29 28 29 27 28 27 28 26 28 25 29 27 29 27 28 27 28 27 28 26 27 25 26 23 26 23 27 25 27 25 27 24 27 24 26 24 26 22 25 22 24 21 22 20 22 20 22 19 22 19 21 19 21 18 19 16 20 15 50–54 55–59 60–64 65–69 70–74 75–79 80–84 ≥85 180 Clinical Manual of Geriatric Psychiatry Source. All rights reserved.” Journal of the American Medical Association 269:2386–2391. . Copyright © 1993. American Medical Association. Anthony JC. Adapted from Crum RM. 1993. Bassett SS.

However. some of the items most sensitive to Alzheimer’s disease (delayed recall and design copying) are minimally affected by ethnicity and educational differences. like the MMSE. In two independent cohorts of older adults being followed up for dementia. a 60-second Animal Naming task performed as well in detecting Alzheimer’s disease as did the MMSE. 2005).. Developed initially for patients in Japan and the United States. 1999). Abbreviated Cognitive Screens There has been an emphasis in recent research on the development and validation of very brief cognitive assessment tools that might be suitable for dementia screening in primary care settings or other situations when time is very limited (Lorentz et al. 1995). and when the Animal Naming task was combined with recall of a five-item name and address (“John Brown 42 Market Street Chicago”). initial screens for dementia of several types. optimal verbal fluency cutoff scores are likely to vary by education . McCurry et al. a cutoff score of less than 14 animals in 60 seconds was highly effective in detecting dementia. have long been included in neuropsychological testing batteries to evaluate retrieval from semantic memory.g. Another study (Duff Canning et al. The CASI (Teng et al. this test has now been used in several large-scale studies that provide normative reference points (e. which mainly included well-educated older adults. 1994) (see Table 5–1) includes 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 testing. and recent studies examining the diagnostic accuracy of such tasks suggest that they could play a role as brief. However. sensitivity to dementia was high. especially Animal Naming. sensitivity and specificity surpassed those of the MMSE (Kilada et al. 2002). Category fluency measures. 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. even among persons with MMSE scores greater than 24. is influenced by age and education in older adults without dementia.Dementia and Alzheimer’s Disease 181 and Hispanic adults. Performance on the CASI. In that study. 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 (Loewenstein et al.

which is the core early deficit in Alzheimer’s disease and certain other dementias. By combining the most sensitive item used in the MMSE and CASI (i. are likely to perform less well. and outcomes usually were not affected by linguistic background. whereas others present a predrawn circle. A practical drawback to clock drawing is the lack of standard procedures for administration and scoring. The Mini-Cog (Borson et al. possibly. 2005). but many patients can complete the task in 1 or 2 minutes. 2000) is composed of a three-item word learning and recall task and a simple clock drawing task. or those with little or no education. A recent review of the performance of cognitive screening tests in diverse groups (Parker and Philp 2004) concluded that. very old persons.182 Clinical Manual of Geriatric Psychiatry level and. Asian American. An additional advantage is that this test was designed for and has been validated with multiethnic elderly populations (black. However. 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. and the visual outcomes can be useful in showing undetected cognitive problems to patients or their family members. and scoring is relatively simple and straightforward. Clock drawing tests also have been widely used for very brief cognitive screening. 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).e.. and care must be taken to use appropriate normative reference points. and Hispanic) and appears less likely to be biased by low education and literacy than is the full MMSE (Borson et al. Because of these drawbacks. A recent review of clock drawing procedures for dementia screening (Shulman 2000) found fairly high sensitivities and specificities (about 85%). Animal Naming is not recommended as a stand-alone cognitive screen. Administration time runs from 2 to 4 minutes. the Clock Drawing Test is generally not used as a stand-alone screening measure. Attempting to re-create such a familiar item is generally acceptable to patients. Another limitation is that clock drawing does not directly test for impaired memory. Administration time varies depending on the version used and the patient’s psychomotor skills. ethnic and linguistic background. in general. Some methods require the patient to draw the circle for the clock face. 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. .

The OMCT correlates highly with the MMSE. a six-item version of the Blessed Information Memory Concentration Test (Katzman et al. the authors provide recommended cutoff scores for use in screening for dementia and for Alzheimer’s disease. and the relative lack of independent validation data is a limitation. and the total score combines both free and cued recall. 2002). most treatment and management decisions revolve around the patient’s functional abilities. 1983). it was found to be more sensitive to mild or subclinical dementia (Brooke and Bullock 1999). both free and cued recall are assessed. The Orientation-Memory-Concentration Test (OMCT). but in at least one study. It taps several skills often affected in dementias of various types. it has not been used widely yet. and memory for verbal narrative (a spoken phrase).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. Advanced age and very low education adversely affect scores. has been adapted for telephone screening. 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 information. Administration time is about 4 minutes. After a delay of about 2 minutes filled with an unrelated task (counting forward and backward from 1 to 20). mental control (counting backward and reciting months backward).g. including temporal orientation. the cue word for “apple” would be “fruit”). 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. Ability to perform everyday activities in an independent fashion is only modestly correlated with outcomes of mental status . For populations with different base rates of disease. Rating Functional Skills Although testing of cognitive function is useful in the detection and diagnosis of dementia. takes approximately 5 minutes to administer.. Although the Memory Impairment Screen is a promising screening tool. and has been translated into Spanish. The Memory Impairment Screen is more effective in identifying Alzheimer’s disease than is the three-word recall task from the MMSE (Kuslansky et al. 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 category cue (e.

a very brief mental status examination. The Direct Assessment of Functioning Scale (Loewenstein et al. It has . The NPI provides frequency and severity ratings for 12 psychiatric and behavior problems commonly observed in dementia. shopping. premorbid ability levels. scores on the IQCODE are relatively unaffected by education.184 Clinical Manual of Geriatric Psychiatry examinations or neuropsychological tests. or language proficiency. Also. Unlike scores on many cognitive screening tests. which consists of eight items assessing areas of function considered crucial for maintaining independent living in the community (e. or telling time—instead of relying on informants’ reports of everyday function. this scale yields generally comparable outcomes for both English. delusions and hallucinations. using the telephone.. 1994) is rated by physicians or trained professionals on the basis of observation of the patient and input from caregivers. because persons with little or no education often perform poorly on mental status examinations. Examples of such scales include the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE.and Spanish-speaking patients. including agitation. The NPI (Cummings et al. The scale measures a single general factor of cognition. may be preferable to more extensive cognitive assessment for screening or diagnosing dementia (Wilder et al. addressing an envelope. and apathy and indifference (see Appendix for NPI items). has high reliability. and thus it is important to assess these skills in addition to testing mental status when dementia or other cognitive impairments are suspected. Other Rating Measures Other observer-rated scales have been developed to aid in screening for dementia or to identify specific psychiatric symptoms that can accompany dementia. A widely used functional scale is the Instrumental Activities of Daily Living measure developed by Lawton and Brody (1969) (see Appendix). combined with functional assessment. Jorm et al. 1989) presents tasks to the patient—such as making change. 1995). Cummings 1997). and performs as well as brief cognitive screening tests in detection of dementia (Jorm 2004). Developed for use with elderly persons with mild to moderate dementia. 1991) and the Neuropsychiatric Inventory (NPI. being responsible for medications).g. Several brief rating scales have been developed for use with family members or other caregivers to identify problems in everyday functioning. The IQCODE relies on observations of caregivers or others familiar with everyday behaviors and abilities of the patient.

Laboratory evaluation of dementia Routine workup Complete blood count Electrolyte panel Screening metabolic panel Thyroid function tests Vitamin B12 and folate levels Tests for syphilis Tests for human immunodeficiency virus antibodies. A modified version for use in nursing homes is also available. normal-pressure hydrocephalus. subcortical or brain-stem pathology Electroencephalogram—to evaluate ictal or episodic features of history or mental status examination Lumbar puncture—to rule out central nervous system infection suggested by physical examination Positron emission tomography and single photon emission computed tomography—to differentiate Alzheimer’s disease from other dementing illnesses . The screening battery presented in Table 5–4 was recommended by Reichman (1994). recent bleed Magnetic resonance imaging of head—same indications as for CT. Laboratory Evaluation Laboratory evaluation is aimed at identifying illnesses known to cause dementia and generally begins with a selected standardized battery of tests with relatively high sensitivity and low specificity. as indicated by history Urinalysis Electrocardiogram Chest X ray Additional studies to rule out specific conditions Computed tomography (CT) of head—to rule out mass lesion.Dementia and Alzheimer’s Disease 185 been translated into several languages for use in cross-cultural investigations and has acceptable validity and reliability (Cummings 1997). is more sensitive for ischemia or infarction. Table 5–4.

. whereas others result in dementia only in some cases. including general intelligence. learning and memory. and impaired recognition are commonly observed in dementia of the Alzheimer’s type but are less often noted in subcortical dementia (e.. However. as declining functional brain reserve reduces the individual’s ability to tolerate physiological derangement. If coexisting psychiatric disturbance is suspected. and irreversible by currently available approaches. The remainder of this chapter and the next chapter are devoted to the differential diagnosis of dementia. Other measures may be useful as well. “Mood Disorders—Diagnosis”). Huntington’s chorea or Parkinson’s disease). language. attention. whereas for other causes of dementia. For example. Alzheimer’s disease). visuospatial performance. Each of these tests has been developed for measures applicable to geriatric populations or has been studied extensively with older patients. but any battery for dementia evaluation should tap a full range of cognitive abilities. For some etiologies. and reasoning or problem solving.g. the pattern of performance on these tests can either strengthen or weaken the case for certain types of dementia. . on tests of learning and memory. symptoms may be arrested or reversed to varying degrees with specific treatments. sharply reduced delayed recall. Neuropsychological testing alone is generally not sufficient to establish a particular etiology of dementia. the list of factors capable of causing dementia increases with the age of the patient. Table 5–6 lists general medical conditions and medications that can produce symptoms of dementia. dementia is chronic. or in major depression. In general. Table 5–5 summarizes some of the tests that we have found useful in diagnostic assessment for possible dementia.186 Clinical Manual of Geriatric Psychiatry 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. a very shallow learning curve. some disorders invariably produce a dementia (e. in frontotemporal dementia. Common Etiologies of Dementia Dementia may result from a diverse set of disorders and conditions. beginning with the most common cause of dementia—Alzheimer’s disease.g. progressive. psychodiagnostic measures also should be included (see Chapter 3.

Table 5–5. forgetfulness suggested by better cued than free recall. and processing speed Interpretation IQ scores lower than estimated baseline or low age-scaled subtest scores may indicate impairment Comment Influenced by education Wechsler Memory Scale—Third Edition (WMS-III) Low scores on immediate Sensitive to mild Orientation. good recognition memory Dementia and Alzheimer’s Disease California Verbal Learning Test (CVLT) 187 . normed to age 80 Short-term and secondary (recent) memory. word pairs. memory span. faces. normed to age 89 Functions assessed Verbal and nonverbal skills. including vocabulary. normed to age 89 immediate and delayed impairment recall of stories. perceptual organization. attention. reasoning. dementia or delayed memory control. and abstract designs Memorization of a 16item shopping list. effect of interference Slow rate of learning or Sensitive to mild cortical and subcortical impaired delayed recall dementia suggests amnestic deficit. mental Battery of verbal and amnesia. strategy use. Examples of neuropsychological assessment instruments Test Wechsler Adult Intelligence Scale— Third Edition (WAIS-III) Description General adult intelligence battery with 14 subtests. nonverbal memory indices may indicate tests. benefits of cues. scenes. recognition.

developed a Registry for and normed for older Alzheimer’s Disease adults (CERAD) Word List Learning Object Memory Evaluation Slow rate of learning or Sensitive to mild dementia of the impaired delayed recall Alzheimer’s type. Examples of neuropsychological assessment instruments (continued) Test Description Functions assessed Interpretation Comment 188 Clinical Manual of Geriatric Psychiatry Consortium to Establish Memorization of a list of Verbal learning and delayed recall 10 words. normed to age 90+ Cutoff scores vary with age and education More sensitive to mild anomic aphasia than is mental status examination Intrusions may be noted in early Alzheimer’s disease. access to Cutoff scores vary with age and education semantic memory. ability to organize rapid retrieval . with low education level suggests amnestic normed for ages 70–90 memory. perseverations or loss of set in subcortical dementias Boston Naming Test (BNT) Controlled Oral Word Association Test (COWAT) Verbal fluency. easier suggests amnestic than CVLT deficit Delayed recall <50% or Good test of secondary Storage and retrieval Memorization of 10 memory for patients very low rate of learning from secondary common objects.Table 5–5. access to semantic objects. normed to age memory 90+ Naming of words beginning with specified letters. delayed recall deficit and recognition Naming of drawings of Confrontation naming.

New York. pp. Spreen O. Wiley. Examples of neuropsychological assessment instruments (continued) Test Description Functions assessed Composite index of visual scanning speed. and Lezak M. 381–416. slowing in subcortical dementia May be more sensitive than memory tests to frontotemporal and subcortical dementias Trail Making Test (TMT) Lines drawn to connect number and letter sequences. normed to age 80 Cutoff scores vary with age and education Dementia and Alzheimer’s Disease Note. For references to tests and further discussion. 4th Edition. mental flexibility. New York. see La Rue A: “Geriatric Neuropsychology: Principles of Assessment. cognitive flexibility Interpretation Cutoff scores vary with age and education Comment Failure on alternating sequence noted in mild brain impairment of various types.” in Handbook of Assessment in Clinical Gerontology. Edited by Lichtenberg PA. Strauss E (eds): A Compendium of Neuropsychological Tests.Table 5–5. New York. Loring D: Neuropsychological Assessment. sequencing. Oxford University Press. 1999. 2nd Edition. 189 . normed to age 80+ Wisconsin Card Sorting Test (WCST) Sorting of multidimensional patterns into categories. 2004. Howieson D. visuomotor integration Inferring concepts. Oxford University Press. 1998.

190 Clinical Manual of Geriatric Psychiatry Table 5–6. General medical conditions and substances that can produce symptoms of dementia General medical conditions Dementia syndrome of depression Endocrine disorders Thyroid diseasea Parathyroid disease Adrenal disease Pituitary disease Infections Acquired immunodeficiency syndromea Creutzfeldt-Jakob disease and other viral and prion encephalitides Cryptococcosis Encephalitis Leptomeningitis Neurosyphilis Progressive multifocal leukoencephalopathy Neurological disorders Alzheimer’s diseasea Amyotrophic lateral sclerosisb Cerebellar and spinocerebellar degeneration Huntington’s chorea Dementia with Lewy bodiesa Multiple system atrophy Normal-pressure hydrocephalus Olivopontocerebellar degeneration Parkinsonism-dementia complex of Guam Parkinson’s diseasea Pick’s diseaseb Progressive subcortical gliosisb Progressive supranuclear palsy Nutritional disorders Folate deficiency Pellagra .

arteriosclerosisa Hypertensiona Repeated episodes of cerebral ischemia or hypoxiaa Vasculitis 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 bPatient Common offender. may present as having “frontotemporal dementia. primary and metastatica Chronic subdural hematoma Obstructive hydrocephalus Systemic disorders Anemia Paraneoplastic dementia Pulmonary disease with hypoxia or hypercarbia Vascular disorders Atherosclerosis.” .Dementia and Alzheimer’s Disease 191 Table 5–6. General medical conditions and substances that can produce symptoms of dementia (continued) Nutritional disorders (continued) Pernicious anemia Thiamine deficiencya Space-occupying lesions Brain tumor.

a substance involved in cholesterol metabolism and probably in neuronal protection and repair. 1 in 4 persons age 80 and older.5 times the risk of developing Alzheimer’s disease (compared with those homozygous for the ε3 allele). The other well-established risk factor for Alzheimer’s disease is the apolipoprotein ε4 allele (APOE4). in another 10%–20% (Langa et al.. possible) cases are included in the survey (see Figure 5–1). and half of persons age 95 and older have Alzheimer’s disease. Because the definitive diagnosis of Alzheimer’s disease requires direct visualization of characteristic neuropathology (i.192 Clinical Manual of Geriatric Psychiatry Alzheimer’s Disease Alzheimer’s disease. accounts for about 50% of all cases of primary dementia and may combine with other conditions. Alzheimer’s disease is at best a probable diagnosis in the living patient. and persons with minimal education are at increased risk (Katzman 1993). ε3. Estimates of prevalence vary depending on the extent of diagnostic workup performed and whether mild (i. neuritic degeneration and loss) in brain tissue of affected patients and brain biopsy is prohibitively risky.to 15fold risk of developing Alzheimer’s disease. The risk of “sporadic” (as opposed to “familial”. amyloid β-peptide–containing senile plaques. obesity.. primarily vascular dementia. Rates of diagnosis of Alzheimer’s disease in women are higher than in men. 2004). and ε4—of the gene on chromosome 19. hypercholesterolemia. accounting for about 1% of all Alzheimer’s disease cases) and late-onset (older than 65) subtypes. which is rare before age 50 and uncommon in early old age. but prevalence climbs steeply after age 65.e. neurofibrillary tangles [NFTs] consisting of hyperphosphorylated tau protein. which codes for the production of apolipoprotein. and other factors also have been associated with increased risk of Alzheimer’s disease. atherosclerotic cerebrovascular disease. Epidemiology—Risk Factors and Protective Factors Age is the major risk factor for Alzheimer’s disease. and presence of two ε4 alleles is associated with a 12. This effect of APOE4 is mediated . including both early-onset (age 65 or younger.e. Presence of one ε4 allele is associated with about 2. Conservative estimates suggest that 1 in 20 persons age 65 and older. hypertension. There are three alleles— ε2. Diabetes. see subsection “Genetics of Alzheimer’s Disease” later in this chapter) disease is increased in persons with a history of head injury and is very high in individuals with Down syndrome who survive to middle age.

1989. and prevalence of cardiovascular disease and tends to worsen response to head trauma. In a meta-analysis of 11 retrospective and prospective studies. Prevalence of Alzheimer’s disease in the Framingham Study and the East Boston Study. 2005). Szekely et al. age-related cognitive decline. The literature reviewed did not allow any conclusions regarding which . decreased longevity. and it is attenuated in black and Hispanic individuals (Harwood et al.Dementia and Alzheimer’s Disease 193 Prevalence of Alzheimer’s disease (%) Age (years) Figure 5–1. (2004) concluded that long-term exposure to nonsteroidal anti-inflammatory drugs (NSAIDS) is associated with a reduced risk for developing Alzheimer’s disease. 1992 and Evans et al. in part by earlier onset of Alzheimer’s disease in those who are APOE4 positive. 2004). increased plasma cholesterol levels. APOE4 is also associated with the presence of concomitant Lewy bodies in autopsy studies of patients with Alzheimer’s disease (Tsuang et al. Data from Bachman et al. Source. and several other disorders (Smith 2000).

2004). Engelhart et al. There was no evidence of an association between intake of β-tocopherol and Alzheimer’s disease risk. over a 3-year follow-up period. (2005). This observational report was contradicted by the Women’s Health Initiative Memory Study. vitamin E and C supplements did not reduce the risk of Alzheimer’s disease. 2001). who found that hormone replacement therapy was protective against the development of Alzheimer’s disease. which reduce cholesterol. (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. 508). older subjects did not sustain the same benefit. Zandi et al. might reduce the risk of Alzheimer’s disease. with reductions in risk of 34% per 5-mg/day increase in α-tocopherol. Several cross-sectional observational studies raised the possibility that statins. and 25% per 1-mg/day increase in δ-tocopherol. according to several investigators. which found that estrogen with or without progestin increased the risk of developing both Alzheimer’s disease and mild cognitive impairment (Shumaker et al. and δ-tocopherols were significantly and inversely associated with incident Alzheimer’s disease. a randomized. . They followed up 1. placebo-controlled primary prevention trial in women age 65 years or older. in food or supplement form. but only in women ages 50–63. γ-. 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.9 years and found that dietary α-. and the most effective duration of treatment or dosage of medication is unknown. However. emphasis added). double-blind. In this study. Morris and colleagues (2005) reported data that may partially resolve the disagreement between the two studies discussed in the prior paragraph. but not either vitamin alone. The risk of developing Alzheimer’s disease also appears to be reduced in people who ingest adequate amounts of the antioxidants vitamin E and vitamin C. 3228. (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).194 Clinical Manual of Geriatric Psychiatry NSAIDs are best. A possible explanation for these discrepant findings was reported by Henderson et al. 40% per 5-mg/day increase in γ-tocopherol. Hormone replacement therapy (estrogen with or without progestins) in postmenopausal women was reported to reduce the risk of developing Alzheimer’s disease (LeBlanc et al.041 subjects age 65 or older for a median of 3.

Utah. at least three pathological criteria for Alzheimer’s disease are internationally acceptable: 1) Braak’s criteria (Braak and Braak 1991). The role of statins in the prevention of dementia and Alzheimer’s disease remains to be determined. and laboratory tests. Neuropathological Criteria At present. Zandi et al. the small number of subjects who reported taking statins. and a history of insidious onset and gradual progression must be present. 1984). dementia of the Alzheimer’s type is diagnosed (Table 5–7). physical examination. dementias associated with other neurological diseases (e. General criteria for dementia must be met. which began in 1995 with the enrollment of 5. Diagnostic Criteria In DSM-IV-TR (American Psychiatric Association 2000). Statin use was less frequent in subjects with prevalent dementia.. the term dementia of the Alzheimer’s type is applied to patients whose condition meets clinical and laboratory criteria for probable Alzheimer’s disease.Dementia and Alzheimer’s Disease 195 To examine this relation. (2005) followed up with 4. This finding is surprising given the known relation between atherosclerosis and cerebrovascular disease.g. The authors acknowledged several methodological and statistical factors that may have obscured a real association. 1991) and their combination. Separate standards are listed for the clinical diagnosis of probable and possible Alzheimer’s disease (Table 5–8). 2) Consortium to Establish a Registry for Alzheimer’s Disease (CERAD) criteria (Mirra et al. and the small number who developed Alzheimer’s disease. among them the short duration (about 3 years) of exposure to statins. Pick’s disease or Creutzfeldt-Jakob disease) are coded separately. 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. an investigation of the genetic and environmental antecedents of dementia among the elderly population of Cache County. and 3) National Institute on Aging and .092 individuals age 65 or older. if all other causes of dementia are ruled out by the history.895 participants in the Cache County Study. but the authors found no association between statin use and subsequent onset of dementia or Alzheimer’s disease.

increase in number there (stage IV). Washington. The deficits do not occur exclusively during the course of a delirium. (1) other central nervous system conditions that cause progressive deficits in memory and cognition (2) systemic conditions known to cause dementia (3) substance-induced conditions E. The CERAD pathological criteria are based on the density of neuritic plaques (also discussed in the subsection “Neuropathology of Alzheimer’s Disease” later in this chapter) in three areas: 1) the second frontal gyrus at the . spread to the entorhinal region (stage II). American Psychiatric Association. and then involve the association neocortex (stage V) and finally the primary cortex (stage VI). extend to the hippocampus proper (stage III). Text Revision. Summary of DSM-IV-TR diagnostic criteria for dementia of the Alzheimer’s type A. Ronald and Nancy Reagan Institute of the Alzheimer’s Association criteria (National Institute on Aging and Reagan Institute Working Group on Diagnostic Criteria for the Neuropathological Assessment of Alzheimer’s Disease 1997). 4th Edition. Copyright © 2000. DC. The course is characterized by gradual onset and continuing cognitive decline. The development of multiple cognitive deficits manifested by both (1) memory impairment (2) one (or more) of the following cognitive disturbances: (a) aphasia (b) apraxia (c) agnosia (d) disturbance in executive functioning B. These deficits cause significant impairment in social or occupational functioning and represent a significant decline from a previous level of functioning. Braak’s criteria are based on the distribution of NFTs (described in the subsection “Neuropathology of Alzheimer’s Disease” later in this chapter) as Alzheimer’s disease progresses: NFTs first appear in the transentorhinal area (stage I). The cognitive deficits are not due to any of the following: Source. F. C. American Psychiatric Association. 2000. Used with permission. D. The disturbance is not better accounted for by another Axis I disorder. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders.196 Clinical Manual of Geriatric Psychiatry Table 5–7.

and patients may present to general psychiatric clinical settings. 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. 2) the first temporal gyrus at the level of the amygdala. delusional disorder. when stage B is seen in patients between 50 and 75 years. even in the early stages. 1995). In some patients with Alzheimer’s disease.. and 11% had hallucinations within the month before evaluation. Clinical Presentation As is true for all dementing illnesses.g. Delusions are usually persecutory in nature and are typically fragmented and inconsistent. along with a definite clinical history of dementia (Murayama and Saito 2004).. including depressive or anxiety disorders. unlike those seen in the common functional disorders (e. or mood disorder with psychosis). psychosis. and this prevalence was not affected by severity of dementia or of depressive symptoms. Table 5–9 summarizes the clinical and laboratory findings typically observed in uncomplicated cases as the disease progresses (Group for the Advancement of Psychiatry 1988). the myriad ways in .3 times the density of neocortical NFTs than did those without psychosis. and stage C = more than 30 neuritic plaques per 100× light microscopic field. hypochondriacal delusions and Capgras’ syndrome are also common (Migliorelli et al. and when stage C occurs in patients older than 75 years. and delirium. Gormley and Rizwan (1998) reported that one-third of Alzheimer’s disease patients had delusions. Density is rated as follows: stage A =less than 2. Alzheimer’s disease is diagnosed when stage A is identified in patients younger than 50 years. 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. stage B =approximately 6. schizophrenia. and 3) the supramarginal gyrus with parieto-occipital sulcus.e. Functional symptoms nearly indistinguishable from those of concomitant psychiatric illness are part of the presentation of Alzheimer’s disease. Common delusional content includes the belief that one is being threatened. the psychosis is clinically prominent enough to obscure the underlying cognitive impairment and delay accurate diagnosis.Dementia and Alzheimer’s Disease 197 level of the caudate-putamen complex. Delusions in Alzheimer’s disease typically do not have the elaborate “connectedness” seen in functional delusions (i. or abused by caregivers or that possessions are being stolen. deprived.

or similar examination. weight loss) Seizures in advanced disease Computed tomography normal for age Probable Alzheimer’s disease uncertain if Sudden onset. language. confirmed by neuropsychological tests Deficits in two or more areas of cognition Progressive loss of memory and cognitive functions No disturbance of consciousness Onset between ages 40 and 90 Absence of systemic disorders or other brain diseases that in and of themselves could account for deficits Diagnosis of probable Alzheimer’s disease supported by Progressive loss of specific cognitive functions (e.g. incontinence. depression.g. perception) Impaired activities of daily living and altered behavior patterns Family history of similar disorders. normal or nonspecific changes on electroencephalogram Computed tomography—cerebral atrophy with progression documented by serial observation Other features consistent with probable Alzheimer’s disease Plateaus in course of progression of illness Associated symptoms (e. especially if neuropathologically confirmed Laboratory results of normal lumbar puncture. Criteria for clinical diagnosis of Alzheimer’s disease from the NINCDS-ADRDA Work Group Probable Alzheimer’s disease Dementia: established by clinical examination. focal neurological findings.198 Clinical Manual of Geriatric Psychiatry Table 5–8.. motor skills. seizures or gait disturbance early in course of illness . documented by Mini-Mental State Examination.. Blessed Dementia Scale.

but full depressive syndromes (e..g. major depression) are relatively rare. which the patient is able to tie the delusional belief to all aspects of his or her experience). olfactory. 1984. gradually progressive. History The history of Alzheimer’s disease is typically one of insidious onset and gradual progression of cognitive and functional impairment..g. parkinsonism) Note. Adapted from McKhann et al. Criteria for clinical diagnosis of Alzheimer’s disease from the NINCDS-ADRDA Work Group (continued) Possible Alzheimer’s disease Dementia syndrome in absence of other causes and in presence of variations in onset. with few of the . or tactile—are intermittent and of varying and usually trivial content. Source. ADRDA =Alzheimer’s Disease and Related Disorders Association. Depressive symptoms and apathy occur in about 20%–25% of Alzheimer’s disease patients at any given time (Lyketsos et al. NINCDS= National Institute of Neurological and Communicative Disorders and Stroke. presentation. lacking the ordered. 2000b). meaningful quality typical of functional hallucinations. and hallucinations—usually auditory but sometimes visual. or clinical course A second systemic or brain disorder sufficient to produce dementia but not considered the cause Single. severe cognitive deficit Definite Alzheimer’s disease Clinical criteria for probable Alzheimer’s disease with neuropathological confirmation Subtypes Familial Onset before age 65 Presence of trisomy 21 Other relevant disorders (e.Dementia and Alzheimer’s Disease 199 Table 5–8.

usually has difficulty counting backward Severe cognitive decline Severe disorientation Can barely count to 10 Unaware of almost all recent experiences 200 Clinical Manual of Geriatric Psychiatry Misplaces items. mild anomia Normal to minimal deficit Limited vocabulary and sentence Fluent aphasia with unintelligible structure. hobbies. may have neurological signs Self-care May require assistance choosing Requires assistance in multiple spheres. occasional or persistent clothing. familiar persons Moderate deficits. Poor knowledge of current and recent events recent events Some deficits in recall of remote Many deficits in recall of remote Almost no recall of any past events events events Word-finding problems. Natural history of Alzheimer’s disease: clinical and laboratory findings Function/test Orientation Concentration Recent memory Remote memory Language and speech Early cognitive decline Fully oriented Mild deficits. can travel to familiar places Cannot feed or toilet self Praxis Visuospatial skills May get lost in unfamiliar settings. poor word-list generation. forgets names. some errors in serial calculation Moderate cognitive decline Frequent mistakes. but usually knows date. may need coaxing to problems with bladder or bowel bathe incontinence . marketing Poor constructions and spatial disorientation. repetitive speech Ideomotor apraxia. difficulty with finances. poor construction on tests Normal Agraphia.Table 5–9.

C. abulia. depression. or irritability Normal Normal Bilateral temporoparietal hypoperfusion Agitation or anxiety.L. 201 . PET=positron emission tomography.Table 5–9. Reproduced by permission of Routledge/Taylor & Francis Group. Source. SPECT= single photon emission computed tomography. Copyright 1988 from The Psychiatric Treatment of Alzheimer’s Disease by Group for the Advancement of Psychiatry. obsessiveness Normal to atrophic cortices and Cortical atrophy and ventricular dilated ventricles enlargement Background slowing Bilateral temporoparietal hypoperfusion Diffuse slowing Bilateral temporoparietal and frontal hypoperfusion Dementia and Alzheimer’s Disease Note. apathy and indifference Severe cognitive decline Cannot perform Personality CT scan EEG PET and SPECT Possible apathy. may withdraw from challenging situations Denial common. Natural history of Alzheimer’s disease: clinical and laboratory findings (continued) Function/test Complex or new tasks Early cognitive decline Decreased performance Moderate cognitive decline Decreased performance. L. CT=computed tomography. EEG= electroencephalogram. psychosis.

deficits in reasoning. and virtually all other aspects of cognition are affected. including anomic or mixed aphasia. with less rapid decline in the early and late stages and relatively more rapid decline in midcourse. Perhaps because of this slow progression. The rate of progression of cognitive impairment varies among individuals. Although relatively synchronous decline in cognitive capacities is the general rule. ability to plan and organize activities. and friends and family who have only superficial interactions with patients may be unaware of relatively major deficits. Sometimes close family members who have observed declining cognition attempt to rationalize away the significance of their observations. apraxia.202 Clinical Manual of Geriatric Psychiatry sharp downward steps in function typical of vascular dementia or the more abrupt onset and rapid progression of the dementia syndrome of depression. Mental Status Examination Some of the major mental status findings typical of each stage of Alzheimer’s disease are included in Table 5–9. whereas instrumental activities of daily living are affected earlier. suspiciousness or social withdrawal may lead to an exaggerated estimate of the degree of cognitive decline in a relatively intact individual. Patients with Alzheimer’s disease rapidly forget new information and often do not benefit from cueing . language disturbance may be severe enough to prevent accurate evaluation of memory and higher cognitive functions. memory impairment (especially the ability to recall new information after a short delay [Welsh et al. multiple sources of historical data may be necessary to establish a reliable history. Unlike frontotemporal dementia. multiple neuropsychological impairments are seen. Functional decline generally parallels cognitive decline. cognitive deficits often can be concealed or compensated for. Later. but a decline of 2–3 points per year on the Folstein MMSE is typical. in some patients. in the early stages. 1991]) is invariably present and is often the presenting symptom. but basic activities of daily living tend to be preserved until cognitive function has reached the “moderately impaired” stage. Neuropsychological Tests In probable Alzheimer’s disease. marked impairments in expressive and receptive language. Some studies find nonlinear progression. and prominent learning and memory impairment. Because of these possibilities. similarly.

the laboratory evaluation of patients with possible Alzheimer’s disease is primarily aimed at ruling out other causes of dementia. List-learning tasks are among the most sensitive for detecting the memory deficits of early Alzheimer’s disease and for differentiating such deficits from the milder memory changes of age-associated memory impairment. as confirmed by subsequent neuropathological diagnosis (Knopman et al. results for individuals must be interpreted relative to normative tables for age and education level. learning and memory. neuropsychological deficits may be restricted to one or two areas—most often. positron emission tomography (PET) measuring glucose metabolism or amyloid burden. Table 5–5 describes three such tasks. If this evaluation does not identify another cause of dementia. Laboratory Evaluation Laboratory evaluation of Alzheimer’s disease is the same as that described earlier in this chapter for dementia (Table 5–4). 1994). measurement of cerebrospinal fluid antigens. (2004) reviewed the diagnostic accuracy of SPECT in Alzheimer’s disease and concluded that “diagnostic accuracy can be improved with SPECT in dementia patients who present with possible comorbid . Advanced and Experimental Diagnostics Research studies that used single photon emission computed tomography (SPECT). Brief versions of tests like those described in Table 5–5 have been combined by CERAD to form a screening battery that may be useful in detecting and staging Alzheimer’s disease (Welsh et al. No single cutoff score can be used to classify impairment on learning tasks. rather. Early in the course of illness. implying deficits in encoding or learning as well as problems with retrieval. and analysis of apolipoprotein alleles all have produced promising results. Despite the promise of the experimental diagnostic procedures discussed in the following subsection. the diagnosis of “probable Alzheimer’s disease” has reasonable sensitivity (approximately 80%) and specificity (approximately 70%). 2001). including Word List Learning from the CERAD battery. magnetic resonance imaging (MRI). and either DSM-IV-TR or NINCDS–Alzheimer’s Disease and Related Disorders Association clinical criteria are applied. Dougall et al. functional magnetic resonance imaging (fMRI) with activation. magnetic resonance spectroscopy.Dementia and Alzheimer’s Disease 203 or memory reminders.

Dickerson and associates (2004) studied memory-associated activation of the medial temporal lobe regions with fMRI in subjects with mild cognitive impairment and found that greater activation was associated with better memory performance. and results were promising but not yet applicable to the clinical setting.204 Clinical Manual of Geriatric Psychiatry symptoms of vascular disease or who do not entirely conform to clinical criteria …especially in ruling in AD [Alzheimer’s disease] as a cause when the SPECT result is positive and vice versa” (p. de Leon and colleagues (2004) conducted a series of studies in which MRI and cerebrospinal fluid biomarkers were used to diagnose Alzheimer’s disease. the subjects who recruited the largest area of the parahippocampal gyrus were the most impaired at baseline.5 years (more than 25% of whom developed probable Alzheimer’s disease) activated significantly larger areas of the parahippocampal gyrus despite similar memory performance. (2003) analyzed the available PET data in light of the risk-benefit ratio of available treatments for Alzheimer’s disease and concluded that cholinesterase inhibitors (discussed in the subsection “Cholinesterase Inhibitors” later in this chapter) should be prescribed on the basis of the history. neuropsychiatric evaluation. although specific indications have yet to be published. Despite their limitations. both SPECT and PET appear to have a role in the evaluation of some cases of suspected Alzheimer’s disease. If treatments entailing more serious risk are developed. thioflavin-T derivative that crosses the blood-brain barrier and binds to amyloid β-peptide. as well as for assessment of anti-amyloid treatment response. the authors found several methodological problems in the studies that they believed limited the validity and therefore the utility of their results. more important. the 44% who deteriorated over the ensuing 2. However. They found PIB to be a reliable marker of amyloid in vivo and proposed a possible future role for the PET-PIB procedure in the diagnosis and staging of Alzheimer’s disease. 562). physical examination. Kulasingam et al. Patwardhan and colleagues (2004) used rigorous inclusion criteria to conduct a meta-analysis of nine studies in which the operating characteristics of PET were assessed in the diagnosis of Alzheimer’s disease. the addition of PET to the diagnostic battery would be warranted. a benzothiazole. Although specificity and sensitivity were both estimated at 86%. without recourse to PET or SPECT imaging and examination. and structural neuroimaging to rule out other causes of dementia. These in- . Klunk and associates (2004) used PET to study the distribution of labeled Pittsburgh Compound-B (PIB).

hypomania. some cases of depression can be particularly misleading. Amnestic Disorders Amnestic disorders can be misdiagnosed as dementia. and diagnostic error is easily avoided. respectively. They include depressive pseudodementia (see Chapter 3.Dementia and Alzheimer’s Disease 205 vestigators concluded that greater activation of the parahippocampal gyrus may be compensating for greater Alzheimer’s disease pathology and could be a diagnostic sign of impending Alzheimer’s disease. Nevertheless. The clinical diagnosis of Alzheimer’s disease had 93% sensitivity and 55% specificity. In addition to sparing of intellect. confabulation is often a prominent feature of this syndrome. These are all discussed in detail in Chapter 6 (“Other Dementias and Delirium”). hysteria. In most patients. these and other experimental approaches have not reached the stage of widespread acceptability in the diagnosis of Alzheimer’s disease.188 patients with dementia who underwent autopsy. and several authorities have recommended antidepressant treatment trials in selected patients (see related discussion in Chapter 4. for APOE4 alone. mania. and the dementias due to general medical conditions and substances. “Mood Disorders—Diagnosis”). intellectual functions other than memory are spared. Finally. personality disorder. adding APOE4 data to the clinical diagnosis increased the specificity to 84% but lowered the sensitivity. the signs and symptoms of functional illness are clear. The most common amnestic disorder in elderly patients is Korsakoff ’s psychosis. compared with 65% and 68%. vascular dementia. and malingering. To date. cognitive impairment is readily identified as secondary. However. high-dose ingestion of alcohol. even though in amnestic disorder. . Ganser syndrome. which is caused by prolonged thiamine deficiency usually associated with long-term. “Mood Disorders—Treatment”). Mayeux and colleagues (1998) studied the diagnostic value of the presence of APOE4 in a sample of 2. Other Dementias Alzheimer’s disease must be distinguished from the other degenerative dementias such as frontotemporal dementia and dementia with Lewy bodies. Differential Diagnosis of Alzheimer’s Disease Functional Disorders Certain functional conditions can mimic Alzheimer’s disease.

. these microfibrils have been shown to consist of paired helical filaments. 2) neuritic plaques. which are composed of dense bundles of amyloid fibrils and dystrophic neurites (usually containing paired helical filaments). Under an electron microscope. and γ-secretase enzymes to generate either nonamyloidogenic or amyloidogenic peptides. but when APP is cut by β-secretase and then by γ-secretase. that are 100 Å wide and twist every 800 Å. senile plaques. However. whereas amyloid β-peptide 1–42. particularly involving anterior frontal and temporoparietal areas. Neuropathology of Alzheimer’s Disease The gross neuropathology of Alzheimer’s disease consists of cortical atrophy. it generates peptides of 39–43 amino acids. and 3) “burned out” plaques. A “primitive” form of neuritic plaque lacking the amyloid component of the core also has been described (Terry et al. which accounts for about 10% of amyloid β-peptide. often requiring reevaluation after potential causes of delirium have been eliminated and the underlying dementia has been allowed to emerge. composed primarily of an abnormally phosphorylated tau protein. APP is a transmembrane protein that is present in almost all tissues. It undergoes proteolytic cleavage by α-. Microscopic findings include NFTs. which has a much more acute onset and progression and entails more severe impairment of attention and concentration and more disorganization of thought. it generates a harmless peptide. Neurofibrillary tangles are densely packed microfibrils found in the cytoplasm of dead neurons. and granulovacuolar degeneration. Senile plaques are extracellular deposits of the 42–amino acid amyloid βpeptide that is derived from the amyloid precursor protein (APP).206 Clinical Manual of Geriatric Psychiatry Delirium Alzheimer’s disease is usually easily differentiated from delirium. which consist of formed filamentous and nonstructured amyloid β-peptide without attached abnormal neurites. 1994). They are 5–150 µm in diameter and appear in three major forms: 1) diffuse plaques. in which a dense amyloid core is surrounded by reactive astrocytes but no abnormal neurites. When full-length APP is cut by α-secretase and then by γ-secretase. of which amyloid β-peptide 1–40 is the most common and considered harmless. delirium superimposed on Alzheimer’s disease may be more difficult to diagnose. β-. is neurotoxic and involved in the formation of senile plaques in Alzheimer’s disease brains (Kamboh 2004).

This analogy ultimately led to the development of tacrine. and autopsy studies have reported a strong correlation (r=0.8) between the degree of choline acetyltransferase loss and premortem measurements of cognitive and functional decline. and volume reduction in the hippocampus that is detectable with MRI (de Leon et al. which catalyzes the synthesis of acetylcholine. both of which are less specific indicators of cholinergic cell activity than is choline acetyltransferase. donepezil. each containing a small granule. Other investigators have identified synaptic loss. However. these findings support a working analogy between Alzheimer’s disease and Parkinson’s disease. also have been found to be reduced in affected brain tissue. “Neurobiochemistry of Alzheimer’s Disease”). in which a single neurotransmitter (dopamine) is also deficient. Altogether. and other acetylcholinesterase inhibitors (see subsection “Cholinesterase Inhibitors” later in this chapter). and generalized loss of neuronal dendrites in affected cortical areas. neuronal loss. less profound abnormalities in .Dementia and Alzheimer’s Disease 207 Granulovacuolar degeneration primarily affects hippocampal pyramidal neurons and consists of groups of intracytoplasmic vacuoles about 5 µm in diameter. 2004). and loss of serotonergic neurons of the dorsal raphe nucleus also have been described. Other histopathological findings in Alzheimer’s disease include congophilic angiopathy. The first two changes have been correlated with reduced cortical tissue levels of choline acetyltransferase and norepinephrine and its metabolites. Neurobiochemistry of Alzheimer’s Disease The first and most thoroughly confirmed neurobiochemical abnormality found in brain tissue affected by Alzheimer’s disease neuropathology was reduced temporoparietal and hippocampal cortical activity of choline acetyltransferase. reduced cortical concentrations of serotonin have been less consistently reported. Biopsy studies have detected significant losses of this enzyme as early as the first symptomatic year. Concentrations of acetylcholinesterase and acetylcholine. consisting of amyloid deposits in the walls of small arteries of the frontal and parietal cortex. loss of noradrenergic neurons of the locus coeruleus. which are modestly effective treatments for Alzheimer’s disease. respectively (discussed in the next section below. an enzyme found only in cholinergic cells. Loss of cholinergic neurons of the nucleus basalis of Meynert.

208 Clinical Manual of Geriatric Psychiatry other neurotransmitter systems have been documented (American Psychiatric Association 2000). activity diversion. because affected twins are not included in the baseline sample. and at least one noncholinesterase inhibitor—memantine—has been shown to be at least modestly effective in Alzheimer’s disease. Psychosocial Therapy for Persons With Alzheimer’s Disease Psychosocial therapies developed for persons with Alzheimer’s disease and other dementias have attempted to minimize disruptive behaviors or increase positive behaviors. Studies of incidence are likely to find a lower concordance rate than are studies of prevalence. whereas the corresponding figure for dizygotic pairs was 22%. found in about half of Alzheimer’s disease families. regardless of whether onset was before or after age 80. several genes are responsible: one (presenilin 1). two others—presenilin 2. Genetics of Alzheimer’s Disease Alzheimer’s disease is transmitted as an autosomal dominant trait in about 2% of all cases. Each of these genes in its pathological variant results in abnormal β-APP processing with resultant overproduction of the amyloid β-peptide 42 (St George-Hyslop 2000). The other 98% of individuals with Alzheimer’s disease have sporadic disease. is on chromosome 14. Pedersen et al. behavior modification approaches using techniques such as time-outs. In these familial cases. which appears to result from an interaction between a genetic vulnerability and environmental factors. In early studies with a single dementia patient or a small number of patients. on chromosome 21—are present in far fewer Alzheimer’s disease families. on chromosome 1. support mood and a sense of well-being. or improve or support memory. (2004) examined incident Alzheimer’s disease in a cohort of 662 twin pairs followed up for 5 years and found a concordance rate of about 32% for monozygotic twins and about 9% for dizygotic twins. and selective reinforcement were shown to be effective in reducing urinary incontinence or reinstating important self-care . (1997) found a concordance rate for prevalence of Alzheimer’s disease among monozygotic twin pairs of 67%. which typically have early onset. Gatz et al. and the gene that encodes for APP.

and results showed either no benefit or very circumscribed benefit. there are also ongoing new investigations of the effects of predetermined training regimens for persons with early Alzheimer’s disease. all of which reported beneficial effects on cognition or mood in comparison with no-treatment or social-contact control subjects. However. events.. usually with the aid of tangible prompts such as photographs or music.g. Early studies of memory training for patients with dementia used techniques developed for normal older adults (e. More recent work addressing behavior problems has used cued recall procedures adapted from the cognitive rehabilitation literature. 1998). Reminiscence therapy. studies were small in size... 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. 2005). has become an increasingly popular intervention. Loewenstein et al. which involves the discussion of past activities. A recent review of the literature on reminiscence therapy in dementia found four controlled trials.Dementia and Alzheimer’s Disease 209 activities such as bathing or walking (Gatz et al. and experiences.g. It can be used by staff at activity centers and long-term-care facilities and lends itself to involvement of family members. especially as an adjunct to cholinesterase inhibitor therapies (e. Clare and colleagues (2001) described 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. group or individual practice of mnemonics such as visual imagery). 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. Bird and colleagues (1995) provide good examples of successes and failures of this approach. with the interval between the cue and the desired response gradually lengthened from immediately to over an hour or more. However.g. more promising results have been demonstrated with the use of specialized training techniques (e. spaced retrieval) that have proven effective in work with memory-impaired braininjured 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. 2004). and all used different types of reminiscence procedures (Woods et al. In an interesting case study. Recently.

particularly if accompanied by practical advice and encouragement. and gentle interpretation may lead to adaptive behavior change. it may be beneficial to view the coping with illness as a partnership between the patient and family members and other key social support persons.g. spending the first minutes of each session reviewing what was last discussed. the patient’s premorbid pattern of ego strengths and vulnerabilities. Increased levels of . with the degree of responsibility for independent behavior gradually shifting from the individual to these supportive others (Judd 1999). individual psychotherapy has more limited goals. sending home for review a short outline of what was covered in each session. Psychosocial Therapy for Dementia Caregivers Caring for a family member with Alzheimer’s disease or other dementia is challenging at best and overwhelmingly stressful at worst. Many patients at this stage of illness use primitive defenses. hypercritical and hostile behavior directed toward family members (denial and displacement). if nonspecific. and.210 Clinical Manual of Geriatric Psychiatry The potential benefits of psychotherapy for persons with Alzheimer’s disease and other dementias are also undergoing a reexamination. For some of these patients. multiple bizarre somatic complaints (somatization). resulting in characteristic symptom complexes such as accusations that family members are stealing from them (denial and projection). The role of individual psychotherapy in the overall medical management of Alzheimer’s disease depends on the stage of illness. and writing out specific suggestions for activities or coping approaches to practice at home) may also increase the effectiveness of psychotherapy. healing authority figure whose attention can have significant. sometimes. Throughout the course of therapy. In general. caring. supportive therapy is most useful in the early stages of illness and is aimed at ameliorating the anxiety and loss of selfesteem accompanying awareness and anticipation of lost cognitive capabilities. and the presence or absence of concomitant functional complications. often limited to provision of a constant. with clinicians beginning to more systematically combine techniques drawn from the rehabilitation literature with general psychotherapy procedures. the capacity for insight is preserved. Adapting the process of therapy to take diminished memory into account (e. Later in the course of illness. anxiety-relieving and mood-elevating effects (Group for the Advancement of Psychiatry 1988)..

and caregivers consistently rated the interventions as helpful (Gitlin et al. telephone-linked computer consultation. Researchers studying caregiver interventions have underscored the diversity of caregiver backgrounds and needs and the persistent. yet changing. or .g. Other recent research has shown that the distress experienced by many caregivers may not be automatically alleviated when help is hired in the home (Pot et al.15 standard deviation). anxiety. The meta-analysis of 6-month outcomes found a significant decrease in caregiver burden for a diverse group of active treatments (e. In general. Another encouraging result was that African American and Hispanic caregivers benefited as much as white caregivers in terms of reduced burden. A second generation of caregiver interventions has included individual and family counseling. In the most ambitious study of caregiver interventions to date in the United States. and some subgroups of caregivers (e. and combinations of these approaches. and professional-enhanced support groups) compared to usual care control (e. skills training. stresses associated with the role.200 caregivers.Dementia and Alzheimer’s Disease 211 depression and anxiety. higher use of psychotropic medications. coping-with-caregiving classes. information packets and referrals). family-based in-home intervention. 2005) or when the family member with dementia enters a nursing home (Schulz et al. Psychiatrists and other mental health professionals can offer the option of family therapy for caregivers who are experiencing depression. men and well-educated persons) did not experience a significant reduction in burden. and they caution against one-size-fits-all approaches. Recognition of caregiver burden has led to numerous psychosocial interventions aimed at alleviating stress and adverse health consequences. 2004). 2004). the effect size associated with interventions was modest (0. Early forms of interventions such as peer support groups and education were found to have only very small benefits when subjected to careful study. poorer physical health. 2003).. case management. 2002). However.g. Spouses may have an especially difficult time adjusting to the nursing home placement of a husband or wife (Schulz et al. skills training.. and increased mortality have all been documented for family caregivers. the multisite Resources for Enhancing Alzheimer’s Caregiver Health (REACH) investigation included a sample of over 1.g.. multicomponent approaches that offer options to fit individual caregivers’ needs and relatively intensive as opposed to brief interventions have been found to be most beneficial (Schulz et al.

212 Clinical Manual of Geriatric Psychiatry

other clinically significant mental health symptoms. Family intervention can be useful at all stages of Alzheimer’s disease (Jarvik and Winograd 1988). Initially, key elements of family therapy include dissemination of practical advice, provision of information and education, referral to appropriate community resources, and opportunities to express emotions and fears related to the diagnosis. Later, family therapy may be more focused on amelioration of caregiver anxiety, demoralization, and depression. In the final stages of illness, consultation and support vis-à-vis the often painful decision to institutionalize and providing assistance with the process of grieving a lost loved one may become the foci of family therapy. Being able to continue a supportive psychotherapeutic relationship with the family over the long haul of caregiving is ideal but often difficult to achieve. Being available by telephone for brief follow-up contacts as the patient’s illness proceeds to advanced stages can help to sustain a sense of support. Systematically assessing the behavioral deficits in the patient and determining which deficits cause the most distress to the caregiver can be helpful in the initial evaluation and in monitoring response to treatment. Brief structured questionnaires such as the Memory and Behavior Problems Checklist and the NPI (see subsection “Other Rating Measures” earlier in this chapter, and Appendix) can be completed by the caregiver or by a professional on the basis of caregiver input. Memory loss per se is generally less distressing to caregivers than are emotional and behavior problems such as depression, delusions, belligerence, and agitation. Treatment of these associated symptoms often can be the difference between continuation of home care and institutionalization for a patient with dementia. In therapeutic work with family caregivers, it is important to keep in mind that the caregiving role, despite its demands, can be a source of gratification and increased self-efficacy. Caregivers may derive satisfaction from repaying older relatives for their own past care or may feel relief from knowing that their loved one is receiving the best possible care (Scharlach 1994). In caring for older relatives who are frail or who have dementia, African American and Hispanic families rely more heavily on relatives and friends than do white families and are less likely to place their older family members in nursing homes. In the REACH study, Hispanic women who were dementia caregivers reported lower levels of caregiving stress, greater perceived benefits of caregiving, and a greater use of religious coping than did their white counter-

Dementia and Alzheimer’s Disease

213

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 institutional 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, especially when used in conjunction with family therapy or other interventions, are included at the end of this chapter, following the references.

Psychopharmacotherapy for Cognitive Decline in Alzheimer’s Disease
Cholinesterase Inhibitors Several cholinesterase inhibitors (tacrine, donepezil, rivastigmine, and galantamine) are available for treatment of the cognitive deficits of mild to moderate Alzheimer’s disease. All of these agents increase central cholinergic neurotransmission by inhibiting breakdown of acetylcholine by acetylcholinesterase. Of these, tacrine is not recommended because of its hepatotoxicity, and the other three are about equally effective and equally tolerable; 10 mg/day of donepezil, 6–12 mg/day of rivastigmine, and 16–18 mg/day of galantamine can be expected to produce, on average, about a three-point improvement on the cognitive subscale of the Alzheimer’s Disease Assessment Scale (Ritchie et al. 2004). Continuation treatment with cholinesterase inhibitors slows the progression of Alzheimer’s disease and reduces the likelihood of nursing home placement. One 36-month follow-up study found that almost 80% fewer cholinesterase inhibitor–treated subjects were admitted to nursing homes compared with untreated subjects (Lopez et al. 2005). Memantine Memantine is the first noncholinesterase inhibitor that has been shown, in randomized controlled clinical trials, to be effective in reversing or slowing cognitive and functional decline in Alzheimer’s disease (Areosa et al. 2005). The drug is an antagonist of the N-methyl-D-aspartate (NMDA)–type glutamate recep-

214 Clinical Manual of Geriatric Psychiatry

tor and appears to exert its effects at the cellular level by reducing glutamatemediated 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 combined with cholinesterase inhibitors (Tariot et al. 2004). Improvement in agitation and mood has been observed in several clinical trials, but cognitive and functional decline in Alzheimer’s disease remains the main indication. The initial 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 unpublished. 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 highdose vitamin E to the treatment regimen of patients with Alzheimer’s disease.

Psychopharmacotherapy for Noncognitive Symptoms of Alzheimer’s Disease
Agitation Perhaps the most common and most debilitating symptom complex seen in patients with Alzheimer’s disease is agitation, a syndrome that occurs in almost all patients with Alzheimer’s disease as they progress into the middle and late stages of illness. Agitation typically presents as restlessness, pacing, irritability, anger, anxiety and fearfulness, and refusal to accept care, often accompanied by persecutory beliefs that may reach delusional severity and verbal or physical aggressiveness. Agitation is often accompanied by impaired attention and concentration, elevated heart rate and blood pressure, and tachypnea.

Table 5–10.
Characteristic

Clinical pharmacology of agents useful for reducing the signs of dementia
Donepezil 3–5 No 70–80 96 2D6, 3A4 5–10 mg/day Cholinesterase inhibitor Rivastigmine 0.5–2 Yes 2a 40 Nonhepatic 1.5–6 mg twice daily Cholinesterase inhibitor Galantamine 0.5–1 Yes 5–7 0–20 2D6, 3A4 4–12 mg twice daily Cholinesterase inhibitor Memantine 3–7 No 60–80 45 Nonhepatic 5–10 mg twice daily NMDA receptor antagonist Dementia and Alzheimer’s Disease

Time to maximal serum concentration (hr) Absorption affected by food? Serum half-life (hr) Protein binding (%) Metabolism (CYP enzyme) Dose (initial/maximal) Mechanism of action

Note. CYP= cytochrome P450; NMDA=N-methyl-D-aspartate. a Rivastigmine is a pseudoirreversible acetylcholinesterase inhibitor that has an 8-hour half-life for the inhibition of acetylcholinesterase in the brain. Source. Adapted from Cummings JL: “Alzheimer’s Disease.” New England Journal of Medicine 351:56–67, 2004. Copyright © 2004 Massachusetts Medical Society. All rights reserved.

215

216 Clinical Manual of Geriatric Psychiatry

Verbalizations range from perseverative expressions of apprehension and fear to pressured incoherence, screaming, and cursing. Episodes of agitation often occur during the late afternoon or early evening (“sundowning”). Before medications are prescribed for agitation, it is important to examine the patient and his or her physical and social environment to determine what, if any, unmet needs are contributing to the agitation. Interventions may include providing optimal levels of sensory stimulation, engaging activities, and social contact; timely toileting; better communication; and adequate treatment of pain. Behavioral interventions based on an operant conditioning model and interventions to reduce overstimulation and stress also have been reported to be effective, but specific guidelines for which intervention is best for which patient remain to be determined (Cohen-Mansfield 2001). When nonpharmacological measures have been applied and symptoms remain, conventional and atypical neuroleptics, benzodiazepines, trazodone, anticonvulsants (including carbamazepine, valproic acid, and gabapentin), or lithium may be prescribed. All of these medications have been reported to be effective, but conventional (Devanand et al. 1998) and atypical (Fujikawa et al. 2004; Rabinowitz et al. 2004) neuroleptic medications have been the beststudied and most commonly used agents for agitation, at least until April 2005. At that time, the U.S. Food and Drug Administration (FDA) issued a public health advisory, citing 17 placebo-controlled trials of olanzapine, aripiprazole, risperidone, and quetiapine in elderly patients with dementia who also had behavior disorders. In 15 of those trials, which included more than 5,106 patients, a 1.6- to 1.7-fold increase in mortality was seen, mainly from “heart-related events,” including heart failure and sudden death, or infections, mostly pneumonia. The atypical antipsychotics fall into three drug classes based on their chemical structure, but because the increase in mortality was seen with medications in all three chemical classes, the FDA concluded that the increased mortality was probably related to the common pharmacological effects of all atypical antipsychotic medications, including those that had not been systematically studied in the dementia population. Accordingly, the FDA requested manufacturers of all atypical antipsychotic medications to add a boxed warning to their drug labeling that describes this risk and that notes that these drugs are not approved for the treatment of behavior disorders in elderly patients with dementia. The FDA is also considering adding a warning to the labeling of older antipsychotic medications because limited

Dementia and Alzheimer’s Disease

217

data also suggested a similar increase in mortality for these agents. Accordingly, clinicians should consider this risk before recommending antipsychotic medications for agitation in elderly individuals with dementia. (The FDA advisory 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 agitation is accompanied by hallucinations, delusions, belligerent and hostile behavior, or physical aggressiveness. In one unreplicated double-blind, randomassignment 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 disturbance, 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 augmenting 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 order or as needed. Refractory symptoms may require treatment with neuroleptics and trazodone. Several rating scales, including the Behavior Pathology in Alzheimer’s Disease 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

Anticonvulsants such as valproic acid also have a role in the pharmacological management of behavioral disturbance in patients with Alzheimer’s disease (Sival et al. 2004) and may be particularly effective in patients with a history of mood instability or those with prominent mood instability as a feature of their agitation. Finally, evidence indicates that cholinesterase inhibitors such as donepezil and rivastigmine, in addition to improving cognitive function in Alzheimer’s disease, have salutary effects on noncognitive symptoms, including agitation, hallucinations, delusions, disinhibition, and apathy (Aupperle et al. 2004; Holmes et al. 2004). Table 5–11 shows the clinical pharmacology of agents useful for the control of symptoms and signs of agitation. 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 apprehension, 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 disorders 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 reuptake 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 principles that guide treatment of depression in elderly patients without dementia apply (see Chapter 4, “Mood Disorders—Treatment”), with the following modifications: • Patients with Alzheimer’s disease, by virtue of cholinergic system disruption, are particularly susceptible to adverse reactions ranging from subtle

Dementia and Alzheimer’s Disease

219

worsening of cognitive function to frank delirium while taking centrally acting anticholinergic agents. Accordingly, tricyclic antidepressants and other anticholinergic agents should be avoided when possible, in favor of selective serotonin reuptake inhibitors and the other nontricyclic antidepressants. Because patients with Alzheimer’s disease may have impaired ability to articulate subjective feelings of sadness, hopelessness, helplessness, or worthlessness, the clinician often must rely more on neurovegetative signs and nonverbal expression of mood as target symptoms for treatment. The latter may include refusal to eat, crying spells, facial expressions of sadness or pain, unexplained episodes of agitation or hostility, and increased confusion. Patients with Alzheimer’s disease also may not be able to describe subjective side effects of medications, such as postural light-headedness or dizziness, so routine measurements of orthostatic blood pressure and careful assessment of gait and balance may be more necessary than in the elderly patient without dementia.

Mood Instability, Insomnia, Apathy Lithium, valproic acid, and other mood-stabilizing agents may be prescribed for patients with Alzheimer’s disease who have concomitant bipolar disorder or its variants, following the considerations listed above. Similarly, benzodiazepine and nonbenzodiazepine hypnotic agents are prescribed for patients with Alzheimer’s disease, as for elderly persons without dementia. The common practice of prescribing diphenhydramine or other antihistamines as hypnotics is particularly inadvisable for patients with Alzheimer’s disease because these agents have significant anticholinergic potency and can cause increased cognitive impairment. Psychostimulants such as methylphenidate and modafinil have a minor role in treatment of Alzheimer’s disease. Although it has been repeatedly documented that these agents do not improve cognitive function, they can be effective for apathy and social withdrawal and are occasionally useful to reverse sedative side effects of other agents.

metabolic syndrome Drowsiness. ataxia Note. psychosis 2.5–2. psychosis Agitation. metabolic syndrome Drowsiness. mood lability 25–200 5–30 25–200 250–1. psychosis Dosage (mg/day) 0. psychosis Agitation. psychosis Agitation Agitation. a All (except trazodone and valproate) may increase risk of death from multiple causes. akathisia. akathisia. drowsiness EPS. . EPS=extrapyramidal side effects. Medication Haloperidol Risperidone Clinical pharmacology of medications for agitation with and without psychosis Indications Agitation. weight gain.0 Side effects and adverse reactions EPS.0 0. drowsiness. metabolic syndrome Drowsiness. tardive dyskinesia. orthostatic hypotension May increase risk of stroke in patients with cerebrovascular disease May increase risk of stroke in patients with cerebrovascular disease Special considerationsa 220 Clinical Manual of Geriatric Psychiatry Olanzapine Agitation. weight gain. metabolic syndrome Drowsiness.5–10 Quetiapine Aripiprazole Trazodone Valproate Agitation.5–2. tardive dyskinesia.500 Drowsiness.Table 5–11. weight gain.

Bullock R: Validation of a 6 item cognitive impairment test with a view to primary care usage. Carter G. Marx MS. Wolf PA. Int J Geriatr Psychiatry 14:936–940. Linn R. Text Revision. Watanabe J. and critique. Acta Neuropathol (Berl) 82:239–259. J Gerontol Med Sci 44:M77–M84. 1997 Areosa SA. 1999 Buschke H. et al: Long-term maintenance of treatment gains following a cognitive rehabilitation intervention in early dementia of Alzheimer type: a single case study.Dementia and Alzheimer’s Disease 221 References American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. Curr Med Res Opin 20:1605–1612. Wilson BA. et al: Long-term effects of rivastigmine treatment on neuropsychiatric and behavioral disturbances in nursing home residents with moderate to severe Alzheimer’s disease: results of a 52-week open-label study. McShane R: Memantine for dementia. Gerontologist 37:342–354. 2000 Borson S. Kuslansky G. Adamowicz J: Success and failure in five case studies: use of cued recall to ameliorate behaviour problems in senile dementia. Neurology 42:117. summary. Braak E: Neuropathological staging of Alzheimer-related changes. 1989 . Am J Geriatr Psychiatry 9:361–381. Neurology 52:231–238. American Psychiatric Association. Neuropsychol Rehabil 11:477–494. Alexopoulos P. Sherriff F. 2001 Cohen-Mansfield J: Nonpharmacologic interventions for inappropriate behaviors in dementia: a review. 4th Edition. Koumaras B. 2001 Cohen-Mansfield J. et al: Prevalence of dementia and probable senile dementia of the Alzheimer type in the Framingham Study. 2005 Braak H. Int J Geriatr Psychiatry 15:1021– 1027. Katz M. Scanlan JM. 1992 Bird M. 2004 Bachman DL. Washington. Scanlan J. et al: Simplifying detection of cognitive impairment: comparison of the Mini-Cog and Mini-Mental State Examination in a multiethnic sample. J Am Geriatr Soc 53:871–874. 2005 Aupperle PM. DC. Rosenthal AS: A description of agitation in a nursing home. Chen M. 2000 Aranda MP. et al: The Mini-Cog: a cognitive ‘vital signs’ measure for dementia screening in multi-lingual elderly. 1991 Brooke P. Knight BG: The influence of ethnicity and culture on the caregiver stress and coping process: a sociocultural review and analysis. 1999 Clare L. Cochrane Database Syst Rev (2):CD003154. Brush M. 1995 Borson S. et al: Screening for dementia with the memory impairment screen. Int J Geriatr Psychiatry 10:5–11.

appraisal. et al: Dietary intake of antioxidants and risk of Alzheimer disease. Neuropsychobiology 49:201–204. JAMA 62:2554. Stuss D.222 Clinical Manual of Geriatric Psychiatry Coon DW. et al: The Neuropsychiatric Inventory: comprehensive assessment of psychopathology in dementia. Ebmeier KP: Systematic review of the diagnostic accuracy of 99mTc-HMPAO-SPECT in dementia. J Gerontol A Biol Sci Med Sci 52:M117–M125. 1989 Farber NB. et al: Heritability for Alzheimer’s disease: the study of dementia in Swedish twins. 2004 Duff Canning SJ. 2004 Devanand DP. Newcomer JW. et al: Increased neocortical neurofibrillary tangle density in subjects with Alzheimer disease and psychosis. Ann Neurol 56:27–35. Arch Neurol 47:49–52. Bruggink S. Klauber MR. 2000 Folstein MF. Solano N. 2004 Dougall NJ. 2004 Cummings JL: The Neuropsychiatric Inventory: assessing psychopathology in dementia patients. 2004 Engelhart MJ. 1998 Dickerson BC. Funkenstein HH. et al: The Mini-Mental State Examination in the early diagnosis of Alzheimer’s disease. et al: Quetiapine treatment for behavioral and psychological symptoms in patients with senile dementia of Alzheimer type. J Intern Med 256:205–223. 2002 Evans DA. Rubin EH. Aging Ment Health 8:330–345. 1997 Cummings JL. et al: A randomized. et al: Diagnostic utility of abbreviated fluency measures in Alzheimer disease and vascular dementia. Neurology 48:S10–S16. Geerlings MI. Arch Gen Psychiatry 57:1165–1173. and coping in Latina and Caucasian female dementia caregivers: findings from the REACH study. J Psychiatr Res 12:189– 198. Salat DH. et al: Prevalence of Alzheimer’s Disease in a community population of older persons: higher than previously reported. Neurology 44:2308–2314. Neurology 62:556–562. Mega J. Hofstetter CR. Gray K. Am J Psychiatry 155:1512–1520. placebo-controlled dosecomparison trial of haloperidol for psychosis and disruptive behaviors in Alzheimer’s disease. Takahashi T. Am J Geriatr Psychiatry 12:554–570. Marder K. Albert MS. DeSanti S. et al: Well-being. Michaels KS. et al: Medial temporal lobe function and structure in mild cognitive impairment. McHugh PR: “Mini-mental state”: a practical method for grading the cognitive state of patients for the clinician. Folstein SE. 2004 Galasko D. 1975 Fujikawa T. Ruitenberg A. Zinkowski R. Leach L. Pedersen N. Kinoshita A. Rubert M. et al: MRI and CSF studies in the early diagnosis of Alzheimer’s disease. 1997 . 1990 Gatz M. JAMA 287:3223–3229. 1994 de Leon MJ. Bates JF. Berg S.

Burgio LD. Dean C. Brown T. 2004 Henderson VW. et al: Empirically validated psychological treatments for older adults. Springer. Psychol Aging 18:361–374. Green RC. 2004 Jorm AF. Mattis S: Dementia Rating Scale–2: Professional Manual. Rizwan MR: Prevalence and clinical correlates of psychotic symptoms in Alzheimer’s disease. Benke KS. 1983 . 1998 Group for the Advancement of Psychiatry: The Psychiatric Treatment of Alzheimer’s Disease. et al: Effect of multicomponent interventions on caregiver burden and depression: the REACH multisite initiative at 6-month follow-up. Barker WW. Int J Geriatr Psychiatry 13:100–108.Dementia and Alzheimer’s Disease 223 Gatz M. Cullen JS. 1988 Jorm AF: The Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE): a review. 1993 Katzman R. Lutz. Kluwer Academic/Plenum. Belle SH. et al: MIRAGE Study Group: postmenopausal hormone therapy and Alzheimer’s disease risk: interaction with age. Int Psychogeriatr 16:275–293. 2001 Kamboh MI: Molecular genetics of late-onset Alzheimer’s disease. 2003 Gormley N. Fox L. Ownby RL. Scott R. J Neurol Neurosurg Psychiatry 76:103–105. Int J Geriatr Psychiatry 13:410–414. 1999 Jurica PJ. Journal of Mental Health and Aging 4:9–45. 2004 Katona CL. 2005 Holmes C. Ann Hum Genet 68 (pt 4):381–404. New York. 1991 Judd T: Neuropsychotherapy and Community Integration: Brain Illness. Winograd CH: Treatments for the Alzheimer’s Patient: The Long Haul. Hunter BN. Psychological Assessment Resources. et al: Validation of a short Orientation-MemoryConcentration Test of cognitive impairment. 1998 Gitlin LN. Am J Psychiatry 140:734–739. New York. Int Psychogeriatr 16:317–326. and Behavior. Neurology 43:13–20. Bray J: A double-blind comparison of the efficacy and safety of paroxetine and imipramine in the treatment of depression with dementia. 1988 Harwood DG. FL. et al: The efficacy of donepezil in the treatment of neuropsychiatric symptoms in Alzheimer disease. New York. Psychol Med 21:785–790. et al: Apolipoprotein E polymorphism and age of onset for Alzheimer’s disease in a bi-ethnic sample. Fiske A. Wilkinson D. Leitten CL. Neurology 63:214–219. Emotions. Brunner/Mazel. Fuld P. et al: Performance of the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE) as a screening test for dementia. 2004 Jarvik LFE. 1998 Katzman R: Education and the prevalence of dementia and Alzheimer’s disease.

Mueller J. Acevedo A. Langston JW. JAMA 292:2901–2908. 1989 Loewenstein DA. Ann Neurol 55:306–319. Ann Intern Med 107:481–485. 2004 Logsdon RG. Becker JT. et al: Alteration of a clinically meaningful outcome in the natural history of Alzheimer’s disease by cholinesterase inhibition. Brody EM: Assessment of older people: self-maintaining and instrumental activities of daily living. et al: A new scale for the assessment of functional status in Alzheimer’s disease and related disorders. Am J Geriatr Psychiatry 12:395–402. 1987 Kilada S. Foster NL. 2004 Knopman DS. et al: When should functional neuroimaging techniques be used in the diagnosis and management of Alzheimer’s dementia? a decision analysis. 2001 Loewenstein DA. Borson S: Brief screening tests for dementia. 1999 Lopez OL. Am J Geriatr Psychiatry 3:300–307. 2004 Lawton MP. 2002 . et al: Use of the Fuld Object-Memory Evaluation in the detection of mild dementia among Spanish and English-speaking groups. Cxaja SJ. Duara R. et al: Assessment of agitation in Alzheimer’s disease: the Agitated Behavior in Dementia scale. Alzheimer’s Disease Cooperative Study. Cummings JL. et al: Brief screening tests for the diagnosis of dementia: comparison with the Mini-Mental State Exam. Duara R. et al: Hormone replacement therapy and cognition: systematic review and meta-analysis.224 Clinical Manual of Geriatric Psychiatry Kiernan RJ. et al: The Neurobehavioral Cognitive Status Examination: a brief but quantitative approach to cognitive assessment. Engler H. Grant EA. J Am Geriatr Soc 47:1354–1358. Arguelles T. 1995 Loewenstein DA. Larson EB: Mixed dementia: emerging concepts and therapeutic implications. Nordberg A. 1969 LeBlanc ES. Weiner MF. 2005 Klunk WE. Teri L. J Am Geriatr Soc 50:1086–1091. et al: Cognitive rehabilitation of mildly impaired Alzheimer disease patients on cholinesterase inhibitors. 2001 Kulasingam SL. 2002 Langa KM. Scanlan JM. DeKosky ST. J Am Geriatr Soc 53:83–87. Amigo E. J Gerontol 44:114–121. Buschke H. JAMA 285:1489–1499. Gerontologist 9:179–186. Chan BKS. Alzheimer Dis Assoc Disord 19:8– 16. et al: Imaging brain amyloid in Alzheimer’s disease with Pittsburgh Compound-B. Samsa GP. Value Health 6:542–550. Saxton J. 2005 Lorentz WJ. Katz M. et al: Practice parameter: diagnosis of dementia (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 56:1143–1153. Can J Psychiatry 47:723–733. Zarin DA. Gamaldo A. 2003 Kuslansky G. et al: Screening for Alzheimer’s disease: the memory impairment screen versus the conventional three-word memory test. Janowsky J.

1984 Migliorelli R. Am J Clin Nutr 81:508– 514. 1998]. Drachman D. Edland SD. Saunders AM. pp 77–121 Mayeux R. in Geriatric Psychiatry. et al: Clinical diagnosis and Alzheimer’s disease: report of the NINCDS-ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer’s Disease. double-blind clinical trial of sertraline in the treatment of depression complicating Alzheimer’s disease: initial results from the Depression in Alzheimer’s Disease study. part II: standardization of the neuropathologic assessment of Alzheimer’s disease. et al: The Cognitive Abilities Screening Instrument (CASI): data from a cohort of 2524 cognitively intact elderly. Teson A. 2005 Murayama S. Tangney CC. Neurology 34:939–944. 1991 Morris MC. New York. Philp I: Screening for cognitive impairment among older people in black and minority ethnic groups. Radiology 231:73–80. Sheppard J-M.Dementia and Alzheimer’s Disease 225 Lyketsos CG. McCrory DC. Karasu TB. Evans DA. 2004 National Institute on Aging and Reagan Institute Working Group on Diagnostic Criteria for the Neuropathological Assessment of Alzheimer’s Disease: Consensus recommendations for the postmortem diagnosis of Alzheimer’s disease. Saito Y: Neuropathological diagnostic criteria for Alzheimer’s disease. 1998 McCurry SM. Steinberg M. Am J Psychiatry 157:1686–1689. Neurobiol Aging 18:S1–S2. et al: Relation of the tocopherol forms to incident Alzheimer disease and to cognitive change. Petracca G. McKeel D. 2000a Lyketsos CG. Matchar DB. 1997 Parker C. Tschanz JT. Neurology 41:479–486. 1976. Am J Psychiatry 157:708–714. Edited by Bellak L. Steele CD. placebo-controlled. Age Ageing 33:447–452. Neuropathology 24:254–260. 2004 . Heyman A. Int J Geriatr Psychiatry 14:882–888. et al: Utility of the apolipoprotein E genotype in the diagnosis of Alzheimer’s disease. 1995 Mirra SS. Psychol Med 25:505–513. Teri L. Shea S. Alzheimer’s Disease Centers Consortium on Apolipoprotein E and Alzheimer’s Disease [published erratum appears in N Engl J Med 338:1325. Grune & Stratton. et al: Mental and behavioral disturbances in dementia: findings from the Cache County Study on Memory in Aging. 1999 McKhann G. Folstein M. N Engl J Med 338:506–511. et al: Randomized. 2000b Mattis S: Mental status examination for organic mental syndrome in the elderly patient. et al: Alzheimer disease: operating characteristics of PET—a meta-analysis. 2004 Patwardhan MB. et al: The Consortium to Establish a Registry for Alzheimer’s Disease (CERAD). et al: Neuropsychiatric and neuropsychological correlates of delusions in Alzheimer’s disease.

et al: A controlled trial of selegiline. Gerontologist 42:589–602. pp 369–388 Reisberg B. American Psychiatric Press. JAMA 291:2947–2958. Belle SH. N Engl J Med 336:1216–1222. Czaja S. et al: How heritable is Alzheimer’s disease late in life? findings from Swedish twins. 2004 Reichman WE: Nondegenerative dementing disorders. Biol Psychiatry 47:183–199. et al: Behavioral and psychological symptoms in patients with dementia as a target for pharmacotherapy with risperidone. Clayton T. et al: Metaanalysis of randomized trials of the efficacy and safety of donepezil. 1997 Scharlach AE: Caregiving and employment: competing or complementary roles? Gerontologist 34:378–385. Psychol Aging 20:211–219. and rivastigmine for the treatment of Alzheimer disease. alpha-tocopherol. Berg S. Duivenvoorden HJ. Washington. Borenstein J. O’Brien A. in The American Psychiatric Press Textbook of Geriatric Neuropsychiatry. Twisk JWR. 1987 Ritchie CW. J Clin Psychiatry 48(suppl):9–15. The Alzheimer's Disease Cooperative Study. et al: Conjugated equine estrogens and incidence of probable dementia and mild cognitive impairment in postmenopausal women: Women’s Health Initiative Memory Study. et al: Dementia caregiver intervention research: in search of clinical significance. 2004 Shulman KI: Clock-drawing: is it the ideal cognitive screening test? Int J Geriatr Psychiatry 15:548–561. 2004 Sano M. 2004 Smith JD: Apolipoprotein E4: an allele associated with many diseases. 1994 Schulz R. et al: Transitions in caregivers’ use of paid home help: associations with stress appraisals and well-being. et al: Behavioral symptoms in Alzheimer’s disease: phenomenology and treatment. J Clin Psychiatry 65:1329–1334. Jansen PA. 2002 Schulz R. Ann Med 32:118–127. 2000 . galantamine. 2005 Rabinowitz J. or both as treatment for Alzheimer's disease. 2000 Shumaker SA. Ernesto C. Am J Geriatr Psychiatry 12:358–369. Edited by Coffey CE. Ames D. Cummings JL. 2004 Sival RC. Katz IR. De Deyn PP. Salob SP. et al: Sodium valproate in aggressive behaviour in dementia: a twelve-week open label follow-up study. Czaja SJ. 1994. Gatz M. Zarit SH. Thomas RG. Legault C. Ann Neurol 55:180–185. 2000 St George-Hyslop PH: Molecular genetics of Alzheimer’s disease. Kuller L.226 Clinical Manual of Geriatric Psychiatry Pedersen NL. et al: Long-term care placement of dementia patients and caregiver health and well-being. 2004 Pot AM. JAMA 292:961–967. DC. Int J Geriatr Psychiatry 19:305–312.

Butters N. V: a normative study of the neuropsychological battery.Dementia and Alzheimer’s Disease 227 Street JS. JAMA 291:317–324. Hansen LA: Structural basis of the cognitive alterations in Alzheimer disease. Neuroepidemiology 23:159–169. Schneider LS. fixed-dose trial of fluoxetine vs. Edited by Terry RD. Katzman R. Wilson RK. Arch Neurol 48:278–281. 1995 Woods B. 1994. Lyketsos C. Psychosomatics 38:246–252. Homma A. Cross P. et al: Alzheimer’s dementia: performance on the Mini Mental State Examination. Thorne JE. Jones C. et al: Operating characteristics of brief screens for dementia in a multicultural population. Gao ZX: Validity of Hasegawa’s Dementia Scale for screening dementia among aged Chinese. 2005 . et al: Reminiscence therapy for dementia. 2004 Teng EL. Arch Gen Psychiatry 57:968–976. Chiu HC. et al: Memantine treatment in patients with moderate to severe Alzheimer disease already receiving donepezil: a randomized controlled trial. Masliah E. et al: Nonsteroidal anti-inflammatory drugs for the prevention of Alzheimer’s disease: a systematic review. amitriptyline in the treatment of major depression complicating Alzheimer’s disease. pp 179–196 Tsai N. Am J Geriatr Psychiatry 5:60–69. 1997 Tariot PN. et al: Genetic association between the APOE 4 allele and Lewy bodies in Alzheimer disease. et al: A double-blind. Neurology 64:509–513. 1989 Tsuang DW. randomized. randomized. Mohs RC. Gannon KS. et al: The Cognitive Abilities Screening Instrument (CASI): a practical guide for cross-cultural epidemiological studies of dementia. Grossberg GT. in Alzheimer Disease. Zandi PP. Am J Geriatr Psychiatry 3:96–107. 2004 Taragano F. Hughes J. Clark WS. Gunay I. Chen J. Mangone CA. et al: Olanzapine treatment of psychotic and behavioral symptoms in patients with Alzheimer disease in nursing care facilities: a double-blind. The HGEU Study Group. 1994 Wilder D. Gray KF. et al: A double-blind comparison of trazodone and haloperidol for treatment of agitation in patients with dementia. et al: The Consortium to Establish a Registry for Alzheimer’s Disease (CERAD). Int Psychogeriatr 6:45–58. placebo-controlled trial. Spector A. Raven. 1987 Teng EL. Farlow MR. Int Psychogeriatr 1:145–152. Hasegawa K. Neurology 44:609–614. New York. 1997 Szekely CA. Bick K. et al: Detection of abnormal memory decline in mild cases of Alzheimer’s disease using CERAD neuropsychological measures. J Consult Clin Psychol 55:96–100. 2005 Welsh KA. Cochrane Database Syst Rev (2):CD001120. 2000 Sultzer DL. Butters N. 1994 Terry RD. Lopez OL. 1991 Welsh KA.

MD. 2005 Resources for Dementia Caregivers Alzheimer’s Association: (800) 272-3900. http://www. MD. Health Professions Press.228 Clinical Manual of Geriatric Psychiatry Zandi PP. Baltimore. Department of Health and Human Services.gov (click on “Elders and Families” for help with locating services and resources for older adults) . Johns Hopkins University Press. et al: Cache County Study Group. 3rd Edition.org American Association of Retired Persons (AARP): http://www. 1999 National Institutes of Health Clinical Trials: http://www. Rabins PV (eds): The 36-Hour Day.aarp. Arch Neurol 61:82–88. Hoffman S (eds): Behaviors in Dementia: Best Practices for Successful Management. Khachaturian AS. Sparks DL. Arch Gen Psychiatry 62:217–224. Baltimore. Reduced risk of Alzheimer disease in users of antioxidant vitamin supplements: the Cache County Study. 2004 Zandi PP.gov (clinical trials that are recruiting patients with Alzheimer’s disease) U.clinicaltrials.aoa. et al: Do statins reduce risk of incident dementia and Alzheimer disease? the Cache County Study. Anthony JC. Khachaturian AS.S.org (information about the Family and Medical Leave Act) Kaplan M. http://www. 1998 Mace NL. Administration on Aging: (800) 677-1116.alz.

England. and the overlap of its clinical features with those of Alzheimer’s disease and vascular dementia. Classic Pick’s disease. Diagnostic Criteria Consensus criteria for diagnosing frontotemporal dementia were published in 1998 (Neary et al. the average age at onset of the frontotemporal dementia was 52. One Swedish study (Andreasen et al. 229 . and found that frontotemporal dementia and Alzheimer’s disease had the same prevalence (15 per 100. and several other histopathologically distinct conditions are the main contributors to this category.000) in patients ages 45–64. it is difficult to estimate its prevalence. 1998) and are presented in Table 6–1. primary progressive aphasia.2 years. Ratnavalli and colleagues (2002) analyzed records from a university hospital in Cambridge. Epidemiology Because of the histopathological heterogeneity of this syndrome (see “Pathology” below).2% in a clinically diagnosed sample of 619 patients referred for diagnostic evaluation (compared with 36.6 Other Dementias and Delirium Frontotemporal Dementia Frontotemporal dementia is a term used to describe a group of disorders that share a common pattern of relatively focal degeneration of the frontal and temporal lobes of the brain. 1999) found a prevalence of 3.9% with Alzheimer’s disease). whereas Gustafson and colleagues (1992) estimated the prevalence as close to 10%.

glabellar) Incontinence Akinesia. snout.g..230 Clinical Manual of Geriatric Psychiatry Table 6–1. rigidity. and tremor Low and labile blood pressure Investigations Neuropsychology: significant impairment on frontal lobe tests in the absence of severe amnesia. Clinical diagnostic features of frontotemporal dementia Core diagnostic features Insidious onset and gradual progression Early decline in social interpersonal conduct Early impairment in regulation of personal conduct Early emotional blunting Early loss of insight Supportive diagnostic features Behavior disorder Decline in personal hygiene and grooming Mental rigidity and inflexibility Distractibility and impersistence Hyperorality and dietary changes Perseverative and stereotyped behavior Utilization behavior Speech and language Altered speech output Aspontaneity and economy of speech Press of speech Stereotypy of speech Echolalia Perseveration Mutism Physical signs Primitive reflexes (e. or perceptuospatial disorder Electroencephalography: conventional electroencephalogram findings are normal despite clinically evident dementia . aphasia. grasp.

with a dominant pattern of inheritance found in the majority (Chow et al. In the frontal variant. and a family history of dementia is present in about half of cases. and apathy (Bozeat et al. 2005) found that after an average of 3 years. 2000). facts. objects. irritability. about 5–7 years after onset. 2004). . Clinical diagnostic features of frontotemporal dementia (continued) Supportive diagnostic features (continued) Investigations (continued) Brain imaging (structural and/or functional): predominant frontal and/or anterior temporal abnormality Source. altered food preferences. ritualized or stereotypical behavior. Some authorities 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. 1999). presents with deficits in the phonological and syntactic components of language (Grossman 2002). and word meanings and is associated with primarily temporal lobe pathology. with disinhibition. A recent longitudinal study (Seeley et al. History. loss of empathy. patients who initially presented with the semantic (left temporal) variant of frontotemporal dementia also developed the symptoms of right frontotemporal deficit (especially emotional flatness. and may progress to corticobasilar degeneration (Gorno-Tempini et al. Progressive nonfluent aphasia is associated with primarily frontal (perisylvian) pathology. and weight gain emerged in both groups later in the disease.Other Dementias and Delirium 231 Table 6–1. and 3) progressive nonfluent aphasia. the main presenting feature is progressive personality change. and Mental Status Examination The typical age at onset of frontotemporal dementia is in the 50s and 60s. Clinical Presentation. and disruption of physiological drives such as sleep and appetite). Disinhibition. Semantic dementia is characterized by progressive loss of knowledge of people. and those with initially prominent behavioral symptoms developed semantic language deficits. 1998. change in eating patterns. compulsions. Adapted from Neary et al.

however. The Frontal Systems Behavior Scale (Grace and Malloy 2001) provides standardized ratings of apathy. schizophrenia. education.g.. 2005). The standardization sample for this measure included participants up to age 95 years. 2000) is completed by a trained professional on the basis of a . 2004). If the referral question concerns differentiation between frontotemporal dementia and Alzheimer’s disease. 1992) and the Frontal Assessment Battery (FAB. referral for neuropsychological assessment should be considered to document impairments and to differentiate changes due to dementia from affective illness or personality disorder. executive skills. The Executive Interview correlates well with neuropsychological measures of executive function and is sensitive to differences in everyday functional level for older adults in residential care (Royall et al. or motor function affected by frontal lobe syndromes. and as a result. The Frontal Systems Behavior Scale has been shown to discriminate dementias with prominent frontal system neuropathology from other dementias and also has been used with psychiatric patients. or major depression). dementia with Lewy bodies.g. these brief screens are a good starting point. In such cases. and it is now used frequently in clinical research (e. 2000). and gender. Informant rating scales also may help to ensure that a thorough picture of frontal deficits in everyday settings is obtained. including the Executive Interview (Royall et al.. brief screening is less likely to differentiate frontotemporal dementia from other syndromes that preferentially affect frontal executive function (e. Mendez et al. The FAB differentiates better between frontotemporal dementia and Alzheimer’s disease than does the Mini-Mental State Examination (MMSE) (Slachevsky et al. 2005). and norms are stratified by age. Dubois et al. individuals with frontotemporal dementia may score in the normal range on brief examinations in the early to middle stages of disease.232 Clinical Manual of Geriatric Psychiatry Screening Instruments and Rating Scales Most brief mental status examinations do not assess frontal executive functions. 1992) and retirement facilities (Royall et al. The Frontal Behavioral Inventory (Kertesz et al. Both measures take about 10 minutes to administer and cover several different aspects of behavior. cognition. and disinhibition and has parallel forms for the patient and informant that can be useful for assessing patients’ self-awareness of behavior changes. Several short batteries have been developed to help clinicians test for frontal lobe changes.

the Trail Making Test).g. grasp. Neuropsychological Tests On neuropsychological examination.” and Appendix) is another behavior rating scale completed by professionals on the basis of a caregiver interview. and education is needed to help with understanding the avolitional nature of specific behavior changes and with developing management strategies. “Dementia and Alzheimer’s Disease.g.g.. The symptoms of frontotemporal dementia. It taps several behaviors that are often affected in frontotemporal dementia and has been used in clinical trials. However. Items for this scale were based on behaviors described in diagnostic consensus reports (e. especially the frontal variant. as well as naming and verbal fluency tests (see Table 5–5 in Chapter 5.. and some patients will develop parkinsonian signs and symptoms or motor neuron abnormalities in the later stages. stereotypy) before notable memory deficits emerge. The Neuropsychiatric Inventory (NPI. norms for clinical use are lacking. and reasoning tasks (e. see Chapter 5. whether based on direct informant ratings or interviews. Neary et al. snout. Neuropsychological tests sensitive to frontal executive dysfunction include motor programming tasks. 1998) for frontotemporal dementia. The heterogeneity that has been noted in frontotemporal dementia is also . but data are limited on the clinical usefulness of this version. “Dementia and Alzheimer’s Disease. frontotemporal dementias can be distinguished in early stages from dementia due to Alzheimer’s disease by the relative salience of executive function deficits as opposed to memory disorder or by the emergence of progressive alterations in speech (e. and glabellar reflexes may be present.. can provide a good starting point for tailoring interventions for caregivers. dysfluency. the Similarities subtest of the Wechsler Adult Intelligence Scale—Third Edition).g. A caregiver-completed form of the NPI has been developed (Kaufer et al.” for test descriptions). A systematic survey of affected behaviors. are often very distressing to family members.. Physical and Neurological Examination As shown in Table 6–1. 2000).Other Dementias and Delirium 233 structured caregiver interview. cognitive speed and flexibility measures (e. The Frontal Behavioral Inventory has good reliability and appears effective in discriminating clearly diagnosed frontotemporal dementia from Alzheimer’s disease or vascular dementia.

234 Clinical Manual of Geriatric Psychiatry apparent on testing. with some affected persons having striking changes in personality and social behavior early on. Laboratory Evaluation Depending on the underlying pathology. (2005) reviewed 433 cases that went to autopsy and found that frontotemporal dementia was correctly identified on the basis of clinical and laboratory findings in 29 of 34 autopsy-verified cases. Creutzfeldt-Jakob disease. Parkinson’s disease. 2001) provides representative norms for interpreting several commonly used executive function tests. Because of the lack of differentiating physical signs. and the tendency for Alzheimer’s disease to include signs and symptoms of frontal lobe involvement. as well as detailed information on qualitative features of performance that may be important diagnostically. frontal and temporal hypoperfusion (on single photon emission computed tomography). and those associated with other general medical conditions all must be ruled out before a diagnosis of frontotemporal dementia is made. and head trauma. reduced glucose metabolism (on positron emission tomography with fluorodeoxyglucose). This finding represents 85% sensitivity. human immunodeficiency virus (HIV) infection. the most challenging distinction is between frontotemporal dementia and Alzheimer’s disease. as follows: . Knopman et al. Table 6–2 summarizes the main differentiating features of these two conditions. but preserved communication skills. the authors also reported 99% specificity. Differential Diagnosis The other degenerative dementias (Alzheimer’s disease and dementia with Lewy bodies). Pathology The typical gross pathological finding is of frontal and anterotemporal atrophy. the dementias associated with Huntington’s disease. Microscopic findings have been subdivided according to the profile of immunohistochemical staining and the pattern of intracellular inclusions. The Delis-Kaplan Executive Function System (Delis et al. and atrophy (on computed tomography or magnetic resonance imaging) may be seen in frontotemporal dementia. vascular dementia. and others showing prominent language deficits with relative preservation of personality.

Other Dementias and Delirium 235 1. 2004). agitation. Tau-positive astrocytic plaques and ballooned achromatic neurons (corticobasal degeneration). The second and third subdivisions above include cases with tau-negative. 2004). Trazodone improved symptoms of irritability. 2003). depression. Treatment There is no specific treatment for the personality or cognitive changes seen in the frontotemporal dementias. Tau-positive argyrophilic grain disease. and eating disorders in one randomized. However. placebo-controlled crossover study (Lebert et al. double-blind. tau-positive. 2004). Its precise nosological status remains controversial because some authorities regard it as a variant of Alzheimer’s disease and others consider it a clearly distinct condition. including senile dementia of the Lewy body type and diffuse Lewy body disease. intraneuronal Pick bodies (Pick’s disease). 2003). including classic argyrophilic. ubiquitin-positive inclusions in the dentate gyrus and in the brain-stem motor nuclei (frontotemporal dementia with motor neuron inclusions) and dementia lacking distinctive histology (Hodges et al. 3. 2. Tau-positive pathology. Tau gene mutations (FTDP17) and diffuse tau-positive neuronal and astrocytic immunoreactivity. a double-blind. rivastigmine (Moretti et al. 2004). placebo-controlled crossover study with paroxetine resulted in worsening cognition and no improvement in behavior (Deakin et al. and 4. suggesting that open-label treatment studies in frontotemporal dementia may be misleading. degenerative dementing condition with clinical and pathological features that overlap with those of Alzheimer’s disease and Parkinson’s disease. and paroxetine (Moretti et al. 1996) is a progressive. This debate has led to the use of various terms for this condition. but several aspects of disturbed behavior have been reported to respond to psychopharmacological treatment. . Dementia With Lewy Bodies Dementia with Lewy bodies (McKeith et al. and similar results have been observed in open-label studies with moclobemide (Adler et al.

tau mutations Presynaptic cholinergic and serotonergic Temporoparietal hypometabolism Neurochemistry Cholinergic deficit Positron emission tomography Postsynaptic cholinergic. 521. Gustavson A: “Alzheimer’s Disease and Frontotemporal Dementia. Edited by Coffey CE. Adapted from Miller BL. . p. American Psychiatric Press.236 Clinical Manual of Geriatric Psychiatry Table 6–2. Used with permission. Copyright © 2000.” in American Psychiatric Press Textbook of Geriatric Neuropsychiatry. American Psychiatric Press. presenilin 1 and 2. bizarre Severe Bizarre Severe Weight gain Spared Variable Severely impaired Severely impaired Semantic (often) No No (except for familial tauopathy) Out of proportion to neuronal loss Frontotemporal dementia Neuropsychological test performance Drawing Impaired Memory Impaired Executive function Impaired Generation Impaired Anomia Lexical Neuropathology Plaques Tangles Gliosis Abnormal genes Yes Yes Proportional to neuronal loss Amyloid precursor protein. DC. 2nd Edition. presynaptic and postsynaptic serotonergic Frontotemporal hypometabolism Source. Differentiation of Alzheimer’s disease from frontotemporal dementia Alzheimer’s disease Symptom Behavior Affect Apathy Delusions Compulsions Eating Socially correct Normal Mild Simple Mild Weight loss Early disinhibition Remote. Washington. 2000. Cummings JL. apolipoprotein ε4.

2005. 1866]. 2005. relative preservation of medial temporal lobe structures on computed tomography/magnetic resonance imaging scan. 1999). If one or more of the following suggestive features are present. hallucinations in other modalities. The diagnosis of dementia with Lewy bodies is less likely if “cerebrovascular disease evident as focal neurological signs or on brain imaging is 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. transient unexplained loss of consciousness. and spontaneous motor features of parkinsonism” (McKeith et al. p. but autopsy series have found it to account for 15%–36% of cases of dementia (Hansen et al. systematized delusions. 1864). depression. p. 1864). which would make it the second most common cause of dementia. p. Diagnostic Criteria Consensus criteria published originally by McKeith et al. 1864). and low dopamine transporter uptake in basal ganglia as demonstrated by [single photon emission computed tomography] SPECT or [positron emission tomography] PET imaging” (McKeith et al. and prominent slow wave activity on electroencephalogram with temporal lobe transient sharp waves” (McKeith et al. generalized low uptake on SPECT/PET perfusion scan with reduced occipital activity. 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. 1990. Holmes et al. p.Other Dementias and Delirium 237 Epidemiology The prevalence and incidence of dementia with Lewy bodies are not well established. p. but without muscle atonia. 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. 2005. Supportive features include “repeated falls and syncope. after Alzheimer’s disease. 2005.” McKeith et al. 2005. abnormal (low uptake) MIBG (metaiodobenzyl guanidine—a measure of postganglionic sympathetic cardiac innervation) myocardial scintigraphy. . recurrent visual hallucinations that are typically well formed and detailed. (1996) and recently revised (McKeith et al. 1864). severe neuroleptic sensitivity.

all of which are also regarded as supportive of the diagnosis of dementia with Lewy bodies. transient loss of consciousness. REM sleep behavior disorder also may be present early in the disease (Ferman et al. 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.238 Clinical Manual of Geriatric Psychiatry Although the consensus criteria have enjoyed widespread acceptance. as well as extrapyramidal reactions to conventional neuroleptics (severe) and atypical neuroleptics (severe in comparison to patients with other conditions). Clinical Presentation and Mental Status Examination The clinical presentation is of a dementia with intellectual changes that generally parallel those of Alzheimer’s disease. systematized delusions. 2002). Serby and Samuels (2001) reexamined their usefulness via a critical analysis of 242 published cases of dementia with Lewy bodies and found visual hallucinations and fluctuating cognition to be of very limited value. The authors suggested that these features often may be a result of treatment rather than “core” features of the disease and concluded that “greater caution should be used in the establishment of a set of diagnostic criteria for DLB [dementia with Lewy bodies]. neuroleptic sensitivity. 215). progressive decline in intellectual function that is almost always eventually accompanied by parkinsonism. silent visual hallucinations that typically appear as animals. as are deficits in executive functions. Deficits in attentional processes are also common in dementia with Lewy bodies. History The history of dementia with Lewy bodies is typically of a gradual. . syncope. The history is likely to include repeated falls. The presence of parkinsonism and. if not diagnostic. and hallucinations in other modalities. its co-occurrence with dementia appear to be the most reliable indicators of the presence of DLB” (p. Although marked day-to-day fluctuations in cognitive function and well-formed. perhaps. except the early memory impairment is more likely to represent a retrieval deficit than the impairment in new learning typically seen in Alzheimer’s disease.

Other Dementias and Delirium 239 Physical and Neurological Examination Physical and neurological examination in dementia with Lewy bodies is likely to detect bradykinesia and rigidity. individuals later . especially if the newly learned information is organized in a natural way (e. 2001). Compared with patients with uncomplicated Alzheimer’s disease. However. forward digit span) is usually preserved in Alzheimer’s disease. there may also be greater benefit from cues and recognition testing formats. no significant differences were seen between diagnostic groups on mental status examinations (either the MMSE or the Dementia Rating Scale. including memory dysfunction. however. 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. delayed recall tends to be better preserved in dementia with Lewy bodies than in Alzheimer’s disease.. 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 pictures (Calderon et al. and patients have greater difficulty with motor programming and executive functions such as shifting from one thought or action to another. Participants in this study were tested early in the course of illness (about 1 year after the onset of memory problems). 2005) provided further support that neuropsychological testing may help in diagnostic differentiation.. In dementia with Lewy bodies. but parkinsonian tremor may be absent. By contrast.g. A recent study comparing autopsy-verified cases of Alzheimer’s disease.g. and executive function. particularly in the later stages of illness. see Table 5–1). 2001). stories) (Calderon et al. and at that point. whereas simple attention (e. dementia with Lewy bodies. Similarly. visuoperceptual processing. more psychomotor slowing occurs early in the course of dementia with Lewy bodies. Typically. individuals with dementia with Lewy bodies may have disproportionate problems with attention and working memory. and combined Alzheimer’s disease and dementia with Lewy bodies (Kraybill et al. Evidence of stroke or other physical conditions that could account for the clinical features should be considered as evidence against a diagnosis of dementia with Lewy bodies. low scores are likely to be seen on nearly all types of attention tasks.

choline acetyltransferase and acetylcholinesterase) of a magnitude even greater than that reported in Alzheimer’s disease. Neurochemical analysis of neocortical brain tissue indicates loss of cholinergic markers (i. including Alzheimer’s disease. as are seen in Alzheimer’s disease. Parkinson’s disease and Alzheimer’s disease. patients with dementia with Lewy bodies had more impairment at baseline on a measure of psychomotor speed and executive function (Trail Making Test) and on an attention test (digit span) (see Table 5–5 for descriptions of these measures). and Parkinson’s disease with dementia.240 Clinical Manual of Geriatric Psychiatry found to have pure Alzheimer’s disease or combined Alzheimer’s disease and dementia with Lewy bodies performed worse on verbal memory measures and confrontation naming than did those with pure dementia with Lewy bodies.e.. and neocortex. cholinesterase inhibitors such as donepezil and rivastigmine have been studied in this condition. 1996]) are widespread in the brain stem. double-crossover study of just seven subjects found donepezil to be statistically significantly superior to placebo. vascular dementia. as measured by the MMSE and the Alzhei- . by contrast. Pathology and Pathogenesis The micropathology of dementia with Lewy bodies involves extensive cortical neuritic plaques. subcortical nuclei. A double-blind. no differences were observed on brief screening measures of attention and executive function (Dementia Rating Scale subscales). Lewy bodies (intracytoplasmic spherical. placebo-controlled. suggesting that referral for detailed neuropsychological testing may be needed to improve antemortem diagnostic accuracy for dementia with Lewy bodies. frontotemporal dementia. Differential Diagnosis The differential diagnosis of dementia with Lewy bodies includes essentially all of the dementing diseases. Interestingly. with relatively few neurofibrillary tangles. limbic cortex. Treatment Because of the relatively severe loss of cholinergic innervation found in dementia with Lewy bodies. eosinophilic neuronal inclusion bodies that can also be visualized via antiubiquitin immunocytochemical detection techniques [McKeith et al.

the prevalence of vascular dementia ranges from 2.to 79-year-old women to 16.Other Dementias and Delirium 241 mer’s Disease Assessment Scale–cognitive subscale. and episodic secondary memory. 2004).2% in 70. working memory. and aripiprazole may therefore be preferable for symptoms of agitation and psychosis that remain after administration of cholinesterase inhibitors. as assessed by a computerized test battery. after 4 weeks of treatment (Beversdorf et al. Treatment of agitation or psychosis in dementia with Lewy bodies is complicated by severe extrapyramidal reactions to conventional neuroleptics. Most treatment effects disappeared 3 weeks after rivastigmine was discontinued. subjects taking rivastigmine (6–12 mg/ day) had significantly improved attention. and 3) the prevalence differs substantially from nation to nation. 2002). A report by Hulette and colleagues . usually Alzheimer’s disease. with prevalence rates doubling every 5 years. In another double-blind. and even the atypical agents risperidone. and this has impeded definitive validation of clinical diagnostic criteria for vascular dementia (Jellinger 2005). Overall. Still. and clozapine have been reported to cause significant extrapyramidal symptoms in dementia with Lewy bodies. community-based studies suggest that 1) the prevalence of clinical vascular dementia is age dependent. ziprasidone. Vascular Dementia Epidemiology The prevalence of vascular dementia is difficult to estimate because no generally accepted and validated neuropathological criteria have been established to date. other atypical agents such as quetiapine. placebo-controlled. 1998). 2) the frequency of vascular dementia is higher in men.3% in men older than 80 (Leys et al. olanzapine. randomassignment study (Wesnes et al. Until a “class effect” is established. compared with those taking placebo. Diagnostic Criteria The nosological status of vascular dementia has been called into question by autopsy studies indicating that the underlying neuropathology in clinical vascular dementia is commonly a “mixture” of vascular lesions and other degenerative conditions.

5) The DSM-IV-TR (American Psychiatric Association 2000) criteria for vascular dementia are summarized in Table 6–3.242 Clinical Manual of Geriatric Psychiatry (1997) indicated that only 6 of nearly 2. alcohol abuse. History The history of the current illness in vascular dementia is classically one of a more abrupt. if not most. cases. (p. may nevertheless contribute to the cognitive changes. . low education level. arterial hypertension. If this figure is at all representative. 1980) (Table 6–4) designed to quantify the probability of underlying infarctions in the patient with dementia has been published on the basis of the clinical signs and symptoms described in the following subsections. eventually causing neuronal death. “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. both previously regarded as markers of AD [Alzheimer’s disease]. stepwise course of cognitive impairment than the more gradual onset and decline typical of “pure” Alzheimer’s disease and other degenerative dementias. but other criteria sets have been proposed that offer different profiles of specificity and sensitivity (Wetterling et al. Risk factors identified by the history in vascular dementia are those associated with stroke—that is. 1996). However. Korczyn (2005) came to a similar conclusion. who reviewed the status of cerebrovascular brain injury (CVBI) in relation to dementia and stated. atherosclerotic disease. although possibly insufficient to fulfill the arbitrary criteria set for the diagnosis of AD. the vascular damage may accumulate slowly and impair neuronal metabolism and function. 51).000 brains of individuals with dementia that were surveyed by pathologists had “pure” vascular pathology. the effects of CVBI may become submerged once AD-pathology arrives at the isocortical stages” (p. This view was supported by Chui (2005). clinical vascular dementia should be thought of as a “vascular complication” superimposed on another dementing illness in many. Demented patients with vascular brain disease frequently have some degree of amyloid deposits and neurofibrillary changes. stating that most patients diagnosed as VaD [vascular dementia] actually have evidence of hippocampal atrophy and cortical cholinergic deficiency. Like the AD changes. which. and heart disease. A rating scale (Rosen et al.

Copyright © 2000. The deficits do not occur exclusively during the course of a delirium. relatively well-preserved memory with severe disturbance of language and praxis. American Psychiatric Association. Source. Focal neurological signs and symptoms or laboratory evidence indicative of cerebrovascular disease that are judged to be etiologically related to the disturbance.g. C. The cognitive deficits in Criteria A1 and A2 each cause significant impairment in social or occupational functioning and represent a significant decline from a previous level of functioning. although certain features such as relative preservation of personality and insight. or signs associated with more global cortical and subcortical damage. Physical and Neurological Examination Patients with vascular dementia may have focal neurological signs associated with ischemic damage to motor cortex and descending tracts. D. and “patchiness” of cognitive deficits on mental status examination are reported to be more common in vascular dementia than in other types of dementia.Other Dementias and Delirium 243 Table 6–3. 2000. Text Revision. . Used with permission. or relatively severe memory impairment with relative preservation of calculating ability and capacity for abstract thought). such as exaggerated deep tendon reflexes or focal weakness or rigidity. emotional lability. American Psychiatric Association. “Patchiness” refers to the phenomenon of relatively well-preserved islands of function concurrent with relatively deteriorated areas of function (e. Washington. DC. Summary of DSM-IV-TR diagnostic criteria for vascular dementia The development of multiple cognitive deficits manifested by both (1) memory impairment (2) one (or more) of the following cognitive disturbances: (a) aphasia (b) apraxia (c) agnosia (d) disturbance in executive functioning B. depressed mood. 4th Edition. somatic complaints. such as gait abnormalities. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. A.. Clinical Presentation and Mental Status Examination Vascular dementia is clinically very similar to other dementias.

or behavioral planning and sequencing). Source. bruits) and signs of poor peripheral circulation (e.g. For those whose cerebrovascular impairment is limited to lacunar infarcts or who have extensive deep white matter disease. Neuropsychological Tests Neuropsychological test findings in vascular dementia vary with the nature and severity of cerebrovascular illness. atrophic skin changes) also may increase the probability that dementia is at least partly of vascular origin. extensor plantar reflex. with impairments expected on tests of psychomotor speed and dexterity. Point value 2 1 1 1 1 2 2 2 dysarthria. dysarthria or reduced verbal output may be present) (Roman et al. deficits are more consistent with subcortical dementia.. frontal executive functions (e. 1993). head trauma (motor or sensory deficits). and signs of “frontal release” such as grasp or snout reflex. impaired gag reflex. A score of 4 or more is consistent with vascular dementia. attentional shifting. cogwheel rigidity. 1980.g. working memory.. and akinesia). atonia and hyperreflexia. frontal release signs). Physical and neurological examination may show abnormal findings associated with Parkinson’s disease (tremor. deficits commensurate with the location and extent of infarction should be expected..g. Clinical features of the Modified Ischemic Score Feature Abrupt onset Stepwise deterioration Somatic complaints Emotional incontinence History or presence of hypertension History of strokes Focal neurological symptoms Focal neurological signs Note. For patients who have had single or multiple large infarcts. difficulties with divided attention. Evidence of systemic atherosclerosis (e. Huntington’s disease (choreoathetoid movements). Subtle frontal-subcortical deficits may precede clinically significant dementia in patients with . and motor aspects of speech (e.g. diminished pulses. ataxia. or Creutzfeldt-Jakob disease (ataxia. HIV infection (tremor.244 Clinical Manual of Geriatric Psychiatry Table 6–4.. myoclonus). Adapted from Rosen et al.

and hypothyroidism. but was not related to the severity of CVD. “Dementia and Alzheimer’s Disease”). such as brain tumor. A high rate of intertest scatter is not specific to vascular dementia and cannot be used to identify this condition or to differentiate it from Alzheimer’s disease or other dementias. have been considered to be adequate to differentiate vascular dementia from other dementing illnesses (which are discussed in detail below). dementia with Lewy bodies. including neuropsychological tests. as presented in Chapter 5 (“Dementia and Alzheimer’s Disease”. and functional disorders (see Table 5–6 in Chapter 5. Computed tomographic or magnetic resonance brain imaging that shows brain infarction is sufficient. the dementias associated with HIV disease. the history. dementia due to other medical conditions. delirium. Table 5–4). head trauma. (p.Other Dementias and Delirium 245 deep white matter disease (leukoaraiosis) or lacunar infarcts. also may be observed in vascular dementia. with or without clear cognitive impairment. physical and neurological examination. Huntington’s disease. Reed et al. mental status examination. and abrupt change in mood and personality. laboratory evidence of cerebrovascular disease is required. but some studies have cast doubt on this claim. frontotemporal dementia. if the number and location of infarcts are judged to account for the observed cognitive deficits. The presence of dementia was predictably related to the level of neurofibrillary pathology. As discussed earlier. and Creutzfeldt-Jakob disease. to establish a diagnosis of vascular dementia in the absence of neurological signs and symptoms. and laboratory evaluation. 63) . even when AD [Alzheimer’s disease] changes were essentially absent. Laboratory Evaluation Laboratory evaluation generally begins with a selected standardized battery of tests with relatively high sensitivity and low specificity. Differential Diagnosis As is true of all of the dementing illnesses. the differential diagnosis of vascular dementia includes Alzheimer’s disease. (2004) studied 18 individuals with autopsy-defined cerebrovascular disease and found that clinical features were quite variable. As indicated in Table 6–3. Parkinson’s disease. normal-pressure hydrocephalus. only 40% of cases with high CVD [cerebrovascular disease] levels had elevated Hachinski Ischemia Scale scores and neither abrupt onset nor stepwise progression was found in most high CVD cases. clinical presentation.

. Increasing evidence suggests that the vascular lesions of vascular dementia may affect . and diabetes usually are cited as the most common causes of thrombotic infarction. “sundowning”) of the type to which patients with vascular dementia are prone. absence of the neurological signs and symptoms and risk factors for vascular dementia) seen in the functional disorders. several functional illnesses can also mimic dementia of any type. hippocampal lesions. An emerging consensus suggests that the “subcortical” pattern of damage is sufficiently homogeneous in terms of clinical.e.246 Clinical Manual of Geriatric Psychiatry Nonetheless. distal field (watershed/borderzone) infarcts. allowing the underlying dementia to be characterized. Generally. and sclerosis (Jellinger 2005). incomplete ischemic injury. As described earlier. Generalized arteriosclerosis secondary to hypertension. Agitation. white matter lesions. including vascular dementia. Accurate diagnosis of vascular dementia in both cases depends on reevaluation when signs or symptoms of delirium or acute agitation have cleared. lacunar infarcts and scars. particularly in the early evening. based on either the number and distribution of lesions or the size of vessels involved (large vs. radiographic. and cardiac disease and carotid atherosclerosis as the most common causes of embolic infarction. cerebral atherosclerosis. and patients with delirium have a disturbance in consciousness that is not seen in patients with uncomplicated vascular dementia. small and medium-sized lesions mainly in functionally important brain areas. Pathogenesis Vascular dementia is caused by varying combinations of vascular insults to the brain. these illnesses are identifiable by the rapid onset and progression of symptoms and the atypical overall clinical picture (i. transient state. However. including arterial territory infarcts.. particularly with respect to treatment trials. delirium is generally distinguishable from vascular dementia in that delirium is characterized by a much more acute onset and more rapid progression than vascular dementia. the diagnostic picture can be clouded in two situations: 1) when vascular dementia and true delirium occur simultaneously and 2) during an episode of acute agitation (e.g. and pathophysiological features to constitute a meaningful subtype. which is usually a self-limiting. Several subtypes of vascular dementia have been described. may have many of the features of delirium without the implications of deranged physiology and poor prognosis characteristic of true delirium. small vessels).

These results are presumably based on the cholinergic deficit that has been identified in vascular dementia. only subjects with “mixed” Alzheimer’s disease and vascular dementia benefited from active treatment). 2002. 2002).Other Dementias and Delirium 247 cholinergic pathways in vascular dementia. 2003). Tzourio et al. Others support the view that ischemia due to vascular pathology triggers the cascade of events leading to the development of plaques and tangles (Casserly and Topol 2004. and prevention of cardiac arrhythmia and prescription of aspirin or other antiplatelet-aggregating agents also may be of benefit (Nelson et al. Treatment of Cognitive Impairment in Vascular Dementia Three studies have reported the efficacy of cholinesterase inhibitors in vascular dementia: two studies with donepezil (Black et al. leading to a hypocholinergic state similar to that observed in Alzheimer’s disease (Mesulam et al. Interestingly. even though such a deficit is not required for cholinesterase inhibitors to be effective (Yesavage et al. in this study. Prevention of Vascular Dementia Treatment aimed at controlling hypertension has been shown to reduce the risk of dementia and cognitive impairment (Forette et al. Wilcock et al. 2002). and it is likely that rivastigmine and yet-to-bedeveloped cholinesterase inhibitors are equally effective. a glial cell modulator that has been shown to interfere with neuroinflammatory processes linked to the pathological activa- .. Wilkinson et al. Roy and Rauk 2005) have hypothesized that both Alzheimer’s disease and vascular dementia are the result of a common pathophysiological process initiated by soluble β-amyloid. 2003. although benefits are minimal (Orgogozo et al. 2002. Some investigators (e. Memantine also has been shown to be effective in vascular dementia. 2003).g. 2002). 2003). Propentofylline. which is the typical pattern seen with cholinesterase inhibitors in Alzheimer’s disease. statin therapy has not been of benefit in trials published to date (Shepherd et al. 2002. Honig et al. 2003). which is toxic to both neuronal and vascular tissue. 2003) and one study with galantamine (Erkinjuntti et al. Dosage and treatment outcomes in vascular dementia are comparable in magnitude to those seen in Alzheimer’s disease but appear to be a result of improvement in cognitive function compared with placebo-treated subjects rather than a reduced rate of cognitive decline.

These findings led the FDA to issue advisories to physicians and led several investigators to conduct confirmatory studies. Mixed Dementia In a review. or death. a subsequent analysis of a comparably large data set led to the same conclusion about olanzapine. multiple lacunar infarctions. the U. (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. 2000).800 elderly patients with dementia that risperidone was associated with an increased risk of ischemic stroke. Treatment of Behavioral Complications. Langa et al.4 million patients age 65 or older and found no increase in the crude rate of stroke when patients taking risperidone or olanzapine were compared with those who received a typical neuroleptic. In 2004. with the following caveat. Herrmann et al. Food and Drug Administration (FDA) concluded on the basis of its review of four randomized trials of risperidone in almost 1. but patients with vascular dementia who are taking atypical agents should be monitored closely for evidence of vascular complications. has been effective in early Phase II trials and warrants watching. and equilibrium and was not associated with an increased incidence of stroke. 2902). balance. They found that olanzapine was equal to conventional neuroleptics for control of behavior problems but produced fewer negative effects on gait. These studies and others like them are reassuring.S. documented either by clinical criteria or by neuroimaging findings” (p. and is- . (2004) studied a Canadian database of more than 1. Moretti et al. Mood Disorder. and half received promazine) or olanzapine. (2005) studied 346 subjects with vascular dementia and “behavioral problems” who were randomly assigned to 12 months of treatment with conventional neuroleptics (about half received haloperidol.248 Clinical Manual of Geriatric Psychiatry tion of microglial cells and reactive astrocytes (Kittner et al. As discussed earlier. and Psychosis in Vascular Dementia Psychosocial and psychopharmacological therapy for behavioral complications of vascular dementia follow the general principles outlined in Chapter 5 (“Dementia and Alzheimer’s Disease”) for Alzheimer’s disease. myocardial infarction. the amyloid plaques and neurofibrillary tangles of Alzheimer’s disease and the large infarctions.

inability to sustain attention to complex tasks. attention. from 25% to 45% of Alzheimer’s disease brains have significant vascular pathology (Langa et al. and other dementing conditions depends on identification of the characteristic physical and laboratory abnormalities associated with each disease entity. these patients progress to a frank frontotemporaltype dementia with apathy. DSM-IV-TR specifically recognizes HIV disease. Despite the benefits of HAART. and Pick’s disease (a form of frontotemporal dementia. Patients with the cognitive impairment associated with acquired immunodeficiency syndrome (AIDS)—the AIDS dementia complex—typically present with forgetfulness. trauma. and plaques and tangles are nearly always present in the brains of individuals with vascular dementia. and generalized mental slowing. frontotemporal dementia. Creutzfeldt-Jakob disease. loss of initiative. or degeneration). head trauma. and significant psychomotor retardation. with preventive efforts aimed at control of blood pressure and other risk factors for vascular dementia. 2004). Parkinson’s disease. 2004). supported by appropriate historical information. Depending on the source of pathological material. most AIDS dementia patients continue to have significant cognitive impairment even when viral counts in brain tissue have declined to relatively low levels. Treatment follows guidelines for Alzheimer’s disease. These characteristics are summarized in Table 6–5. Highly active antiretroviral therapy (HAART) has been reported to improve memory. described earlier in the “Pathology” subsection of “Frontotemporal Dementia”) as capable of causing dementia via direct damage to brain structures (by infection.” Table 5–6). Huntington’s disease. all of which leads to the conclusion that vascular dementia is actually mixed dementia in a large percentage of cases.Other Dementias and Delirium 249 chemic periventricular leukoencephalopathy of vascular dementia are often found together in the brains of individuals with dementia. Differentiation of each of these conditions from Alzheimer’s disease. and other cognitive functions in AIDS dementia (Robertson et al. . even though HAART agents poorly penetrate the blood-brain barrier. “Dementia and Alzheimer’s Disease. vascular dementia. Dementia Due to General Medical Conditions Although many other conditions can cause impairment in cognition severe enough to meet criteria for dementia (see Chapter 5. dementia with Lewy bodies.

anomia. required personality common incontinence) for diagnosis if focal neurological signs absent Elevated CSF protein. depression. lacunae in basal Patchy impairment.. ataxia. Neurological signs and mild lymphocytosis slowness. Neurological signs and ganglia. enlargement on CT. history of hypertension.g. hypoperfusion on deficits early SPECT Stroke. gait periventricular lesions preservation of abnormalities. falls. neuroimaging tremor. atherosclerosis HIV dementia HIV-positive blood test. ± family history Physical findings Typically none until middle to late stages Cognitive and behavioral function Imaging and laboratory findings 250 Clinical Manual of Geriatric Psychiatry Vascular dementia Abrupt onset. apathy.. gradual onset of cognitive changes Cortical atrophy. present (e. poor symptoms may be concentration common may be present. “frontal release” nonspecific. white matter. very common. Language deficits early ventricular (word finding. relative symptoms (e. temporal/parietal not helpful with hypometabolism on retrieval.Table 6–5. Differentiating the common dementias Type Alzheimer’s disease History Gradual onset and progression. visuospatial PET. fluent aphasia). HIV signs) usually present in CSF . clues MRI. stepwise decline. Forgetfulness.g.

hemiparesis common Cognitive and behavioral function Imaging and laboratory findings Parkinson’s disease Dementia in later stages of neurological syndrome Extrapyramidal signs (e..g. perseveration. tremor. dysarthria. Differentiating the common dementias (continued) Type Head trauma History Head injury Physical findings Depends on location of injury. memory hypometabolism impairment later. impulse extent of injury dyscontrol. (e. gait disturbance. ventricular decreased word-list enlargement) common. frontal signs intercaudate distance.. PET may show striatal early. poor Subcortical atrophy on CT (e. bradykinesia) Huntington’s disease “Fidgeting” progressing Autosomal dominant to choreoathetosis pattern of inheritance.g. nonprogressive unless head trauma repeated (e. irritability striatal atrophy. in dementia pugilistica) Cognitive slowing.g. rigidity. loss CT or MRI may show of judgment. irritability. personality change may be seen.. onset generally in 30s– 40s. clues diminished on PET helpful with memory retrieval Personality change. offspring of affected parent 50% likely to be affected Depends on location. impaired global cerebral behavioral metabolism also may be sequencing).g..Table 6–5. increased recall. psychosis common Other Dementias and Delirium 251 . Memory impairment usually present. generation.

can be transmitted by corneal transplant or contact with infected brain tissue or CSF CT and MRI may be normal. CSF= cerebrospinal fluid. PET= positron emission tomography. 1-year cognitive deficits late) present course) typical. . global disturbance variably progression (i. rapid appetite early. MRI=magnetic resonance imaging. Differentiating the common dementias (continued) Type Pick’s disease History Onset in 50s–60s Physical findings Cognitive and behavioral function Imaging and laboratory findings CT or MRI may show frontal and temporal atrophy.. HIV=human immunodeficiency virus. 5%– Myoclonus early. memory impairment.Table 6–5. PET may show frontal hypometabolism 252 Clinical Manual of Geriatric Psychiatry Creutzfeldt-Jakob disease Frontal release signs (e.g. grasp reflex) deterioration of social common skills. fatigue. emotional blunting. EEG =electroencephalogram.g. triphasic synchronous discharges at 0. dyspraxia later Onset in 40s–60s. visual 15% have family diminished sleep and symptoms. language deficits early. Personality change. later.e.. gait history. SPECT= single photon emission computed tomography. EEG may show sharp.5–2 Hz Note. CT= computed tomography. seizures Nonspecific symptoms (e. snout.. ataxia.

Functionally significant cognitive deficits in Parkinson’s disease are quite variable. 2003). Neuropsychological profiles of patients with Parkinson’s disease and dementia with Lewy bodies are similar. However. but executive dysfunction is generally less severe in Parkinson’s disease. others remain free of all but minor executive deficits for 5–10 years. but problems with retention of learned material may be absent or mild. visuoperceptual skills. verbal fluency. 2002. or other neurological disorders. 2001. 2004) and similar positive results found in several open-label studies (Masanic et al. The dementias of Parkinson’s disease and Huntington’s disease. As the disease progresses. Emre et al. and attentional fluctuations may be less pronounced. no effective treatment for the dementia of Huntington’s disease has yet been developed. treatment trials with cholinesterase inhibitors have reported efficacy in Parkinson’s dementia comparable to that seen in Alzheimer’s disease (Aarsland et al. A substantial proportion of patients with Parkinson’s disease (20%– 45%. Giladi et al. 2003). placebocontrolled crossover study (Zhang et al. double-blind. impaired learning and retrieval efficiency appears. are sometimes described as “subcortical” because they are characterized by a cluster of clinical features (relative preservation of language function. except in those who have concomitant Alzheimer’s disease. with improvement in short-term memory and sustained attention reported in one random-assignment.Other Dementias and Delirium 253 Dementia associated with head trauma has been reported to respond to cholinesterase inhibitors. including attention. Family members caring for older adults with Parkinson’s disease. response inhibition. and ability to do mathematical calculations. and many never show the level of cognitive deficit that would be detected on mental status examinations. patients may have subtle changes in executive functions (especially problems in maintaining or shifting set) but do not yet meet criteria for dementia. Some patients with Parkinson’s disease develop noticeable cognitive deficits within a year or two of the onset of motor symptoms. In the early stages of these illnesses. or other . Morey et al. such as Alzheimer’s disease. 2004. Despite the differences in pathophysiology between Alzheimer’s disease and Parkinson’s disease. with comparatively severe deficits in frontal executive functions. according to Rickards [2005]) have significant depressive symptoms that can compound mild cognitive impairments. dementia with Lewy bodies. Huntington’s disease. like some forms of vascular dementia. and ability to plan and execute multistep actions) that are relatively less common in dementing illnesses with primarily cortical pathology.

Extracerebral pathology. Accurate diagnosis usually depends on recognition of the characteristic clinical and laboratory features of the underlying illness. 2002). usually in the context of severe and prolonged alcohol intake. and various conditions (e. focal lobar atrophy) with mainly frontal lobe–type behavioral manifestations. including psychotherapy for marked caregiver strain (e. dorsomedial nucleus of the thalamus. The syndrome is caused by thiamine deficiency. 2005) in case reports but not in a placebo-controlled. . Secker and Brown 2005). Some patients with a diagnosis of alcoholic dementia have Korsakoff ’s syndrome. progressive subcortical gliosis. Dementia Due to Other General Medical Conditions Dementia also may be caused by other diseases with primarily central nervous system pathology. single-blind study of malnutrition-related disease (Sahin et al. amyotrophic lateral sclerosis. and periaqueductal gray matter. subdural hematoma. and dementia per se. Substance-Induced Persisting Dementia Certain substances with central nervous system activity can produce both intoxication. with varying amounts of cortical atrophy and ventricular enlargement. which persists for months or years after the substance use is terminated (see Table 5–6). “Dementia and Alzheimer’s Disease”).. Alcohol is perhaps the classic example of such a substance. which is a pure amnesia due to damage to the mammillary bodies.254 Clinical Manual of Geriatric Psychiatry progressive neurological disorders may benefit from some of the same interventions as caregivers of patients with Alzheimer’s disease (see Chapter 5.g.g. such as multiple sclerosis. both intracranial (brain tumor.. during which cognitive impairment severe enough to otherwise qualify as dementia may be present. and has been reported to be responsive to cholinesterase inhibitors (Cochrane et al. also can cause dementia via mechanical and biochemical effects on brain function. hypercalcemia. hypoglycemia) processes. hydrocephalus) and extracranial (hypothyroidism. Other cases of “alcoholic dementia” are probably cases of concomitant Alzheimer’s disease or vascular dementia or reflect the effects of continued intoxication (Lishman 1987). The battery suggested in Table 5–4 in Chapter 5 (“Dementia and Alzheimer’s Disease”) is designed to have relatively high sensitivity for this purpose.

Reversible Dementia Some dementias (mainly those due to a general medical condition). older adults with alcohol-related dementia have relatively prominent subcortical dementia features.Other Dementias and Delirium 255 However. or at least stabilize. Clarfield (1988) re- . For patients with Korsakoff ’s syndrome. memory deficits dominate the profile and may include tendencies to confabulate or intrude irrelevant but related information into recall attempts. On neuropsychological testing. 2. at least in principle. stabilization or improvement of the cognitive impairment. especially of the vermis. improvement of neuroimaging evidence of sulcal or ventricular dilatation after 60 days of abstinence. ataxia or peripheral sensory polyneuropathy. pancreatic). evidence indicates that substantial cognitive deficits beyond “pure” amnesia are common in people who drink heavily and that even though these deficits tend to remit after drinking is discontinued. for older patients with alcohol-related dementia if they remain abstinent (Oslin and Cary 2003) underscores the importance of screening for alcohol problems in primary care and psychiatric settings. and some may show learning and memory problems similar to those of patients with Alzheimer’s disease at comparable levels of dementia severity. A clinical diagnosis of dementia at least 60 days after the last exposure to alcohol. and neuroimaging evidence of cerebellar atrophy.. Oslin and colleagues (1998) also proposed that supportive features include alcohol-related organ system damage (e. renal. as defined by a minimum average of 35 standard drinks per week for men (28 for women) for more than 5 years. Significant alcohol use. including reduced mental control and executive function impairments. can be arrested or reversed if the underlying condition is successfully treated before significant brain damage occurs.g. The period of significant alcohol use must occur within 3 years of the initial onset of dementia. some deficits may persist for years and may in fact be permanent. Oslin and colleagues (1998) reviewed the literature and proposed the following diagnostic criteria for probable alcohol-related dementia: 1. hepatic. The observation that cognition and functional status may improve.

minimal language disturbance. substance-induced persisting dementia. 2003). 2004). but only 11% partially and 3% fully reversed. or brain tumor were reversible. In 2003. 0.6% of the dementia cases actually reversed (0. as declining functional brain reserve reduces the individual’s ability to tolerate physiological derangement. Clarfield attributed the decline to improved selection criteria and more rigorous methodology. resulting in the proportion of truly reversible dementias declining toward its “true” very low value. Osimani and colleagues (2005) confirmed the reversibility of the dementia due to vitamin B12 deficiency and suggested that neuropsychological evaluation could distinguish this syndrome from Alzheimer’s disease. 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. cerebral amyloid inflammatory vasculopathy (Harkness et al. In general. cases of reversible dementia also have been reported involving cerebral Whipple’s disease (Rossi et al.31% fully). Delirium Epidemiology The prevalence of delirium depends on the population at risk and the diagnostic criteria used. with occlusion of the right sigmoid sinus (Bernstein et al. Clarfield updated his meta-analysis and found that of more than 5. Since Clarfield’s last review. cryptococcal meningitis (Ala et al.256 Clinical Manual of Geriatric Psychiatry viewed several studies and found that 13% of dementias were potentially reversible. potentially reversible causes were seen in 9%. and the rate is even higher among nursing home patients. 2005). 2004). 2004).29% partially. metabolic dementia (including thyroid and vitamin B12 [cobalamin] deficiency). subdural hematoma. bromide intoxication (Yu et al. and dementia secondary to normal-pressure hydrocephalus. Clarfield found that other than the dementia syndrome of depression. The high- . systemic lupus erythematosus (Lee et al. only 8% reversed at all. 2004). and dural arteriovenous fistula of the right transverse sinus and torcula. and only 0. and absence of ideomotor apraxia in dementia due to vitamin B12 deficiency as compared with Alzheimer’s disease. They found more frequent psychosis.000 cases reviewed. With more conservative criteria (excluding the dementia syndrome of depression). the list of organic etiologies that can cause dementia increases with the age of the patient.

the patient with delirium usually cannot give a reliable history of the current illness. 2001. History and Clinical Presentation Four specific subtypes of delirium are recognized in DSM-IV-TR: 1) delirium due to a general medical condition. sustain. and dehydration as risk factors. and a history of abrupt discontinuation of prolonged. 2) delirium due to substance intoxication. the patient’s recent history is critical in distinguishing among these possibilities. Table 6–7 reviews the key differences between the two syndromes. hospital personnel. McNicoll et al. For obvious reasons. Because delirium occurs as an emergent complication of several life-threatening illnesses. and the medical history is typically that of the primary illness. and 4) delirium due to multiple etiologies. or the medical record. it is important to complete the evaluation rapidly. Mental Status Examination As indicated in Table 6–6.Other Dementias and Delirium 257 est prevalence of delirium is in intensive care units. use of bladder catheter. where rates of 70%–87% have been reported (Ely et al. family. which is obtained from friends. but studies also have identified visual impairment. addition of more than three medications while in the hospital. high-dose ingestion will be present in cases of substance withdrawal delirium. A recent history of drug or alcohol ingestion will be present in cases of substance intoxication delirium. 2003). Well-established risk factors include age and cognitive impairment. Delirium due to a general medical condition usually develops over hours to days. severe illness. 3) delirium due to substance withdrawal. Delirium frequently coexists with dementia and sometimes can be mistaken for dementia. Diagnostic Criteria DSM-IV-TR diagnostic criteria for delirium due to a general medical condition are summarized in Table 6–6. DSM-IV-TR recognizes the most prominent features of delirium as “reduced clarity of awareness of the environment” with “reduced ability to focus. malnutrition. or shift attention” (American Psychiatric . Obviously. and use of physical restraints. with a superimposed history of the development of disturbance in consciousness and cognition. and iatrogenic events as precipitating factors that sequentially increase the risk of delirium (Inouye 2000).

Used with permission. C. There is evidence from the history. or language function. 4th Edition. Disturbance of consciousness (i. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. or laboratory findings that the disturbance is caused by the direct physiological consequences of a general medical condition.” In both types. 2001). with comparable reliability and validity (Trzepacz et al. Ross and colleagues (1991) found hallucinations and delusions to be far more common in patients with “activated” than with “somnolent” delirium. 2000. the Confusion Assessment Method (CAM. A change in cognition or the development of a perceptual disturbance that is not better accounted for by a preexisting. More commonly. memory. or evolving dementia. B. DC. or “perceptual disturbance that is not better accounted for by…dementia” (American Psychiatric Association 2000. Inouye et al. 143).. such as a deficit in orientation. American Psychiatric Association. particularly when the delirium is mild or accompanied by significant somnolence. Text Revision. Association 2000. 1988) developed a 10-item Delirium Rating Scale. D. sustain. the patient has either cognitive impairment. or shift attention. p. the patient with delirium cannot participate in a thorough mental status examination. established. which can be used to quantify delirium severity and treatment response and may help to differentiate delirium from psychotic episodes or dementia. Another instrument. 1990) . Several authorities on delirium have further subdivided the disorder into the following categories: 1) “somnolent or hypoactive” and 2) “activated or hyperactive. American Psychiatric Association. Trzepacz and colleagues (Trzepacz and Dew 1995. the cognitive deficits in delirium are rarely disguised by the patient’s attempts to cover or minimize deficits but may nonetheless be overlooked by clinicians. and the syndrome is identified indirectly.258 Clinical Manual of Geriatric Psychiatry Table 6–6. Unlike uncomplicated dementia. Source. physical examination. this scale was updated to a 16-item version that has increased flexibility and breadth of symptom coverage. p. in 2000. and our clinical experience is the same. Copyright © 2000. The disturbance develops over a short period of time (usually hours to days) and tends to fluctuate during the course of the day. 143). Trzepacz et al. reduced clarity of awareness of the environment) with reduced ability to focus.e. Washington. Summary of DSM-IV-TR diagnostic criteria for delirium due to a general medical condition A.

and Psychiatry 76:i31–i38.Other Dementias and Delirium 259 Table 6–7.e. which can be administered to intubated patients and does not require verbal responses. often intact early Source. delusions Slow/rapid. >90%) positive predictive accuracy for the recognition of delirium. Reproduced with permission from the BMJ Publishing Group. 2005). 2005). (Table 6–8). The relatively shorter and easier to administer CAM and the Delirium Rating Scale (original 10-item version) showed good to very good agreement in the classification of delirium among older acutely ill hospital inpatients in a study of 94 subjects (Adamis et al. Adapted from Butler C. is based on diagnostic criteria from DSM-III-R (American Psychiatric Association 1987) and has very high (i. Differentiating delirium from dementia Feature Onset Course Duration Alertness Sleep-wake Attention Orientation Working memory Episodic memory Thought Speech Perception Behavior Delirium Abrupt/subacute Fluctuating Hours to weeks Abnormally high or low Disrupted Impaired Impaired Impaired Impaired Disorganized. An even shorter version of the CAM.” Journal of Neurology. 2005. including a complete physical and neurological examination and laboratory . Neurosurgery. Zeman AZ: “Neurological Syndromes Which Can Be Mistaken for Psychiatric Conditions. incoherent Illusions and hallucinations common Withdrawn or agitated Dementia Insidious Slow progression Months to years Typically normal Typically normal Relatively normal Intact in early dementia Intact in early dementia Impaired Impoverished Word finding difficulty Usually intact in early dementia Varies. agreement was strongest with the more sensitive Delirium Rating Scale cutoff point of 10.. has been developed and appears to have specificity and sensitivity comparable to the “standard” version (McNicoll et al. Laboratory Evaluation Proper evaluation of delirium requires comprehensive medical evaluation.

easily aroused) Stupor (difficult to arouse) Coma (unarousable) Note. 2. 1990. Inattention Indicated by a positive response to the following question: Does the patient have difficulty focusing attention—for example. Acute onset and fluctuating course Indicated by positive responses to the following questions: Is there evidence of an acute change in mental status from the patient’s baseline? AND Did this behavior fluctuate during the past day—that is. laboratory evaluation may have been substantially completed before consultation was requested. with rambling or irrelevant conversation. how would you rate this patient’s level of consciousness? Alert (normal) Vigilant (hyperalert) Lethargic (drowsy. being easily distractible or having difficulty keeping track of what is being said? 3. Altered level of consciousness Indicated by any response other than alert (normal) to the following question: Overall. unclear or illogical flow of ideas. Disorganized thinking Indicated by a positive response to the following question: Is the patient’s speech disorganized or incoherent. or unpredictable switching from subject to subject? 4. Confusion Assessment Method (CAM) algorithm 1.260 Clinical Manual of Geriatric Psychiatry Table 6–8. depending on the differential diagnosis of the primary illness. after nonpsychiatric personnel have done the physical examination. the battery of tests listed in Table 6–9 is rather broad and usually can be narrowed in the actual clinical situation. The diagnosis of delirium requires a present or abnormal rating for criteria 1. Similarly. and 3 or 4. Adapted from Inouye et al. Source. tend to come and go or increase and decrease in severity? 2. . Delirium is usually discovered by psychiatrists in a consultation role. tests as needed.

American Psychiatric Press.Other Dementias and Delirium 261 Table 6–9. Washington. 1996. As mentioned earlier. dementia can mimic delirium. calcium. Wise MG. Trzepacz PT: “Delirium (Confusional States). Adapted from Wise MG. or anxiety is superimposed. white blood cell count and differential. Copyright © 1996. American Psychiatric Press. liver function tests Drug levels (toxic screen. medication levels) Arterial blood gases Urinalysis. albumin. in light of above studies Blood studies Heavy metals Thiamine and folate levels Thyroid function tests Lupus erythematosus preparation Antinuclear antibodies Urinary porphobilinogen Lumbar puncture Computed tomography or magnetic resonance imaging of the head Electroencephalogram Source. particularly when agitation. including acetone and glucose Chest X ray Electrocardiogram Additional studies based on clinical judgment. p. serum urea nitrogen. 267. the clinician must rule out other psychiatric illnesses that have signs and symptoms similar to those of true delirium. Laboratory evaluation of delirium Screening studies Blood studies Complete blood count (hematocrit. In these circumstances. psychosis. confused patient with poor attention and concentration is virtually indistinguishable . DC. aroused. sedimentation rate) Electrolytes. Edited by Rundell JR. mean corpuscular volume. ammonia (NH4). glucose. Used with permission.” in The American Psychiatric Press Textbook of Consultation-Liaison Psychiatry. the clinical picture of a disorganized. Differential Diagnosis In addition to identifying the primary illness underlying delirium.

it is not surprising that age is a major risk factor for the development of delirium. also can present with a clinical state that can be difficult to distinguish from delirium caused by a general medical condition or a psychoactive substance. Cognitive impairment is also a major risk factor for the development of delirium. . which are fairly potent clinical causes of delirium. However. are ruled out. the pathogenic activity of which may be partially blocked by benzodiazepine antagonists such as flumazenil. he or she is often obliged to conduct a rapid “mini-evaluation” in which potential causes of delirium. and other common dementing illnesses (Korevaar et al. hysteria. including mania. is not accompanied by alterations in the level of consciousness. and even when the clinician knows that the patient has dementia. other mechanisms also have been proposed. and schizophrenia. vascular dementia. depression. in the delirium of hepatic encephalopathy. 2005). and the observation that centrally acting anticholinergic drugs can produce a delirium in otherwise intact individuals that can be reversed by cholinergic-enhancing agents (Kobayashi et al. Pathogenesis The precise mechanism underlying the clinical picture of delirium is not known. Indirect evidence for this hypothesis includes the fact that cholinergic neurons appear to be the most sensitive to cerebral ischemia and hypoxia. Noyan et al. particularly in the severe manifestations known as manic delirium and catatonic excitement. 2004. the role of an endogenous benzodiazepinelike substance is evident. particularly medications with central anticholinergic effects and infection.262 Clinical Manual of Geriatric Psychiatry from that of delirium. This “pseudodelirium” is usually self-limited and of very brief duration (minutes to hours). rendering them susceptible to ischemia and hypoxia. probably because of the reduced central cholinergic tone common to Alzheimer’s disease. Functional disorders. 2003). although a final common pathway involving a disturbed balance between central cholinergic and dopaminergic neurons that mediate attention and arousal has been postulated (Trzepacz 2000). and may be rapidly responsive to simple reassurance or other behavioral interventions. hypomania. Because aging is accompanied by reduced central cholinergic tone and many elderly patients have compromised cardiovascular and pulmonary functions.

encephalitis. Specific Psychopharmacotherapy Two subtypes of delirium call for specific pharmacological therapy. or barbiturates can produce a characteristic delirium (delirium tremens.. 1998). acid–base or electrolyte imbalance. functional decline. in more acute situations. or combinations thereof. acute withdrawal of alcohol or other central nervous system depressants. benzodiazepines are the treatment of choice and are usually administered parenterally until symptoms are under control. even when corrected for severity of underlying illness) at the time of admission adversely affects rates of posthospitalization mortality. and nursing home placement (Inouye et al. intracranial hemorrhage or infarction. “thyroid storm”). further amelioration of symptoms can be attained with oral administration of cholinesterase inhibitors such as donepezil or parenteral administration of physostigmine. intravenous administration provides more rapid onset of action. acute hyperthyroidism (i. First.e. infection of the central nervous system (meningitis. Lorazepam. conjugation) that is relatively insensitive to the presence of liver disease.5 mg every hour until symptoms are under control. Lorazepam may be administered in doses of 0. When withdrawal of the offending agent and supportive therapy are ineffective. and hypertensive encephalopathy.Other Dementias and Delirium 263 Treatment The first priority is to identify emergent. or anticholinergic agents. acute intoxication with central nervous system depressants.e. in its most severe form) that is rapidly responsive to replacement therapy with any of the three agents. treatment of delirium is important even if the underlying causes are not immediately life threatening because evidence shows that the presence of delirium per se (i. Practically. abscess).. stimulants. at which time oral administration can be initiated..e. has the additional advantages in elderly patients of having no active metabolites and undergoing one-step hepatic metabolism (i. a more rapidly acting cholines- . benzodiazepines. life-threatening causes of delirium and correct them if possible. The second type of delirium responsive to specific psychopharmacotherapy is that caused by centrally acting anticholinergic agents. a benzodiazepine with the most reliable absorption after intramuscular injection. withdrawal of alcohol. The most hazardous of these causes are acute cerebral ischemia or hypoxia. However. hypoglycemia and hyperglycemia with or without ketoacidosis.

Because physostigmine has a duration of action of only about 60 minutes.0 mg of haloperidol or risperidone administered orally is effective (Han and Kim 2004). alternatively.5 mg of lorazepam is usually very effective.5–5. Dosages and routes of administration vary depending on the severity of the clinical situation.264 Clinical Manual of Geriatric Psychiatry terase inhibitor. rivastigmine. and most of the literature in this area is disease specific. 0.5–2. whereas most anticholinergic agents are somewhat longer acting. When symptoms are refractory. the dosage of physostigmine is 2 mg administered intramuscularly or by slow intravenous push. . 1994).5–1.0 mg of haloperidol or intramuscular administration of 2. The long-term prognosis of delirium is primarily determined by the underlying illnesses. they can control agitation and thereby reduce the danger of self-inflicted injury. however. Although neuroleptics may not correct the pathophysiology underlying delirium. a switch to oral agents may be warranted after acute reversal of symptoms with physostigmine. reduced awareness of the environment. The typical dose of donepezil is 5–10 mg/day administered orally. additional doses of physostigmine may be administered until the situation has stabilized. a growing body of case reports suggests that empirical administration of oral cholinesterase inhibitors (donepezil. Prognosis One-quarter or more of elderly patients who develop delirium during acute hospitalization continue to have symptoms such as inattention. most studies agree that delirium per se increases the risk of functional decline and death. or olanzapine as necessary. augmentation with 0. and temporal disorientation for up to 6 months after discharge (Levkoff et al. exhaustion.0 mg of olanzapine is appropriate when rapid control of symptoms is required. risperidone. galantamine) should be followed by administration of a high-potency neuroleptic agent such as haloperidol. Nonspecific Psychopharmacotherapy In most other situations in which rapid control of symptoms of delirium is desired. In a less acute situation. Intravenous or intramuscular administration of 0. or disconnection from vital extracorporeal supports and render the patient more cooperative with appropriate diagnostic and therapeutic interventions.

et al: Efficacy and tolerability of donepezil in vascular dementia: positive results of a 24-week. Erzinclioglu SW. 2002 Adamis D. 2001 Casserly I. Gustafson Y. Geldmacher DS. MacDonald AJ. placebo-controlled clinical trial. 1999 Calderon J. Stroke 34:2323–2330. et al: Donepezil for cognitive impairment in Parkinson’s disease: a randomised controlled study. 2004 Black S. Sullivan CJ: Reversible dementia: a case of cryptococcal meningitis masquerading as Alzheimer’s disease. Drach LM: Pharmacological treatment of frontotemporal dementia: treatment response to the MAO A inhibitor moclobemide. Teufel M. Sandberg O: Epidemiology of delirium.Other Dementias and Delirium 265 References Aarsland D. et al: Prevalence and incidence of clinically diagnosed memory impairments in a geographically defined general population in Sweden: the Piteå Dementia Project. 2004 American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. Text Revision. 2003 Bozeat S. 2004 . 2003 Beversdorf DQ. Sjodin C. J Alzheimers Dis 6:503–508. Treloar A. Laake K. attention. Doss RC. Neuroepidemiology 18:144–155. Román GC. Gress DR: Rapidly reversible dementia. Blennow K. 4th Edition. Gregory CA. Davis RA. Dement Geriatr Cogn Disord 10:315–318. Dowd CF. Int J Geriatr Psychiatry 18:653–655. J Neurol Neurosurg Psychiatry 72:708– 712. Washington. 2005 Adler G. Washington. Age Ageing 34:72–75. Topol E: Convergence of atherosclerosis and Alzheimer’s disease: inflammation. 1987 American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. and misfolded proteins. American Psychiatric Association. DC. 2003 Ala TA. J Neurol Neurosurg Psychiatry 70:157–164. Larsen JP. DC. cholesterol. Lancet 363:1139–1146. Am J Geriatr Psychiatry 12:542–544. et al: Perception. et al: Which neuropsychiatric and behavioural features distinguish frontal and temporal variants of frontotemporal dementia from Alzheimer’s disease? J Neurol Neurosurg Psychiatry 69:178–186. Warner JL. American Psychiatric Association. Lancet 361:392. 3rd Edition. 2000 Andreasen N. 1999 Bernstein R. Revised. multicenter. et al: Donepezil in the treatment of dementia with Lewy bodies. Ralph MA. international. et al: Concurrent validity of two instruments (the Confusion Assessment Method and the Delirium Rating Scale) in the detection of delirium among older medical inpatients. randomized. Perry RJ. and working memory are disproportionately impaired in dementia with Lewy bodies compared with Alzheimer’s disease. 2000 Bucht G.

2003 Gorno-Tempini ML. Gurevich T. Rankin KP. Hayashi VN. Murray RC. Psychopharmacology (Berl) 172:400–408. Staessen JA. Slachevsky A. et al: Dementia with Lewy bodies may present as dementia and REM sleep behavior disorder without parkinsonism or hallucinations. et al: Paroxetine does not improve symptoms and impairs cognition in frontotemporal dementia: a double-blind randomized controlled trial. N Engl J Med 9:2509–2518. JAMA 286:2703–2710. San Antonio. TX. Litvan I. 2002 Forette F. Shabtai H. Arch Intern Med 163:2219–2229. 2001 Emre M. 2003 Cochrane M. Boeve BF. et al: Acetylcholinesterase inhibitors for the treatment of Wernicke-Korsakoff syndrome—three further cases show response to donepezil. Alzheimer Dis Assoc Disord 19:45–52. Rahman S. 2002 Ferman TJ. cognitive and anatomical evolution from nonfluent progressive aphasia to corticobasal syndrome: a case report. Smith GE. 2004 . 1999 Chui H: Neuropathology lessons in vascular dementia. et al: Inheritance of frontotemporal dementia. 2003]. Nestor PJ. et al: The FAB: a Frontal Assessment Battery at bedside. Kramer J: Delis-Kaplan Executive Function System. Bernard GR. Kurz A. Acta Neurol Scand 108:368–373. 2005 Deakin JB. Seux ML. et al: Rivastigmine for dementia associated with Parkinson’s disease. 2001 Dubois B. Jauhar P. Psychological Corporation. Neurology 55:1621–1626. et al: The prevention of dementia with antihypertensive treatment: new evidence from the Systolic Hypertension in Europe (Syst-Eur) study [published erratum appears in Arch Intern Med 163:241. Neurocase 10:426–436. Kaplan E. Gauthier S. et al: Efficacy of galantamine in probable vascular dementia and Alzheimer’s disease combined with cerebrovascular disease: a randomised trial.266 Clinical Manual of Geriatric Psychiatry Chow TW. Alcohol Alcohol 40:151–154. Inouye SK. 2004 Delis DC. 2005 Clarfield AM: The reversible dementias: do they reverse? Ann Intern Med 109:476– 486. Cochrane A. et al: Clinical. et al: Rivastigmine (Exelon) for dementia in patients with Parkinson’s disease. 1988 Clarfield AM: The decreasing prevalence of reversible dementias: an updated metaanalysis. J Int Neuropsychol Soc 8:907–914. Arch Intern Med 162:2046–2052. 2004 Erkinjuntti T. Arch Neurol 56:817–822. Albanese A. Miller BL. Aarsland D. 2002 Giladi N. Lancet 359:1283–1290. et al: Delirium in mechanically ventilated patients: validity and reliability of the Confusion Assessment Method for the Intensive Care Unit (CAM-ICU). 2000 Ely EW.

Cairns N. 2000 Inouye SK. 2004 Hansen L. 2001 Grossman M: Frontotemporal dementia: a review. Coles A. J Int Neuropsychol Soc 6:460– 468. et al: Clinical-neuropathologic findings in multiinfarct dementia: a report of six autopsied cases. 2004 Hodges JR. et al: Clinicopathological correlates in frontotemporal dementia. 1992 Han CS. Foreman MD. Xuereb JH. Lantos P. Ann Intern Med 113:941– 948. Tang M-XAS. J Gen Intern Med 13:234–242. Am J Psychiatry 161:1113–1115. J Neuropsychiatry Clin Neurosci 12:233–239. vascular dementia and dementia with Lewy bodies. 1990 Inouye SK. et al: Validity of current clinical criteria for Alzheimer’s disease. 2002 Gustafson L. et al: Stroke and the risk of Alzheimer disease. Cummings JL. Davidson W. J Int Neuropsychol Soc 8:566–583. Pohl U. Galasko D. 1997 Inouye SK: Prevention of delirium in hospitalized older patients: risk factors and targeted intervention strategies. Davies RR. 2004 Holmes C. Ann Neurol 56:399–406. 1990 Harkness KA. 1999 Honig LS. Mamdani M. et al: The Lewy body variant of Alzheimer’s disease: a clinical and pathologic entity. Lutz. van Dyck CH. et al: Validation of the NPI-Q. J Neurol Sci 229–230:57–63. et al: Does delirium contribute to poor hospital outcomes? a three-site epidemiologic study. Lanctôt KL: Atypical antipsychotics and risk of cerebrovascular accidents. Neurology 40:1–8. Rushing JT. Ketchel P. 1998 Jellinger KA: Understanding the pathology of vascular cognitive impairment. 2003 Hulette C. Psychological Assessment Resources.Other Dementias and Delirium 267 Grace J. Kim YK: A double-blind trial of risperidone and haloperidol for the treatment of delirium. 2000 . a brief clinical form of the Neuropsychiatric Inventory. Neurology 48:668–672. McKeel D. Passant U: Frontal lobe degeneration of non-Alzheimer type. 2000 Kertesz A. Nadkarni H. Psychosomatics 45:297–301. Malloy PF: Frontal Systems Behavior Scale: Professional Manual. Ann Med 32:257–263. Baillieres Clin Neurol 1:559–582. Br J Psychiatry 174:45–50. 2005 Kaufer DI. et al: The Frontal Behavioral Inventory in the differential diagnosis of frontotemporal dementia. Albert S. Brun A. et al: Rapidly reversible dementia in cerebral amyloid inflammatory vasculopathy. Salmon D. Arch Neurol 60:1707–1712. Nochlin D. Eur J Neurol 11:59–62. 2004 Herrmann N. FL. et al: Clarifying confusion: the confusion assessment method: a new method for detection of delirium. Alessi CA.

et al: Open-label study of donepezil in traumatic brain injury. Mutou K. Rheumatol Int 24:305– 308. Blackwell Scientific.268 Clinical Manual of Geriatric Psychiatry Kittner B. placebo-controlled trials. Foster NL. Lowe J. J Neurol Sci 229–230:3–6. et al: Delirium in the intensive care unit: occurrence and clinical course in older persons. BMC Geriatr 5:6. 2000 Knopman DS. Haemostasis 28:134–150. J Am Geriatr Soc 51:1–9. et al: Antemortem diagnosis of frontotemporal lobar degeneration. Arch Phys Med Rehabil 82:896–901. et al: Diagnosis and management of dementia with Lewy bodies: third report of the DLB Consortium. JAMA 292:2901–2908. Higashima M. 2003 . Neurology 65:1863–1872. Pisani MA. 2005 Korevaar JC. De Deyn PP. Parisi JE. 2004 Levkoff SE. Ann Neurol 7:480–488. Lewy body pathology. et al: Cognitive differences in dementia patients with autopsy-verified AD. Kosaka K. Pasquier F. UK. Larson EB: Mixed dementia: emerging concepts and therapeutic implications. Larson EB. Evans DA. Hasenbroekx C. Yoo WH: Reversible dementia in systemic lupus erythematosus without antiphospholipid antibodies or cerebral infarction. 2005 Kobayashi K. 2004 Lebert F. 2004 Korczyn AD: The underdiagnosis of the vascular contribution to dementia. Erkinjuntti T: Investigating the natural course and treatment of vascular dementia and Alzheimer’s disease: parallel study populations in two randomized. Galasko D. Am J Geriatr Psychiatry 2:230–238. 1987 Masanic CA. 1996 McKeith IG. van Munster BC. Parnetti L: Epidemiology of vascular dementia. 2001 McKeith IG. Neurology 47:1113–1124. 2005 Kraybill ML. VanReekum R. controlled trial with trazodone. Oxford. Tsuang DW. et al: Frontotemporal dementia: a randomised. Dickson DW. Dement Geriatr Cogn Disord 17:355–359. 1994 Leys D. Prog Neuropsychopharmacol Biol Psychiatry 28:1189–1194. Bayley MT. et al: Severe delirium due to basal forebrain vascular lesion and efficacy of donepezil. Ann N Y Acad Sci 903:535–541. or both. et al: Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB): report of the consortium on DLB international workshop. Jeon HS. Zhang Y. 2004 Lee SI. 2005 Langa KM. Liptzin B. Neurology 64:2069– 2073. de Rooij SE: Risk factors for delirium in acutely admitted elderly patients: a prospective cohort study. 2005 McNicoll L. 1998 Lishman WA: Organic Psychiatry. et al: Progression and resolution of delirium in elderly patients hospitalized for acute care. Boeve BF. Stekke W.

Friedman J. Antonello RM. Beilin L. Am J Geriatr Psychiatry 11:441–447. 1998 Nelson M. 2003 Moretti R. et al: Acquired sociopathy and frontotemporal dementia. Reid C. Pisani MA. Chen AK. Shapira JS. et al: Rivastigmine in frontotemporal dementia: an open-label study. 2003 Noyan MA. Dawson K. Antonello RM. Drugs Aging 21:931–937. 2003 Oslin D[W]. Brayne C. Snowden JS. J Geriatr Psychiatry Neurol 18:33–38. Cary MS: Alcohol-related dementia: validation of diagnostic criteria. J Am Geriatr Soc 53:495–500. Drugs Aging 20:897–903. et al: Olanzapine as a possible treatment of behavioral symptoms in vascular dementia: risks of cerebrovascular events: a controlled. Prog Neuropsychopharmacol Biol Psychiatry 27:885–887. Atkinson RM. Antonello RM. Torre P. et al: Detection of delirium in the intensive care unit: comparison of Confusion Assessment Method for the Intensive Care Unit With Confusion Assessment Method ratings. Stroke 33:1834–1839. et al: Alcohol related dementia: proposed clinical criteria. 2005 Morey CE. 2004 Moretti R. Cohen B: Cholinergic denervation in a pure multi-infarct state: observations on CADASIL. 2002 Osimani A. Eur Neurol 49:13–19. 2005 Mesulam M. Elbi H. Rigaud AS. et al: Efficacy and safety of memantine in patients with mild to moderate vascular dementia: a randomized. 2003 Orgogozo JM. et al: The effect of Aricept in persons with persistent memory disorder following traumatic brain injury: a pilot study. Smith DM. et al: Rationale for a trial of low-dose aspirin for the primary prevention of major adverse cardiovascular events and vascular dementia in the elderly: Aspirin in Reducing Events in the Elderly (ASPREE). 2003 Neary D. Torre P. 2002 . Gustafson L. 2005 Mendez MF. Int J Geriatr Psychiatry 13:203–212. Neurology 60:1183–1185. Siddique T. et al: Neuropsychology of vitamin B12 deficiency in elderly dementia patients and control subjects.Other Dementias and Delirium 269 McNicoll L. 2005 Oslin DW. Berry J. Neurology 58:1615–1621. open-label study. Dement Geriatr Cogn Disord 20:99–104. Neurology 51:1546–1554. et al: The prevalence of frontotemporal dementia. Berger A. et al: Frontotemporal dementia: paroxetine as a possible treatment of behavior symptoms. Stoffler A. Cilo M. Aksu H: Donepezil for anticholinergic drug intoxication: a case report. 1998 Ratnavalli E. Torre P. J Neurol 252:1186–1193. et al: Frontotemporal lobar degeneration: a consensus on clinical diagnostic criteria. Brain Inj 17: 809–815. 2003 Moretti R. placebo-controlled trial (MMM 300). Ely EW.

270 Clinical Manual of Geriatric Psychiatry

Reed BR, Mungas DM, Kramer JH, et al: Clinical and neuropsychological features in autopsy-defined vascular dementia. Clin Neuropsychol 18:63–74, 2004 Rickards H: Depression in neurological disorders: Parkinson’s disease, multiple sclerosis, and stroke. J Neurol Neurosurg Psychiatry 76 (suppl 1):i48–i52, 2005 Robertson KR, Robertson WT, Ford S, et al: Highly active antiretroviral therapy improves neurocognitive functioning. J Acquir Immune Defic Syndr 36:562–566, 2004 Roman GC, Tatemichi TK, Erkinjuntti T, et al: Vascular dementia: diagnostic criteria for research studies: report of the NINDS-AIREN International Workshop. Neurology 43:250–260, 1993 Rosen WG, Terry RD, Fuld PA, et al: Pathological verification of ischemic score in differentiation of dementias. Ann Neurol 7:486–488, 1980 Ross CA, Peyser CE, Shapiro I, et al: Delirium: phenomenologic and etiologic subtypes. Int Psychogeriatr 3:135–147, 1991 Rossi T, Haghighipour R, Haghighi M, et al: Cerebral Whipple’s disease as a cause of reversible dementia. Clin Neurol Neurosurg 107:258–261, 2005 Roy S, Rauk A: Alzheimer’s disease and the ‘ABSENT’ hypothesis: mechanism for amyloid beta endothelial and neuronal toxicity. Med Hypotheses 65:123–137, 2005 Royall DR, Mahurin RK, Gray KF: Bedside assessment of executive cognitive impairment: the Executive Interview. J Am Geriatr Soc 40:1221–1226, 1992 Royall DR, Palmer R, Chiodo LK, et al: Executive control mediates memory’s association with change in instrumental activities of daily living: the Freedom House study. J Am Geriatr Soc 53:11–17, 2005 Sahin HA, Gurvit IH, Bilgic B, et al: Therapeutic effects of an acetylcholinesterase inhibitor (donepezil) on memory in Wernicke-Korsakoff ’s disease. Clin Neuropharmacol 25:16–20, 2002 Secker DL, Brown RG: Cognitive behavioural therapy (CBT) for carers of patients with Parkinson’s disease: a preliminary randomised controlled trial. J Neurol Neurosurg Psychiatry 76:491–497, 2005 Seeley WW, Bauer AM, Miller BL, et al: The natural history of temporal variant frontotemporal dementia. Neurology 64:1384–1390, 2005 Serby M, Samuels SC: Diagnostic criteria for dementia with lewy bodies reconsidered. Am J Geriatr Psychiatry 9:212–216, 2001 Shepherd J, Blauw GJ, Murphy MB, et al: Pravastatin in elderly individuals at risk of vascular disease (PROSPER): a randomised controlled trial. Lancet 360:1623– 1630, 2002

Other Dementias and Delirium

271

Slachevsky A, Villalpando JM, Sarazin M, et al: Frontal Assessment Battery and differential diagnosis of frontotemporal dementia and Alzheimer disease. Arch Neurol 61:104–107, 2004 Trzepacz PT: Is there a final common neural pathway in delirium? focus on acetylcholine and dopamine. Semin Clin Neuropsychiatry 5:132–148, 2000 Trzepacz PT, Dew MA: Further analyses of the Delirium Rating Scale. Gen Hosp Psychiatry 17:75–79, 1995 Trzepacz PT, Baker RW, Greenhouse J: A symptom rating scale for delirium. Psychiatry Res 23:89–97, 1988 Trzepacz PT, Mittal D, Torres R, et al: Validation of the Delirium Rating Scale— Revised–98: comparison with the Delirium Rating Scale and the Cognitive Test for Delirium. J Neuropsychiatry Clin Neurosci 13:229–242, 2001 Tzourio C, Anderson C, Chapman N, et al, for the PROGRESS Collaborative Group: Effects of blood pressure lowering with perindopril and indapamide therapy on dementia and cognitive decline in patients with cerebrovascular disease. Arch Intern Med 163:1069–1107, 2003 Wesnes KA, McKeith IG, Ferrara R, et al: Effects of rivastigmine on cognitive function in dementia with Lewy bodies: a randomised placebo-controlled international study using the Cognitive Drug Research computerised assessment system. Dement Geriatr Cogn Disord 13:183–192, 2002 Wetterling T, Kanitz RD, Borgis KJ: Comparison of different diagnostic criteria for vascular dementia (ADDTC, DSM-IV, ICD-10, NINDS-AIREN). Stroke 27:30–36, 1996 Wilcock G, Mobius HJ, Stoffler A, for the MMM 500 Group: A double-blind, placebo-controlled multicentre study of memantine in mild to moderate vascular dementia (MMM500). Int Clin Psychopharmacol 17:297–305, 2002 Wilkinson D, Doody R, Helme R, et al: Donepezil in vascular dementia: a randomized, placebo-controlled study. Neurology 61:479–486, 2003 Yesavage JA, Mumenthaler MS, Taylor JL, et al: Donepezil and flight simulator performance: effects on retention of complex skills. Neurology 59:123–125, 2002 Yu CY, Yip PK, Chang YC, et al: Reversible dysphagia and dementia in a patient with bromide intoxication. J Neurol 251:1282–1284, 2004 Zhang L, Plotkin RC, Wang G, et al: Cholinergic augmentation with donepezil enhances recovery in short-term memory and sustained attention after traumatic brain injury. Arch Phys Med Rehabil 85:1050–1055, 2004

This page intentionally left blank

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 colleagues. 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 particularly difficult because of the great overlap between symptoms of anxiety disorders and anxiety symptoms seen in other Axis I conditions, particularly depression, dementia, and late-onset psychosis. A Dutch study of 3,056 individuals 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 conditions (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 permanent 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 attack 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 apprehension 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 associated with a significantly increased risk of suicide attempts and completed suicide, even in the absence of other mental disorders (Khan et al. 2002). Geriatric depression is often slower to remit when the clinical picture is complicated by comorbid general anxiety symptoms, panic disorder, or posttraumatic stress disorder (Hegel et al. 2005; Steffens and McQuoid 2005). Anxiety also may be a predictor of cognitive decline, especially when accompanied by complaints of loss of memory (Sinoff and Werner 2003).

Anxiety Rating Scales
Both observer-rated measures, such as the Hamilton Anxiety Rating Scale (Hamilton 1959), and self-rated instruments, such the Spielberger State-Trait Anxiety Inventory (Spielberger et al. 1970) and the Worry Scale (Wisocki et al. 1986), assess severity and type of anxiety symptoms. The Hamilton scale, which consists of 14 items to assess 89 symptoms, has been the most widely used test in psychiatric research, and a few studies support its utility with el-

Anxiety Disorders and Late-Onset Psychosis 275

Table 7–1. Autonomic and psychomotor features of anxiety
Generalized anxiety disorder Restlessness or feeling keyed up or on edge Being easily fatigued Difficulty concentrating or mind going blank Irritability Muscle tension Sleep disturbance (difficulty falling or staying asleep, or restless unsatisfying sleep) Panic attacka Palpitations, pounding heart, or accelerated heart rate Sweating Trembling or shaking Sensations of shortness of breath or smothering Feeling of choking Chest pain or discomfort Nausea or abdominal distress Feeling dizzy, unsteady, light-headed, or faint Derealization (feelings of unreality) or depersonalization (being detached from oneself ) Fear of losing control or going crazy Fear of dying Paresthesias (numbness or tingling sensations) Chills or hot flushes
aPanic

attack is diagnosed if four or more of these symptoms develop abruptly and reach a peak within 10 minutes.

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 interventions to reduce anxiety in both young adult and elderly subjects but has been less widely applied in pharmacological research. The Worry Scale was specifically developed for use with older adults; the 35 items reflect severity of worry about financial, health, and social concerns. It is useful in assessing severity 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 appropriate 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 diagnosis 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 diagnosis. 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 similar to those that affect adults of all ages. These situations include those conventionally 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 significantly 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 after 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

Table 7–2. General medical conditions and medications that can produce symptoms of anxiety
General medical conditions Hyperadrenocorticism Hyperthyroidisma Hypoadrenocorticism Hypoglycemia (any cause) Insulinoma with hypoglycemia Pheochromocytoma Medications Anticholinergics—atropine, scopolamine Antidepressants—fluoxetine,a tranylcypromine Caffeinea Psychostimulants—amphetamine, cocaine, methylphenidate Sympathomimetics Decongestants—phenylephrine, phenylpropanolamine, pseudoephedrine, ephedrine Bronchodilators—albuterol, epinephrine, isoproterenol, metaproterenol Xanthine derivatives—theophylline,a aminophyllinea Medication withdrawal—alcohol,a benzodiazepines (especially short-acting agents),a other central nervous system depressantsa
aRelatively

common offenders in the authors’ experience.

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 precipitate 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 include 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

The authors interpreted this finding as enhancing the rationale for longterm treatment of GAD. and financial concerns predominating.” few differences were found between early. Frequency and uncontrollability of worry. In another recent study (Le Roux et al. Although 47% had onset “later in life. whereas late-onset patients reported more functional limitations resulting from physical problems. depending on inclusion criteria and the period of . with a reported prevalence between 0. subsyndromal anxiety. with results of most studies falling in the 3%–12% range. Taken together. whereas subjects with comorbid major depressive disorder tended to have recurrent depressive episodes. greater psychotropic use.and late-onset cases. muscle tension. 2005). and agoraphobia without history of panic disorder.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 associated with a higher level of suicidality. GAD tended to be a single. About one-third of older individuals in each group reported worries about community or world affairs. (2005a) found that GAD tends to persist. An earlier report based on the same sample compared frequency of DSM-IV (American Psychiatric Association 1994) anxiety symptoms for older adults with GAD. or no mental disorder (Wetherell et al. social phobia. phobias constitute the most common anxiety disorder among elderly individuals. with spontaneous remission (without treatment) unlikely even if comorbid major depressive disorder remits. degree of distress or impairment associated with worry. older adults with onset of GAD before age 50 years were found to have a higher rate of psychiatric comorbidity. worries about minor matters. and 90% with GAD). with health concerns. whereas worries about oneself were elevated in the GAD group. Worrying about family members was common in all groups (endorsed by 69% of control subjects with no mental disorder.8. and more severe worry compared with GAD patients with later ages at onset. chronic episode. 2003b). Phobias Phobias include the DSM-IV-TR categories of specific phobia. and sleep disturbance were the symptoms most likely to distinguish GAD from the other conditions. and Lenze et al. Lenze and colleagues (2005a) found that the average age at onset of GAD in 103 elderly subjects was 48. 91% with subsyndromal anxiety. In a follow-up study. The most common lifetime pattern of comorbidity was GAD preceding major depressive disorder.7% and 12%.

Summary of DSM-IV-TR diagnostic criteria for generalized anxiety disorder A. Used with permission. Obsessive-Compulsive Disorder Late onset of OCD appears to be quite rare. or other important areas of functioning. and the anxiety and worry do not occur exclusively during posttraumatic stress disorder. occupational.. because rates of specific phobia and social phobia are more consistently reported at about 2%–6% and 0. Washington. about a number of events or activities (such as work or school performance). F. C. B. older patients may become reluctant to join friends for a game of bridge because they fear being unable to follow the action or having an episode of incontinence. The disturbance is not due to the direct physiological effects of a substance or a general medical condition and does not occur exclusively during a mood disorder or a psychotic disorder. with at least some symptoms present for more days than not for the past 6 months. DC. DSMIV-TR criteria for specific phobia are summarized in Table 7–4. American Psychiatric Association. For example. with the prevalence in elderly females about twice that in elderly males (Krasucki et al.e. being embarrassed in public. Excessive anxiety and worry (apprehensive expectation) occurring more days than not for at least 6 months. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. and subsequent investigation by the clinician may detect for the first time that such mishaps have actually occurred. Ritchie et al.. Most of the variability in prevalence seems to stem from different ways to define agoraphobia. the fear actually may not be so unreasonable. or being contaminated). 1–6 months) studied. Text Revision. worry. with a predominance of females that is . prevalence (i. Copyright © 2000. 2004). The anxiety and worry are associated with three (or more) of the six symptoms listed under generalized anxiety disorder in Table 7–1. New onset of phobic symptoms in elderly patients requires thorough clinical investigation because in some cases.6%–1.g. The anxiety.2%. The person finds it difficult to control the worry. Source. 2000. with most epidemiological studies reporting rates in the 1% range. 1998. D. 4th Edition. respectively. E. The focus of the anxiety and worry is not confined to features of an Axis I disorder (e. the anxiety and worry are not about having a panic attack. American Psychiatric Association. or physical symptoms cause clinically significant distress or impairment in social.Anxiety Disorders and Late-Onset Psychosis 279 Table 7–3.

Washington. The avoidance. and counting rituals. the duration is at least 6 months. Philpot and Banerjee 1998. occupational functioning. B. Weiss and Jenike 2000). the likelihood that compulsive rituals have become ego-syntonic and are no longer seen as irrational is increased. In this situation. The pattern of symptoms is similar to that seen in younger patients. 4th Edition. Several reports suggested that late-onset OCD is frequently associated with organic brain disease. Transient outbreaks of obsessive thoughts and compulsive rituals are not uncommon among elderly patients with major depression with or without psychosis. such as obsessive-compulsive disorder or posttraumatic stress disorder. Some older patients with chronic OCD seek medical attention only when supervening age-related changes or superimposed mood disorder or dementia forces them into treatment.280 Clinical Manual of Geriatric Psychiatry Table 7–4. DC. or distress in the feared situation interferes significantly with the person’s normal routine. 2000. Exposure to the phobic stimulus almost invariably provokes an immediate anxiety response. Copyright © 2000. or social activities or relationships. 2002. The anxiety. Summary of DSM-IV-TR diagnostic criteria for specific Marked and persistent fear that is excessive or unreasonable. The person recognizes that the fear is excessive or unreasonable. Source. transient ischemic attack. The phobic situation is avoided or else is endured with intense anxiety or distress. anxious anticipation. or phobic avoidance associated with the specific object or situation is not better accounted for by another mental disorder. Text Revision. which may take the form of a situationally bound or situationally predisposed panic attack. In individuals under age 18 years. significantly less pronounced than in other anxiety disorders. or there is marked distress about having the phobia. Used with permission. with a few minor differences: elderly patients have fewer concerns about symmetry. panic attacks. and the clinician may need to explore the early history of the disorder to obtain a less misleading picture. including stroke. C. American Psychiatric Association. E. 1997). whereas hand washing and fear of having sinned are more common in elderly patients (Kohn et al. DSM-IV-TR allows a diag- . cued by the presence or anticipation of a specific object or situation. G. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. phobia A. need to know. F. American Psychiatric Association. and organophosphate poisoning (Carmin et al. D.

and external resources diminish with age. whereas exposure to traumatic events or illnesses increases. particularly of late onset. Some researchers believe that elderly people are more vulnerable to traumatic events than are younger people (Lyons and McClendon 1990). or supportive psychotherapy results in more complete relief of symptoms. who is likely to initiate an evaluation for possible myocardial infarction. Patients and family members are often reluctant to accept that something as terrifying as a panic attack can be “mental.” and patients may avoid evaluation by the mental health professional because they fear that they are “losing their minds” or “going crazy. life-threatening physical illness. Posttraumatic Stress Disorder The literature on posttraumatic stress disorder (PTSD) in elderly individuals presents conflicting views. and older patients with late-onset panic disorder report less distress related to panic symptoms than do elderly patients with early-onset panic disorder (Sheikh et al. and higher levels of functioning than do middle-aged patients with panic disorder. the “inoculation hypothesis” proposed by Eysenck (1983) maintains that exposure to stress or a previous crisis could increase resistance to subse- . coping resources. present first to their family physician or internist.Anxiety Disorders and Late-Onset Psychosis 281 nosis of OCD in this circumstance if the content of the obsessions or compulsions is not mood congruent (Table 7–5). lower levels of depression. the diagnosis of panic disorder requires the occurrence of panic attacks and significant anticipatory anxiety.” As defined by DSM-IV-TR (Table 7–6). The “differential vulnerability hypothesis” suggests that adaptive capacities. It may require several panic attacks accompanied by negative laboratory test results before the primary care physician identifies the correct diagnosis and seeks psychiatric consultation. Many older patients with panic disorder. On the other hand. behavioral. Anticipatory anxiety itself. without panic attacks. 2004b). less anxiety and arousal. and successful pharmacological amelioration of panic attacks is only part of the therapeutic challenge. Panic Disorder Elderly patients with panic disorder (with or without agoraphobia) report less severe and fewer panic symptoms. or other episodic. can be quite disabling. transient ischemic attack. and evidence is accumulating that combining pharmacotherapy with cognitive-behavioral.

occupational functioning. (2). quent stress and enable elderly people to develop the coping strategies to adapt successfully to traumatic events. impulses. suggest that neither the vulnerability hypothesis . impulses. or significantly interfere with the person’s normal routine. and (4): (1) recurrent and persistent thoughts. At some point during the course of the disorder. the content of the obsessions or compulsions is not restricted to it. repeating words silently) that the person feels driven to perform in response to an obsession. counting. (3). Text Revision. at some time during the disturbance. A. or usual social activities or relationships. E. However. Source. are time-consuming (take more than 1 hour a day). or according to rules that must be applied rigidly (2) the behaviors or mental acts are aimed at preventing or reducing distress or preventing some dreaded event or situation. impulses. Washington. Used with permission. Summary of DSM-IV-TR diagnostic criteria for obsessive-compulsive disorder Either obsessions or compulsions: Obsessions as defined by (1). DC. or images or to neutralize them with some other thought or action (4) the person recognizes that the obsessional thoughts. American Psychiatric Association.. American Psychiatric Association. If another Axis I disorder is present. these behaviors or mental acts either are not connected in a realistic way with what they are designed to neutralize or prevent or are clearly excessive B. 4th Edition. or images are not simply excessive worries about real-life problems (3) the person attempts to ignore or suppress such thoughts. The disturbance is not due to the direct physiological effects of a substance or a general medical condition. 2004). Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. The obsessions or compulsions cause marked distress. the person has recognized that the obsessions or compulsions are excessive or unreasonable. data from a more recent study of 148 survivors of two traumatic events.282 Clinical Manual of Geriatric Psychiatry Table 7–5. as intrusive and inappropriate and that cause marked anxiety or distress (2) the thoughts. or images are a product of his or her own mind (not imposed from without as in thought insertion) Compulsions as defined by (1) and (2): (1) repetitive behaviors or mental acts (e. praying.g. impulses. C. Copyright © 2000. or images that are experienced. 2000. however. an airplane crash and a train crash (Chung et al. D.

2000. Source.Anxiety Disorders and Late-Onset Psychosis 283 Table 7–6. greater functional impairment. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. Washington. dysthymia. and subsequent general health problems were similar across age groups. The panic attacks are not better accounted for by another mental disorder. DC. Mood Disorder With Anxiety Anxiety symptoms are often a prominent part of major depression. and a lower quality of life (Hegel et al. bipolar disorder. co-occurrence of full mood and anxiety syndromes is common. Diagnostic criteria for PTSD are summarized in Table 7–7. coping strategies used. Text Revision. Copyright © 2000. Patients with comorbid panic disorder or PTSD were more likely to report suicidal thoughts at baseline and had a higher prevalence of chronic medical illnesses. and as described earlier. One large-scale study of elderly primary care patients with major depression or dysthymia found that patients with comorbid panic disorder or PTSD had substantially greater psychiatric and medical illness than did those without comorbid anxiety. American Psychiatric Association. A. Summary of DSM-IV-TR diagnostic criteria for panic disorder with or without agoraphobia Both (1) and (2): (1) recurrent unexpected panic attacks (2) at least one of the attacks has been followed by 1 month (or more) of one (or more) of the following: (a) persistent concern about having additional attacks (b) worry about the implications of the attack or its consequences (c) a significant change in behavior related to the attacks B. Used with permission. American Psychiatric Association. 2005). The panic attacks are not due to the direct physiological effects of a substance or a general medical condition. Instead. C. the investigators found that levels of intrusive thoughts. avoidance behavior. Presence or absence of agoraphobia. Differentiation of dysphoric states into depressed mood or anxiety may be particularly difficult with the current generations of elderly individu- . 4th Edition. such as social phobia or specific phobia. D. and cyclothymia. nor the inoculation hypothesis applied to this cohort of community residents.

. Summary of DSM-IV-TR diagnostic criteria for posttraumatic stress disorder A. does not expect to have a normal life span) B. including images. or was confronted with an event or events that involved actual or threatened death or serious injury. or a threat to the physical integrity of self or others. . and dissociative flashback episodes. or perceptions (2) recurrent distressing dreams of the event (3) acting or feeling as if the traumatic event were recurring (includes a sense of reliving the experience. unable to have loving feelings) (7) sense of a foreshortened future (e. thoughts. or conversations associated with the trauma (2) efforts to avoid activities. helplessness.284 Clinical Manual of Geriatric Psychiatry Table 7–7. including those that occur on awakening or when intoxicated) (4) intense psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event (5) physiological reactivity on exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event Persistent avoidance of stimuli associated with the trauma and numbing of general responsiveness (not present before the trauma). The person has been exposed to a traumatic event in which both of the following were present: (1) The person experienced. C. or people that arouse recollections of the trauma (3) inability to recall an important aspect of the trauma (4) markedly diminished interest or participation in significant activities (5) feeling of detachment or estrangement from others (6) restricted range of affect (e.g. as indicated by three (or more) of the following: (1) efforts to avoid thoughts. illusions.. or horror. places. hallucinations. The traumatic event is persistently reexperienced in one (or more) of the following ways: (1) recurrent and intrusive distressing recollections of the event.g. witnessed. (2) The person’s response involved intense fear. feelings.

as indicated by two (or more) of the following: (1) difficulty falling or staying asleep (2) irritability or outbursts of anger (3) difficulty concentrating (4) hypervigilance (5) exaggerated startle response E. 4th Edition. and bizarre behavior typical of schizophrenia and delusional disorder are clearly not a part of uncomplicated anxiety disorder.g. Schizophrenia With Anxiety Although the characteristic hallucinations. “Mood Disorders— . Text Revision. Summary of DSM-IV-TR diagnostic criteria for posttraumatic stress disorder (continued) D. 2000. Extra effort to establish rapport and develop the patient’s trust can be very important in this situation. many of whom are uncomfortable with introspection and unfamiliar with conventional terms for subjective states. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. neurovegetative signs and symptoms of mood disorder and the autonomic and psychomotor features of anxiety disorder facilitate accurate diagnostic classification. and D) is more than 1 month. als. The disturbance causes clinically significant distress or impairment in social. F. or other important areas of functioning. In most cases.. American Psychiatric Association. Copyright © 2000. Used with permission. American Psychiatric Association. projective psychological tests (e. Washington. Duration of the disturbance (symptoms in criteria B. If doubt persists. C. Specify if: Acute: if duration of symptoms is less than 3 months Chronic: if duration of symptoms is 3 months or more With delayed onset: if onset of symptoms is at least 6 months after the stressor Source. elderly patients with these conditions may be quite secretive about their psychotic experiences and can appear to have anxiety alone. thought disorder. DC. Persistent symptoms of increased arousal (not present before the trauma). see Chapter 3. the Rorschach Inkblot Test.Anxiety Disorders and Late-Onset Psychosis 285 Table 7–7. hospitalized elderly patients often connect with a particular staff member (usually on the night shift) whom they trust and with whom they share their inner psychic content. the Thematic Apperception Test. occupational. delusions.

and the limitations imposed by circumstances. . One subsystem is composed of noradrenergic innervation arising from cell bodies in the locus coeruleus.e. the increasing likelihood of mental and physical incompetence. p.. Another diagnostic challenge is confronted in the differentiation between obsessive thoughts (Simpson et al. and other subcortical structures. a bilateral nucleus of cell bodies located in the central gray matter of the isthmus on the floor of the fourth ventricle. They also impinge on cells in the hypothalamus. thalamus. and cerebellum. allowing the clinician to distinguish them from manifestations of psychosis (American Psychiatric Association 2000. they remain relatively vulnerable to challenge by evidence or logic (i. “overvalued ideas” (in which case the specifier “with poor insight” is applied). 461). or nonspecific illness. these aspects of aging (Gurian and Miner 1991). Pathogenesis Psychodynamic Theories The general psychodynamic literature on the pathogenesis of anxiety is too voluminous to attempt to summarize here. DSM-IVTR indicates that even when obsessions become ego-syntonic. which are postulated to account for anxiety throughout the life span. Axons from these cells provide the main noradrenergic input to the ipsilateral cortex. Anxiety related to these concerns may emerge directly into consciousness. reality testing is intact). septal nuclei. 1999) and schizophrenic delusions. memory impairment. the demands of conscience. In support of this hypothesis. and ability to come to terms with. although relatively little consideration has been given to anxiety in late life. elderly individuals face anxiogenic circumstances unique to senescence. Neurobiological Theories Contemporary hypotheses about neurobiological substrates of anxiety and fear focus on several interconnected subsystems of the central nervous system. wherein it can be relatively easily identified. These include the growing discrepancy between past and present capabilities. and the encroaching reality of death. or may remain unconscious and be expressed indirectly as somatic dysfunction. improved emotional well-being is often associated with increased conscious awareness of. In addition to intrapsychic conflict between libidinal impulses and emotions.286 Clinical Manual of Geriatric Psychiatry Diagnosis”) can help to identify suppressed psychotic thought content. cingulate gyrus. hippocampus.

together with the amygdala. early experiences. Binding of a benzodiazepine molecule to this receptor facilitates the ability of the GABAreceptor complex to open chloride channels. focusing on dopaminergic input to the amygdala from the ventral tegmental area (Gelowitz and Kokkinidis 1999) and lateralized serotonergic neurotransmission within the nondominant amygdala (Andersen and Teicher 1999). constitute a component of the system that mediates the startle response. 1987) and a chloride ion channel. Hypothesized pathogenic influences on this system include genetic mechanisms. These receptors appear to be linked to a “supramolecular receptor complex” that includes a receptor for γ-aminobutyric acid (GABA) (Hommer et al. and the interaction of the two. and the substantia nigra. in order of increasing intensity. More recent animal studies have examined the role of the medial prefrontal cortex–amygdala circuit in the pathogenesis of anxiety disorders. moreover. Evidence indicates that brain . Anatomical and pharmacological manipulation of this system in animal models provides convincing evidence of its role in regulating aspects of cerebral arousal. including the superior colliculus. anxiety. studies of the noradrenergic system in elderly subjects suggest that an age-related decrease in central noradrenergic function may increase these subjects’ susceptibility to anxiety (Sunderland et al. all of which. 1991). allowing negatively charged chloride ions to enter the cell and produce hyperpolarization. Investigators theorize that early experiences lead to structural and functional alterations in the responsiveness of this system. and pathological influences on its function have been postulated to underlie anxiety disorders in humans (Hommer et al. Another major area of investigation focuses on benzodiazepine receptors localized to central neurons. which ultimately lead to pathological states of anxiety (Redmond 1987). This response has been extensively studied in animal models. 1987). fear.Anxiety Disorders and Late-Onset Psychosis 287 where their influence is augmented by input from noradrenergic cells in the lateral tegmental nuclei. or panic. the ventral nucleus of the lateral lemniscus. This arousal is postulated to be experienced as vigilance. thereby reducing the cell’s reactivity to stimulation and its likelihood of conducting an impulse. Autoradiographic studies have shown benzodiazepine receptors in brain-stem structures. Findings of these studies have been partially supported by clinical evidence of the efficacy of serotonin reuptake inhibitors and dopamine receptor blockers in anxiety disorders.

desensitization techniques that typically pair a state of induced relaxation with a real or imagined feared situation or object. 2000). However. Finally. 1991). 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 receptor (5-HT1A receptor knockout) show increased anxiety-like behavior in a variety of conflict tests. Treatment Psychosocial-Behavior Therapy Although definitive studies in geriatric patients are lacking. and graded exposure approaches that attempt to extinguish anxiety. there is little clinical basis to doubt the efficacy of traditional psychotherapeutic approaches to anxiety in the elderly. 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. . septum.288 Clinical Manual of Geriatric Psychiatry levels of GABA are reduced in older subjects. fear responses. a key role for serotonin receptors in the development of “normal” anxiety behavior in humans has been delineated by Gross et al. or compulsive rituals gradually by increasingly prolonged and intense exposure to feared situations. cost considerations often favor use of more focused. The 5-HT1A receptor is expressed in two distinct neuronal populations in the brain: as an autoreceptor on serotonin-containing neurons of the raphe nuclei and as a heteroreceptor on nonserotonin-containing neurons of the forebrain (mainly the hippocampus. time-limited techniques such as cognitive-behavioral therapy (CBT). which could result in an increased propensity to anxiety with age (Sunderland et al. including OCD (Simpson et al. 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 anxiety-like behavior. The more purely behavioral therapies are also preferred for reasons of cost and include relaxation techniques aimed at generalized reduction of muscle tension and anxiety. and cortex). and panic disorder (Barlow et al. 2000). social phobia (Cottraux et al. 1999). (2002). which has been shown to be effective in nonelderly patients with anxiety disorders.

however. or a wait-list condition. Effect sizes associated with treatment were somewhat smaller than those that have been reported for CBT with younger GAD patients. techniques such as hypnosis. meditation. perhaps reflecting different levels of commitment and skill among therapists (Wetherell et al. an active alternative psychosocial treatment (a discussion group addressing anxiety-evoking themes). and by 6month follow-up. but limited access and variability in treatment delivery were noted as drawbacks to systemwide provision of this therapy. one-half had achieved a high state of function. supportive therapy]” (p. including CBT and several antidepressants (Heuzenroeder et al. A recent well-controlled intervention randomly assigned older adults with GAD to short-term (12-week) CBT. Patients who received active treatment showed clear improvements relative to those on the waiting list. The author noted that the modest results in a trial of CBT may be related to learning difficulties in older patients and suggested that “age-appropriate principles of learning may need to be integrated to increase potency” (p. results with exposure and response prevention are best when patients can clearly describe the situations that provoke anxiety or ritualistic behavior. Although few outcome studies have been done. Successful treatment of a case of late-onset OCD with exposure and response prevention was described by Carmin et al. An Australian public health investigation of randomized controlled trials for the general adult population compared efficacy and cost of different interventions for GAD and panic disorder. the elderly participants in this study may well have been treatment resistant because they had experienced anxiety for an average of more than 30 years and almost 90% had tried other psychological or pharmacological therapies. Reduction in anxiety was clinically significant for one-third of the treated patients. 2004). (2002). 161). with slightly greater benefit observed with CBT compared with the discussion group. and guided imagery may have a role.g. sig- . The conclusion was that CBT had greater total health benefits than drug interventions alone for both anxiety disorders. For patients whose anxiety is generalized or pervasive. 149). 2003a).. The authors noted that outcomes in some CBT groups were better than in others. albeit with some persisting anxiety.Anxiety Disorders and Late-Onset Psychosis 289 A review by Mohlman (2004) of psychosocial treatment of GAD in the elderly concluded that “the existing body of work does not clearly indicate the superiority of CBT over alternative interventions [e. but large-scale studies in the elderly remain to be published. In general.

E. when treatment is required on a daily or neardaily basis for up to 4–6 weeks. one author of this book (J. However.290 Clinical Manual of Geriatric Psychiatry nificant reductions in subjective anxiety have been reported for elderly patients in response to both progressive and imaginal relaxation procedures (Scogin et al. these symptoms are severe enough to render these agents intolerable. are generally preferable. similarly.) has had excellent results with clonazepam.5–1. the longer-acting agents such as diazepam can be used safely. which is long-acting but does not give rise to clinically significant amounts of active metabolite. some elderly patients experience acute withdrawal symptoms between doses of short-acting benzodiazepines. 1997).S. For very short-term anxiety associated with specific situations such as airplane travel. pharmacological treatment of depression should be initiated before or during the application of behavior therapy. Most therapists who use behavior techniques in the treatment of anxiety advocate the adjunctive use of antianxiety agents with behavior therapy. Therefore. the shorter-acting benzodiazepines such as lorazepam or oxazepam. Psychopharmacotherapy Benzodiazepines remain the treatment of choice for anxiety of acute or subacute duration (Table 7–8). which undergo single-step conjugation in the liver and have no active metabolites. making it the only long-acting benzodiazepine free of this disadvantage. 1992). Following specific procedures for relaxation training (Bernstein and Borkovec 1973) is important to ensure an effective intervention and to compare results for a given patient with results of clinical investigations. when phobic or obsessivecompulsive behaviors emerge as part of a depressive syndrome. In this situation. daily use of the longer-acting agents in elderly patients will lead to accumulation of clinically significant blood levels of long-acting active metabolites. Several rating scales have been designed to assess the effectiveness of relaxation interventions (Crist et al. Chronic GAD and the other anxiety disorders generally require continuous therapy beyond 4–6 weeks. 1989).0 mg by mouth twice daily (Calkin et al. such as in adjustment disorder with anxiety or in acute GAD. at which point the effectiveness of benzo- . most of which have half-lives of several days or longer. Typical dosages are 0. These agents have the additional advantage of being relatively well tolerated by patients with even fairly advanced liver disease. in these situations.

American Psychiatric Association. Source.5–30 0. Used with permission. Washington. producing inactive metabolites. Approximately 100% longer in elderly (i.Table 7–8. cApproximately 50% longer in elderly. dDominant metabolic pathway is nitroreduction.25–4 0.5–3 Drug Chlordiazepoxide Diazepam Clorazepate Alprazolam Lorazepam Oxazepam Temazepam Clonazepam aApproximate b Trade name Librium Valium Tranxene Xanax Ativan Serax Restoril Klonopin Anxiety Disorders and Late-Onset Psychosis range. Adapted from American Psychiatric Association: “Treatment With Antianxiety Agents. a minor oxidative pathway producing potentially active metabolites also has been identified.” in Treatments of Psychiatric Disorders: A Task Force Report of the American Psychiatric Association. DC. 1989. American Psychiatric Association. Pharmacological properties of benzodiazepines Rate of absorption Intermediate Fast Fast Intermediate Intermediate Slow Slow Fast Duration of action Long Long Long Intermediate Short Short Short Long Active metabolites Yes Yes Yes Yes No No No Nod Elimination half-life (hours) 5–30b 20–50b 36–200b 12–15c 10–14 5–10 10–20 20–50 Therapeutic dosage range (mg/day)a 10–40 2–20 7. Vol. longer in men than in women. use high end of range).5–6 15–60 15–90 0.. Copyright © 1989. pp. 2036–2052. some patients may require higher or lower dosages. 291 . 3.e.

and one small. whereas only 4 of 17 in the placebo group did. In the citalopram group. Controlled trials in the elderly are scant. In each group. and monoamine oxidase inhibitors) have been shown to be effective in nonelderly patients. the remaining 4 had panic disorder (3) and PTSD (1). and peak effects on anxiety tend to occur sooner than peak antidepressant effects. in a doubleblind. It has several advantages over benzodiazepines: no sedative effects. found that 25–200 mg/day of sertraline (average dosage= 92.5 mg) eliminated panic attacks in 9 of 10 subjects by the end of the 12-week study .e. serotonin-norepinephrine reuptake blockers. in general. therefore. Lenze et al. Dosages are similar to those required for treatment of depression. (2005b) administered citalopram. Heterocyclic antidepressants (including selective serotonin reuptake inhibitors.292 Clinical Manual of Geriatric Psychiatry diazepines may diminish and more reliable results may be obtained with heterocyclic antidepressants such as nortriptyline. Buspirone is contraindicated in patients taking monoamine oxidase inhibitors (presumably because of its serotonergic properties) and is less effective in patients who have been treated with benzodiazepines. open-label study of 10 subjects (average age =72. neuroleptics have a very minimal role in the treatment of uncomplicated GAD.4). and no tendency to produce dependence or withdrawal symptoms. Although efficacy of alprazolam in nonelderly adults with panic disorder has been reported. 15 subjects had GAD. citalopram. paroxetine. sertraline. benzodiazepines and buspirone are both relatively ineffective in inhibiting panic attacks. but Morinigo et al. average dosage of about 1. mirtazapine.. placebo-controlled. Treatment of panic disorder and OCD is somewhat more specific. prescription follows the guidelines for treatment of mood disorder outlined in Chapter 4 (“Mood Disorders—Treatment”). otherwise. no interaction with alcohol.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. or venlafaxine. In general. escitalopram. buspirone has little or no abuse potential. and usually several weeks of daily dosage are required before effects are observed. A disadvantage is that it has little or no acute efficacy. with or without agoraphobia. random-assignment design to 34 subjects (average age=69. 11 of 17 responded. 20–30 mg/day.5) who had panic disorder. (2005) reported excellent results with lowdose risperidone (i. Buspirone is another nonbenzodiazepine that has been shown to be an effective anxiolytic agent in elderly patients (Goldberg 1994).

Similarly. which did not allow onset of schizophrenia after age 45. and cautions listed in Chapter 4 (“Mood Disorders—Treatment”) for treatment of depression apply. 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.) In the National Institute of Mental Health Epidemiologic Catchment Area Program (Regier et al. following ICD-9-CM [World Health Organization 1978] convention. DSM-IV also allowed dementia.1% of individuals age 65 or older were given a diagnosis of schizophrenia with DSM-III (American Psychiatric Association 1980) criteria. 10% had onset of psychotic symptoms after age 65. dosages of antidepressants are similar to those used for depressive disorders. including schizophrenia. A similar diagnostic distribution was found by Webster and Grossberg (1998).8% had mood disorder with psychosis. 0. 2. to be coded as “with delusions. 2004a). Generally. has a codable subtype of “with delusions” for vascular dementia only. and although they are generally well tolerated and should be effective in the elderly. . Besides these “functional” disorders. and the most common diagnoses were dementia of the Alzheimer’s type.4% had organic mental disorder (mainly primary degenerative or vascular dementia) with psychosis. delusional disorder. definitive studies are lacking. the adult literature has convincingly documented the efficacy of selective serotonin reuptake inhibitors for the treatment of OCD. and 1. DSM-IV recognized the possibility of late onset in all psychotic illnesses. mood disorder with psychotic features. The diagnostic breakdown was as follows: 3.7% had disorders that would be diagnosed by DSM-III-R (American Psychiatric Association 1987) criteria as schizophrenia (10 of 15 patients) or delusional disorder (4 of 15 patients).Anxiety Disorders and Late-Onset Psychosis 293 (Sheikh et al. and psychotic disorder due to a general medical condition.” (DSM-IV-TR. including Alzheimer’s type and vascular dementia. Late-Onset Psychosis Epidemiology The prevalence of late-onset psychosis is difficult to estimate because of a lack of diagnostic consistency across investigations. 1988). In their group.700 consecutive admissions to a psychogeriatric unit. who reported on 1. substance-induced psychotic disorder.

more commonly have sensory deficits (particularly conductive hearing loss). Compared with earlyonset schizophrenia patients. and schizoaffective disorder. VLOSLP appears to be a stable entity and not merely the harbinger of a progressive dementing condition. British investigators found that the incidence of VLOSLP was significantly higher in African. the typical picture of VLOSLP follows DSM-IV-TR diagnostic criteria for schizophrenia: there are . 2001). 1995]). and Rabins and Lavrisha (2003). patients with VLOSLP are less likely to have a family history of schizophrenia. The International Late-Onset Schizophrenia Group (Howard et al. (2003). and less commonly have negative symptoms. respectively.and Caribbean-born elders than in indigenous elders (Reeves et al. Despite the age association. 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.294 Clinical Manual of Geriatric Psychiatry followed by major depression. delirium. delusional disorder. medical or toxic causes. and dementia with psychosis is discussed in Chapter 5 (“Dementia and Alzheimer’s Disease”). bipolar disorder. Mood disorder with psychosis is described in Chapter 3 (“Mood Disorders—Diagnosis”). female gender. Diagnostic Criteria DSM-IV-TR diagnostic criteria for schizophrenia and delusional disorder are summarized in Tables 7–9 and 7–10. (2004) and Barak et al. concluded that onset after age 40 of psychotic symptoms typical for schizophrenia should be called late-onset schizophrenia-like psychosis. Rodriguez-Ferrera et al. and onset after age 60 should be called very-late-onset schizophrenia-like psychosis (VLOSLP). Palmer et al. as indicated by follow-up studies conducted by Mazeh and colleagues (2005). (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 schizophrenia patients. and ethnic minority immigrant status. 2000). schizophrenia. based on extensive review of the literature. Clinical Presentation The clinical presentation of late-onset psychosis depends in large part on the underlying diagnosis.

or selfcare are markedly below the level achieved prior to the onset. If there is a history of autistic disorder or another pervasive developmental disorder. Summary of DSM-IV-TR diagnostic criteria for schizophrenia Two (or more) of the following. active-phase symptoms) and may include periods of prodromal or residual symptoms. each present for a significant portion of time during a 1-month period (or less if successfully treated): (1) delusions (2) hallucinations (3) disorganized speech (4) grossly disorganized or catatonic behavior (5) negative symptoms. i. Schizoaffective disorder and mood disorder with psychotic features have been ruled out because either (1) no major depressive. Source. or mixed episodes have occurred concurrently with the active-phase symptoms. A. 4th Edition. Continuous signs of the disturbance persist for at least 6 months. C. For a significant portion of the time since the onset of the disturbance. affective flattening. the additional diagnosis of schizophrenia is made only if prominent delusions or hallucinations are also present for at least a month (or less if successfully treated). Copyright © 2000. or avolition Note: Only one Criterion A symptom is required if delusions are bizarre or hallucinations consist of a voice keeping up a running commentary on the person’s behavior or thoughts. American Psychiatric Association. including at least 1 month of symptoms (or less if successfully treated) that meet Criterion A (i. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. Text Revision. E. B. .e. alogia. Washington. During these prodromal or residual periods. one or more major areas of functioning such as work. manic. or two or more voices conversing with each other.. interpersonal relations. their total duration has been brief relative to the duration of the active and residual periods. American Psychiatric Association. D.e.. Used with permission. F. or (2) if mood episodes have occurred during active-phase symptoms. DC. The disturbance is not due to the direct physiological effects of a substance or a general medical condition.Anxiety Disorders and Late-Onset Psychosis 295 Table 7–9. 2000. the signs of the disturbance may be manifested by only negative symptoms or two or more symptoms listed in Criterion A present in an attenuated form.

2000.296 Clinical Manual of Geriatric Psychiatry Table 7–10. If mood episodes have occurred concurrently with delusions. Text Revision. B. and the remainder of this chapter follows suit. Nonbizarre delusions of at least 1 month’s duration. Criterion A for schizophrenia has never been met. (2003). Source. They concluded that “the validity of the distinction between late-onset schizophrenia and other paranoid psychoses of old age would thus seem to be lacking at the descriptive as well as the predictive and construct levels. and a relative absence of formal thought disorder and affective blunting. American Psychiatric Association. most notably Riecher-Rossler et al. because published articles on late-onset psychosis in recent years are essentially all focused on VLOSLP. Researchers in geriatric psychiatry seem to have agreed with this assessment. delusions that may be bizarre. their total duration has been brief relative to the duration of the delusional periods. American Psychiatric Association. Washington. The presentation of delusional disorder similarly follows DSM-IV-TR. C. 4th Edition. D. In a study of community-residing outpatients with schizophrenia (Heaton et al. who studied hospital case registers of more than 1. although hallucinations are nonbizarre and functioning is relatively intact. Neuropsychological Tests Most patients with schizophrenia spectrum disorders have neuropsychological deficits. 2001). Rather. hallucinations (which are more likely to be visual than in early. Used with permission. 602). Copyright © 2000. the distinction between VLOSLP and delusional disorder has been called into question by several investigators. the average global neuropsychological score was 1. However. 352 of whom had onset after age 40. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. E. there would appear to be a broad overlap between the two diagnostic categories” (p. Apart from the impact of the delusion(s) or its ramifications. functioning is not markedly impaired and behavior is not obviously odd or bizarre. Summary of DSM-IV-TR diagnostic criteria for delusional disorder A.62 stan- .or late-onset cases).100 patients with schizophrenia or paranoid psychosis. The disturbance is not due to the direct physiological effects of a substance or a general medical condition. DC. with severity ranging from mild frontal executive deficits to clinical dementia.

with and without psychotic symptoms. 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. in a retrospective chart review study (Dwork et al. retest scores also remained stable or even slightly improved for both early. patients with Alzheimer’s disease.. mean changes over time and test-retest reliabilities were the same for schizophrenic patients and control subjects across a wide range of cognitive measures. The investigators speculated that individuals with schizophrenia may have lowered cognitive reserve.Anxiety Disorders and Late-Onset Psychosis 297 dard deviations (SDs) lower for patients compared with control subjects. see Chapter 5. have found higher dementia rates. In this study. For example. Both older and younger patients had this stable pattern.and lateronset schizophrenic-like disorder groups. . however. mainly with older institutionalized samples. 19%). whereas significant decline was noted for patients with Alzheimer’s disease. Longitudinal neuropsychological data for VLOSLP patients (e. late-onset schizophrenia-like psychosis patients (onset after age 45 years). The cognitively impaired schizophrenic patients had higher rates of Alzheimer-type brain changes (especially neocortical neuritic plaques) than did those without cognitive deficit. most studies have found schizophrenia-related cognitive deficits to be stable over time. age 75 and older) are scant. study. in contrast to neurodegenerative disorders such as Alzheimer’s disease and dementia with Lewy bodies. 1998) that examined brain autopsy findings for patients who had been institutionalized for severe mental disorder or dementia. and about 30% of the patients had “very impaired” cognitive scores (>3 SDs below the level of nonschizophrenic control subjects). Deficits of this magnitude contribute in significant ways to the functional and social limitations associated with schizophrenia-like conditions. A related study compared performance on cognitive mental status examinations (the Mini-Mental State Examination and Dementia Rating Scale. and control subjects without mental disorders across retest intervals of 1–2 years. However. but the extent of these changes generally fell short of pathological criteria for Alzheimer’s disease. a few studies.g. Also. a higher proportion of schizophrenic patients than those with severe depression were rated as having significant cognitive impairment prior to death (68% vs. “Dementia and Alzheimer’s Disease”) for older early-onset schizophrenia spectrum patients. In the Heaton et al. and more research is needed. for example. which predisposes them to clinically significant cognitive changes at lesser levels of Alzheimer’s disease pathology.

It is important to remember that performance on neuropsychological tests may be impaired in the absence of organic brain disease if attention. low-potency neuroleptic medications with potent central anticholinergic effects) can lead to this potentially hazardous misdiagnosis. anhedonia. dysphoria. 1979). but medications or combinations of medications that produce psychomotor slowing and toxic hallucinations (e. pseudodementia). Finally.e. Delirium. For instance.” functioning to help maintain psychic equilibrium threatened by peculiar or frightening experiences. and irritability are usually apparent enough to lead diagnostic efforts in the right direction. Accordingly. when these features are obscured by psychotic manifestations. retesting after these symptoms are at least partly controlled may avoid false-positive findings suggestive of degenerative or vascular disease. Again. including medical records. In psychotic mood disorder. concentration. Late-onset hypomania and mania can present a clinical picture very similar to that of VLOSLP (Spar et al. although none has focused on late-onset disorders. also should be considered. correct diagnosis may require a detailed history obtained from multiple sources. along with inpatient observation.. These hypotheses assume that delusions are “secondary. and motivation are negatively affected by functional illness (i. particularly if induced by medications. delirium is rarely mistaken for VLOSLP. the common delusion expressed by pa- ..298 Clinical Manual of Geriatric Psychiatry Differential Diagnosis The major diagnostic entities to be ruled out before diagnosing VLOSLP include mood disorder with psychosis and dementia with psychosis. Dementia with psychosis may be identified by mental status examination supplemented with neuropsychological tests (see Chapter 5. the diagnosis may rest on identification of the characteristic neurovegetative signs and symptoms of depression and careful determination of a sequence of onset of symptoms in which mood and neurovegetative changes occur before delusions and hallucinations. Pathogenesis Psychodynamic Theories Several plausible psychodynamic theories have been proposed to explain the development of delusions in mental illness. sadness. “Dementia and Alzheimer’s Disease”).g.

g. . More recent attention has been paid to the role of glutamate. and flat affect. mood-congruent delusions of bodily malfunction (“I can’t eat because the food doesn’t go into my stomach anymore”) and delusional guilt (“The president has lost his veto power. each of which is a feature of DSM-IV-TR schizophrenia. Schwartz (1963) proposed that an inner sense of meaninglessness or insignificance results in a self-aggrandizing delusion of “centrality” (e. both internal and external stimuli for the development of persecutory delusions have been described. a dysfunction in a “phylogenetically old apparatus of a memory of situations” results in familiar perceptions being experienced as novel. Similarly. The psychoses associated with long-term ingestion of dopaminergic agents such as amphetamine or cocaine have led to the hypothesis that “endogenous” dopaminergic hyperactivity causes functional psychosis. and the Communists are going to take over because of me”). and alien. delusional beliefs often seem designed to explain hallucinatory experiences. are generally inadequately articulated in the literature. vague. Similarly.. and helplessness. catatonic behavior.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 actually moved around by the patient. Psychic equilibrium is sustained by explaining these changes as the results of the covert hostile actions of others. “The ill-intended actions of many other people are oriented around me. help the individual to explain and understand his or her pervasive sense of dysphoria. for example. commonly seen in psychotic major depression. degradation. In late-onset schizophrenia and delusional disorder. whereas psychotic symptoms associated with ingestion of serotonergic hallucinogens such as lysergic acid diethylamide (LSD) have implicated serotonergic dysfunction. Arnold (1999) proposed that in schizophrenia. uncertain. Psychodynamic explanations of hallucinations. who has no recall of the events. Neurobiological Theories Neurobiological explanations of delusions and hallucinations are partly based on analogy with well-known drug-induced mental changes. The delusion enables the individual to avoid the awareness of severely impaired memory function. so I must be a powerful and important person”). “The neighbors are pumping poison gas into my apartment” is a belief that might accompany olfactory hallucinations. in which intellectual deficits and mood disturbance are absent.

. Hirsch and colleagues reported findings of 1) a marked decrease in pyramidal cell dendritic spines in layer III of the frontal and temporal cortex and 2) a correlation greater than 0.37 (SD=0. which is modest at best. 797). Moreover.300 Clinical Manual of Geriatric Psychiatry Hirsch and colleagues (1997) proposed that “schizophrenia and phencyclidine psychosis are similar. but to date no widely accepted neurobiological theory of “functional” psychosis has yet been articulated. and to a later developed intermittent hyperactivity of the dopaminergic system superimposed on a basal hypodopaminergic state. A changed neuroplastic response to environmental stimulation due to dopaminergic sensitization can explain how an episodic. The authors noted that clinical and experimental studies point to a primary/early cortical defect involving the glutamatergic system. He . (p. . subcortical hyperactivity can act on a basic glutamatergic and dopaminergic hypofunction to produce psychotic symptoms. 24) Glenthøj and Hemmingsen present a hypothesis for spontaneous mesolimbic dopaminergic sensitization and progressive evolution of psychosis on the basis of their own clinical and experimental findings and those of others—the “filter” hypothesis for schizophrenia and the state dependence of schizophrenic symptoms. These findings support the hypothesis proposed by Glenthøj and Hemmingsen (1997). Other theorists have focused on structural abnormalities observed in the brains of schizophrenic patients (Harrison 1999).. who observed that most abnormalities postulated to underlie schizophrenia “involve the cortico-striato-thalamo-cortical circuits. and phencyclidine is known to block the N-methyl-D-aspartate (NMDA) subtypes of glutamate (receptor). Treatment Psychosocial-Behavior Therapy Tarrier (2005) reviewed 20 controlled studies of CBT in schizophrenic patients and found an overall effect size of 0.90 between decrease in mRNA for the NMDA glutamate receptor and cognitive deterioration in elderly patients with schizophrenia. studies of messenger RNA [mRNA] suggest that glutamate receptor deficiencies occur in schizophrenia and are regionally and specifically distributed” (p.39). 24). which are central for attention and information processing” (p.

Although none of the controlled trials in these reviews focused on elderly patients per se. but the greater increase in cognitive insight with combined treatment was significantly correlated with greater reduction in positive symptoms. facilitating the flow of clinical data from the patient. The Beck Cognitive Insight Scale (Beck et al. 131). 2004). The overall group effect was not significant for symptoms. A recommended therapeutic stance toward the patient’s delusional belief is “respectful disagreement. 520) Rector and Beck (2002) described in detail how cognitive therapists conceptualize and treat positive and negative symptoms of schizophrenia. there is little reason to expect that CBT would be significantly less effective in older patients. Turkington et al. open disagreement invites the patient to incorporate the therapist into the delusion. “There is consistent evidence that CBT reduces persistent positive symptoms in chronic patients and may have modest effects in speeding recovery in acutely ill patients” (p. and maximizing compliance with somatic therapy can be an effective component of the overall treatment program for VLOSLP. A randomized controlled trial of cognitive-behavioral social skills training for middle-aged and older outpatients (average age=approximately 54) with chronic schizophrenia conducted by Granholm et al. which measures the ability to observe and question one’s own cognitive processes. Patients receiving cognitive behavioral social skills training achieved significantly greater cognitive insight…and demonstrated greater skill mastery. thereby thwarting ef- . Besides CBT. as long as cognitive impairment were not present..” wherein the therapist 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. 2004). (p.g. and they may become suspicious and distrustful of the treating professional who does. Other reviewers (e. although general skill at social functioning activities did not differ significantly. individual supportive psychotherapy aimed at building trust.Anxiety Disorders and Late-Onset Psychosis 301 concluded. However. 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) have emphasized the value of CBT as an adjunct to antipsychotic medications and socially based remedial approaches such as social skills training. (2005) found that patients receiving combined treatment performed social functioning activities significantly more frequently than the patients in treatment as usual.

(2004) surveyed 52 “American experts on treatment of older adults. These agents’ main advantages over the typical antipsychotic medications are their relative lack of extrapyramidal side effects. insight-oriented psychotherapeutic approaches are usually discouraged in favor of approaches that focus on more dynamically superficial content. and olanzapine has anticholinergic effects that are usually well tolerated in therapeutic dosage . fear. Although some elderly patients are capable of a degree of detachment from their delusions and can gain insight into their defensive function. “Quetiapine (100–300 mg/day). such as conscious concerns and feelings.25–3. 2000.5–15 mg/day). Consistent with these recommendations. in which case the therapy should be aimed at the accompanying anxiety. Although sessions without the patient can be productive. and somewhat lower propensity to impair cognition. Family therapy may be extremely useful. or anhedonia. although some patients can use the group situation to initiate social contact with other patients and appear to benefit indirectly. the natural history and prognosis of the disorder.302 Clinical Manual of Geriatric Psychiatry forts to establish a mutually respectful. psychotic patients often refuse to cooperate with treatment aimed at the delusions or hallucinations per se. and details of the treatment plan. Madhusoodanan et al. olanzapine (7. sleeplessness. In this regard. 2000) to be effective and well tolerated in elderly patients with psychoses. and aripiprazole (15–30 mg/day) were high second-line [choices]” (p. Acute side effects of risperidone and olanzapine are usually limited to sedation and orthostatic hypotension. Psychopharmacotherapy Controlled studies are lacking. trusting relationship. but Alexopoulos et al.” The experts’ first-line recommendation for late-life schizophrenia was risperidone (1.5 mg/day). particularly in situations in which family members have been alienated by psychotic behavior. somewhat greater efficacy for negative symptoms of schizophrenia. several open studies have shown risperidone (Davidson et al. 1999) and olanzapine (Madhusoodanan et al. Work with family members focuses on education about the patient’s condition. the family therapist also attempts to enlist family support for the inpatient and outpatient components of the treatment plan. 5). Group therapy is generally of little value in the acute phase of psychotic illness. inviting the patient to participate each time may avoid exacerbating feelings of mistrust and paranoia.

dyslipidemia. xerophthalmia. Alternatively. may be effective in controlling agitation and hallucinations but is typically less effective than neuroleptic medications in reversing thought disorder and delusions. insulin resistance and diabetes. (p.5 mg administered orally three times a day. the experts prefer risperidone. akinesia. constipation. One or two doses of an antiparkinsonian agent such as benztropine or trihexyphenidyl hydrochloride may be useful for diagnostic purposes when akathisia is suspected. which can be increased up to threefold. side effects are usually limited to sedation. For patients with cognitive impairment. or obesity. 5) Of the typical antipsychotic agents. and cogwheel rigidity. Alexopoulos et al. Clozapine. diabetic neuropathy. and anticholinergic delirium. low-dose. but longterm administration of anticholinergic agents should be avoided whenever possible because of the increased susceptibility of elderly patients to memory impairment. long-term side effects of significant weight gain. dyslipidemia. However. high-potency medications such as haloperidol and fluphenazine still have a role in VLOSLP. confusion. particularly in patients whose symptoms are nonresponsive to the atypical agents or who cannot tolerate the tendency of these agents to stimulate weight gain. clonazepam. (2004) would avoid clozapine. ziprasidone. the experts surveyed by Alexopoulos et al.and midpotency) should be avoided in patients with QTc prolongation or congestive heart failure.and mid-potency) for patients with diabetes. which produces no extrapyramidal side effects. olanzapine. and conventional antipsychotics (especially low. and conventional antipsychotics (especially low. but the risk of blood dyscrasia necessitates a pretreatment complete blood count followed by periodic retesting. Accordingly. Acute side effects to be anticipated with typical agents include sedation. A typical starting dosage of clonazepam is 0. stated the following: Quetiapine is first line for a patient with Parkinson’s disease.Anxiety Disorders and Late-Onset Psychosis 303 ranges. Moreover. and xerostomia. At these dosages. with quetiapine high second line. Adjunctive treatment with lorazepam or other short-acting benzodiazepines often allows the total dosage of neuroleptic to be reduced below levels that cause these side effects. and dyslipidemia are seen in varying degrees of severity with all of the atypical antipsychotic agents. diabetes. akathisia. Dosages of atypical and typical antipsychotic medications required to achieve symptom remission in VLOSLP typically range around 33%–100% .

5 100 5 75 40 15 +++ +++ ++ + + + + + +++ ++ + ++ + ++ +++ 0/+ + 0/+ 0 0/+ 0 +++ ++ + + 0 ++ + +++ ++ ++ +++ +++ + 0/+ 0/+ 0/+ 0/+ 0/+ +++ (im) ++ + + ++ 0/+ + + ++ + + + + . and side-effect profiles Equivalent dose (mg/day) Sedation Anticholinergic effects Extrapyramidal effectsa Hypotensive effects 304 Clinical Manual of Geriatric Psychiatry Typical agents Chlorpromazine Thioridazineb. dose equivalences. Drug Antipsychotic drugs.c Perphenazine Trifluoperazine Thiothixene Haloperidol Fluphenazine Atypical agents Risperidone Clozapined Olanzapine Quetiapine Ziprasidonec Aripiprazole 100 100 8 5 5 2 2 1.Table 7–11.

Anxiety Disorders and Late-Onset Psychosis 305 . bMaximal dosage is 800 mg/day. Rundell JR: “Delirium (Acute Confusional States) and Dementia. especially at night. and side-effect profiles (continued) Note.” in Concise Guide to Consultation Psychiatry. and perioral tremor (“rabbit syndrome”). p. 0/+ =absent or very weak effect. higher dosages may cause pigmentary retinopathy. akathisia. dHypersalivation is common. is contraindicated in patients with preexisting QTc interval>500 msec or various forms of cardiac illness. Adapted from Wise MG. 1994.Table 7–11. Washington. ++= moderate effect. Used with permission. +++= strong effect. im=intramuscular. aInclude acute dystonia. DC. American Psychiatric Press. Copyright © 1994. c Causes increase in QT/QTc interval. 41. Antipsychotic drugs. 2nd Edition. += weak effect. pseudoparkinsonism. dose equivalences. Source. American Psychiatric Press.

Table 7–11 presents dose equivalences and relative side-effect potencies of the commonly prescribed atypical and typical antipsychotic medications. DC. J Clin Psychiatry 65 (suppl 2):5–99. An effective dosage titration approach is to prescribe one-third to one-half the adult dosage on a standing basis and to add a similar dosage on an as-needed basis once or twice a day for agitation. 3rd Edition. Aizenberg D. or delusion-driven behavior (e. Mirecki I. Text Revision. 1999 Arnold OH: Schizophrenia—a disturbance of signal interaction between the entorhinal cortex and the dentate gyrus? the contribution of experimental dibenamine psychosis to the pathogenesis of schizophrenia: a hypothesis. at which point the dosage is increased slightly and maintained. DC. 4th Edition.306 Clinical Manual of Geriatric Psychiatry of the recommended dosage for schizophrenic adults. Neuroreport 10:3497–3500. 1994 American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. the patient will not eat because the food “comes from the toilet” or “is poisoned”). Neuropsychobiology 40:21–32. hallucinations. et al: Very late-onset schizophrenia-like psychosis: clinical and imaging characteristics in comparison with elderly patients with schizophrenia. 2000 Andersen SL. 3rd Edition. 1999 Barak Y. J Nerv Ment Dis 190:733–736. Washington. Carpenter D.g. 1987 American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. Washington. Streim J. 2004 American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. Washington. American Psychiatric Association. Because delusional thought content may persist for weeks or months after delusions are no longer driving the patient’s affect and behavior. it is usually impractical to use delusional thought content per se as a target symptom of acute therapy. Teicher MH: Serotonin laterality in amygdala predicts performance in the elevated plus maze in rats. American Psychiatric Association. Washington. 2002 . DC. References Alexopoulos GS. American Psychiatric Association. 1980 American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. After acute symptoms subside. Revised. dosages can be gradually reduced until symptom breakthrough occurs. et al: Using antipsychotic agents in older patients.. DC. 4th Edition. American Psychiatric Association.

Easthope Y. Int J Geriatr Psychiatry 19:333–343. imipramine. Kunik ME. 2000 Beck AT. Epstein N. New York. Edited by Lichtenberg P. New York. New York. et al: An inventory for measuring clinical anxiety: psychometric properties. Susser ES. Wiegartz PS. Orengo CA. van Balkom AJ. 2004 Beekman AT. Brown G. Harvey PD. open-label study of risperidone in elderly patients with psychosis. Wiley. 1999. et al: Cognitive behavior therapy versus supportive therapy in social phobia: a randomized controlled trial. Depress Anxiety 15:87–90. Behav Res Ther 34:225–234. 2004 Cottraux J. Schizophr Res 68:319–329. 1983. 1988 Beck JG. 1996 Beck AT. 1973 Blazer D. and personality: the ‘inoculation’ effect. in Stress Research. de Beurs E. et al: Anxiety and depression in later life: co-occurrence and communality of risk factors. Zebb BJ: Characteristics of generalized anxiety disorder in older adults: a descriptive study. middle-aged and elderly comparisons. et al: The Relaxation Inventory: self-report scales of relaxation training effects. pp 59–90 Carmin CN. multicenter. or their combination for panic disorder: a randomized controlled trial. Wiley. pp 17–30 Calkin PA. et al: A long-term. Springer. Int J Geriatr Psychiatry 15:506–514. 1998 Eysenck H: Stress. 2000 Crist DA. Rickard HC. 2000 Bernstein DA. Stanley MA. Borkovec TD: Progressive Relaxation Training: A Manual for the Helping Professions. Albuisson E. Champaign. Edited by Cooper CJ. 1991. in Handbook of Assessment in Clinical Gerontology. Baruch E. George LK. et al: Cognitive-behavioral therapy. Yunus U. Am J Psychiatry 157:89–95. Psychother Psychosom 69:137–146. et al: Coping with post-traumatic stress: young. Am J Psychiatry 155:1536–1543. 1989 Davidson M. J Pers Assess 53:716–726. Note I. et al: Senile degeneration and cognitive impairment in chronic schizophrenia. Werrett J. Balter JM. Research Press. Gillock KL: Assessment of anxiety disorders in the elderly.Anxiety Disorders and Late-Onset Psychosis 307 Barlow DH. 2002 Chung MC. Edited by Salzman C. 2000 Dwork AJ. Hughes D: The epidemiology of anxiety disorders: an age comparison. et al: A new instrument for measuring insight: the Beck Cognitive Insight Scale. Lebowitz BD. Gorman JM. IL. Pollard CA. Vervarcke J. disease. J Consult Clin Psychol 56:893–897. On behalf of the Risperidone Working Group. JAMA 283:2529–2536. Int J Geriatr Psychiatry 12:745–749. Shear MK. in Anxiety in the Elderly: Treatment and Research. Keilp JG. et al: Treatment of late-onset OCD following basal ganglia infarct. Prentice-Dunn S. 1997 Carmin CN. et al: Tolerability of clonazepam in demented and non-demented geropsychiatric patients. pp 121–146 .

Unützer J. Journal of Clinical Psychiatry Monograph Series 12:31–36. 1999 Glenthøj BY. Reas DL. 2003 . Haby MM. Stark K. Brain 122 (pt 4):593–624. J Neurosci 19:RC41. New York. 2005 Gross C. Hemmingsen R: Dopaminergic sensitization: implications for the pathogenesis of schizophrenia. 1991. et al: Cost-effectiveness of psychological and pharmacological interventions for generalized anxiety disorder and panic disorder. pp 977–983 Hopko DR. 1999 Heaton RK. in Anxiety in the Elderly: Treatment and Research. 1959 Harrison PJ: The neuropathology of schizophrenia: a critical review of the data and their interpretation. controlled trial of cognitive behavioral social skills training for middle-aged and older outpatients with chronic schizophrenia. Palmer BW. Garey LJ. Psychol Assess 15:173–183. Prog Neuropsychopharmacol Biol Psychiatry 21:23–46. Zhuang X. in Psychopharmacology: The Third Generation of Progress. Am J Geriatr Psychiatry 13:48–58. Edited by Meltzer H. Br J Med Psychol 32:50–55. Gladsjo JA. Tang L. 1987. Arch Gen Psychiatry 58:24–32. Nature 416:396–400. et al: Assessing worry in older adults: confirmatory factor analysis of the Penn State Worry Questionnaire and psychometric properties of an abbreviated model. et al: Serotonin-1A receptor acts during development to establish normal anxiety-like behaviour in the adult. Pharmacol Biochem Behav 56:797– 802. et al: Stability and course of neuropsychological deficits in schizophrenia. Am J Psychiatry 162:520–529. et al: A pivotal role for glutamate in the pathogenesis of schizophrenia. Kokkinidis L: Enhanced amygdala kindling after electrical stimulation of the ventral tegmental area: implications for fear and anxiety. Miner JH: Clinical presentation of anxiety in the elderly. Raven. 1997 Hommer D. et al: Impact of comorbid panic and posttraumatic stress disorder on outcomes of collaborative care for late-life depression in primary care. Paul D: The benzodiazepine/GABA receptor complex and anxiety. McQuaid JR. Stanley MA. and its cognitive dysfunction. pp 31–44 Hamilton M: The assessment of anxiety states by rating. 2005 Heuzenroeder L. et al: A randomized.308 Clinical Manual of Geriatric Psychiatry Gelowitz DL. Springer. Edited by Salzman C. 1994 Granholm E. McClure FS. New York. Aust N Z J Psychiatry 38:602–612. Lebowitz BD. Das I. 2001 Hegel MT. 1997 Goldberg RJ: The use of buspirone in geriatric patients. Skolnick P. 2002 Gurian BS. 2004 Hirsch SR. Donnelly M.

Am J Psychiatry 157:722–728. Mulsant BH. Bondi MW. 2005 Mohlman J: Psychosocial treatment of late-life generalized anxiety disorder: current status and future directions. Mulsant BH. Mann A: The relationship between anxiety disorders and age. Int J Geriatr Psychiatry 13:79–99. 1999 Madhusoodanan S. et al: Clinical features of obsessive-compulsive disorder in elderly patients. Wetherell JL: Age at onset of generalized anxiety disorder in older adults. 2005b Le Roux H. et al: Patients with very-late-onset schizophrenia-like psychosis: a follow-up study. Seeman MV. Clin Psychol Rev 24:149–169. Suresh P. Mohlman J. Shear MK. Brecher M. 1990 Madhusoodanan S. Am J Geriatr Psychiatry 13:417–419. 1985 Lyons J. 2003 . placebo-controlled trial. Zemishlani C. The International LateOnset Schizophrenia Group. McClendon O: Changes in PTSD symptomatology as a function of aging. Khan S. et al: Risperidone in the treatment of elderly patients with psychotic disorders [published erratum appears in Am J Geriatr Psychiatry 7:268. J Nerv Ment Dis 173:488–494. 2000 Mazeh D. 2000 Khan A. et al: Efficacy and tolerability of olanzapine in elderly patients with psychotic disorders: a prospective study.Anxiety Disorders and Late-Onset Psychosis 309 Howard R. Gatz M. et al: Comorbid anxiety disorders in depressed elderly patients. Brenner R. Am J Geriatr Psychiatry 7:132–138. Ann Clin Psychiatry 12:11–18. Shear MK. 1999]. Mulsant BH. J Affect Disord 68:183–190. Howard R. Am J Geriatr Psychiatry 13:23–30. J Neuropsychiatry Clin Neurosci 15:45–52. Leventhal RM. Brenner R. Westlake RJ. Am J Geriatr Psychiatry 5:211–215. Aizenberg D. 2004 Morinigo A. 2002 Kohn R. 2005a Lenze EJ. et al: Generalized anxiety disorder in late life: lifetime course and comorbidity with major depressive disorder. 2005 Leuchter AF. 2005 Palmer BW. Am J Psychiatry 157:172–178. et al: Late-onset schizophrenia and very-late-onset schizophrenia-like psychosis: an international consensus. Nova-Psy Newsletter 8:13–18. et al: Risperidone for resistant anxiety in elderly persons. Am J Geriatr Psychiatry 13:81–82. Am J Psychiatry 162:146–150. Am J Geriatr Psychiatry 13:77–80. et al: Are late-onset schizophrenia spectrum disorders neurodegenerative conditions? annual rates of change on two dementia measures. Spar JE: The late-onset psychoses: clinical and diagnostic features. Twamley EW. 2000 Lenze EJ. Blanco M. 1997 Krasucki C. 1998 Lenze EJ. Rabins PV. Rasmussen SA. et al: Efficacy and tolerability of citalopram in the treatment of late-life anxiety disorders: results from an 8-week randomized. Labrador J. et al: Suicide risk in patients with anxiety disorders: a meta-analysis of the FDA database.

McQuaid JR. Psychol Aging 7:419–424. 2003 Ritchie K. 2004 Philpot MP. New York. Arch Gen Psychiatry 4:349–361. Haque S: Older people with schizophrenia: a community study in a rural catchment area. Stewart R. Edited by Meltzer H. Int J Geriatr Psychiatry 19:1181–1187. 1998 Rabins PV. 2001 Regier DA. et al: Increased first-contact rates for very-late-onset schizophrenia-like psychosis in African. 1963 Scogin F.and Caribbean-born elders. Can J Psychiatry 47:39–48. Lavrisha M: Long-term follow-up and phenomenologic differences distinguish among late-onset schizophrenia. et al: Measuring cognitive insight in middleaged and older patients with psychotic disorders. and risk factors. 1992 Sheikh JI. et al: Progressive and imaginal relaxation training for elderly persons with subjective anxiety. 2004 Schwartz DA: A review of the “paranoid” concept. Am J Geriatr Psychiatry 12:230. 2004 Rodriguez-Ferrera S. Banerjee S: Obsessive-compulsive disorder in the elderly. Rickard HC. Br J Psychiatry 184:147–152. Vassilas CA. Beluche I. Burke JJ. Schizophr Res 71:297–305. Boyd JH. Am J Geriatr Psychiatry 11:589–594. pp 967–975 Reeves SJ. Lauderdale SA. et al: One-month prevalence of mental disorders in the United States: based on five Epidemiologic Catchment Area sites. Hafner-Ranabauer W. Raven. in Psychopharmacology: The Third Generation of Progress. Sauer J. Br J Psychiatry 179:172–174. Carlson EB. Swales PJ. et al: Prevalence of DSM-IV psychiatric disorder in the French elderly population. Granholm E. et al: Aging and panic disorder: phenomenology. 2004b Simpson HB. Arch Gen Psychiatry 45:977–986. 2002 Redmond DJ: Studies of the nucleus locus coeruleus in monkeys and hypotheses for neuropsychopharmacology. late-life depression. comorbidity.310 Clinical Manual of Geriatric Psychiatry Pedrelli P. 1988 Riecher-Rossler A. Am J Geriatr Psychiatry 12:102–109. Artero S. Behav Neurol 11:117–121. J Clin Psychiatry 60:584–590. 1987. and progressive dementia. 2004a Sheikh JI. Liebowitz MR: Cognitive-behavioral therapy as an adjunct to serotonin reuptake inhibitors in obsessive-compulsive disorder: an open trial. Hafner H. 2003 Rector NA. Cassidy EL: Efficacy of sertraline for panic disorder in older adults: a preliminary open-label trial (letter). et al: Late-onset schizophrenia versus paranoid psychoses: a valid diagnostic distinction? Am J Geriatr Psychiatry 11:595–604. 1999 . Gorfinkle KS. Keith S. Beck AT: Cognitive therapy for schizophrenia: from conceptualization to intervention.

Behavior Therapist 9:91–95. Am J Geriatr Psychiatry 6:196–202. Dudley R. New York. Psychol Aging 18:622– 627. 1979 Spielberger C. Clinical Modification. 2003 Spar JE. Craske MG: Treatment of generalized anxiety disorder in older adults. Grossberg GT: Late-life onset of psychotic symptoms. 1970 Steffens DC. Lebowitz BD. Werner P: Anxiety disorder and accompanying subjective memory loss in the elderly as a predictor of future cognitive decline. Palo Alto. Le Roux H. 2000 Wetherell JL. 2004 van Os J. 9th Revision. Warman DM. J Psychiatr Pract 10:5–16. 2003b Wisocki PA. 1978 . Morse C: The Worry Scale as a measure of anxiety among home bound and community active elderly. MI. 2005 Turkington D. et al: Increasing age is a risk factor for psychosis in the elderly. McQuoid DR: Impact of symptoms of generalized anxiety disorder on the course of late-life depression. Consulting Psychologists Press. Am J Geriatr Psychiatry 13:40–47. Takei N. Ford CV. J Neuropsychiatry Clin Neurosci 12:265–268. Liston EH: Bipolar affective disorder in aged patients. 1995 Webster J. Ann Arbor. Jenike MA: Late-onset obsessive-compulsive disorder: a case series. Int J Geriatr Psychiatry 18:951–959. et al: Anxiety in the elderly: neurobiological and clinical interface. 1998 Weiss AP. Howard R. pp 105–129 Tarrier N: Cognitive behaviour therapy for schizophrenia—a review of development. Soc Psychiatry Psychiatr Epidemiol 30:161–164. Martinez RA. in Anxiety in the Elderly: Treatment and Research. Gatz M: DSM-IV criteria for generalized anxiety disorder in older adults: distinguishing the worried from the well. CA. Lawlor BA. Gatz M. 2005 Sunderland T. Springer. Lushene R: State-Trait Anxiety Inventory. J Consult Clin Psychol 71:31–40. 1991. Edited by Salzman C. 1986 World Health Organization: International Classification of Diseases. Handen B. et al: Cognitive-behavioral therapy for schizophrenia: a review. Psychother Psychosom 74:136–144.Anxiety Disorders and Late-Onset Psychosis 311 Sinoff G. Commission on Professional and Hospital Activities. 2003a Wetherell JL. evidence and implementation. J Clin Psychiatry 40:504–507. Gorsuch R.

This page intentionally left blank .

more time is required to fall asleep. The differential diagnosis of insomnia in the elderly includes the conditions listed below. and physiological measures such as polysomnography. 313 . rating scales that assess sleep behaviors and related issues. and people tend to spend more time in bed. relatively less deep (Stage IV) sleep is experienced. more awakenings occur. despite nursing observations of 6–8 hours of apparent sleep. complete with snoring. Normal Aging Changes In general. The subjective impression produced by these changes is unsatisfying sleep. Trevorrow (1999) has provided recommendations of topics to cover in a sleep assessment interview (Table 8–1) and a description of sleep questionnaires and rating scales.8 Other Common Mental Disorders of the Elderly Insomnia Assessment In addition to conducting thorough interviews of the patient and a sleep partner. which may be reported as insomnia. Differential Diagnosis Almost half of the 29 million Americans age 65 and older complain of inadequate amount or quality of sleep (Monane 1992). it is not uncommon for elderly hospitalized patients to report not sleeping at all. sleep becomes more fragmented. procedures that can be useful in establishing a diagnosis of insomnia include sleep diaries. with advancing age.

sleep onset. nightmares) Current sleep-wake schedule History of sleep complaint (transient disturbance vs. other psychological maladjustment) Stressful circumstances (currently and when sleep problems began) Information about antecedents.g. Inc. daytime fatigue. thought disorder.” in Handbook of Assessment in Clinical Gerontology. satisfaction with daily routines) Naps (frequency. . disruption of sleep-wake schedule) Symptoms of sleep-disordered breathing (disturbed breathing at night. functioning. Edited by Lichtenberg P.. precipitating factors.. early-morning wake-up. Inc. Copyright © 1999 John Wiley & Sons. routines. fatigue. Wiley. Adapted from Trevorrow T: “Assessing Sleep Functioning in Older Adults. length) Sleep hygiene (daytime activity. Insomnia Associated With Axis I Psychiatric Illness Sleep disturbance is associated with almost all of the major syndromes discussed in this book. psychosis. narcolepsy.314 Clinical Manual of Geriatric Psychiatry Table 8–1. and adjustment disorder. sleep maintenance. activities (sleepiness. mood. gastroesophageal reflux. Reprinted with permission of John Wiley & Sons.g. parasomnias. mood disorders. complaints of snoring. periodic limb movements. sleep environment. activity in bed. 331–350. Areas to consider in a sleep assessment interview Nature of the complaint—what the problem is and when it occurs (e. New York. 1999. restless legs. see Table 8–3) History of professional treatment of the sleep complaint and a review of what the patient has tried to remedy the sleep problem Medical or physical problems Use of prescription and nonprescription drugs Psychiatric history and mental status review (symptoms of depression. perpetuating factors Source. exercise. headache on waking. time of day. pp. partner sleeps in another room) Daytime states. anxiety. use of stimulants or depressants. secondary gains. including anxiety disorders. consequences. activities. dementia and delirium. The normal disruptions in mental life caused by stressful or grief-producing situations must be added to this list. diet. long-standing complaint) Symptoms of sleep disorders that may not be initially volunteered (e.

..g. higher doses of mirtazapine). hypnotic medications can produce sleep disturbance after prolonged use (sometimes in as little as 3 weeks of nightly ingestion) or during the acute withdrawal phase after repeated ingestion (the so-called rebound effect). Muscle movements that cause brief awakenings are most likely to be indicative of this condition. it is particularly important to identify and treat breathing-related sleep disorder because taking sedative-hypnotic drugs can exacerbate this condition and create a . dosage.g. or with immobility (e. Sleep apnea has been found in about 30%–40% of elderly patients evaluated in sleep laboratories and is typically associated with obesity and snoring. Also. Treatment—General and Behavioral Interventions In light of the differential diagnosis of insomnia described earlier in this section. arthritis).g. psychostimulants. particularly if they are ingested late in the evening. DSM-IV-TR (American Psychiatric Association 2000) diagnostic criteria for primary insomnia are summarized in Table 8–2. and timing of medications that can cause insomnia before prescribing hypnotic agents. Of the physical illnesses that can disturb sleep. certain antidepressants (fluoxetine. methylxanthine derivatives (such as theophylline and aminophylline). congestive heart failure or chronic obstructive pulmonary disease). and medications containing caffeine (as well as caffeinecontaining beverages such as coffee and many cola drinks) can interfere with sleep. bupropion. Frequent awakenings also may be associated with urinary obstruction secondary to prostatism or chronic urinary tract infection.. Substance-Induced Insomnia Sympathomimetic agents (including decongestants and bronchodilators). usually manifested as leg twitches and jerks. if not all. Nocturnal myoclonus. stroke or Parkinson’s disease) can severely disturb sleep. the proper diagnosis is primary insomnia. experimental and clinical evidence indicates that most.Other Common Mental Disorders of the Elderly 315 Insomnia Associated With Physical Illness Physical conditions associated with pain (e. with difficulty breathing (e. Primary Insomnia When the causes of insomnia listed above have been ruled out. it is important whenever possible to treat mental and physical illness and to adjust the type. is diagnosed somewhat less frequently and may be observed without using sophisticated electronic equipment.

may last well beyond the termination of treatment” (p. However. American Psychiatric Association. occupational. C. potentially lethal situation. 1993). The predominant complaint is difficulty initiating or maintaining sleep. the review also pointed out that few clinicians are trained in the use of CBT for chronic insomnia. The sleep disturbance does not occur exclusively during the course of narcolepsy. for at least 1 month. Text Revision. Table 8–3 lists the features regarded by The International Classification of Sleep Disorders (American Sleep Disorders Association 1997) as diagnostic of inadequate sleep hygiene. The disturbance is not due to the direct physiological effects of a substance or a general medical condition. DC. optimization of sleep hygiene should always be attempted before hypnotic agents are prescribed for other than occasional use. Interventions as simple as systematically restricting time spent in bed and providing education about normal variability in sleep patterns and age-related changes have been effective in increasing sleep efficiency and reducing daytime sleepiness in older patients with insomnia (Riedel et al. or other important areas of functioning. breathing-related sleep disorder. in contrast to those produced by medications. A recent state-of-the-science conference (National Institutes of Health 2005) on the manifestations and management of chronic insomnia in adults concluded that a cognitive-behavioral treatment package is “as effective as prescription medications are for brief treatment of chronic insomnia” (p. Washington. The disturbance does not occur exclusively during the course of another mental disorder. The sleep disturbance (or associated daytime fatigue) causes clinically significant distress or impairment in social. 4th Edition. circadian rhythm sleep disorder.. Similarly. 1995).g.316 Clinical Manual of Geriatric Psychiatry Table 8–2. Source. D. Copyright © 2000. 8) and that “beneficial effects of CBT [cognitive-behavioral therapy]. or a parasomnia. 8 hours of sleep per night is not necessary for everyone) is an example of a cognitive-behavioral intervention that may also be useful in treating insomnia in old age (Morin et al. 2000. 8). Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. Summary of DSM-IV-TR diagnostic criteria for primary insomnia A. E. or nonrestorative sleep. Used with permission. American Psychiatric Association. Modifying thoughts about “good” and “poor” sleep (e. B. .

to occur in bed Source. such as thinking. American Sleep Disorders Association. Rochester. or in some way not conducive to sleep 10. inadequate blankets) 9. but most elderly patients will experience less morning “hangover” with the short-acting agents. 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. lorazepam. such as temazepam. whereas triazolam is very . too stuffy. tobacco. Features of inadequate sleep hygiene 1. television watching. such as diazepam or flurazepam. Engaging in exciting or emotionally upsetting activities too close to bedtime 7. reading.g. or oxazepam. Scheduling exercise too close to bedtime 6. almost any of the available agents are effective. Sleeping on an uncomfortable bed (e. Revised. all agents of this class have hypnotic activity and are essentially interchangeable. MN.. Performing activities demanding high levels of concentration shortly before bed 11. snacking) 8. 1997. poor mattress. alprazolam is intermediate in duration of action and in desirability.. Treatment—Psychopharmacotherapy Benzodiazepine anxiolytic and hypnotic medications and the nonbenzodiazepine medications zolpidem. or caffeine in the period preceding bedtime 5.Other Common Mental Disorders of the Elderly 317 Table 8–3. For occasional use. Allowing mental activities. Frequently using the bed for nonsleep-related activities (e. too hot. Allowing the bedroom to be too bright. In this regard. than with the long-acting agents. too cluttered. and reminiscing. planning. Daytime napping at least two times each week 2. zaleplon. too cold. Experiencing frequent periods (two to three times per week) of extended amounts of time spent in bed 4.g. studying. even though minor interindividual differences in susceptibility to one or more of their effects are the rule. Having variable wake-up times or bedtimes 3. Routinely using products containing alcohol. Adapted from American Sleep Disorders Association: The International Classification of Sleep Disorders: Diagnostic and Coding Manual.

The following case is illustrative: A 76-year-old woman was admitted to the hospital for evaluation of mental cloudiness and lethargy. Sedative-hypnotics.5–5 0. and the fact that she had started taking 5 mg of diazepam per night for sleep about 2 months before admission .250 0.5–1 50–100 50–500 500–1. paradoxical agitation. and mild but sometimes disturbing amnesia in some elderly patients.5–2 15–30 2.318 Clinical Manual of Geriatric Psychiatry Table 8–4. with dosage and duration of action Generic name (trade name) Benzodiazepine hypnotics Flurazepam (Dalmane) Temazepam (Restoril)a Triazolam (Halcion) Benzodiazepine anxiolytics Lorazepam (Ativan)a Oxazepam (Serax)a Diazepam (Valium) Alprazolam (Xanax) Barbiturates Pentobarbital (Nembutal) Secobarbital (Seconal) Others Chloral hydrate (many) Glutethimide (Doriden) Methyprylon (Noludar) Zolpidem (Ambien)a Zaleplon (Sonata)a Eszopiclone (Lunesta)a a Dose (mg) Duration of action 15–30 15–30 0. the short-acting agents named above (temazepam. or oxazepam) are much preferred over long-acting agents (diazepam or flurazepam) because of the risk with the latter of building up potentially intoxicating blood levels of very long-acting active metabolites.125–0. lorazepam.000 25–250 100–200 5–10 5–10 1–2 Long Short Ultrashort Short Short Long Intermediate Intermediate Intermediate Intermediate Intermediate Intermediate Short Ultrashort Short Agents recommended for use in elderly persons. Comprehensive medical and neurological workup failed to identify a cause of her symptoms. For long-term use. short acting but should be avoided because of its propensity to cause ataxia.

Some clinicians attempt to avoid the development of tolerance by prescribing two or three different benzodiazepines concurrently. Zolpidem has a half-life of about 2 hours. has no active metabolites. 2000).Other Common Mental Disorders of the Elderly 319 was initially ignored. 2005. Nonbenzodiazepine Hypnotics Three nonbenzodiazepine agents have been shown to be safe and effective for elderly patients with primary insomnia: zolpidem (Shaw et al. 1996) suggested that zolpidem is safe to administer to patients with chronic obstructive pulmonary disease. Each agent produces sleep by selectively binding to the γ-aminobutyric acid (GABA)A1 receptor. It is as effective as zolpidem and produces even less next-day psychomotor impairment. One study (Girault et al. zaleplon (Hedner et al. It has little anxiolytic or anticonvulsant effect and causes few side effects beyond mild dizziness and nausea. Zammit et al. 2004). and eszopiclone (R. as measured by wake time . with some reporting minor increases in delta sleep. although this may be largely because of its more rapid elimination. but definitive data have not yet been published. The nonbenzodiazepine agents. Because benzodiazepine hypnotic agents begin to lose effectiveness after several weeks of nightly ingestion. no formal research data supporting this practice have yet been published. with emphasis on the advantages of irregular administration. and each is comparable to benzodiazepine hypnotics in terms of efficacy but produces somewhat less next-day drowsiness and cognitive impairment. and “rebound” insomnia after the drug has been eliminated has not been observed. Rosenberg et al. Although this approach has been successful in certain instances. it is important to provide detailed instructions on their use. particularly eszopiclone. 1992). Subsequent consultation with a geriatric psychopharmacologist led to discontinuation of the diazepam and rapid amelioration of her symptoms. with instructions to the patient to alternate between the medications weekly. Controlled studies have not identified any side effects in excess of those produced by placebo. Neither zolpidem nor zaleplon has consistently shown sleep maintenance efficacy. and does not accumulate during repeated administration. may be effective for longer than a few weeks. Zaleplon has a half-life of about 1 hour and also has no active metabolites to accumulate. Studies of its effects on sleep architecture are equivocal.

and because the currently middle-aged cohort has an increased incidence of substance abuse. but in low doses (i. Eszopiclone is rapidly absorbed. like the benzodiazepine hypnotics. The trend is already occurring: Grant et al. and restorative sleep—and studies in the elderly suggest that it is safe and effective at dosages up to 2 mg/night. It should also be noted that insomnia remains an “off-label” (i. Among primary care patients. which some sleep researchers believe are the most refreshing stages of sleep.S. eszopiclone. As the elderly population increases in the next decade. indication for use of trazodone. However. trazodone. not approved by the U. It has been shown to be an effective hypnotic in patients with selective serotonin reuptake inhibitor–induced insomnia (Kaynak et al. is associated with next-day somnolence and mild impairment on some measures of cognitive function. less strict criteria lead to higher estimates.e. the absolute number of older people with substance abuse problems will rise.. Alcohol Abuse and Dependence Epidemiology The prevalence of alcohol abuse and dependence in community-dwelling elderly persons ranges from 2% to 4% (Adams and Cox 1995) when DSMIII (American Psychiatric Association 1980) criteria are used. the frequency of problems among elderly persons is expected to increase as well. the prevalence is 8%–15% (Oslin 2004). 50–75 mg) it is well tolerated and effective in inducing sleep and has the theoretical advantage over several of the agents listed above of maintaining or actually increasing delta sleep (Stages III and IV) (Scharf and Sachais 1990). Trazodone Trazodone is not marketed as a hypnotic. It has been shown to produce improvement in all four domains of insomnia—including sleep onset. unlike the newest entry in the nonbenzodiazepine hypnotic category. sleep maintenance.. and surveys of hospitalized elderly persons and those in nursing homes have produced prevalence estimates from 8% to around 50% (Johnson 2000). 2004). with a time to peak concentration of approximately 1 hour and a half-life of 5–6 hours. (2004) con- .320 Clinical Manual of Geriatric Psychiatry after sleep onset.e. which is a single-isomer cyclopyrrolone agent. sleep duration. although widely recognized. Food and Drug Administration).

Cognitive impairment severe enough to meet DSM-IV-TR criteria for dementia is common in active elderly drinkers but typically resolves during the first few weeks of abstinence as the acute effects of intoxication.8-fold increase in the rate of alcohol abuse in people age 65 and older. which is defined in Table 8–5. from the generally less severe syndrome of substance (alcohol) abuse. Associated Psychiatric Conditions Besides intoxication and withdrawal.. but one survey (Moos et al. Most elderly alcoholic patients began drinking in young adulthood. The proper diagnosis of cognitive deficits that persist in the sober elderly alcoholic person may be challenging. these deficits are often attributed to varying combinations of age-associated memory impairment. but in clinical practice. one done in 1991–1992 and the other in 2001–2002. 2005) found that increased health problems in elderly individuals predicted reduced alcohol consumption 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. Risk Factors Risk factors for development of alcohol abuse or dependency in late life have been difficult to pin down. Korsakoff-type amnesia (i. but a significant proportion (up to 30%) do not develop a problem with alcohol until late life.25% in 1991–1992 to 1. compromised liver function. and found a 4.e. All studies find that men are much more likely to be problem drinkers than are women. from 0.Other Common Mental Disorders of the Elderly 321 trasted alcohol abuse prevalence rates from two comparable national surveys. 49). which is defined in Table 8–6. poor nutrition. Diagnostic Criteria DSM-IV-TR distinguishes substance (alcohol) dependence.21% in 2001–2002. and alcohol-induced mood changes diminish. isolated short-term mem- . the major mental syndromes associated with alcohol abuse and dependence in the elderly are cognitive impairment and depression. and several patterns of relation to age at onset have been identified.

322 Clinical Manual of Geriatric Psychiatry

Table 8–5. Summary of DSM-IV-TR criteria for substance dependence
A maladaptive pattern of substance use, leading to clinically significant impairment or distress, as manifested by three (or more) of the following, occurring at any time in the same 12-month period: (1) tolerance, as defined by either of the following: (a) a need for markedly increased amounts of the substance to achieve intoxication or desired effect (b) markedly diminished effect with continued use of the same amount of the substance (2) withdrawal, as manifested by either of the following: (a) the characteristic withdrawal syndrome for the substance (b) the same (or a closely related) substance is taken to relieve or avoid withdrawal symptoms (3) the substance is often taken in larger amounts or over a longer period than was intended (4) there is a persistent desire or unsuccessful efforts to cut down or control substance use (5) a great deal of time is spent in activities necessary to obtain the substance, use the substance, or recover from its effects (6) important social, occupational, or recreational activities are given up or reduced because of substance use (7) the substance use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by the substance
Source. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision. Washington, DC, American Psychiatric Association, 2000. Copyright © 2000, American Psychiatric Association. Used with permission.

ory deficit), and underlying focal or diffuse vascular and/or degenerative brain disease. Oslin and colleagues (1998) reviewed the literature on this topic and proposed a set of research diagnostic criteria for “alcohol-related dementia” (see Table 8–7), which they then validated in a later study of 192 institutionalized veterans (Oslin and Cary 2003). The 10.1% of the veterans with dementia who met criteria for alcohol-related dementia were younger (mean age=66.8 years) than those with Alzheimer’s disease, vascular dementia, or mixed dementia (mean age= 74.7, 74.3, and 73.2 years, respectively)

Other Common Mental Disorders of the Elderly 323

Table 8–6. Summary of DSM-IV-TR criteria for substance abuse
A. A maladaptive pattern of substance use leading to clinically significant impairment or distress, as manifested by one (or more) of the following, occurring within a 12-month period: (1) recurrent substance use resulting in a failure to fulfill major role obligations at work, school, or home (2) recurrent substance use in situations in which it is physically hazardous (3) recurrent substance-related legal problems (4) continued substance use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of the substance The symptoms have never met the criteria for substance dependence for this class of substance.

B.

Source. Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision. Washington, DC, American Psychiatric Association, 2000. Copyright © 2000, American Psychiatric Association. Used with permission.

and, unlike subjects with Alzheimer’s disease, vascular dementia, or mixed dementia, did not show declines in cognitive or physical functioning over a 24month 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 depressive 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 depression or suicidality, and a family history of depression (Atkinson 1999).

Assessment
Accurate histories of alcohol use in adults can often be augmented by embedding 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 Identification Test (AUDIT; Saunders et al. 1993), and the five-item AUDIT-5

324 Clinical Manual of Geriatric Psychiatry

Table 8–7. Classification of probable alcohol-related dementia (ARD)
Criteria for the clinical diagnosis of probable ARD include the following: 1. A clinical diagnosis of dementia at least 60 days after the last exposure to alcohol 2. Significant alcohol use, as defined by a minimum average of 35 standard drinks per week for men, and 28 for women, for a period greater than 5 years. The period of significant alcohol use must occur within 3 years of the initial onset of cognitive deficits. B. The diagnosis of ARD is supported by the presence of any of the following: 1. Alcohol-related hepatic, pancreatic, gastrointestinal, cardiovascular, or renal disease; that is, other end-organ damage 2. Ataxia or peripheral sensory polyneuropathy (not attributable to other specific causes) 3. Beyond 60 days of abstinence, the cognitive impairment stabilizes or improves. 4. After 60 days of abstinence, any neuroimaging evidence of ventricular or sulcal dilatation improves. 5. Neuroimaging evidence of cerebellar atrophy, especially of the vermis C. The following clinical features cast doubt on the diagnosis of ARD: 1. The presence of language impairment, especially dysnomia or anomia 2. The presence of focal neurological signs or symptoms (except ataxia or peripheral sensory polyneuropathy) 3. Neuroimaging evidence of cortical or subcortical infarction, subdural hematoma, or other focal brain pathology 4. Elevated Hachinski Ischemia Scale score D. Clinical features that neither are supportive nor cast doubt on the diagnosis of ARD include 1. Neuroimaging evidence of cortical atrophy 2. The presence of periventricular or deep white-matter lesions on neuroimaging, in the absence of focal infarct(s)
Source. Adapted from Oslin and Cary 2003; Oslin et al. 1998.

A.

(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’Connell et al. (2004) reported that the CAGE Questionnaire “performed poorly

Other Common Mental Disorders of the Elderly 325

in psychiatric populations” but were more enthusiastic about the AUDIT-5, which, they stated, “may prove more useful in older people with psychiatric illness.”

Treatment—Brief Counseling and Psychotherapy
Simple advice and counseling provided by primary care physicians have been shown to be effective in reducing problem drinking among high-risk (i.e., heavy-drinking) older adults (Fleming et al. 1999). In this study, two 10- to 15-minute counseling sessions resulted in a 34% reduction in 7-day alcohol use, 74% reduction in mean number of binge-drinking episodes, and 62% reduction in the percentage of patients drinking more than 21 drinks per week in the intervention group compared with the control group. The research literature generally suggests that treatment of established alcohol abuse and dependence in the elderly follows principles appropriate for young and middleaged adults and depends on the severity of the problem, the financial and social resources of the patient, and the patient’s motivation. Combinations of individual and group counseling, treatment of associated physical and mental conditions, and referral to outpatient, partial hospital, and inpatient programs can be expected to result in outcomes as good as or better than in younger individuals.

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 improvement was seen in total abstinence, but half as many naltrexone-treated subjects relapsed to significant drinking compared with those who received placebo. The medication was well tolerated and had few side effects beyond nausea and dizziness. Acamprosate (calcium acetylhomotaurinate) is the newest pharmacological agent approved for the treatment of alcoholism. It is a derivative of the essential amino acid taurine and is structurally similar to GABA. Acamprosate 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

for alcohol dependence in adults and “appears to be especially useful in a therapeutic approach targeted at achieving abstinence” (p. 811). Side effects are minimal and include diarrhea, headaches, nausea, and pruritus. Disulfiram is the best-studied agent for promoting abstinence but is seldom used in elderly patients because of the risks of serious adverse reactions.

Other Psychoactive Substance Abuse and Dependence
Epidemiology
Abuse and dependence (as defined in DSM-IV-TR) involving substances other than alcohol appear to be quite rare in elderly individuals, but a prospective, blinded observational study of patients age 60 years or older who presented to a large urban emergency department over a 6-month period found that 2% of these patients had positive urine test results for cocaine (Rivers et al. 2004). Cocaine-positive patients were older, more frequently male, and more than five times as likely to have alcohol or drug abuse diagnoses as those with negative urine test results. This rate is three times higher than the 0.6% rate for all illicit drug use in this age group estimated by the National Household Survey on Drug Abuse (Substance Abuse and Mental Health Services Administration 2001) and suggests that official surveys may underestimate the actual prevalence of illicit drug use among the elderly. More typical findings emerged from a study of 100 elderly patients hospitalized for substance abuse: female sex was a risk factor for drug dependence, almost all cases involved sedative-hypnotics (primarily benzodiazepines), and physical health problems involving chronic pain were common (Finlayson and Davis 1994). This extreme version of a pattern of misuse has been termed nonmedical use and is defined as use of pain relievers, tranquilizers, stimulants, or sedatives that were not prescribed for the individual, or use of the drug only for the experience or feeling it caused (Zarba et al. 2005). According to a study by Zarba et al. (2005), such use among those 65 or older declines in comparison to those ages 50–64, but the likelihood increases among those who smoke cigarettes and drink alcohol and is highest among older Americans who smoke, drink, and use cannabis. The authors interpreted this finding as “carrying habits into old age” because the association between cannabis use and other drug

Other Common Mental Disorders of the Elderly 327

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 substances. In this regard, acetaminophen-containing compounds, such as hydrocodone 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 transplantation was necessitated by addiction to opioid-acetaminophen preparations.

Common Patterns of Abuse
Table 8–8 lists drugs that are abused or misused by elderly patients and that should be inquired about in any suspect cases. In addition to simple overuse or underuse of prescribed and over-the-counter drugs, the clinician should inquire about timing of drug ingestions, because significant problems could arise from combining several agents in the following list: • • • Benzodiazepine anxiolytics and antihistamines (additive sedation) Narcotic analgesics and antihistamines (additive sedation, constipation) Decongestants and caffeine (additive stimulation)

Distinguishing Use From Abuse
Distinguishing use from abuse is difficult in any age group, but it is particularly challenging in elderly patients, which may partially explain why so many cases—more than 95% in one study (McInnes and Powell 1994)—are overlooked by physicians. Several of the factors discussed earlier regarding the negative effects of alcohol apply here as well: 1) adverse consequences of medication misuse such as falls, burns, generalized weakness, and sleep disturbance may be misattributed to other medical conditions or may not be reported because of age-related memory impairment exacerbated by the effects of the abused substance itself; 2) obvious mental status changes due to medication abuse (e.g., somnolence, depression, poor attention and concentration) may be ascribed to other causes (age, vascular or degenerative dementia, functional

328 Clinical Manual of Geriatric Psychiatry

Table 8–8. Psychoactive substances abused by elderly patients
Cold preparations containing anticholinergic antihistamines Chlorpheniramine Diphenhydramine Cold preparations containing stimulating sympathomimetics Ephedrine Phenylephrine Phenylpropanolamine Pseudoephedrine Narcotic analgesics Codeine Oxycodone Propoxyphene Nonnarcotic analgesics Acetaminophen Aspirin Other nonsteroidal anti-inflammatory agents Over-the-counter products containing caffeine or alcohol Sedative-hypnotics Barbiturates Benzodiazepines Chloral hydrate Over-the-counter antihistamines

mood disorder); and 3) other negative consequences of substance abuse may be disregarded entirely (e.g., symptom breakthrough caused by skipped doses of medications prescribed for chronic physical illness, such as congestive heart failure) or may be recognized but inappropriately considered an acceptable side effect of or adverse reaction to an otherwise effective medication regimen.

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) recommends physicians consider before prescribing potentially addictive medica-

Other Common Mental Disorders of the Elderly 329

tions to elderly patients. Recognition of the existence of a substance abuse problem and the necessity of its treatment is also important: Brennan and colleagues (2001) found that fewer than 25% of elderly Medicare beneficiaries whose substance abuse had been identified in the hospital obtained outpatient treatment in the 4 years following hospital discharge. These researchers suggest that treating professionals need to take an active role in follow-up with these patients. Once substance abuse or dependence has been identified and acknowledged, the specific approach is dictated by clinical circumstances. Detoxification in the hospital is often the first step and should be considered whenever drug effects are obvious and the precise identity of the drugs and their dosages cannot be reliably ascertained. After detoxification, communitybased programs that incorporate home visits, individual and family counseling, recommendations for medication changes, and involvement in a peer support or education group have been shown to be effective (Brymer and Rusnell 2000) in reducing misuse of prescription medications. The clinician should attempt to enlist the spouse, other family members, the patient’s other physicians, and, when possible, the local pharmacist to help maintain surveillance and control of availability of substances. Sponsors of nursing homes and administrators at retirement hotels are often willing and able to assist in this manner as well, and a firm therapeutic alliance with the patient, in the context of which are discussed the patient’s fears that his or her real or imagined symptoms will go untreated if abused substances are not available, can be extremely important and may in itself obviate the need for specific intervention.

Sexual Dysfunction
Sexual Dysfunction Versus Normal Aging Changes
In general, the diagnosis of sexual dysfunction is based on reduced function in one or more of the first three phases of the sexual response cycle: 1. The desire phase (DSM-IV-TR hypoactive sexual desire disorder) 2. The excitement phase (DSM-IV-TR male erectile disorder, female sexual arousal disorder) 3. Orgasm (DSM-IV-TR male or female orgasmic disorder)

hoarding of drugs. or obtaining drugs from multiple physicians)? Is other drug-related impairment evident (e. The investigators reported consistent declines in frequency of intercourse. and disability warrant the drug use? Have appropriate nonpharmacological therapies been used when indicated? Have pharmacological agents with less potential for long-term problems and dependence been used if appropriate (e. The probability of minimal erectile dysfunction was constant at 17% throughout the age range.. The Massachusetts Male Aging Study found that the probability of complete erectile dysfunction tripled from 5% to 15%. This study also surveyed changes in male sexual activity over a 9-year follow-up period. however (Levine 2000). Adapted from Juergens SM: “Prescription Drug Dependence Among Elderly Persons. but the largest declines were in men ages 60–70 at entry into the study (Araujo et al. 1994. between ages 40 and 70 years. These data indicated that as men age.g. sexual arousal will take more time and more stimulation. sexual desire.330 Clinical Manual of Geriatric Psychiatry Table 8–9. and that of moderate erectile dysfunction doubled from 17% to 34%.” Mayo Clinic Proceedings 69:1215–1217. Similar results were found in the Global Study of Sexual Attitudes and Behaviors (Laumann et al.. uncontrolled dose escalation. they should expect that sexual desire will gradually diminish. erections .g. particularly in men. Because normal aging is associated with reduced function in all three areas. 2005). frequency of erections. if not. distress. Factors to consider before prescribing potentially addictive substances for elderly patients Do the diagnosis. and. have the diagnosis and treatment been reconsidered? Has the patient had other drug or alcohol dependence or abuse problems in the past (a major relative contraindication to use of addictive drugs)? Do any findings suggest addiction to the prescribed drug (e. 2004). memory or psychomotor disturbance)? Can a family member or significant other confirm the effectiveness of the drug as well as the absence of impairment and addiction? Would tapering the dose of the drug (after an appropriate trial) help determine whether problems are related to the drug or whether further treatment is needed? Source.. and satisfaction with sex in all age groups. diagnosis of the above sexual dysfunctions in elderly patients requires that the clinician take normal aging changes into account.g. buspirone hydrochloride for anxiety or nonopioid analgesics for pain)? Is the drug yielding an acceptable therapeutic response with use of appropriate doses (often lower in elderly than in younger patients).

almost all of which increase in prevalence with age. This relative “immunity” to age-related problems notwithstanding. ejaculation may be diminished in vigor. Nevertheless.000 men with erectile dysfunction and found that more than 60% of those ages 65–85 had hypertension. the reported prevalence of sexual activity in older women is somewhat lower than in elderly men and appears to be influenced more by the availability of a secure partner (Mooradian and Greiff 1990). with the percentage declining to 43% in men older than 75 (Diokno et al. (2004) analyzed medical records of more than 272. hyperlipidemia. premature ejaculation is somewhat less likely to occur late in life but can occur in men at any age. less vaginal lubrication (which can contribute to the development of the sexual pain disorders dyspareunia and vaginismus). peripheral vascular disease. Sexual Dysfunction and Physical Illness One of the most common causes of physiological erectile dysfunction in men is prostate surgery. Seftel et al. the Global Study of Sexual Attitudes and Behaviors found that increased age among women was not reliably associated with any sexual dysfunction except lubrication difficulties (Laumann et al. 1990). and several other conditions. in one survey. and orgasm may not occur during every episode of intercourse. Erectile dysfunction is also strongly associated with hypertension. Despite these possible problems. more than 50% had hyperlipidemia. Because of the natural lengthening of the plateau phase of arousal. Perineal prostatectomy is the most likely cause of impotence. About 13% had the triad of hypertension.Other Common Mental Disorders of the Elderly 331 will be softer and not last as long. The authors concluded that “ED [erectile dysfunction] is a pathophysiological event that shares common . diabetes mellitus. followed by retropubic prostatectomy and transurethral prostatectomy. with some reporting increased ease of orgasm with age. The ability to have orgasm per se is more inconsistently affected. Women may notice several changes with advancing age: reduced desire for sex. reduced clitoral and breast sensitivity. and reduced intensity of the muscular phase of orgasm (due to reduced perineal muscle tone). 2005). and 6% had depression. about 25% had diabetes. and diabetes. almost 74% of the married men older than 60 reported being sexually active. ischemic heart disease. about two-thirds of men remain potent after retropubic procedures. Despite these age-related changes. hyperlipidemia.

treatment of underlying physical and mental illnesses. all of which can impair erectile and ejaculatory function. “Mood Disorders—Treatment”). clonidine. particularly guanethidine. Treatment Adjustment of offending medications. 2344) and advised physicians to view erectile dysfunction as a clinical marker for detecting and treating these conditions at an early stage. and optimization of general health are the treatments of first choice for diminished libido and anorgasmia in elderly men and women. often. testosterone therapy in the low-dose regimens is efficacious for the treatment of low libido in postmenopausal women who are adequately estrogenized. When these steps are ineffective. Psychopharmacological agents. Sexual side effects of psychopharmacological agents are common in patients with severe mental illness and are a major cause of noncompliance.P.) Whether age is a risk factor for these adverse effects is not clear. Clinical studies support the idea that androgens stimulate sexual desire and satisfaction and demonstrate improved sexual enjoyment and well being in women who switched from estrogen alone to estrogen–androgen therapy. but a complete sexual history should address the potential contribution of these agents. patients are reluctant to discuss these side effects with their doctors (K. Trazodone has been reported in a relatively small number of patients to cause painful and prolonged erection (priapism) that can require surgical reduction and result in permanent damage. also have been implicated in erectile and ejaculatory dysfunction. (p. According to a review by Bolour and Braunstein (2005). 406) . monoamine oxidase inhibitors. diabetes and depression” (p. and dosage adjustment or replacement should be attempted before more specific therapy is prescribed.332 Clinical Manual of Geriatric Psychiatry etiological factors with hypertension. (Adverse medication effects are discussed more fully in Chapter 4. hyperlipidemia. methyldopa. and venlafaxine can also cause anorgasmia in men and women. including cyclic antidepressants and neuroleptics. treatment with testosterone may be effective. 2003). and the β-blockers. Rosenberg et al. Sexual Dysfunction and Medications The worst drug offenders vis-à-vis sexual dysfunction appear to be antihypertensive medications. and selective serotonin reuptake inhibitors (see Chapter 4.

but testosterone replacement enhances the response. or masturbation frequency. but Gray et al. high cholesterol. and is likely to be effective in hypogonadal men as well. 2005). Although response rates of up to . and libido but not correlated with changes in spontaneous erections. and is probably not within the range of expertise of the typical geriatric psychiatrist. intercourse frequency. at least in diabetic men (Kalinchenko et al. high blood pressure.Other Common Mental Disorders of the Elderly 333 The results of testosterone therapy in elderly men are somewhat more complex. Smoking cessation. and tadalafil. cigarette smoking. a procedure that was the most common medical therapy for erectile dysfunction before the approval of sildenafil. Second-line treatment options for erectile dysfunction include intracavernosal self-injection. 3845).libido and erectile function” (p. Other risk factors are thought to include tightly bundled nerves and blood vessels in the back of the eye (which are apparently detectable via ophthalmoscopic examination). (2005). Treatment of erectile dysfunction has been revolutionized by the phosphodiesterase-5 inhibitors. although not studied. 2000) have shown improvements in libido and erectile function with testosterone therapy. waking erections. The patient injects a vasoactive drug. 2003) and erectile dysfunction (Jain et al. Hypogonadism. Studies in men with hypogonadism (Steidle et al. All seem to be safe and generally effective in elderly men (Salonia et al. studying healthy elderly men with experimentally manipulated testosterone levels. is another promising approach to suboptimal response to sildenafil and probably vardenafil and tadalafil as well.. found improved libido only in subjects who received high doses of testosterone and who were sexually active at the beginning of the study. In addition to the precautions listed by the manufacturers. such as alprostadil or prostaglandin E1. directly into the penis to relax cavernous and arterial smooth muscle. vardenafil. 2003). and diabetes. recent reports of the new onset of nonarteritic anterior ischemic optic neuropathy (NAION). warrant additional caution in those with preexisting NAION. including sildenafil. Testosterone therapy for sexual dysfunction is not without risks. 2005). The authors concluded “that testosterone supplementation in older men can dose-dependently improve.. Total testosterone levels were significantly correlated with changes in overall sexual function. a type of blindness in men taking phosphodiesterase-5 inhibitors. especially in men with incipient prostate cancer. and more severe erectile dysfunction at baseline predict a poor response to sildenafil (Park et al. all conditions common among elderly men.

note that the presence of delirium or dementia rules out this condition. DSM-IV-TR criteria for this syndrome are summarized in Table 8–11.334 Clinical Manual of Geriatric Psychiatry 85% have been reported. In the medicated urethral system for erection. another 5 had “subclinical” organic personality syndrome. Each has advantages and disadvantages. a transurethral preparation of alprostadil was developed that does not require needle injections into the penis. penile fibrosis. penile pain. Koponen et al. This prevalence is similar to that reported by other investigators (Franulic et al. the patient uses a polypropylene applicator to insert a semisolid pellet containing alprostadil into the urethra. positionable. Definite personality disorder that would have met DSM-IV-TR’s broader criteria for personality change due to a general medical condition was diagnosed in another 14. and side effects include prolonged erection. 1997). Psychiatric Illness Related to a General Medical Condition Personality Change Due to a General Medical Condition Although personality changes are common in Alzheimer’s disease and vascular dementia and nearly universal in frontotemporal dementia. which was reported after 10. The three types of implants are semirigid. or 47% of the sample. and hematoma or ecchymosis. and consultation with a urologist experienced with these devices is recommended.7% of men (Padma-Nathan et al.9% of patients. personality change due to a general medical condition as defined in DSM-IV-TR is relatively rare. for an inclusive total of 28 of 60. the rate of treatment discontinuation is high. . and efficacy was similar regardless of age or the cause of erectile dysfunction. 2000). Because of the high dropout rate. The medicated urethral system for erection produced erections sufficient for intercourse in 65. The most common complaint was mild penile pain. Treatment of erectile dysfunction is summarized in Table 8–10.8% of alprostadil administrations in the home setting and by 32. (2002) diagnosed definite organic personality syndrome (by DSM-III-R [American Psychiatric Association 1987] criteria) in 9 of 60 patients evaluated an average of 30 years after sustaining head trauma. and multicomponent inflatable. The third-line intervention for treatment-resistant erectile dysfunction is surgical implantation of a penile prosthesis.

Determine patient and partner preferences C. in which the circuit connecting the anterior cingulate gyrus and ventral striatum is involved. and psychosocial history B.” International Journal of Impotence Research 11:59–74. Personality change due to a general medical condition without cognitive impairment (per DSM-IV-TR) has also been described in Sydenham’s chorea and in two prefrontal disconnection syndromes: 1) orbitofrontal syndrome. Sexual. and in which apathy is common (Mega and Cummings 1994). Intraurethral alprostadil B. 1999. if above is ineffective A. Change or discontinue offending medications B. Consultation with patient and partner A. Modify lifestyle D. Initial intervention A. Couples therapy V. for example. and 2) anterior cingulate syndrome. Physical examination C. vardenafil. prostaglandin E1) VI.Other Common Mental Disorders of the Elderly 335 Table 8–10. Replace hormones C. Assessment and treatment of erectile dysfunction I. Vacuum constriction devices C. if above is ineffective A. Although orbitofrontal syndromes may be classified as without cognitive def- . Corrective surgery IV. in which limbic structures and orbital prefrontal cortex are damaged by. Review findings B. disinhibition. Adapted from Process of Care Consensus Panel: “Position Paper: The Process of Care Model for Evaluation and Treatment of Erectile Dysfunction. Laboratory tests II. stroke. and mood elevation are common. trauma. First-line therapy. medical. Intracavernosal self-injection (alprostadil. Educate about erectile dysfunction III. tadalafil) B. if above is ineffective A. Second-line therapy. or tumor. Third-line therapy. and in which irritability. Oral agents (sildenafil. Diagnostic process A. Surgical prosthesis Source.

Source. or other important areas of functioning. D. 1993). The disturbance does not occur exclusively during the course of a delirium. DC. Beneficial effects of behavioral interventions have been reported in some patients with frontal lobe impairment. or completion of complex tasks). Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. poor planning. Summary of DSM-IV-TR diagnostic criteria for personality change due to a general medical condition A. American Psychiatric Association. or laboratory findings that the disturbance is the direct physiological consequence of a general medical condition. Washington. impairments in everyday executive functions are common (e. physical examination. There is evidence from the history. The disturbance causes clinically significant distress or impairment in social. however. Used with permission. treatment of personality change due to a general medical condition is aimed at amelioration of the specific medical condition judged to be causative in each case. C. Text Revision. whereas altering the environment to reduce the need for self-initiation is emphasized in more severely impaired patients (Sohlberg et al. reflecting the lability. If midline brain structures are involved (orbitomedial frontal syndrome). impulsivity. monitoring.. memory deficits and problems with inhibition may be observed on careful testing. 2000. Pearlson (2000) argued that multiple infarctions . Psychotic Disorder Due to a General Medical Condition Many general medical conditions have been identified as being capable of causing hallucinations or delusions. retraining of cognitive strategies is emphasized in mildly impaired patients. and distractibility that characterize this disorder. icit by DSM-IV-TR criteria. In general. particularly if the temporal lobe and limbic structures are affected. 4th Edition. These deficits may be less apparent on structured neurological or neuropsychological examination than in natural problem-solving situations. occupational. American Psychiatric Association. B. Copyright © 2000. E.g.336 Clinical Manual of Geriatric Psychiatry Table 8–11. A persistent personality disturbance that represents a change from the individual’s previous characteristic personality pattern. A review by Plotkin (1989) suggested that the most likely general medical causes of delusions in elderly patients are cerebral lesions associated with stroke or trauma. The disturbance is not better accounted for by another mental disorder.

potential endogenous causes are appropriately treated. that is. 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). and in delirium. allowing functional psychosis to be ruled out. cognitive disturbance will be present. and delirium. Psychosis has been reported as a consequence of vitamin B12 deficiency. these complaints can be exacerbated by depression and . a complete medical evaluation will identify the general medical condition judged to be etiologically related to the disturbance. dementia. In dementia. meningioma. and complex partial seizures have been associated with olfactory hallucinations and delusions. In most cases. Treatment of psychotic disorder due to a general medical condition is very similar to treatment of mood disorder due to a general medical condition. occasional frank clouding of consciousness. and variable cognitive disturbance will be seen. prominent deficits in attention and concentration. Some specific delusion-like false beliefs also have been observed in patients with damage to the occipital lobe (denial of blindness) and parietal lobe (denial of hemiparesis). the correct diagnosis of psychosis with sensory loss may be difficult to establish with confidence.Other Common Mental Disorders of the Elderly 337 that do not necessarily cause dementia (“multi-infarct disease”) are associated with late-life onset of schizophrenia. sometimes tactile. Inasmuch as sensory deficits have been cited as contributing factors in the development of functional psychosis in elderly patients. In this syndrome. Whether this syndrome should be thought of as a psychotic disorder secondary to a general medical condition or as lateonset schizophrenia cannot be determined from the available data. Blindness and deafness have been associated with visual and auditory hallucinations. hallucinations occur in an otherwise clear sensorium and are typically accompanied by persecutory delusions. and antiretroviral therapy. The differential diagnosis of psychotic disorder due to a general medical condition includes functional psychosis. and then therapy for residual symptoms is administered according to the guidelines for treatment of functional psychosis described in Chapter 7 (“Anxiety Disorders and Late-Onset Psychosis”). Alcoholic hallucinosis is a specific syndrome that occurs within 2–3 days after termination of drinking. frightening auditory or visual.

physical therapy.338 Clinical Manual of Geriatric Psychiatry anxiety and can be applied consciously or unconsciously as a means to gain attention and care. with some insight into the synergistic effects of mood state on pain. a mixed norepinephrine and serotonin reuptake blocker. 2005). Tramadol is a weak agonist of the mu opiate receptor and is indicated for treatment of moderate to moderately severe pain. may have antidepressant properties (Rojas-Corrales et al. Acetaminophen and tramadol. and persistent limitations in activities because of pain are likely (Moosey and Gallagher 2004). including relaxation techniques (e. However. despite evidence that the great majority of individuals who take opioids chronically for pain do not become addicted to these drugs (even though physical dependency may develop) and evidence that increased age is associated with reduced rate of development of tolerance to opioid medications (Buntin-Mushock et al. when chronic pain is combined with depression. It has weak opiate-like effects. Therefore. Duloxetine. It is not surprising that evidence suggests that elderly patients manage chronic pain quite well with available agents and that chronic pain is not a major determinant of the use of medical services (Cook and Thomas 1994). and pharmacological management (Schneider 2005). and has been reported to produce serotonin syndrome in combination with selective serotonin reuptake inhibitors. and evidence indicates that other mixed norepinephrine. 2002). Patients with no significant memory problems. Some clinicians are reluctant to prescribe chronic opioids because of the fear of addiction.. has been approved for the treatment of chronic pain due to diabetic neuropathy.and serotonin-enhancing agents are also effective for neuropathic pain (Bomholt et al. blocks reuptake of norepinephrine and serotonin. proper management of chronic pain entails assessment and manipulation of social support networks. are good candidates for such interventions. recognition and treatment of associated depressive and anxiety syndromes. nonsteroidal anti-inflammatory drugs (NSAIDs. Some elderly patients can also benefit from behaviorally oriented pain management training. topical agents. not the least of which is the challenge of assessing pain and its response to treatment when the patient is unable to . use of medical services is increased. 2005). Treatment of chronic pain in patients with dementia poses several problems.g. Ersek et al. 2003). and opioids are the mainstay of pharmacological treatment of chronic pain. particularly the selective cyclooxygenase-2 [COX-2] inhibitors).

more frequent and longer episodes. Bowie et al. 2000). 2001). (2005) found few differences in clinical characteristics between elderly patients with early-onset and elderly patients with late-onset (i. (2005) used a word-list-generating task to distinguish phonemic word fluency from semantic word fluency (semantic=generate words in a category—e.. Several visual analogue scales have been shown to be useful in this situation (Pautex et al.. phonemic= generate words starting with a particular letter—e. some differences in presentation of unipolar major depression in late life have been reported.. whereas negative symptoms are more variable. and more rapid cycling (Cutler and Post 1982) compared with younger bipolar patients. after age 50) bipolar disorder. 794). leading to the impression that their clinical status is improving. Bowie et al. However. (2005) concluded that “thought disorder does not appear to ‘burn out’ in chronic schizophrenia” (p. (2005) reported that verbal productivity declines with age and is correlated with worsening in Mini-Mental State Examination scores. animals. Some geriatric patients with schizophrenia may lose the skills necessary to report symptoms. Elderly patients with bipolar disorder have been reported to have generally less severe symptoms and less religiosity (Broadhead and Jacoby 1990).Other Common Mental Disorders of the Elderly 339 provide reliable information about the pain.8 times more likely to be female. and Rubey (2005) provides a good overview of chronic pain management in elderly patients with dementia. f) and found that the decline in elderly schizophrenic patients was in phonemic and not semantic fluency.g. Schizophrenia Positive symptoms tend to diminish in aging schizophrenic patients. but the trend among elderly schizophrenic patients seems to be toward improved social adaptation (Cohen et al. 2005). Kosmidis et al. except that those with late-onset bipolar disorder were 2. Sajatovic et al. Patients with schizophrenia have more age-related decline in cognitive function than do age-matched control subjects but much less than do patients with Alzheimer’s disease (Friedman et al.g. Influence of Aging on Disorders of Early Onset Mood Disorders As described in Chapter 3 (“Mood Disorders—Diagnosis”).e. .

most were crosssectional prevalence studies in community and treatment populations that used variable diagnostic criteria and inconsistent methodology. 2001). dependent. histrionic. Agronin and Maletta (2000) found that published studies generally agreed with the prognostic scheme proposed by Solomon (1981). However. Regarding the natural history of personality disorders. histrionic. 1994). schizoid. and schizotypal) either remain the same or worsen in late life. which claimed that individuals with PD [personality disorder] characterized by affective and behavioral lability (antisocial. and older depressed patients with personality disorder have more persistent declines in function and quality of life despite treatment (Abrams et al. and narcissistic) (Kunik et al. and obsessive-compulsive) among older adults than either Cluster A disorders (paranoid. (2003). borderline. and demonstrate persistent characteristics of rigidity and suspiciousness.340 Clinical Manual of Geriatric Psychiatry Personality Disorders Agronin and Maletta (2000) reviewed the literature on personality disorders in late life and found not more than “several dozen articles”. thereby allowing few reliable generalizations. 1994). narcissistic. 1994). schizoid. Molinari et al. individuals with PD characterized by overcontrol of affect and impulses (obsessive-compulsive. paranoid. but with depression and hypochondriasis as common endpoints. (p. Studies typically report a higher prevalence of DSM-IV-TR Cluster C personality disorders (avoidant. personality disorders are as prevalent among elderly patients in geropsychiatric inpatient units as in a young adult comparison sample (Ames and Molinari 1994. borderline. avoidant. and schizotypal) or Cluster B disorders (antisocial. On the other hand. Personality disorder as a comorbid condition appears to be significantly more common in patients hospitalized for depression than in those hospitalized for disorders of cognition (Kunik et al. Studies that used structured interviews suggested that the prevalence of personality disorders tends to decline with age in community-dwelling subjects. 7) A study by Engels et al. and dependent) demonstrate less impulsivity and aggression and have a tendency to improve in late life. which found that “community residents in the oldest age group reported more schizoid and more obsessive-compulsive characteristics compared to one or more of the younger age groups (and)…older mental health patients showed more schizoid disorder characteristics and fewer high-energy disorder characteristics compared to one or .

Neuropharmacology 48:252–263. Mikkelsen JD. For an excellent overview of the effects of personality factors on mental disorders in later life. Brower KJ. 4th Edition. MN. Am J Geriatr Psychiatry 9:67–71. Cox NS: Epidemiology of problem drinking among elderly people. Washington. Washington. see Seidlitz (2001). DC. Rochester. 447). duloxetine. 3rd Edition. 2000 American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. American Sleep Disorders Association. Alcohol Clin Exp Res 16:1029–1034. persistent and neuropathic pain. Int J Addict 30:1693–1716. Mohr BA. mirtazapine and citalopram in animal models of acute. American Psychiatric Association. et al: Personality disorder symptoms predict declines in global functioning and quality of life in elderly depressed patients. DC. Revised. Int J Geriatr Psychiatry 14:905–910. 2005 . American Psychiatric Association. Molinari V: Prevalence of personality disorders in community-living elderly. References Abrams RC. 1987 American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. 1997 Ames A. McKinlay JB: Changes in sexual function in middle-aged and older men: longitudinal data from the Massachusetts Male Aging Study. 1994 Araujo AB. 2001 Adams WL. 2005 Bomholt SF. Int J Impot Res 17:399–408. 1992 Bolour S. Schulenberg JE. J Am Geriatr Soc 52:1502–1509. Am J Geriatr Psychiatry 8:4–18. J Geriatr Psychiatry Neurol 7:189–194. alcoholism and ageing: a brief review.Other Common Mental Disorders of the Elderly 341 more of the younger patient groups” (p. provided further support for Solomon’s scheme. Blackburn-Munro G: Antinociceptive effects of the antidepressants amitriptyline. Washington. American Psychiatric Association. Spielman LA. Maletta G: Personality disorders in late life: understanding and overcoming the gap in research. 3rd Edition. 1999 Blow FC. DC. 2000 American Sleep Disorders Association: The International Classification of Sleep Disorders: Diagnostic and Coding Manual. 1980 American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. 1995 Agronin ME. 2004 Atkinson R: Depression. Braunstein G: Testosterone therapy in women: a review. Text Revision. Revised. et al: The Michigan Alcoholism Screening Test— Geriatric Version (MAST-G): a new elderly specific screening instrument. Alexopoulos GS.

Thomas MR: Pain and the use of health services among the elderly. J Geriatr Psychiatry Neurol 13:106–114. 2003 Finlayson RE. Turner JA. 2001 Broadhead J. 2003 Ersek M. McCurry SM. 2000 Conigliaro J. Herzog AR: Sexual function in the elderly. et al: Efficacy and safety of naltrexone and acamprosate in the treatment of alcohol dependence: a systematic review. De Broe ME: Analgesic abuse in the elderly: renal sequelae and management. Am J Psychiatry 162:793–795. Addiction 99:811– 828. Am J Geriatr Psychiatry 8:19–28. Haringsma R. Anesth Analg 100:1740–1745. et al: Personality disorders in the elderly compared to four younger age groups: a cross-sectional study of community residents and mental health patients. Brown MB. Moriyama K. et al: The longitudinal course of thought disorder in geriatric patients with chronic schizophrenia. 2005 Cohen CI. J Am Geriatr Soc 40:662–665. Friedman J. Munoz A. Buchanan RG. Welsh J. Can J Clin Pharmacol 7:161–166. Davis LJ Jr: Prescription drug dependence in the elderly population: demographic and clinical features of 100 inpatients. et al: Efficacy of a self-management group intervention for elderly persons with chronic pain. Clin J Pain 19:156–167. Jacoby R: Mania in old age: a first prospective study. Post RM: Life course of illness in untreated manic-depressive patients. 2000 Buchsbaum DG. 2000 Cook AJ. Phillip L. 1982 Diokno AC. Mayo Clin Proc 69:1137– 1145. Arch Intern Med 150:197–200. Blank K. J Aging Health 6:155–172. 1994 Cutler NR. Med Care 39:39–49. 1994 . Tsapelas I. Geppert JJ. Compr Psychiatry 23:101–115. 2005 Brennan PL. 2004 Bowie CR. Angeles M. Rusnell I: Reducing substance dependence in elderly people: the side effects program. McNeil M: Screening and identification of older adults with alcohol problems in primary care. et al: Schizophrenia and older adults: an overview: directions for research and policy. Kraemer K. Kagay CR. Int J Geriatr Psychiatry 5:215–222. Cohen GD. Drugs Aging 12:391–400. J Personal Disord 17:447–459. 1990 Elseviers MM. et al: Screening for drinking disorders in the elderly using the CAGE Questionnaire. Duijsens IJ. et al: Age-dependent opioid escalation in chronic pain patients.342 Clinical Manual of Geriatric Psychiatry Bouza C. et al: Predictors and outcomes of outpatient mental health care: a 4-year prospective study of elderly Medicare patients with substance use disorders. 1992 Buntin-Mushock C. 1998 Engels GI. 1990 Brymer C.

Horta E. vigilance. Kaynak D. Singh AB. Mihaltan F. Emilien G. Muir JF. et al: Six-year follow-up study of cognitive and functional status across the lifespan in schizophrenia: a comparison with Alzheimer’s disease and normal aging. Barry KL. Harvey PD. anatomic and psychosocial factors: a 6 month follow-up. Maturana R. 2004 Gray PB. 2000 Friedman JI. 1999 Franulic A. et al: Oral testosterone undecanoate reverses erectile dysfunction associated with diabetes mellitus in patients failing on sildenafil citrate therapy alone. Taiminen T. Gontcharov NP. et al: The effects of trazodone on sleep in patients treated with stimulant antidepressants. et al: Dose-dependent effects of testosterone on sexual function. The Zaleplon Clinical Investigator Study Group. DICP 24:971–975. et al: Effects of repeated administration of zolpidem on sleep. Raschko RR: A profile of alcohol and prescription drug abuse in a high-risk community-based elderly population. Kozlov GI. Dawson DA. Int J Geriatr Psychiatry 15:575–581. 2001 Girault C. 2004 Koponen S. 2005 Hedner J. mood. 2000 Juergens SM: Prescription drug dependence among elderly persons. 1991–1992 and 2001– 2002. Gozukirmizi E. 2002 Kosmidis MH. Portin R. Am J Psychiatry 159:1315–1321. Rademaker AW. et al: Brief physician advice for alcohol problems in older adults: a randomized community-based trial. et al: Verbal fluency in institutionalized patients with schizophrenia: age-related performance decline.Other Common Mental Disorders of the Elderly 343 Fleming MF. diurnal and nocturnal respiratory function. Psychiatry Res 134:233–240. Stinson FS. J Urol 164:371–375. McVary KT: Testosterone supplementation for erectile dysfunction: results of a meta-analysis. Chest 110:1203–1211. and visuospatial cognition in older men. J Clin Endocrinol Metab 90:3838–3846. Bozikas VP. 2005 . Vlahou CH. and physical performance in patients with COPD. Woodhouse LJ. 2003 Kaynak H. Mayo Clin Proc 69:1215–1217. Sleep Med 5:15–20. 1994 Kalinchenko SY. Manwell LB. J Fam Pract 48:378–384. Drug Alcohol Depend 74:223–234. Aging Male 6:94–99. 2000 Jinks MJ. 1990 Johnson I: Alcohol problems in old age: a review of recent epidemiological research. Brain Inj 14:431–439. Yaeche R. et al: Axis I and II psychiatric disorders after traumatic brain injury: a 30-year follow-up study. Int J Geriatr Psychiatry 15:704–712. et al: Zaleplon shortens subjective sleep latency and improves subjective sleep quality in elderly patients with insomnia. et al: The 12-month prevalence and trends in DSM-IV alcohol abuse and dependence: United States. Am J Psychiatry 158:1441–1448. 2000 Jain P. 1996 Grant BF. Coleman T. et al: Organic personality disorder after traumatic brain injury: cognitive.

Curr Gastroenterol Rep 1:42–49. 1997 . J Neuropsychiatry Clin Neurosci 6:358–370. et al: Diagnostic rate of comorbid personality disorder in elderly psychiatric inpatients. 2003 Oslin D. 1994 Monane M: Insomnia in the elderly. 2000 McClain CJ. GSSAB Investigators’ Group. Barry T. Rifai AH. 2005. Am J Geriatr Psychiatry 12:571–583. J Consult Clin Psychol 61:137–146. Ames A. Am J Geriatr Psychiatry 11:441–447. et al: Older adults’ health and changes in latelife drinking patterns. 1994 Molinari V. Liberto JG.nih. O’Brien J. Greiff V: Sexuality in older women. Kowatch RA. Am J Geriatr Psychiatry 5:324–332. et al: Naltrexone as an adjunctive treatment for older patients with alcohol dependence. Cummings JL: Frontal-subcortical circuits and neuropsychiatric disorders (comments). 1993 National Institutes of Health: NIH State-of-the-Science Conference Statement on Manifestations and Management of Chronic Insomnia in Adults (final statement). Chin AV. 1990 Moos RH. et al: A systematic review of the utility of selfreport alcohol screening instruments in the elderly. 1994 Laumann EO. Available at http://consensus. et al: Sexual problems among women and men aged 40–80 y: prevalence and correlates identified in the Global Study of Sexual Attitudes and Behaviors.344 Clinical Manual of Geriatric Psychiatry Kunik ME. Mulsant BH. Int J Impot Res 17:39– 57. Nicolosi A. Aging Ment Health 9:49–59. J Geriatr Psychiatry Neurol 7:209–215. O’Connell H. et al: Acetaminophen hepatotoxicity: an update. Essa M: Prevalence of personality disorders in two geropsychiatric inpatient units. Int J Geriatr Psychiatry 19:1074–1086. 1999 McInnes E. Powell J: Drug and alcohol referrals: are elderly substance abuse diagnoses and referrals being missed? BMJ 308:444–446. 1992 Mooradian AD. 1994 Mega MS. Accessed September 25. 2005 Moosey JM. 2004 Oslin DW. Arch Intern Med 150:1033–1038. 2004 Morin CM. Am J Psychiatry 151:603–605. Gallagher RM: The longitudinal occurrence and impact of comorbid chronic pain and chronic depression over two years in continuing care retirement community residents. J Clin Psychiatry 53(suppl):23–28. Hamilton F. et al: Cognitive-behavior therapy for late-life insomnia. Brennan PL. 2004 Oslin DW: Late-life alcoholism: issues relevant to the geriatric psychiatrist. Pain Med 5:335–348. August 18. Cary MS: Alcohol-related dementia: validation of diagnostic criteria. Barve S. 2005 Levine LA: Diagnosis and treatment of erectile dysfunction. Glasser DB.htm. Am J Med 109 (suppl 9A):3S–12S. Schutte KK. Price S. 2005.gov/2005/ 2005InsomniaSOS026html.

2002 Rosenberg KP. Campbell EA. in The American Psychiatric Press Textbook of Geriatric Neuropsychiatry. Gibert-Rahola J. 2005 . Life Sci 72:143–152. in helpless rats. 1997 Park K. 2005 Salonia A. for the Medicated Urethral System for Erection (MUSE) Study Group: Treatment of men with erectile dysfunction with transurethral alprostadil. 2000. 1998 Padma-Nathan H. 2004 Rojas-Corrales MO. American Psychiatric Association. et al: Alcohol related dementia: proposed clinical criteria. Lichstein KL. pp 831–839 Riedel BW. Montorsi P. et al: Safety and tolerability of oral erectile dysfunction treatments in the elderly. Acad Emerg Med 1:874–877. 2003 Rosenberg R. J Nerv Ment Dis 193:417–419. Caron J. Smith DM. et al: Feasibility and reliability of four pain selfassessment scales and correlation with an observational rating scale in hospitalized elderly demented patients. 1995 Rivers E. Edited by Coffey CE. DC. 2005 Rubey RN: Treatment of chronic pain in persons with dementia: an overview. et al: An assessment of the efficacy and safety of eszopiclone in the treatment of transient insomnia in healthy adults. Dwyer WO: Sleep compression and sleep education for older insomniacs: self-help versus therapist guidance. Cummings JL. et al: Screening for problem drinking in older people referred to a mental health service: a comparison of CAGE and AUDIT. pp 329–346 Philpot M. Berrocoso E. Pearson N. et al: Bipolar disorder in older adult inpatients. Ku JH. 2003 Plotkin DA: Organic delusional syndrome and organic hallucinosis. et al. Briganti A. Psychol Aging 10:54–63. 2005 Pearlson GD: Late-life–onset psychoses. Hellstrom WJ. et al: Cocaine use in elder patients presenting to an inner-city emergency department. Int J Geriatr Psychiatry 13:203–212. J Gerontol A Biol Sci Med Sci 60:524–529. American Psychiatric Press. et al: Antidepressant-like effects of tramadol and other central analgesics with activity on monoamines reuptake. Roth T. Koscis J.Other Common Mental Disorders of the Elderly 345 Oslin D. Sleep Med 6:15– 22. Shirazi E. Aurora T. et al: Survey of sexual side effects among severely mentally ill patients taking psychotropic medications: impact on compliance. 2005 Sajatovic M. Atkinson RM. Kaiser FE. Bleiberg KL. Herrmann F. Am J Alzheimers Dis Other Demen 20:12–20. 2005 Pautex S. Kim SW. J Sex Marital Ther 29:289–296. Petratou V. et al: Risk factors in predicting a poor response to sildenafil citrate in elderly men with erectile dysfunction. Drugs Aging 22:323–338. Aging Ment Health 7:171–175. Washington. in Treatments of Psychiatric Disorders: A Task Force Report of the American Psychiatric Association. DC. BJU Int 95:366–370. Le Lous P. Washington. 1989. N Engl J Med 336:1–7. Bingham CR.

1992 Sohlberg MM. 2004 Zarba A. Sun P. in Personality Disorders. Babor TF. et al: Development of the Alcohol Use Disorders Identification Test (AUDIT): WHO Collaborative Project on Early Detection of Persons With Harmful Alcohol Consumption—II. Jacoby K. comparative study of zolpidem and placebo in the treatment of insomnia in elderly psychiatric in-patients. 1993 Scharf MB. 1981. Available at: http:// oas. in National Household Survey on Drug Abuse. Edited by Lion JR. pp 310–338 Steidle C. Curson H. 1993 Solomon K: Personality disorders in the elderly. 1999. 2005 . Trevorrow T: Assessing sleep functioning in older adults. 30–31. Schwartz S. Caron J.samhsa. Baltimore. McNabb LJ. J Urol 171:2341–2345. 2004 Seidlitz L: Personality factors in mental disorders of later life. J Int Med Res 20:150–161. diabetes mellitus and depression in men with erectile dysfunction.age.346 Clinical Manual of Geriatric Psychiatry Saunders JB. J Clin Psychiatry 51(suppl):13–17. Am J Geriatr Psychiatry 9:8–21. Curr Med Res Opin 20:1979–1991. Addiction 89:791–804. Stuss DT: Contemporary approaches to the management of executive control dysfunction. and Management. 2005 Seftel AD. what now? Geriatrics 60:26–28. in Handbook of Assessment in Clinical Gerontology. Miller F: Unrecognized drug dependence in psychiatrically hospitalized elderly patients. J Clin Endocrinol Metab 88:2673–2681. Edited by Lichtenberg P. Sachais BA: Sleep laboratory evaluation of the effects and efficacy of trazodone in depressed insomniac patients. pp 331–350 Whitcup SM. J Am Geriatr Soc 35:297–301. Coquelin JP: A double-blind. New York. J Head Trauma Rehabil 8:45–58. J Am Geriatr Soc 53:170–171.htm#2. Wagner FA: Carrying habits into old age: prescription drug use without medical advice by older American adults.gov/nhsda/2k1nhsda/vol1/chapter2. 2006. hyperlipidemia. et al: Efficacy and safety of eszopiclone across 6weeks of treatment for primary insomnia. Diagnosis. MD. Wiley. 1990 Schneider JP: Chronic pain management in older adults: with coxibs under fire. 2003 Substance Abuse and Mental Health Services Administration: Illicit drug use. 1987 Zammit GK. Accessed February 28. Mateer CA. Swindle R: The prevalence of hypertension. Williams & Wilkins. et al: AA2500 testosterone gel normalizes androgen levels in aging males with improvements in body composition and sexual function. 2001. Storr CL. Aasland OG. 2001 Shaw SH.

We first discuss decisional competency.9 Competency and Related Forensic Issues The issue of competency arises in many contexts involving cognitively im- paired elderly individuals. expert consultation and testimony on competency. The chapter covers decisional competency. In this chapter. 347 . determination of competency to drive. gifts. and concerned friends or relatives may recommend that durable powers of attorney be executed or may contemplate guardianship or conservatorship. competency to care for oneself and manage one’s finances. and trusts. Attorneys may become concerned about future challenges to the provisions of wills. and elder abuse. Health care providers may question the patient’s ability to give informed consent for medical treatment or to make end-of-life decisions regarding resuscitation and life support. we address the specific social contexts in which the geriatric psychiatrist is most likely to perform a contemporaneous or retrospective evaluation of competency. or the ability to make an acceptably rational and self-interested single decision at a particular point in time. The main types of decisional competency are 1) to give informed consent for medical care. undue influence.

4. this chapter refers to California law. shelter. . The four components involve the ability to 1. readers are strongly urged to check the law applicable to their jurisdiction.e. 1636]) Decisional competency is only one of three equally important components of informed consent for medical care.) Decisional Competency Competency to Give Informed Consent for Medical Care Four components of decisional competency in the medical setting were distinguished by Appelbaum and Grisso (1988) and have been accepted by most authors. 2. 3) to give informed consent for enrollment in a research study. Functional competency entails multiple types of decisional capacity but adds the requirement of executive function. and medical care) and manage one’s finances.348 Clinical Manual of Geriatric Psychiatry 2) to execute an advance directive. and 5) to execute a will (testamentary capacity) or trust. Because statutory and governing case laws differ considerably from state to state. including motivation. it cannot be a result of coercion or threats (discussed in “Undue Influence: The Question of Voluntariness” later in this chapter). This requires both weighing the risks and benefits of a single option and the usually more complex process of weighing multiple options simultaneously.. and execution of goal-oriented sequences of behavior over time. 4) to enter into (and be held accountable for) a contract (contractual capacity). planning. “to reach conclusions that are logically consistent with the starting premises. The President’s Commission for the Study of Ethical Problems in Medicine and Biomedical and Behavioral Research (1982) concluded that the patient must be provided with appropriate information about the recommended medical intervention (the categories of information required by California law are listed in Table 9–1) and that the consent must be given voluntarily—that is.” [p. Communicate a choice Understand relevant information Appreciate the situation and its consequences Manipulate information rationally (i. prioritization. 3. or the ability to provide self-care (provide oneself with food. Next we discuss functional competency. clothing. (Note: For purposes of illustration and discussion.

the physician may administer appropriate emergency treatment until the patient is able to consent. in the case of a violent patient) if the intervention were delayed so that consent could be obtained. or defect that the person has The nature of the medical treatment that is being recommended by the person’s health care providers The probable degree and duration of any benefits and risks of any medical intervention that is being recommended by the person’s health care providers and the consequences of lack of treatment The nature. Simple consent similarly requires that the patient be competent and that the consent be voluntary but does not require the provision of a predetermined body of information to the patient by the physician.. the principle of implied consent applies: that is. a nonemergent situation in which no competent decision maker is available requires a specific court order for medical intervention (Cal Prob. and benefits of any reasonable alternatives Source. Competency to Execute an Advance Directive Advance directives are legal instruments intended to ensure that appropriate decisions regarding medical care are made when a patient becomes incompetent to give informed consent.” usually obtained at the time a patient engages a new physician or during the admission process (the “Terms and Conditions of Admission” typically include simple consent). attorney-in-fact for health care. Prob. risks. which are performed on the basis of “simple consent. Informed consent is generally not required for the great majority of medical interventions. and no substitute decision maker (e. next of kin) or advance directive is available.Competency and Related Forensic Issues 349 Table 9–1. disorder. Similarly. Code §813. In California. in which significant harm would come to a patient (or to others. or. Adapted from Cal. Neither informed nor simple consent is required in an emergent situation. given the opportunity. if the patient is unconscious or otherwise incompetent to participate in the consent process. Code §3201). self-interested patient would consent.g. guardian or conservator. The Patient Self-Determination Act of 1990 . Under these circumstances. the physician may perform the intervention to which a reasonable. Requirements of informed consent: what patients must be told about a proposed treatment The nature and seriousness of the illness. in some jurisdictions.

to give or withhold consent for medical care for the principal if the principal becomes incompetent. the preference to die at home). nursing homes. as well as particular preferences regarding treatment and the end of his or her life (e.350 Clinical Manual of Geriatric Psychiatry (P. (Uniform Durable Power of Attorney Act 1983. and other health care organizations provide information to patients about availability and use of these instruments. There are clear advantages and disadvantages to both types of directives. mandates that hospitals. “This power of attorney shall not be affected by disability of the principal. and the likely risks and burdens of treatment outweigh the expected benefits.” “some consciousness and in an irreversible condition of complete. such as the durable power of attorney for health care or health care proxy.L. specifying the limits of care to be given by health care providers if the individual “cannot make or communicate a choice regarding a particular health care decision. loss of ability to think or communicate with others. Legally defined. and a proxy can . 101-508). 3960) Some states have enacted similar laws creating the health care proxy. 1991. including “permanent unconsciousness. and instruction directives.” or “This power of attorney shall become effective upon the disability or incapacity of the principal” or similar words showing the intent of the principal that the authority conferred shall be exercisable notwithstanding the principal’s subsequent disability or incapacity.” It also has a section in which the individual can specify particular treatments that he or she does not want. usually a family member or spouse (the attorney-in-fact or agent). There are generally two types of advance directives: proxy directives. p. a durable power of attorney is a power of attorney by which a principal designates another his attorney in fact and the writing contains the words. A proxy has much more flexibility than an “instructive” has. which became federal law on December 1. such as the living will.. or nearly complete. and a section containing instructions regarding organ donation. A living will is a document that is created by an individual when he or she is of sound mind. Durable power of attorney for health care allows an individual (the principal) to authorize another person.” and “no more than some ability to think or communicate with others.” 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.g.

p.Competency and Related Forensic Issues 351 respond to circumstances that may not have been anticipated by the principal. Prob. Prob. psychosurgery. if the principal objects to the health care or to the withholding or withdrawal of the health care. a living will and durable power of attorney for health care or health care proxy can be combined. as much as possible. in accordance with the wishes. even if they are incompetent to make other medical decisions. The prevailing view is known as the doctrine of “substituted judgment. Conversely. Because advance directives are intended to be executed when the principal is competent to give or withhold consent for medical care. Much has been written about the question of which rules should govern the decisions of substitute decision makers such as attorneys-in-fact. California law prohibits the attorney-in-fact from consenting to placement in a mental health treatment facility. 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. the case is governed by the law that would apply if there were no durable power of attorney for health care” (Cal. 924). 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. different standards for competency to execute an advance directive may obtain in other states. values. Code §4120). In such a case. The court in a New Jersey case (In re Conroy 1985) spelled out a three-step protocol for analyzing the patient’s . Yet California law states. “A natural person having the capacity to contract may execute a power of attorney” (Cal. Code §4724). a proxy also can betray the trust of the principal by making decisions that the principal would not have endorsed. the powers of the attorney-in-fact differ from state to state. and goals of the principal. However. convulsive treatment.” according to which the substitute decision maker should act. sterilization. Prob. This section appears to reflect the will of the California legislature that individuals retain the authority to make end-of-life decisions. Code §4722) and also prohibits the attorney-in-fact from consenting to health care or consenting to the withholding or withdrawal of health care “necessary to keep the principal alive. In some states. or abortion (Cal. The alternative “best interests” approach calls on the substitute decision maker to perform an “objective assessment of the burdens and benefits for this patient” as the basis for his or her decision (Fellows 1998. In a similar vein.

hhs. Title 45 (Public Welfare). In making this assessment the IRB should take into account the purposes of the research and the setting in which the research will be conducted and should be particularly cognizant of the special problems of research involving vulnerable populations. with 21 recommendations. the President’s Commission clearly spelled out the disclosures required under ordinary circumstances (Table 9–2). pregnant women. In 1982. “When some or all of the subjects are likely to be vulnerable to coercion or undue influence. additional safeguards have been included in the study to protect the rights and welfare of these subjects” (italics added. Part 46 (Protection of Human Subjects). then attempt to deduce the patient’s wishes from his or her more generally held values. prisoners.S. the U.352 Clinical Manual of Geriatric Psychiatry wishes: First. . such as children. Specifically.gov/ ohrp/humansubjects/guidance/45cfr46. Food and Drug Administration published an “exception to informed consent” rule intended to govern research conducted in medically emergent circumstances. and the Code of Federal Regulations now includes minimal language aimed at protection of cognitively impaired subjects. if these steps leave the issue in doubt. Finally. pregnant women. In 1998. voluntary consent must have been obtained. revert to what a person in the patient’s situation might reasonably choose. Competency to Consent to Enrollment in a Research Study The considerations discussed earlier regarding competency to consent to medical care generally apply to competency to consent to enrollment in a study. the National Bioethics Advisory Commission (created by President Clinton in 1995) issued a lengthy report. (a) 3 states. the subject must have been supplied with appropriate information. original available at http://www. If these are not conclusive. and so on. “Research Involving Persons With Mental Disorders That May Affect Decisionmaking Capacity. mentally disabled persons.111 (criteria for Institutional Review Board [IRB] Approval of Research). religious beliefs. consider any statements or other directives made by the patient. prisoners. such as children. Before an investigator can claim to have secured informed consent.” whereas section (b) states. or economically or educationally disadvantaged persons. and in 1996. and the subject must have been considered competent.111). section 46. or economically or educationally disadvantaged persons. “Selection of subjects is equitable. mentally disabled persons.” but few recommendations were adopted. entitled.htm#46.

and appropriate alternatives A statement about the maintenance of confidentiality An explanation about possible compensation if injury occurs. indicating that refusal to participate involves no penalties or loss of benefits Source. but competency to enter into a contract and competency to give a gift during one’s lifetime (inter vivos) are treated as essentially the same in contemporary legal literature (Meiklejohn 1988–1989). oddly. in cases of research involving more than minimal risk Information about how the subject can have pertinent questions answered A statement about voluntary participation. or to retrieve assets already transferred per the terms of the contract or gift. reasonably expected benefits. on the basis of mental incapacity. Disclosures required for research subjects The fact that research is being performed and the purposes of the research Reasonably foreseeable risks. allows conservatees to marry). to manage his or her finances or resist fraud or undue influence. President’s Commission for the Study of Ethical Problems in Medicine and Biomedical and Behavioral Research 1982. Competency to Enter Into a Contract or Make a Gift The traditional view of contract versus property law distinguishes between the “future orientation” of contracts and the “present orientation” of a gift. Restatement of the Law Second. the establishment of a conservatorship generally creates an irrebuttable presumption that the conservatee lacks contractual and donative (but not testamentary) capacity (although California. Definitions of contractual capacity vary widely by jurisdiction. and 2) when the establishment of a conservatorship of estate (discussed in “Competency to Care for Oneself and Manage One’s Finances” later in this chapter) is under contemplation by a court because a proposed conservatee is thought to be unable. Geriatric psychiatrists are likely to confront the issue of contractual capacity in two situations: 1) when an individual who has entered into a contract or made a gift (the grantor) attempts to escape responsibility for the future performance demanded by the contract. Although courts have the authority to grant exceptions in specific cases. Contracts 2d (American Law Institute 1981) provides as follows: . on the basis of the claim that he or she lacked contractual competency at the time.Competency and Related Forensic Issues 353 Table 9–2.

In other words. but not entirely without understanding. spouse. and parents. typically elderly and cognitively impaired.354 Clinical Manual of Geriatric Psychiatry A person incurs only voidable contractual duties by entering into a transaction if by reason of mental illness or defect (a) he is unable to understand in a reasonable manner the nature and consequences of the transaction. and the other party to the contract must prove that the elderly individual possessed contractual capacity (Hankin 1995). made before his incapacity has been judicially determined. “A person entirely without understanding has no power to make a contract of any kind” (Cal. Civ. and remember and understand his or her relations to his or her living descendants. If it can be proved that a conservatorship could have been established. Competency to Make a Will Most states define testamentary capacity as the capacity to “understand the nature of the testamentary act. the usual assumption that every adult is competent for all legal purposes is reversed. Code §39).. Code §38) and “A conveyance or other contract made by a person of unsound mind. courts tend to give substantial weight to facts besides the degree of mental impairment of the grantor.. Civ. the terms of the contract or gift. (p. This statute provides a partial remedy for situations in which an individual. the fact that the grantor agreed to an obviously bad deal may be regarded as evidence supporting the claim that the grantor was incompetent. for unneeded home improvements) because of impaired judgment. and those whose interests are . 41) California law states. When a claim of contractual or donative incompetency is adjudicated.e. who qualifies for but has not (yet) been provided a conservator of estate has entered into an unwise contract (e. is subject to rescission” (Cal. or (b) he is unable to act in a reasonable manner in relation to the transaction and the other party has reason to know of his condition. Code §39).g. as opposed to the procedural fairness) of the transaction in question. The vagueness of these sections is partially remedied by the next section: “A rebuttable presumption affecting the burden of proof that a person is of unsound mind shall exist if the person is substantially unable to manage his or her own financial resources or resist fraud or undue influence” (Cal. such as the substantive fairness (i. understand and recollect the nature and situation of his or her property. Civ.

it is presumed that his will has been made during a time of lucidity” (Estate of Goetz 1967). Testamentary capacity is generally recognized as “only a modest level of competence (‘the weakest class of sound minds’)” (Estate of Rosen 1982). many judges. Although it is common knowledge among psychiatrists that a diagnosis alone does not imply any particular level of intellectual function or automatically determine the presence or absence of any type of competency. attorneys. the entire will or codicil (modification to an existing will) is invalid. all things else being equal. Accordingly. The trend of more recent cases. In many will contests. if lack of testamentary capacity is proved. Despite the fact that testamentary capacity is a low standard. such as Alzheimer’s disease and vascular dementia. it is almost always at the request of a competent testator or of his or her anticipated beneficiaries). and legal presumptions relating to this competency have traditionally also helped to set the bar fairly low. 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). even for brief periods. and juries are not in possession of this insight and may need to be educated through expert testimony. but the remainder remains valid if the will . he or she would not have done” (Cal. 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. In general. and because prospective evaluation of the testator is rarely performed (and if it is. except for the existence of the delusions or hallucinations. once testamentary capacity has been lost. 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. Prob. Any part of a will that is proved to be a result of undue influence is overturned. and a medical record containing the mere diagnosis of a neuropsychiatric illness is almost always enough. Code §6100. to encourage contestants to proceed. wills are vulnerable to challenge if an aggrieved party can produce any evidence of mental impairment in the testator.” Some states require only one or two of these criteria to be met.Competency and Related Forensic Issues 355 affected by the will. however. Because testamentary capacity is such a low standard. Besides the general presumption that the testator was competent at the time the will was executed. allegation of undue influence often proves to be the stronger case for the contestant. it is unlikely to return. has been toward increasing recognition that at least in the case of progressive illnesses. it has also been stated that “when one has a mental disorder in which there are lucid periods.5).

including discussion of the role of other parties (especially those affected by the decision). with more. provisions. and what alternatives to the decision the subject recognizes. But even if that standard did apply. Some courts have differentiated the standards of competency for trusts and wills on the basis of the fact that establishing a trust entails a step in addition to merely signing a set of instructions: the creator of the trust must also transfer his or her property to the trust. This interview should include discussion of the social. which is widely but not universally regarded as a higher level of competency than mere testamentary capacity.e.356 Clinical Manual of Geriatric Psychiatry without the influenced provisions still makes sense and the testator otherwise had testamentary capacity. the creator of the trust (who is usually the trustee) should possess contractual capacity. Moreover. medical circumstances surrounding the decision at issue (i. “Greater mental capacity is required to make a deed than is required to execute a will. (For example. This act would seem to require contractual or donative capacity. the testamentary standard of understanding the nature of the testamentary act would almost always require more intact intellectual function for a trust than that required for a will because trusts are generally more complicated than wills. Undue influence is discussed later in this chapter. Assessing Decisional Competency Clinical Interview The cornerstone of the assessment of decisional capacity is the clinical interview with the subject. and more detailed. a will is simply a piece of paper with a set of instructions. a trust serves the same function as a will. how the . whereas a trust is a more abstract entity that requires relatively intact higher intellectual functions to grasp. For example. in Citizen’s National Bank v. how the subject arrived at the decision. economic. and the relatively low standard for testamentary capacity should apply. Pearson [1978]..”) Another path to the same conclusion is the argument that because the trustee is endowed with the authority to enter into contracts involving the trust assets. if appropriate. who is affected by the decision. and how that party is affected). the discussion of a proposed trust amendment should include inquiry about what assets are entailed. and to that extent. Competency to Execute a Trust Trusts are increasingly popular instruments with which to determine the disposition of one’s assets after death. the court stated. and.

.Competency and Related Forensic Issues 357 trustee(s). anxiety. One author of this book (J. 2005). 2004) and for the fact that equally qualified experts often provide conflicting opinions under oath. and whether delusional thinking affected the decision. the extent to which the decision was influenced by interactions with others.” and so forth. it should be clear to the examiner whether the subject has the requisite understanding and appreciation of the consequences of the decision for the subject and all others affected. how the decision comports with previously held values and goals. and scores on tests of cognitive 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. Impairment in other domains of mental function (e.E. By the end of this discussion.g.” “recall and recollect. successor trustees.. in part. either spontaneously or in response to inquiry.) routinely administers a Folstein Mini-Mental State Examination (MMSE). Vellinga et al. and beneficiaries were selected.g. abnormal mood. the examiner is advised to administer a battery of standardized tests of cognitive function along with the clinical interview. . for the often observed lack of agreement between examiners in published studies of decisional competency (e. The conclusion 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 ability to “understand and appreciate. negatively affect competency. 1997. thought disorder) can.S. does the examiner require that the subject produce key information from memory. Tests of Cognitive Function To help mitigate the effects of the interrater variables described earlier. and what events and considerations led to the decision to amend the trust. That is. 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. or is the ability merely to recognize information acceptable (e. The discussion of a proposed medical intervention should cover the risks and benefits of the proposed intervention and the most reasonable alternatives and should include inquiries of the subject that allow her or him to paraphrase and manipulate the information provided and ask whatever questions that arise.. Marson et al. general information items from the Wechsler Adult Intelligence Scale. but cognitive ability is the most consistent correlate of decisional competence (Palmer et al. a 12-item Boston Naming Test. in principle. tests of remote memory (list the presidents.g.

tests of verbal comprehension.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?”). They include the MacArthur Competence Assessment Tool—Treatment (Grisso et al. including similarities. 2004). proverb interpretation. and gifts. the testator had no previous intention to leave the estate to anyone else. contracts. and other more focused tests as indicated. as compared with a situation in which a will contest is likely. and tests of frontal executive function. Susceptibility to undue influence is . Similarly. Undue Influence: The Question of Voluntariness As mentioned earlier. the threshold for competence should be adjusted according to the degree of harm associated with the subject’s choice. alternating design copying. and clock drawing. the question of undue influence is commonly raised in conjunction with a claim of lack of testamentary capacity and in connection with contested wills. in part because of their inability to adjust to unique situational factors. For example. 1997) and the Competence Assessment Tool for Psychiatric Advance Directives (Srebnik et al. including the consequences of the decision at issue. Standardized Tests of Decisional Competency The literature on competency generally agrees that standardized tests have had a limited role in competency determination. Several of the more recently developed standardized tests of competency allow the rater to adjust the threshold and may be useful as adjuncts to the clinical interview. 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. As Grisso and Appelbaum (1998) indicated. this battery is augmented with a “shopping list” test of new learning. The result is several subscale scores that can be incorporated into a competency determination. word-list generation. and the testator now intends to leave his or her estate entirely to that heir. When indicated. as compared with one that has a low ratio. These instruments assess a patient’s capacity for understanding. and reasoning by providing a body of information and then requiring the patient to respond to questions about that information. a lower level of understanding would be acceptable when a patient is consenting to a medical procedure with a high benefit-risk ratio. appreciation.

may be enough to shift the burden of proof to the recipient. or if the recipient unduly benefits from the gift or bequest. or spiritual adviser who fails to ascertain that a donor has received competent and independent advice.. and the underlying question of voluntariness is also relevant to the issue of informed consent for medical care.” as in the testamentary context. even evidence that the donor is passive or manipulable will suffice. The presumption of undue influence is strengthened if the donor is mentally weak. provisions in the will that are inconsistent with prior or subsequent expressions of the testator’s intentions. if the recipient actively procures the gift or bequest.e. or restraint. by themselves. Code §1575) In some jurisdictions. with regard to contracts. who then must prove that undue influence did not occur. church. merely consist 1) in the use. These include “unnatural provisions in the will. 2) in taking an unfair advantage of another’s weakness of mind. compulsion. A diagnosis of psychiatric illness in the allegedly influenced party will generally support a . was the testator’s mind so controlled by another person that his or her will is actually the will of another person? Depending on the situation. by one in whom a confidence is reposed by another. establish a presumption) of undue influence in a testamentary context. this “will substitution” may require an element of “coercion. or. p. A somewhat weaker set of factors are widely regarded as indicia (i. and a relationship between the testator and the beneficiary that created an opportunity to control the testamentary act” (Spar and Garb 1992. Civ. In the legal literature. 170). or who holds a real or apparent authority over him. of such confidence or authority for the purpose of obtaining an unfair advantage over him. and in some cases. The presumption of undue influence is also strengthened if the recipient is a clerical. 3) in taking a grossly oppressive and unfair advantage of another’s necessities or distress. the question of undue influence tends to be reduced to the “will substitution test”—that is. a diagnosis of mental illness or retardation is generally adequate to support this claim. or. such as that between an elderly patient with psychiatric illness and his or her primary caregiver.Competency and Related Forensic Issues 359 also one of the criteria for establishment of a conservatorship of estate in California and some other states. (Cal. they serve to strengthen a claim of undue influence but do not. the mere existence of a confidential and trusting relationship. Yet undue influence is a complex and poorly defined legal concept at best.

and even late-life marriages are typical results of this situation. it may be an easy matter for the younger person to create several of the circumstances listed by Singer (1992).” They are the production of isolation. That is. Particularly if there is no close family. 8) These factors notwithstanding. absent the influence. the creation of the ‘siege mentality. Inappropriate gifts. is not undue if it does not change the preexisting disposition of the testator. Geriatric psychiatrists are likely to become involved in undue influence evaluations in the clinical setting when an individual is believed by friends or family members to be vulnerable to exploitation and a conservatorship or guardianship of estate is under consideration. especially if the patient has substantial assets.’ the fostering of dependence. Singer (1992) identified six additional factors that “are prominent in undue influence situations. Competency to Care for Oneself and Manage One’s Finances Laws exist in all 50 states and the District of Columbia providing for the appointment by a court of a guardian or conservator for persons found in- . both of which responses may facilitate the creation of the siege mentality. Naïve family members may exacerbate the situation by opposing the relationship or by suggesting that mental impairment is present. if the bequest or gift would have been made anyway. the use of fear and deception. knowledge of the testator’s long-term wishes and intentions is critical to the establishment of this defense. but such a diagnosis is rarely more than just one consideration of many. even that which is clearly coercive. the creation of powerlessness.360 Clinical Manual of Geriatric Psychiatry claim of undue influence. or if preexisting family dynamics are distant or conflictful. excessive payments for services rendered. (p. then no undue influence has occurred. it is important to remember that influence. has even become romantically involved with the elderly person. A typical situation involves an elderly divorced or widowed person with vascular or Alzheimer’s dementia who has fallen under the sway of a much younger individual who has gradually taken over many caregiving functions and. 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. in some cases. new trusts and wills. Obviously.

This competency may be regarded as a form of decisional capacity. measures of frontal executive function are also more critical in the assessment of these “downstream” functions than are the simpler tests of language. Accordingly.us/bills/mca/72/5/ 72-5-101. a perfectly normal individual or one with severe. Chen et al. judgment. and the . memory. Other than at the extremes of cognitive function (i. “a conservator of the person may be appointed for a person who is unable to provide properly for his or her personal needs for physical health. chronic intoxication. which defines an incapacitated individual as someone who is “impaired by reason of mental illness. 2003)... or shelter” (Cal.mt. in California. everyday function is difficult to predict from an office interview. 1997. see http://data. In addition to this ancillary information. Prob. given that such informants are subject to bias and may themselves not be perfectly reliable (Wadley et al. physical illness or disability.htm). 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 assumed by the same person). and other executive functions. food. Alaska. add the requirements of sustained motivation. However. and comprehension that are typically used in the assessment of decisional capacity (Brekke et al. Code §1801a). Colorado. the powers of the conservator of person and the conservator of estate are quite broad: the conservator of person has the power to make decisions regarding place of residence and administration of medical care.state. as mentioned earlier. chronic use of drugs. Functional criteria such as these subsume simple decisional capacity and. multiple sources are desirable. mental deficiency. or other cause (except minority) to the extent that he lacks sufficient understanding or capacity to make or communicate responsible decisions concerning his person or which cause has so impaired the person's judgment that he is incapable of realizing and making a rational decision with respect to his need for treatment” (for an example. 1998).opi. In general. 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.e. Code §1801b). at least in those states that use the Uniform Probate Code (e. end-stage dementia). clothing. Prob.Competency and Related Forensic Issues 361 competent to care for themselves or manage their finances. Montana).g. 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.

the conservatee can still execute a will). in fact. A complete psychiatric evaluation and formal mental status exam are rarely included. wherein only some of the powers discussed earlier are granted to the conservator. unless the court has granted general or specific medical power—that is. Conservatorship and guardianship are clearly radical solutions to the competency problems occasioned by psychiatric and other illnesses.…Typically. (Rosoff and Gottlieb 1987. and the rest remain with the conservatee. But even this approach is costly and demeaning to the patient and. most states have provision for limited conservatorship and guardianship. assets. 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. … Far too often.362 Clinical Manual of Geriatric Psychiatry conservator of estate has the power to manage property. Clearly. pp. evidence is limited to a brief letter from a physician stating that the patient is incompetent. . and disagreement over the need for conservatorship and the motivations of those who support or resist it may lead to long-lasting intrafamilial conflict and resentment. and fortunately several are available (Table 9–3). is sometimes conducive to fiduciary and even physical abuse by guardians. the conservator of person can consent to medical care. despite court oversight. The process of appointment of a guardian or conservator is often demeaning and embarrassing to the conservatee. Armstrong (2000) has collected a series of cases that poignantly illustrate the consequences of abuse of the conservatorship system. In California. they simply restate the circular and conclusory language of the statutory definitions of incompetency. but not over the objection of the conservatee. and income (this includes the power to enter into contractual arrangements on behalf of the principal). The establishment of a conservator of estate automatically renders the conservatee legally incompetent to contract or to transfer property but does not establish lack of testamentary capacity (i. And the process of adjudication of conservatorship and guardianship itself has been criticized. In response to these shortcomings. as determined by the court on a case-bycase basis. The appointment is also expensive and time-consuming.. Guardianship petitions often recite minimal facts in support of the claim of incompetence. 15–16) As if to document this claim. often. [courts] are satisfied with only a perfunctory assessment of the alleged incompetent’s mental capacity. alternatives to conservatorship and guardianship are desirable.e.

certain treatments 363 . make wishes. Surrogate decision-makers available to older persons in California (may vary in other states) Capacity necessary to establish Personal decisionmaking Contractual Durable power of attorney for health care (DPAHC) Yes Makes medical May revoke DPAHC decisions when as long as competent. may not reflect changed values Conservator may not respect May refuse medical May determine care. principal cannota may refuse medical care despite agent’s consent Specifies certain Not applicable limits of care Agent may not make “substituted judgment”. court is recourse (psychiatric medical decisions hospitalization).Table 9–3. court is recourse Competency and Related Forensic Issues Survives Powers of agent incapacity or conservator Powers retained by individual Risks and recourse Living will Contractual Yes Probate conservatorship of person (guardianship) None Yes May not anticipate all situations. civil commitment conservatee’s values and residence.

court is recourse (psychiatric medical decisions hospitalization). make wishes. sterilization) Conservator may not respect May refuse civil May determine conservatee’s values and commitment residence. certain treatments (e.. civil commitment Survives Powers of agent incapacity or conservator Powers retained by individual Risks and recourse 364 Clinical Manual of Geriatric Psychiatry Probate conservatorship for persons with dementia Mental health conservatorship of person None Yes None Yes . court is recourse (including civil only. including commitment).g. certain treatments May refuse physical but Conservator may not respect May consent to conservatee’s values and mental health care not mental health care wishes.Table 9–3. Surrogate decision-makers available to older persons in California (may vary in other states) (continued) Capacity necessary to establish Personal decisionmaking (continued) None Probate conservatorship of person with general medical powers Yes Conservator may not respect May refuse civil May determine conservatee’s values and commitment residence. make wishes. psychosurgery. court is recourse (psychiatric medical decisions hospitalization). abortion.

S.) opinion. May revoke as long as contract competent May expend funds. . May marry Variably reliable court contract oversight. yet court is only recourse Competency and Related Forensic Issues Survives Powers of agent incapacity or conservator Powers retained by individual Risks and recourse Personal trusts Probate conservatorship of estate Mental health conservatorship of estate a bAuthor Contractual to establish.E. May contest most powers Variably reliable court contract of conservator of estate oversight. Surrogate decision-makers available to older persons in California (may vary in other states) (continued) Capacity necessary to establish Financial decisionmaking Power of attorney Durable power of attorney Contractual Contractual No Yes May expend funds. some are values and wishes: court is revocable recourse May expend funds. yet court is only recourse May expend funds. testamentary to modifyb None Yes Yes None Yes 365 Typically is a “springing power” that comes into effect after the principal becomes incompetent. May revoke as long as contract when competent principal cannota Principal must monitor use of funds: court is recourse No oversight of use of funds (“a license to steal”) since principal is incompetent: court is recourse Trustee (if not the settlor) Trustee can manage May modify as long as may not respect settlor’s trust assets competent. (J.Table 9–3.

who hears all of the admissible evidence. Rule 703 particularly applies when the psychiatrist’s expert opinion is based on retrospective evaluation. If of a type reasonably relied upon by experts in the particular field in forming opinions or inferences upon the subject. First. and so on is or would have been affected by that impairment. testimony on whether particular decisions made by the impaired individual are the direct result of such manipulation and persuasion also may be justified and may be permitted. it is recommended that the medical expert avoid testifying on the issue of undue influence per se. In this regard. medical expert testimony should be restricted to the question of the presence and severity of mental impairment and how the patient’s vulnerability to influence. Accordingly. The second revision is based on Rule 703 of the Federal Rules of Evidence. the facts or data need not be admissible in evidence in order for the opinion or inference to be admitted. geriatric psychiatrists need to be familiar with local statutes and case laws defining the various forms of competency. in part. which states. two revisions to those guidelines are suggested. Guidelines for such evaluations in the testamentary context have been published previously (Spar and Garb 1992) and are applicable to each of the forms of decisional competency discussed in this chapter but are not reviewed here.366 Clinical Manual of Geriatric Psychiatry Expert Consultation and Testimony on Competency Geriatric psychiatrists are particularly qualified to provide expert forensic consultation and testimony regarding questions of competency and susceptibility to undue influence.” a judgment that does not require medical expertise and is therefore not a proper part of expert testimony. However. manipulation. simply because undue influence is a complex finding that requires the judgment that a particular benefit is “undue” or “unfair. If circumstances permit. being taken advantage of. persuasion. that the facts or data in the particular case upon which an expert bases an opinion or inference may be those perceived by or made known to the expert at or before the hearing. the only “expert” on the issue of undue influence per se is the trier of fact. Rather. The psychiatric expert may be asked to perform a contemporaneous evaluation of an individual’s competency or susceptibility to undue influence or to state an opinion on the competency and susceptibility to undue influence of an individual who has since died. which always depends on information derived from .

relatives. is therefore not “protected” by Rule 703. This explanation may be important testimony if the court is inclined to believe. and somewhat different ethical principles pertain.to 74-years old and are the second leading cause (after falls) among drivers ages 75. and visuospatial and executive functions. and is of highly questionable probative value. uncooperative. as some clearly are. Here it may be prudent to elicit testimony on direct examination that clinical assessment and diagnosis of psychiatric illness in the elderly are commonly reliant on information from sources (such as spouses. and declining decisional competence resulting from slowing of cognitive processes and reaction time and deficits in attention. including declining visual and auditory acuity. effects of physical and neuropsychiatric illnesses and their treatments. 4 and 3. . that retrospective evaluation is not part of reasonable clinical practice. respectively. male and female drivers are. one in four drivers in the United States will be older than 65. Multiple age-related factors are likely to contribute to this phenomenon. Anticipating and correcting this misperception can be of great value in preserving the proper weight of expert testimony. especially if the patient is severely cognitively impaired. and it is estimated that by the year 2024. On the basis of estimated annual travel. 2003). Motor vehicle injuries are the leading cause of injury-related deaths among drivers ages 65. 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. or catatonic. to express that opinion in a convincing manner. Older drivers have a higher fatality rate per mile driven than any other age group except drivers under age 25. Competency to Drive The fraction of the American population that drives is rapidly aging. caregivers.to 84-years old.Competency and Related Forensic Issues 367 sources other than the testator. The clinician’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. However it is performed. the expert role is substantially different from the role of clinician. By age 80. Because the two obligations can easily conflict. it is usually not recommended for one individual to assume both roles for the same patient. mute. and medical records) other than direct examination of the patient. concentration. in the testimonial context.1 times more likely than 20-year-olds to die as a result of a motor vehicle crash.

the relation between cognitive measures and on-road or nonroad driving measures was significant for all reported domains. issued a “practice parameter” stating that individuals with Alzheimer’s disease whose CDR score is 1. the Trail Making Test Part B (Uc et al. the Driving Scenes test. with mean correlations ranging from 0. 5). measures of visuospatial abilities were the best predictors.” and those with a CDR score of 0. 2005). ability to divide attention. which is part of the new Neuropsychological Assessment Battery (Stern and .35 to 0.65. [1994]) “have an increased risk of accidents similar to that which society accepts for 16 to 19 year old drivers and for those drivers intoxicated with alcohol at a (blood alcohol concentration) <0. 2003). (2004) conducted a meta-analysis of the literature correlating neuropsychological test performance with driving ability and found that in studies that included a control group. 1993). (2000) reviewed the literature on behalf of the American Academy of Neurology and concluded that drivers with early Alzheimer’s disease (MMSE score between 19 and 25 or Clinical Dementia Rating [CDR.5 (approximately corresponding to an MMSE score of 25. In a study published since that review. Dubinsky et al. correlates with driving abilities in individuals with dementia. and ability to distinguish target from background.08%” (p. Three component functions contribute to the UFOV: speed of visual processing. which refers to the area of the visual field in which information can be rapidly extracted without eye and head movements. appears to be of value in this context.368 Clinical Manual of Geriatric Psychiatry Available data are not adequate to determine the precise contribution of each of these factors. a measure called the Useful Field of View (UFOV). but some generalizations are possible. including mazes (Ott et al.0) had a relative crash risk “greater than our society tolerates for any group of drivers. and clock drawing (Freund et al. In studies without a control group.0 or greater should not drive. In particular. 2004). even in the early stages of illness. Morris 1993] score of 1. and those with a CDR score of 0. as does performance on tests of visual attention and visuoperception. Dementia clearly increases the risk of crashing.5 should be referred for a driving performance evaluation by a qualified examiner and should be reassessed every 6 months. Performance on tests of executive function. Ball et al. Reger et al. impairments in each of these functions can result in diminished UFOV (Ball 1997. Several investigators have examined the ability of various off-road assessment tools to predict on-road driving ability of cognitively impaired elders. Dubinsky et al. according to Reisberg et al.

(2005). or unsafe after an on-road driving test.” “marginal. R. Dobbs (1997) studied cognitively impaired seniors who were all still driving and observed three types of driving errors. which “could have resulted in a crash had the driving instructor not taken control of the vehicle or the . Subjects with very mild dementia (CDR score=0. particularly during the more complex stages of the course. and specific tests of visuospatial ability.” and “unsafe. and the tests included in his diagnostic dementia evaluation were 74% accurate in predicting which patients would be classified as safe. but those whose predictions were most accurate placed more weight on duration of dementia. the single physician rater was an experienced neurologist and specialist in dementia. In this study. A.” It may have advantages over the other tests discussed here in ease and convenience of administration and acceptableness to older adult examinees.Competency and Related Forensic Issues 369 White 2003). (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%. His judgments. 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. based on an extensive clinical interview that included specific questions about any recent history of driving problems. 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. Participating physicians based their predictions on almost 20 clinical variables. and executive function.0) did not differ significantly in driving performance. marginal. The most serious errors. measures of dementia severity (CDR and MMSE scores). praxis. was examined for its predictive value. Fitten et al.5) or mild dementia (CRD score=1. On-road evaluation remains the gold standard for assessing the safety of drivers with dementia. the physician was more accurate than either a family member “informant” or the patient in predicting driving safety. In a similar study by Brown et al. (1995) found that subjects with dementia not only performed significantly more poorly on a driving test than did control subjects but also committed more serious driving errors. but both groups were significantly worse than control subjects without dementia. with the accuracy of the general practitioners ranging from 62% to 64% and that of the dementia specialists ranging from 72% to 78%. Ott et al.

which all would seem likely to increase crash risk.9. Subjects with Alzheimer’s disease identified a significantly smaller percentage of restaurant and traffic signs than did neurologically normal control subjects and made significantly more at-fault driving errors. Ray et al. Foley et al. cancer. (1994) looked at stroke. was associated with an increased relative risk (odds ratio) of 1.6) were associated with increased crash risk. (1994) found that hearing impairment did not increase crash risk. Dobbs concluded that diminished driving competence among subjects 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. were made almost exclusively by subjects with dementia. 25% of the subjects with dementia showed driving competence within the range of the normal drivers. including heart attack. osteoarthritis. rheumatoid arthritis.5. coronary disease. Uc and colleagues (2005) studied subjects with mild Alzheimer’s disease (average MMSE score= 26. Certain medications. asthma. to have dementia or other cognitive impairments. In this study. in fact did not. however. McCloskey et al. (1992) found that current use of benzodiazepines was statistically significantly associated with injurious crashes among older drivers in Tennessee.5. which did not reach statistical significance. (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. angina. Glaucoma. Older drivers are at risk for other medical conditions that can impair driving ability. macular degeneration. as expected. and coronary surgery. and diabetes and found that only coronary disease in general (odds ratio=1. Koepsell et al. the UFOV. and monocular vision. The task was to identify and verbally report traffic signs and restaurants along the route. 10).1 years) using several measures of cognitive function.4) and diabetes (odds ratio=2. (1994) found that retinal disorders. and visual acuity and then had subjects drive along a 1-mile stretch of four-lane divided highway. myopia and presbyopia.370 Clinical Manual of Geriatric Psychiatry traffic adjusted” (p. and McCloskey et al. average age = 76. and three of the four control subjects who made errors of this type were subsequently determined. are also important contributors to crash risk. whereas current use of cyclic antidepres- .9. at a relative risk of 1. but wearing a hearing aid while driving increased the risk of crashing by a relative risk of 1. on the basis of cognitive testing. chronic obstructive pulmonary disease.

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. few states have laws mandating that physicians report drivers with dementia or other neuropsychiatric conditions that could impair driving. But every physician has the right and the obligation to attempt to convince dangerously impaired drivers to stop driving. Elder Abuse Epidemiological and clinical studies suggest that for every 100 older adults. a physician’s decision not to report impairment may result in adverse legal consequences for the physician. B. Foley et al. and more seriously. (1995) reported the surprising finding that the use of opioids or antihistamines was not associated with increased crash risk but use of nonsteroidal anti-inflammatory agents was (relative risk =1. even if these admonitions are not always effective.M. for example. These figures may well be underestimates. Despite the evidence that dementia is a major contributor to crash risk. as would physicians in states that do not provide immunity for a breach of confidentiality. Improvements in the ability to predict dangerous driving on the basis of office evaluations are likely to exacerbate this aspect of the physician’s dilemma. Even here. In 2002. because most cases are likely to go undetected. In the National Elder Abuse Incidence Study. as of this writing. Responding to evidence that a patient has become a dangerous driver may be fraught with conflicts for the physician. Physicians practicing in states with laws mandating reporting of impaired drivers would seem somewhat better off in this regard.Competency and Related Forensic Issues 371 sants was associated with a twofold increased risk. and the physician is obligated to protect the patient from that loss whenever it is reasonable to do so. between 2 and 10 individuals are victims of abuse (Lachs and Pillemer 2004). though. But the physician is also obliged to protect the patient and others from the possible consequences of the patient’s impairment. there are conflicts of obligation. Conversely. 84% . only 28 states had laws providing immunity for breach of confidentiality for physicians who report medically unfit drivers. A physician’s official report to authorities of the patient’s impairment may result in an angry patient who chooses another physician. because many patients perceive the loss of “the right to drive” as an intolerable deprivation of autonomy and freedom.4).

The risk of abuse increases sharply with age. Nonetheless. However. including the following generally recognized categories: • • • • • Physical—acts done to cause physical pain or injury Psychological—acts done to cause emotional pain or injury Sexual assault Material exploitation—including misappropriation of money or possessions Neglect—failure to meet the needs of a dependent person Neglect is by far the most commonly identified condition. 2001). Other factors that increase an older person’s risk for abuse include dementia or other forms of cognitive deficit and a shared living situation. The American Medical Association (1992) guidelines on elder abuse suggest routine screening for family violence of all outpatients. 51% reflected general neglect (85% selfneglect. In the Texas study. 2001) of all allegations of neglect in the state of Texas in 1997. After reviewing the domestic violence literature.372 Clinical Manual of Geriatric Psychiatry of the cases were not reported to adult protective service agencies (Administration on Aging 1998).S. in part because there have been no systematic investigations of the effectiveness of interventions for older adults who have been victims of mistreatment. Elder abuse can occur in several forms. including many cases of self-neglect. including sexual abuse (12%). see Fulmer et al. practitioner surveys continue to indicate that physicians rarely do formal screening for elder abuse and often do not inquire about this topic at all. and two-thirds of perpetrators are adult children or spouses (Administration on Aging 1998). there is widespread recognition . Perpetrators of elder mistreatment often have mental illness or alcohol abuse and may be dependent on the abused person for material support (Lachs and Pillemer 2004). and several screening tools have been developed (for a review. with the remainder involving physical abuse. Preventive Services Task Force (2004) declined to endorse routine screening for elder abuse. 14% neglect by others) and 21% involved medical neglect. the U. and emotional abuse (6%). rates of reported elder abuse doubled with each 10-year increase in age (Pavlik et al. In about 9 of every 10 cases of elder abuse. for example. perpetrators are family members. In a study (Pavlik et al. 2004). exploitation (8%). especially within a socially isolated family.

Excellent case examples illustrating issues in intervention can be found in a recent edited volume by Anetzberger (2004). References Administration on Aging: The National Elder Abuse Incident Study. or in the case of a mentally ill perpetrator. given the diverse forms and circumstances that may give rise to concern. cognitive. The National Center on Elder Abuse (http://www. Bergeron (2004) provides a thoughtful and practical discussion of obligation to report issues for mental health professionals. 2005. Final Report. A home interview can also yield valuable information.gov/eldfam/Elder_Rights/ Elder_Abuse/AbuseReport_Full.pdf. . in addition to functional. In most cases. Medication to reduce agitation in an older person with dementia may help to control triggers for abuse by a caregiver.Competency and Related Forensic Issues 373 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 (Bonnie and Wallace 2002. In their tutorial for physicians. World Health Organization 2002). Interventions for abused older adults need to be tailored to the symptoms and situation. Prepared by the National Center on Elder Abuse in collaboration with Westat. In the context of a comprehensive geriatric assessment. it is recommended that the patient be interviewed separately from caregivers or family members whenever abuse is suspected. treatment focused on the abuser may have the greatest effect. Available at http://www.aoa. Many older patients are reluctant to divulge abuse. Lachs and Pillemer (2004) emphasize the need for in-depth but flexible examinations when elder abuse is suspected. and those with cognitive impairment may be unable to recall or report their experiences. physical.elderabusecenter. Accessed September 25. as well as state-specific guidelines for case substantiation and reporting requirements. direct inquiries about abuse and neglect are recommended. and social assessment. September 1998. 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.org/) provides links to bibliographies on detection and management of elder abuse.

IL. Cal Prob Code §1801a.ca.gov/calaw.html. NY. 2006. 1997 Brown LB. Grisso T: Assessing patients’ capacities to consent to treatment [published erratum appears in N Engl J Med 320:748. Alzheimer Dis Assoc Disord 11 (suppl 1):42–47.public. Cal Prob Code §1801b. Wallace R (eds): Elder Abuse: Abuse. 1989].public. Paul. NY. Neglect.ca. American Law Institute. Haworth. Edited by Kendall-Tackett K. Accessed March 8. Cal Prob Code §813. 2006.gov/calaw.public. St.public. Available at http://leginfo.public. DC. 2006. Sloane ME. N Engl J Med 319:1635– 1638. 2006. Accessed March 8. Invest Opthalmol Vis Sci 34:3110–3123.ca. in Health Consequences of Abuse in the Family.html.ca. 1993 Bergeron L: Clinical assessment and the obligation to report. 1981 American Medical Association: Diagnostic and Treatment Guidelines on Elder Abuse and Neglect.public.html. Available at http://leginfo. National Academy Press. Papandonatos GD. Amherst.html. Accessed March 8. 1992 Anetzberger G (ed): The Clinical Management of Elder Abuse.gov/calaw.public. 2004 Appelbaum PS. 1988 Armstrong DG: Retirement Nightmare: How to Save Yourself From Your Heirs and Protectors.ca.374 Clinical Manual of Geriatric Psychiatry American Law Institute: Restatement of the Law Second. 2006. DC.ca. et al: Neuropsychological and psychophysiological correlates of psychosocial functioning in schizophrenia. 2000 Ball K: Attentional problems and older drivers. Ansel M. Binghamton. Owsley C. Contracts 2d.html. Accessed March 8.gov/calaw. 2002 Brekke JS. 2005 Cal Civ Code §38. Prometheus Books. 2004. Cal Civ Code §39. Accessed March 8.html. Available at http://leginfo. 2006. et al: Prediction of on-road driving performance in patients with early Alzheimer’s disease. Raine A.gov/calaw.gov/calaw. MN. Ott BR.ca. Washington. Cal Prob Code §3201.html. Accessed March 8. et al: Visual attention problems as predictor of vehicle crashes in older drivers.gov/calaw. Chicago. Available at http://leginfo. Available at http://leginfo. American Psychological Association. J Am Geriatr Soc 53:94–98. American Medical Association. Schizophr Bull 23:19–28. Cal Civ Code §1575. Available at http://leginfo. Available at http://leginfo. Accessed March 8. 2006. pp 109–128 Bonnie R. and Exploitation in an Aging America. Washington. 1997 Ball K. .

Report of the Quality Standards Subcommittee of the American Academy of Neurology. et al: Executive dysfunction in Alzheimer’s disease: association with neuropsychiatric symptoms and functional impairment. 1995 Foley DJ. 1997 Dubinsky RM. Appelbaum PS. Neurology 54:2205–2211.house. Wallace RB. 2000 Estate of Goetz. Chen ST. et al: Progress in elder abuse assessment instruments. Accessed March 8.gov/calaw. Cal Prob Code §4722 Cal Prob Code §4724 Cal Prob Code §6100.ca. Available at http://leginfo. Clinical Geriatrics 12:33–36. Perryman KM. 1998 Citizen’s National Bank v Pearson. 1997 Hankin MB: A brief introduction to the Due Process in Competence Determinations Act: a statement of legislative intent. 253 Cal App 2d 107 1 (1967) Estate of Rosen. Cincinnati. Ferris R. Accessed March 8. Hill-Fotouhi C: The MacCAT-T: a clinical tool to assess patients’ capacities to make treatment decisions. 2004 Grisso T.gov/media/pdfs/printers/ 109th/evid2005. OH. J Neuropsychiatry Clin Neurosci 10:426–432. California Trusts and Estates Quarterly 1:36– 50. Available at http://judiciary. Eberhard J: Risk factors for motor vehicle crashes among older drivers in a rural community. et al: Clock Drawing Test tracks progression of driving performance in cognitively impaired older adults: case comparisons. Stein AC. J Am Geriatr Soc 43:776–781. Wilkinson CJ.public. Dyer C. Gravenstein S. Fellows LK: Competency and consent in dementia. et al: Alzheimer and vascular dementias and driving: a prospective road and laboratory study. 1998 Fitten LJ. Alzheimer Dis Assoc Disord 11 (suppl 1):8–12. Appelbaum PS: Assessing Competence to Consent to Treatment: A Guide for Physicians and Other Health Professionals. 447 A2d 1220. Lyons K: Practice parameter: risk of driving and Alzheimer’s disease (an evidence-based review). 1995 Freund B. November 14–18. 1995 .html. 1997 Dobbs BM: Driving and dementia: consequences of evaluation and de-licensing. 2004 Fulmer T. 1222 (Me 1982) Federal Rules of Evidence.pdf. J Am Geriatr Soc 52:297–304. J Am Geriatr Soc 46:922–926.Competency and Related Forensic Issues 375 Cal Prob Code §4120. Sultzer DL. 2006.public. 2006.gov/calaw.ca. Paper presented at the 50th annual scientific meeting of the Gerontological Society of America. Psychiatr Serv 48:1415–1419. Guadano L. Hinkin CH. JAMA 273:1360–1365. 1998 Grisso T. Available at http://leginfo.html. New York. Oxford University Press.5. 2006. Accessed March 8. 67 III App 3d 457 43N55 (1978) Dobbs AR: Evaluating the driving competence of dementia patients.

Alzheimer disease. Koepsell TD. Wolf ME. McCloskey L. Heindel WC. guardianship. Case West Reserve Law Rev 39:307–387. Decker MD: Psychoactive drugs and the risk of injurious motor vehicle crashes in elderly drivers. and 1388-204 [classified respectively at 42 USC 1395cc(t) (Medicare) and 1396a(w) (Medicaid)] (1991) Pavlik VN. 1388. et al: Consistency of physician judgments of capacity to consent in mild Alzheimer’s disease. U. 1994 Meiklejohn AM: Contractual and donative capacity. 9N24A1 (1985) Koepsell TD. 1993 Ott BR. et al: Maze test performance and reported driving ability in early dementia. Festa NA. Am J Epidemiol 136:873–883. 2005 Patient Self-Determination Act of 1990. J Am Geriatr Soc 45:453–457. J Am Geriatr Soc 49:45–48. 2003 Ott BR. Appelbaum PS. 1388-115.S. Hawkins L. J Leg Med 8:1–47. J Am Geriatr Soc 42:695–700. Wolf ME. Papandonatos GD. 2001 President’s Commission for the Study of Ethical Problems in Medicine and Biomedical and Behavioral Research: Making Health Care Decisions. Dunn LB. or diabetes mellitus: comparison of a 3-item questionnaire with a comprehensive standardized capacity instrument. §4206 and 4751. 1987 . Whelihan WM. J Geriatr Psychiatry Neurol 16:151–155. 1994 Rosoff AJ. J Am Geriatr Soc 53:829–833. Age Ageing 23:267–273. Neurology 43:2412–2414. Vol 1: A Report on the Ethical and Legal Implications of Informed Consent in the Patient-Practitioner Relationship. 104 Stat. et al: Clinician assessment of the driving competence of patients with dementia. 1988–1989 Morris JC: The Clinical Dementia Rating (CDR): current version and scoring rules. 1994 Lachs MS. Lancet 364:1263–1271. 2004 Marson DC. Fought RL. No. L.376 Clinical Manual of Geriatric Psychiatry In re Conroy. 2005 Palmer BW. et al: Assessment of capacity to consent to research among older persons with schizophrenia. Sclan SG. 1982 Ray WA. et al: Dementia staging in chronic care populations. Welsh RK. Franssen E. Arch Gen Psychiatry 62:726–733. Neuropsychology 18:85–93. 1997 McCloskey LW. competency. et al: Motor vehicle collision injuries and sensory impairments of older drivers. and Alzheimer’s disease. Watson GS. Gottlieb GL: Preserving personal autonomy for the elderly. Pillemer K: Elder abuse. Pub. Hyman DJ. et al: The relationship between neuropsychological functioning and driving ability in dementia: a meta-analysis. McInturff B. Anthony D. DC. 2004 Reisberg B. 101-508. Washington. Government Printing Office. et al: Medical conditions and motor vehicle injuries in older adults. et al: Quantifying the problem of abuse and neglect in adults—analysis of a statewide database. Alzheimer Dis Assoc Disord 8 (suppl 1):S188–S205. 1992 Reger MA.

2002. Appelbaum PS. 2006. Suite 1300. Available at: http://www. Available at: http:// www. Food and Drug Administration: Protection of human subjects: informed consent. Geneva. 1992 Srebnik D. Compr Psychiatry 45:239–245. White T: Neuropsychological Assessment Battery.S. in Physicians Guide to Assessing and Counseling Older Drivers. 2003 Uc EY. Accessed February 28. 2003 Wang CC. Int J Geriatr Psychiatry 19:645–654. IL 60611. Smit JH. . 211 E. Ontario Street.wi. Lutz. Accessed February 28. Schwartzberg JG.pdf. 2004 Wadley VG. 2006. Garb AS: Assessing competency to make a will. Accessed February 28.int/ violence_injury_prevention/violence/world_report/en. U.state. Journal of Questioned Document Examination 1:4–13. March 2004.ahrq. Anderson SW.Competency and Related Forensic Issues 377 Singer M: Undue influence and written documents: psychological aspects. 61 Federal Register 51498 (1996) U. Preventive Services Task Force: Screening for family and intimate partner violence: recommendation statement. 2005 Uniform Durable Power of Attorney Act. Psychological Assessment Resources. Kosinski CJ. 2006. MD. Also available from the National Conference of Commissioners on Uniform State Laws.legis. 2003. Available at: http://www.us/statutes/1983/83stat0243.who. Available at: http//:www. et al: Driver landmark and traffic sign identification in early Alzheimer’s disease. 1992 Spar JE. et al: Competence to consent to treatment of geriatric patients: judgments of physicians. Vellinga A. World Health Organization. §1 8U2 (1983). Reynolds SL: Rethinking alternatives to guardianship. National Highway Traffic Safety Administration. Accessed February 28. Washington. Agency for Healthcare Research and Quality. Marson DC: Self. Russo J: Assessing competence to complete psychiatric advance directives with the Competence Assessment Tool for Psychiatric Advance Directives. Rizzo M. Chicago. DC.htm. 2006. Van Leeuwen E. 1995 World Health Organization: World report on violence and health.S. Rockville.and informant report of financial abilities in patients with Alzheimer’s disease: reliable and valid? J Am Geriatr Soc 51: 1621–1626. Harrell LE.gov/people/injury/olddrive/OlderDriversBook/pages/ Chapter1. Am J Psychiatry 149:169– 174. FL. 2004 Stern RA. J Neurol Neurosurg Psychiatry 76:764–768.html#Anchor-33096). Wilber KH. Gerontologist 35:248–257.nhtsa.gov/clinic/ 3rduspstf/famviolence/famviolrs. family members and the vignette method. et al: Safety and the older driver: an overview.

This page intentionally left blank .

Appendix Clinical Assessment Instruments 379 .

30. 26.380 Clinical Manual of Geriatric Psychiatry Geriatric Depression Scale Choose the best answer for how you felt over the past week. Are you basically satisfied with your life? Have you dropped many of your activities and interests? Do you feel that your life is empty? Do you often get bored? Are you hopeful about the future? Are you bothered by thoughts you can’t get out of your head? Are you in good spirits most of the time? Are you afraid that something bad is going to happen to you? Do you feel happy most of the time? Do you often feel helpless? Do you often get restless and fidgety? Do you prefer to stay home. 29. 10. 12. 11. 28. 16. 23. 4. 13. 21. 14. 19. 6. 27. 24. 8. 9. rather than going out and doing new things? Do you frequently worry about the future? Do you feel you have more problems with memory than most? Do you think it is wonderful to be alive now? Do you often feel downhearted and blue? Do you feel pretty worthless the way you are now? Do you worry a lot about the past? Do you find life very exciting? Is it hard for you to get started on new projects? Do you feel full of energy? Do you feel that your situation is hopeless? Do you think that most people are better off than you are? Do you frequently get upset over little things? Do you frequently feel like crying? Do you have trouble concentrating? Do you enjoy getting up in the morning? Do you prefer to avoid social gatherings? Is it easy for you to make decisions? Is your mind as clear as it used to be? yes/no yes/no yes/no yes/no yes/no yes/no yes/no yes/no yes/no yes/no yes/no yes/no yes/no yes/no yes/no yes/no yes/no yes/no yes/no yes/no yes/no yes/no yes/no yes/no yes/no yes/no yes/no yes/no yes/no yes/no . 18. 25. 2. 5. 17. 1. 22. 20. 15. 7. 3.

19. 4. 7. 30 Scores ≥ 11 raise a question of depression. 23. Washington. 12.” Journal of Psychiatric Research 17:37–49. 15. 11.” in Handbook for Clinical Memory Assessment of Older Adults. 29. 1983. pp. 8. 10. Yesavage J. 27. DC. Edited by Poon L. 25. 20. Source. et al. 213–217. 22. American Psychological Association. 28 “no”: Items 1. 6. 3. Rose T. 9. . Brink T. 14. 26. 5. See also Yesavage JA: “The Use of Self-Rating Depression Scales in the Elderly. 16. 1986. 18. 17. 24.Appendix: Clinical Assessment Instruments 381 Geriatric Depression Scale (continued) Critical responses: “yes”: Items 2.: “Development and Validation of a Geriatric Depression Screening Scale: A Preliminary Report. 21. 13.

382 Clinical Manual of Geriatric Psychiatry Six-Item Orientation-Memory-Concentration Test Item What year is it now? What month is it now? Repeat this phrase after me: “John Brown. Fuld P. Copyright 1983.” American Journal of Psychiatry 140:734– 739. Source. Total weighted error scores > 10 suggest cognitive impairment. Chicago” About what time is it? Count backward from 20 to 1 Say the months in reverse order Repeat the memory phrase Maximum error 1 1 Weight Score ×4 ×3 = _____ = _____ 1 2 2 5 ×3 ×2 ×2 ×2 Total = _____ = _____ = _____ = _____ = _____ Note. Brown T. 42 Market Street. Adapted from Katzman R. One point is scored for each incorrect response and then multiplied by the weighing factor. et al. 1983.: “Validation of a Short OrientationMemory-Concentration Test of Cognitive Impairment. American Psychiatric Association. . Used with permission.

ORI= orientation. LOC = level of consciousness. SIM= similarities. Adapted from Northern California Neurobehavioral Group: Manual for Cognistat (The Neurobehavioral Cognitive Status Examination). 1995. 12. NAM= naming. ATT= attention. p. Northern California Neurobehavioral Group. COMP= comprehension. Fairfax. REP= repetition. 383 . CA. CALC= calculation. Note. MEM= memory. Used with permission.Appendix: Clinical Assessment Instruments Cognistat profile of an 82-year-old woman with probable Alzheimer’s disease. JUD= judgment. CONST= construction. Source.

or prepares meals but does not maintain an adequate diet Prepares adequate meals if supplied with ingredients Plans. Food preparation Needs to have meals prepared and served Heats and serves prepared meals. depends on others for large items Does personal laundry completely F. Shopping Completely unable to shop Needs to be accompanied on any shopping trip Shops independently for small purchases Takes care of all shopping needs independently C.384 Clinical Manual of Geriatric Psychiatry Instrumental Activities of Daily Living (IADL) Scale A. Mode of transportation Does not travel at all Travel limited to taxi or automobile with assistance of another Travels on public transportation when assisted or accompanied by another Travels independently on public transportation. prepares. taxi. Laundry All laundry must be done by others Launders a few small items Does most small items. Housekeeping Unable to participate in any housekeeping tasks Needs help with all home maintenance tasks Performs light daily tasks such as dishwashing Maintains house alone or with occasional assistance E. Ability to use the telephone Does not answer the telephone at all Answers telephone but does not dial Dials a few well-known numbers Operates telephone on own initiative B. or drives own car 1 2 3 4 1 2 3 4 1 2 3 4 1 2 3 4 1 2 3 4 1 2 3 4 . and serves adequate meals independently D.

Manages financial matters independently but. collects and keeps track of income I. drives poorly. . driving a car) or who have no opportunity to perform a particular activity.” The Gerontologist 9:179–186. etc. Ability to perform household repairs or chores Unable to do even simple household repairs or chores Can only do very simple tasks such as hanging a picture or mowing the lawn With some help and direction can do moderately difficult household repairs such as fixing a leaky faucet Is able to independently perform most household chores or repairs Skill in driving an automobile Is unable to drive an automobile Drives when someone is present to give directions. Note. Reprinted from Lawton MP. has good sense of direction. Copyright ©The Gerontological Society of America. Responsibility for own medications Is not capable of dispensing own medication Takes responsibility if medication is prepared in advance in separate dosages Takes independent responsibility but occasionally forgets a dosage Is responsible for taking medication in correct dosages at correct times H. on occasion.. Ability to handle finances Incapable of handling money Manages day-to-day purchases but needs help with banking.g. Reproduced by permission of the publisher. Brody EM: “Assessment of Older People: Self-Maintaining and Instrumental Activities of Daily Living. Source. and good driving skills 1 2 3 4 1 2 3 4 1 2 3 4 1 2 3 4 J. has forgotten to pay a bill or has been overdrawn in bank account Manages financial matters independently. or drives very slowly and cautiously Drives alone but has some tendency to get lost or has occasional driving problems Drives alone.Appendix: Clinical Assessment Instruments 385 Instrumental Activities of Daily Living (IADL) Scale (continued) G. Items can be rated as “not applicable” for persons who have never performed a particular activity (e. 1969. major purchases.

Waking you or other family members up at night 11. If so. Appears anxious or worried 012349 012349 012349 012349 012349 012349 012349 012349 012349 012349 012349 012349 Reaction 012349 012349 012349 012349 012349 012349 012349 012349 012349 012349 012349 012349 . but not finishing things 7.g. items in the newspaper or on TV) 3. Destroying property 9. Trouble remembering significant past events 4. Asking the same question over and over 2. Frequency ratings 0=never occurred 1=not in the past week 2=1 to 2 times in the past week 3=3 to 6 times in the past week 4=daily or more often 9=don’t know/not applicable Reaction ratings 0=not at all 1=a little 2=moderately 3=very much 4=extremely 9=don’t know/not applicable Frequency 1. Forgetting what day it is 6. Starting. Losing or misplacing things 5. Talking loudly and rapidly 12. how much has this bothered or upset you when it happened? Please rate the frequency of the problem and your reaction to it by circling a number from 0 to 9 for both frequency and reaction. Trouble remembering recent events (e. Doing things that embarrass you 10. Please indicate if any of these problems have occurred during the past week. Difficulty concentrating on a task 8..386 Clinical Manual of Geriatric Psychiatry Revised Memory and Behavior Problems Checklist Instructions The following is a list of problems patients sometimes have.

Threats to hurt others 16. Adapted from Teri L. “Life isn’t worth living. Comments about feeling worthless or being a burden to others 23.” “I never do anything right”) 19. Comments about feeling like a failure or about not having worthwhile accomplishments in life 24. et al. 1992. Commenting about death of self or others (e.. “Nothing worthwhile ever happens. Engaging in behavior that is potentially dangerous to self or others 14. Logsdon R.” Psychology and Aging 7:622–631.Appendix: Clinical Assessment Instruments 387 Revised Memory and Behavior Problems Checklist (continued) Frequency 13. Expressing feelings of hopelessness or sadness about the future (e.g. Used with permission. Arguing. and/or complaining 012349 012349 012349 012349 012349 Reaction 012349 012349 012349 012349 012349 012349 012349 012349 012349 012349 012349 012349 012349 012349 012349 012349 012349 012349 012349 Source. Crying and tearfulness 20. Talking about feeling lonely 22.” “I’d be better off dead”) 21. . Truax P.: “Assessment of Behavior Problems in Dementia: The Revised Memory and Behavior Problems Checklist. Threats to hurt oneself 15.g. Appears sad or depressed 18. Aggressive to others verbally 17. irritability..

Frequency: 1= less than once/week.g.: “The Neuropsychiatric Inventory: Comprehensive Assessment of Psychopathology in Dementia. or response misleading for any reason).” Neurology 44:2308–2314. Severity: 1= mild. 2 =about once/week. et al. caregiver does not appear to understand the item. Mega M.. 1994.388 Clinical Manual of Geriatric Psychiatry Items Rated on the Neuropsychiatric Inventory Item Delusions Hallucinations Agitation Depression/dysphoria Anxiety Euphoria/elation Apathy/indifference Disinhibition Irritability/lability Aberrant motor behavior Nighttime behavior Appetite/eating change N/A X X X X X X X X X X X X Absent 0 0 0 0 0 0 0 0 0 0 0 0 Frequency 1234 1234 1234 1234 1234 1234 1234 1234 1234 1234 1234 1234 Severity 123 123 123 123 123 123 123 123 123 123 123 123 Note. 4= daily or continuously. Source. 3 =severe. 3 =several times/week but less than daily. Reprinted from Cummings JL. 2 =moderate. Used with permission. N/A =not applicable (e. Gray K. .

276–277 bereavement and. Very old people biological factors in. 313 social context of. 258 Activities of daily life Alzheimer’s disease and. Karl. 183–184. 202 cognitive changes of normal aging and. 327. See Black Americans Age and aging. 21–23 delirium and. 193 processing resource model of cognitive abilities and.Index Page numbers printed in boldface type refer to tables or figures. 69 Advance directives. 249 Activated or hyperactive subtype. 115 Acamprosate. 367– 368 Acetaminophen. 37 389 . 262 diversity in patterns of. 38–43 prevalence of Alzheimer’s disease by. 329–331 sleep and advancing. 78 Acetylcholinesterase. 48–61 conceptual issues in. and dementia. See also Age of onset. 1–2 influence on mental disorders of early onset. 180 personality and emotional changes in. Older adults. 163–165 Adjustment anxiety and. and competency. 328. 35–36. and motor vehicles. 43–48 Age-associated memory impairment (AAMI). 23–38 psychosis and. 12–15 elder abuse and. 338 Acetazolamide. of delirium. 384– 385 Acute treatment. for bipolar disorder. 207 Acquired immunodeficiency syndrome (AIDS). 108. 25–28 increase in older adults as percentage of population. 339–341 Mini-Mental State Examination and. 181–183 Abraham. 372 general trends in. Abbreviated cognitive screens. 32–34 rating scales and. 349–352 African Americans. 294 sexual dysfunction and. 325–326 Accidents.

78 treatment of. 206–207 psychopharmacotherapy for. 263 diagnosis of. 192–195 frontotemporal dementia and. See also Substance abuse assessment of. 383 competency to drive and. 254–255 symptoms of depression induced by. 195–205. 325–326 Alcohol Use Disorders Identification Test (AUDIT). 178–179 neurobiochemistry of.390 Clinical Manual of Geriatric Psychiatry Age of onset. 214. 92 frontotemporal dementia and. 220 vascular dementia and. 250 depression and. 249 Alcohol and alcohol abuse. 192 anxiety disorders and. 199 Cognistat profile and. 147 Agitated Behavior in Dementia scale. 370 dementia and. 73–74. 90 diagnosis of. 246 AIDS dementia complex. 232. 216–218. 334 Alternative approaches. 213. 278 bipolar disorder and. 321 epidemiology of. Late onset Alzheimer’s disease and. 317. 350. to treatment of depression. 239–240. 207–208 neuropathology of. 197. 372 Amitriptyline. 113 dysthymic disorder and. 236 genetics of. 321 substance-induced dementia and. 323–325 associated psychiatric conditions and. 292 insomnia and. 234. 321–323 delirium and withdrawal from. 210– 213 Alzheimer’s Disease Assessment Scale. 368. 134 . 291. 88. See also Age and aging. 208–210 psychotherapy for caregivers. Early onset. 91. 231 major depression and. 161–162 Alzheimer’s Association. 241 American Academy of Neurology. 198–199 differential diagnosis of. 7. 323–324 Alprazolam anxiety disorders and. 213 Alzheimer’s disease clinical presentation of. 83 psychopharmacotherapy for depression and. 368 American Medical Association. 213– 220 psychosocial theory of. 217–218 Agitation psychopharmacotherapy for Alzheimer’s disease and. 208 Mini-Mental State Examination and. 250 epidemiology of. 205–206. 320–321 risk factors for. 318 Alprostadil.

137. 277 delirium and. 78 Antihistamines Alzheimer’s disease and. 148 management of side effects of. 56 substance abuse and. 194 Antiparkinsonian agents medication-induced mental disorders and. 205 Amnestic mild cognitive impairment. 149 Anticipatory anxiety. 219 anxiety disorders and. See also Selective serotonin reuptake inhibitors. 332 symptoms of depression induced by. 153–155 Antiepileptic agents. 335 Anticholinergic agents anxiety symptoms and. 264 . 175. 287 Animal Naming task. 138 Amphetamines. 303 Antipsychotics. See also Atypical antipsychotics anxiety disorders and. 140 delirium and. 218 cytochrome P450 system and. 370–371 cytochrome P450 system and. 219 drug-drug interactions and. and Alzheimer’s disease. and depression. 147 receptor affinities of. and depression. See also Narcotic analgesics. 148– 149 predictors of response to. 332 treatment resistance and. for pathogenesis of anxiety disorders. 281 Anticonvulsants Alzheimer’s disease and. 36 Amoxapine. 277 automobile driving and. Tricyclic antidepressants advantages and disadvantages of. 139 medication-induced mental disorders and. 78 Antioxidants.Index 391 Amnestic disorders. and panic attacks. 181– 182 Anorexia. 206 Analgesics. Nonsteroidal anti-inflammatory agents substance abuse and. 136–137 Alzheimer’s disease and. of tricyclic antidepressants. 153 Amyloid precursor protein (APP). 292 anxiety symptoms induced by. 327. 140 Antidepressants. 163 cytochrome P450 system and. 174. 328 Antihypertensive agents sexual dysfunction and. 140– 141 dosages of. and depression. and Alzheimer’s disease. 263–264 Anticholinergic effects. 327. 78 Animal models. and Alzheimer’s disease. 328 symptoms of depression induced by. 292 bipolar disorder and. 90 Anterior cingulate syndrome. 56 psychosis and. 134–135 sexual dysfunctions and.

328 Assessment. 304 Arteriosclerosis. 332 symptoms of depression induced by. 276 pathogenesis of. 192– 193. 107 Attorney-in-fact. 154– 155 Automobiles. 24 Augmentation. 276–286 epidemiology of. 285 schizophrenia with. 79 Aspirin. 274 diagnosis of. 275–276 Beck Cognitive Insight Scale. 283. of antidepressants. and normal aging. See also Antipsychotics Alzheimer’s disease and. 313. and vascular dementia. 248 Anxiety Alzheimer’s disease and. 241 late-onset psychosis and. 350. 218 mood disorder with. 303–306 psychotic depression and. 323–324 Auditory acuity. and major depression. 83 Aripiprazole Alzheimer’s disease and. 373 of erectile dysfunction. 216–217 dementia with Lewy bodies and. and Alzheimer’s disease. 356–358 elder abuse and. 351 Atypical antipsychotics. 241 psychosis and. 274–276 treatment of. 218 symptoms of depression and. 304 AUDIT-5 (five-item Alcohol Use Disorders Identification Test). 220 dementia with Lewy bodies and. 301 . 314 of suicidality in elderly. 328 symptoms of depression induced by. 323–325 of competency. 273–274 laboratory evaluation of. 78 Apathy. 285–286 Anxiety disorders autonomic and psychomotor features of. 286–288 rating scales for. 79 Beck Anxiety Inventory. 191. 335 of insomnia. 79 Barbiturates delirium and withdrawal from. 275 clinical presentation of. 241 psychosis and. 288–293 Anxiolytic agents Alzheimer’s disease and. 205 Appetite. 302–303. 78 vascular dementia and. 246 Asparaginase. See also Diagnosis of alcohol abuse or dependency.392 Clinical Manual of Geriatric Psychiatry Antipsychotics (continued) dementia with Lewy bodies and. 219 APOE4. and Alzheimer’s disease. See Driving Baclofen. 263 substance abuse and. 156 sexual dysfunctions and. 105–106. 216.

for depression. 357 . 339 clinical presentation of. of aging. 211. 162–163 Black Americans caregivers for dementia patients and. 56 substance-induced mood disorder and. 103 Beck Depression Inventory for Primary Care (BDI-PC). 100. 128 late-onset psychosis and. 288–290 geriatric depression and. 161– 162 Biology. 101. 263 insomnia and. See also Genetics. 216 anxiety disorders and. 317–319 psychosis and.” 68–70 loss and. 78 Boston Naming Test (BNT). 248 interventions for insomnia. 183 β-Blockers medication-induced mental disorders and. 291 competency to drive and. 163–166 treatment of. See also Hypomania. 90–91 Behaviorally oriented pain management training. 338 Behavior Pathology in Alzheimer’s Disease Rating Scale (BEHAVEAD). Mania aging and early-onset. 12– 14 poverty rates and. See also Cognitivebehavioral therapy Alzheimer’s disease and. 102. 219 anxiety disorders and. 46–47 Bibliotherapies. 216. 106 Behavior. See also Agitation. 45 Blessed Information Memory Concentration Test. 80. 326. 315– 316 major depression and regression of. 328 symptoms of depression induced by. 78 Bereavement depression compared to “normal. 113 pathogenesis and theories of. 327. 370 delirium and withdrawal from. 300–302 Benzodiazepines Alzheimer’s disease and. 48–61. 212 patterns of health and aging in. Neurobiological theories Bipolar disorder. 217–218 Behavior therapy. 303 substance abuse and. 115– 116 psychopharmacotherapy for. 77 symptoms of depression induced by. 290–292. 105 Beck Hopelessness Scale. 111. Behavior therapy complications of vascular dementia and.Index 393 Beck Depression Inventory (BDI). 108 widowhood and. 113 epidemiology of. 188. 157.

215. 326–327 Capacity. 134 Buspirone. 354–356 Carbamazepine. 218 delirium and. 56 Bupropion advantages and disadvantages of. 351. 363–365 California Verbal Learning Test (CVLT). 354. 349. 51 of insomnia. 138. 2 Chloral hydrate. 52. 78 California. 245 Chemotherapeutic agents. 277 medication-induced mental disorders and. 85–86 of psychotic depression. 48 Case examples of biology of aging.394 Clinical Manual of Geriatric Psychiatry Braak’s criteria. 148 receptor affinities of. 196 Brief dynamic therapy. 253 dementia with Lewy bodies and. 242. 164–165. 181–182 Center for Epidemiologic Studies Depression Scale. 166 Cardiovascular system. 69–70 resources for. 210–213 relief after death of patient. 361. 291 Chlorpheniramine. 130 Bronchodilators anxiety symptoms induced by. 136 depression and. 237 vascular dementia and. 69–70. 263. 348. 207 Cholinesterase inhibitors Alzheimer’s disease and. 328 Chlorpromazine. for Alzheimer’s disease. 318. Stroke. 93 Cerebrovascular disease. 228 social context of aging and. 328 CAGE Questionnaire. Vascular lesions Caregivers psychotherapy for dementia and. for geriatric depression. See also Heart disease. 195. and biological aging. See also Competency contracts and. and bipolar disorder. 323–325 Calcium channel blockers. and laws on competency. 214. 304 Choline acetyltransferase. 187 Cannabis. 318–319 of major depression. 213. 90. and symptoms of depression. 362. Vascular disorders. 264 dementia due to general medical conditions and. 143–144. 292 Caffeine anxiety and. 84 Category fluency measures. 328 Chlordiazepoxide. See also Stroke dementia with Lewy bodies and. 240–241 . and symptoms of depression. 351 testamentary. 78–79 China. 277 substance abuse and. 327. older adults as percentage of population of. and Alzheimer’s disease.

257 of dementia with Lewy bodies. 78 Clorazepate. 160 Clinical implications. See also Executive functions. 292 depression and. 71–72.Index 395 substance-induced persisting dementia and. 134 Clinical Dementia Rating (CDR). 254 vascular dementia and. 243 Clock Drawing Test. See also Treatment of biology of aging. of depression. 199 of anxiety disorders. See also Behavior therapy for anxiety disorders. 238 of frontotemporal dementia. 291 psychosis and. 108–109 Cognitive-behavioral therapy. Memory aging effects on performance and. 182. 181 Cognitive and behavioral theories. 356–357 Clinical presentation of age-associated memory impairment. 128–129 for insomnia. 291 Clozapine. 328 symptoms of depression induced by. 274 of bipolar disorder. 368 Clinical Global Impression (CGI). 37 of Alzheimer’s disease. 174. 148 receptor affinities of. 296 of social context of aging. Learning. 294. 34–35 of personality and emotional changes in aging. 303. 326 Code of Federal Regulations. 139. 143. 357– 358 delirium and. 113 of delirium. 231 of psychosis. See also Medical conditions Chronic pain. 78 Cognistat. 316 for late-onset psychosis. 368 Clonazepam pharmacological properties of. 303 Clonidine. 176. 247 Chronic illness. and late-onset psychosis. 42–43 Clinical interview. 352 Codeine substance abuse and. 321–323 competency assessment and. 262 . 288–289 for geriatric depression. 79 Citalopram anxiety disorders and. 175. 175. 26–27 alcohol abuse or dependency and. 337–339 Cimetidine. 197. and major depression. and assessment of competency. 304 Cocaine. 48 of vascular dementia. 300–302 Cognitive impairment. 383 Cognitive Abilities Screening Instrument (CASI). 50–61 of cognitive change in aging. pharmacological properties of.

367–371 enrollment in research studies and. See Web sites Confusion Assessment Method (CAM) algorithm. 237 frontotemporal dementia. 356–358 caring for oneself and management of finances. 354–356 Compliance. 129 personality disorders and. in personality. 71 Computed tomography. 23–38 psychopharmacotherapy for Alzheimer’s disease and. 329 Comorbidity. 360–362 contracts and gifts. 29 Combined treatment. 196–197. 247– 248 Cohen-Mansfield Agitation Inventory. 321–323 diagnosis and treatment of depression and. 97 of hypomania or mania. 358 Competency advance directives and. 87–91. in diagnosis of Alzheimer’s disease. 72 Conservators and conservatorship. 361–362. 198. with treatment for depression.396 Clinical Manual of Geriatric Psychiatry Cognitive impairment (continued) depression and. on cognition in normal aging. 250–252 dementia with Lewy bodies. 250 of delirium. 29 vascular dementia and. 128. 195. 243. 234 vascular dementia. 200–201. 349 surrogate decision-makers and. 353 informed consent for medical care and. 258–259. 363–365 trusts and. 261 of dementias. 297 processing resource model of. 174–183 variables of in normal aging. 340 Competence Assessment Tool for Psychiatric Advance Directives. 147 evaluation of Alzheimer’s disease and. 348–349. 116 Computers. 202 late-onset psychosis and. 217–218 Cohort effects. 260 Congestive heart failure. 353–354 definition of. 132. 347–348 driving and. of psychiatric disorders alcohol abuse or dependency and. 39 . 185. 352. 349–352 assessment of. 131–132 Complicated grief. 363–365 Consortium to Establish a Registry for Alzheimer’s Disease (CERAD) Word List Learning. 203 Continuity. 83. 213– 220 risk of in older adults. 7 standardized measures for rating. 356 wills and. 70. 245 of depression. 188. 201. for geriatric depression. for substance abuse. 155 Community-based programs.

41. Dementia with Lewy bodies. 205 . 246 Delirium Rating Scale. 322. 42 Controlled Oral Word Association Test (COWAT). 143. 259 Delis-Kaplan Executive Function System. 325 Creutzfeldt-Jakob disease. and competency. 199 diagnostic criteria for. of aging. 206 diagnostic criteria for. 3. 14 caregivers for dementia patients and. 139. Frontotemporal dementia. and psychotropic medications. 264 psychosis and. 296 late-onset psychosis and. 259. and emotional changes during aging. 337 treatment of. 197. 258 differential diagnosis of. 138. of health care for older adults. 261 mental status examination and. 359 Contraindications. 5– 6 Counseling. 257–259 pathogenesis of. 263–264 vascular dementia and. 56 substance abuse and. 256–257 laboratory evaluation of. 298. and alcohol abuse and dependency. 142. 257 prognosis in. 353– 354. 101.Index 397 Contracts. 84 psychotic disorder due to a general medical condition and. See also Dementia due to general medical conditions. for tricyclic antidepressants. Vascular dementia alcohol-related. 327 Delirium Alzheimer’s disease and. 351. 306 psychotic depression and. 299. 104–105 Costs. 188 Coping. 336 Dementia. 262 patient history and clinical presentation of. Reversible dementia. See also Mortality Decisional competency. 144 Death. leading causes of in older adults. 213 Cytochrome P450 system. 259–260. 40–42 Cornell Scale for Depression in Dementia. Mixed dementia. Substance-induced persisting dementia. 22 Culture access to mental health services and. 140–141. and emotional changes during aging. 138 Control. 258. 252 Cross-sectional view. 324 Alzheimer’s disease and. 277 medication-induced mental disorders and. 347–348 Decongestants anxiety symptoms induced by. 234 Delusions and delusional disorder Alzheimer’s disease and. and dementia. 261– 262 epidemiology of.

371 delirium and. 340 problems in diagnosis and treatment of. 92– 93. See also Major depression aging and early-onset. 38 Dexamethasone. 161–162 dementia and. 368. 146 Detoxification. 323 Alzheimer’s disease and. 35–38 of alcohol abuse or dependency. 218–219 chronic pain and. 87–88 Depression. 96–97 psychopharmacotherapy for. 237– 241 Dementia Rating Scale (DRS).398 Clinical Manual of Geriatric Psychiatry Dementia (continued) chronic pain and. 132– 156. 198–199 of anxiety disorders. and substance abuse. 178 Dementia syndrome of depression (DSD). and depression. 89 experimental therapies for. 95–96. 337 psychotherapy for caregivers. 176. 190–191 major depression and. 67 laboratory evaluation of. 67–68 Depressive personality disorder. and depression. Differential diagnosis. 95 Depressive pseudodementia. 339 alcohol abuse or dependency and. 249–254 Dementia with Lewy bodies. 7–8. 107–110 undertreatment of. 36–38 psychosis and. 173–186. 329 Developmental optimism. 94–95 normal grief and. 218–219 psychotherapy for. 68–70 personality disorders and. 97 medical conditions and. 261–262 diagnosis of. 210– 213 resources for caregivers. 187–189 differentiation of common forms. 369– 370. See also Assessment. 195–197. 97–105 theories of. Underrecognition of age-related cognitive change and mild cognitive impairment. 159–160 importance of in older adults. 186. 87 Desipramine. DSM-IVTR. 129 psychological tests for. 338–339 competency to drive and. 89 mild cognitive impairment and progression to. 235. 79. 70–76 minor or subthreshold forms of. 276–286 . 250–252 etiologies of. 127–130 rating scales and. 259. 321 of Alzheimer’s disease. Rating scales. 134. 338 complementary and alternative approaches to treatment of. 96 Diagnosis. 174. 228 Dementia due to general medical conditions.

217 for bipolar disorder. 184 Disability. 247 Dosage. 318 pharmacological properties of. 261–262 dementia with Lewy bodies and. 258 of dementia with Lewy bodies. 241–242. 229. 76–80 of vascular dementia. 236 insomnia and. 12–15 Doctor-patient relationship. 240 frontotemporal dementia and. for posttraumatic stress disorder. 3–4 Disulfiram. 34 Donepezil Alzheimer’s disease and. in patterns of health and aging. 91–92 of frontotemporal dementia. 328 Direct Assessment of Functioning Scale. 70–76 of depressive personality disorder. 205–206 delirium and. 240–241 vascular dementia and. 164 . 234. 165. 218 delirium and. 55 of delirium. 213. 117 of substance-induced mood disorder. 219 substance abuse and. and bipolar disorder. See also Diagnosis Alzheimer’s disease and. 92–95 of mixed mood disorder. and agerelated cognitive changes. 259. 166 Diversity. 264 dementia with Lewy bodies and. 95 of dysthymic disorder. 303– 306 of carbamazepine. 245–246 Differential vulnerability hypothesis. 337 vascular dementia and. 79 Divalproex. 230–231 of hypomania and mania. 215. 281–283 Digoxin. 243 Diazepam insomnia and. 313–315 normal grief and bereavement. 148 of antipsychotics for Alzheimer’s disease. 263. 164. 298. 237– 238 of dementia with unspecified cause. 163 for late-onset psychosis.Index 399 biological aging and guidelines for. 79 Diphenhydramine Alzheimer’s disease and. 110–117 of major depression. See also Psychopharmacotherapy of antidepressants for geriatric depression. 129 of minor depression. 80–91. 173–186 of depression due to a general medical condition. 68– 70 psychosis and. rates of in older adults. 291 Differential diagnosis.

293 schizophrenia and. 295 substance abuse and. 35. 322. 94–95 obsessive-compulsive disorder and. 367–371 Drop-out rates. 139. 33 competency to. 296 dementia due to general medical conditions and. 283 personality change due to a general medical condition and. 139. 257. 243 Duloxetine advantages and disadvantages of. 258 delusional disorder and. 83 Economics. 117 minor depressive disorder and. 321. 82. 282 panic disorder and. 152 Double depression. 131–132 Drug-drug interactions monoamine oxidase inhibitors and. 286. 316 major depression and. 242. 323 substance-induced mood disorder and. 274. 152–153. See Costs. 85 mania and hypomania in. 91 Doxepin. 134 Driving cognitive changes of aging and. 336 phobias and. 165 of monoamine oxidase inhibitors. Financial status . 76 vascular dementia and. 114–115. 155 selective serotonin reuptake inhibitors and. 36 alcohol abuse or dependency and. 196. 322 Alzheimer’s disease and. 145 chronic pain and. See also Diagnosis age-related cognitive changes and. 155 DSM-III-R. 91 insomnia and. Financial decision making. 293 DSM-IV-TR. 91–92 Early onset. 280 posttraumatic stress disorder and. 363 Dysthymic disorder. 338 receptor affinities of. 203 anxiety disorders and. and late-onset psychosis.400 Clinical Manual of Geriatric Psychiatry Dosage (continued) of lamotrigine. 136. 134 Durable power of attorney for health care (DPAHC). 279 delirium and. 95 dysthymic disorder and. 68 depressive personality disorder and. See also Age of onset influence of aging on disorders of. 281. 339–341 of major depression. from treatment for depression. 249 depression due to a medical condition and. 284–285 psychiatric illness related to a general medical condition and. 334 psychosis and. 195.

See also Cognitive impairment aging effects on cognitive performance and. 156 Electroencephalogram diagnosis of Alzheimer’s disease. 161– 162 Elder abuse. 273–274 of bipolar disorder. 237 frontotemporal dementia. 186. 198. See also Learning cognition in normal aging and. 232 Exercise. 252 delirium. 165. 371–373 Electrocardiogram in laboratory evaluation of delirium. 114. 318. 230 in laboratory evaluation of dementia. 333. 161 Experimental therapies. 192–195 of anxiety disorders. 139. 148 Estrogen. 145 Electroconvulsive therapy (ECT) major depression and. 32 competency assessment and. 185 lithium and.Index 401 Education. 331– 332. and changes in normal aging. 185 Emotions. 6. for depression. 111. of dementia. 117 psychotic depression and. 201 Creutzfeldt-Jakob disease. 320 Etiology. 159–160 Explicit memory. 44 treatment of depression and. 113 of delirium. 241 Erectile dysfunction (ED). See also Pathogenesis and pathology Executive functions. and Alzheimer’s disease. 157–159 manic episodes following. 261 of dementia. 27. 335 Escitalopram. and depression. 29 Mini-Mental State Examination and. 320–321 of Alzheimer’s disease. 229 of major depression. 111. 190 Endocrine system. 40–42 Endocrine disorders. 190–191. 261 dementia with Lewy bodies. and treatment of depression. and dementia. and insomnia. 194 Eszopiclone. 53 Ephedrine. and biological aging. 334. 92. 43–45. 330. 256–257 of dementia with Lewy bodies. 80 of substance abuse. 180 social context of aging and. 358 Executive Interview. 111. 166 tricyclic antidepressants and. 319. 328 Epidemiologic Catchment Area (ECA) Study. 30 . 237 of frontotemporal dementia. 273 Epidemiology of alcohol abuse and dependency. 326–327 of vascular dementia.

108 Friendship. 303. 75. 204 Galantamine Alzheimer’s disease and. 300 Financial decision making. 39 pharmacogenetics and. 232–233 Frontal lobe hypothesis. 290. 247 Gastrointestinal system. 215 vascular dementia and. 302 Fatality rate. 203. and neuropsychological model of normal aging. 53 Geriatric Depression Scale (GDS). 348 Functional magnetic resonance imaging (fMRI). 47–48 substance abuse and. 213. 232 Frontal Behavioral Inventory. 45–47 social context of aging and. and cognition in normal aging. 192–193. 29 personality and. Sigmund. 134 Fluphenazine. 318 Fluvoxamine. 236 Functional competency. 47–48 Frontal Assessment Battery (FAB). and legal surrogates. 292 Genetics. 216–217. for older drivers. See also Women Generalized anxiety disorder autonomic and psychomotor features of. 360 marriage and. 162 Filter hypothesis. 58 Genitourinary system. 100.402 Clinical Manual of Geriatric Psychiatry Family. 139. 248. 130 late-onset psychosis and. and social context of aging. 49–50 cognition in normal aging and. 231. for schizophrenia. 25 Frontal Systems Behavior Scale. 273 treatment of. 208 biological aging and. 29. 52 Gender. 142 Food and Drug Administration (FDA). 289. 75 . 103. 367. See also Caregivers grandparents and. 352 Freud. 277–278. 365 Financial status. 229–235. of frontotemporal dementia. 304 Flurazepam. 232 Frontotemporal dementia. 101. See also Family history Alzheimer’s disease and. and Alzheimer’s disease. 48 legal issue of undue influence and. 14. 329 Family history. 211–212 geriatric depression and. See also Mortality Fatigue. and social context of aging. 83 Feeling Good (Burns 1999). 275 diagnosis of. 279 prevalence of. 43–45 Fluoxetine depression and. 380–381 Geriatric Mental State Schedule. and depression. See also Genetics Family therapy dementia caregivers and. and biological aging. and depression. and psychosis. 142 receptor affinities of. 139. and biological aging.

130. 217. Complicated grief Group therapy geriatric depression and. Medical conditions. 251. 336 Haloperidol Alzheimer’s disease and. 353–354 Gingko biloba. 249 Hispanic Americans caregivers for dementia patients and. 104. 55–61 Hallucinations late-onset psychosis and. 3–6 Health and Retirement Study. 318 Grandparents. 264 psychosis and. 12– 14 poverty rates and. See Bereavement. 249. 363 Guidelines for diagnostic process with older adults. 220 bipolar disorder and. 45 HIV dementia. 181 patterns of health and aging in. and geriatric depression. 274– 275 Hamilton Rating Scale for Depression (Ham-D). and caregiving. 81. 214 Global Study of Sexual Attitudes and Behaviors. 78 Hamilton Anxiety Rating Scale. 7 Heart disease. 163 delirium and. 194 . 304 symptoms of depression induced by. and dementia. 101. 48 Grief. and competency. and Alzheimer’s disease. See also Health care. 331 Glutethimide. and Alzheimer’s disease. and depression. 49 Head injury dementia and. 211. 112 Health. Primary care physicians informed consent and. personality and perceptions of. See also Hospitalization. 296 psychotic depression and. 78 Guardians and guardianship. Public health Health care. 191 Heterogeneity. 330.Index 403 Gifts. 22– 23 Highly active antiretroviral therapy (HAART). 40. 212–213 Mini-Mental State Examination and. 349 overview of for older adults. 253 secondary mania and. 72–73 Heavy metals. 303. 348–349. 55 for treatment of older adults. Medicare. 128 Hormone replacement therapy. Nursing homes. 161 late-onset psychosis and. 132. 361–362. 250 Home visits. 302 Guanethidine. Insurance. 84 psychotic disorder due to a general medical condition and. 160 Hasegawa Dementia Scale. in patterns of aging. and depression. 181 Hayflick phenomenon. Medical evaluation.

See Web sites Interpersonal psychotherapy. 251. and aging effects on cognitive performance. 348–349. 219 insomnia and. for late-onset psychosis. 105. 319–320 Hypochondriasis. for medical care. See also Medicare Intelligence. 316 differential diagnosis of. 149 Hypnotic agents. 302 Insomnia. 3 Huntington’s disease. 86 Hypomania. 165–166 and side effects of monoamine oxidase inhibitors. 294 Internet. 26 International Classification of Sleep Disorders. 349 Incidental recall. 30 Implied consent. and dementia. 314 diagnostic criteria for. The (American Sleep Disorders Association 1997). 131 Implicit memory. 110–117 psychosis and. 54 IMPACT (Improving MoodPromoting Access to Collaborative Treatment) project. 112 Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE). 253 Hypertension caution with lithium and. 281– 283 Insight-oriented psychotherapy. Sedativehypnotics Alzheimer’s disease and.404 Clinical Manual of Geriatric Psychiatry Hospitalization anorexia and depression. 313. See also Benzodiazepines. 162 Imipramine. See also Sleep disturbance Alzheimer’s disease and. 30 Infectious diseases dementia and. and major depression. and barriers to geriatric mental health care. 352 Instruction directives. 11–12. 315–320 Institutional Review Board (IRB). and biological aging. 350 Instrumental Activities of Daily Living (IADL) Scale. 298 treatment of. 384–385 Insurance. 313–315 sleep hygiene and. 129–130 Intracavernosal self-injection. 316 International Late-Onset Schizophrenia Group. 90 rates of for older adults. 317 treatment of. 349 Inoculation hypothesis. 190 secondary mania and. 152 tricyclic antidepressants. 333–334 Isotretinoin. 219 assessment of. for geriatric depression. 184. 79 . 316. 184 Informed consent. for posttraumatic stress disorder. See also Bipolar disorder diagnosis of. 134 Immunological system.

360–362. 347–358 driving and. 245 Lamotrigine bipolar depression and. 240 dementia with. 203 of anxiety disorders. 95–96. 237–241 Life expectancy. 255 Korsakoff-type anemia. 181 Keep Your Brain Young (McKhann and Albert 2002). 358–360 Levodopa. 276 of delirium. 1–2. 254. 203 Lithium advantages and disadvantages of. 116 of vascular dementia. and depression. 2004). for treatment of depression. 165 Language aging effects on cognitive performance and. 234 of hypomania and mania. 164. 261 of dementia of unspecified type. 185 of depression. 97. 83 of psychosis. 371–373 surrogate decision-makers and. 259–260. 367–371 elder abuse and. 31 Legal issues caring for oneself and management of finances. 31 Knowledge. 30– 31. 137 Alzheimer’s disease and. 205. 79 Levonorgestrel implant. See also Age of onset of major depression. 157 bipolar disorder and. 108–109 Learning. See also Cognitive impairment.Index 405 Japan. and Hasegawa Dementia Scale. 202 Mini-Mental State Examination and. and Alzheimer’s disease. 154–155 . 235. 293–306 Learned helplessness. 128 Learning Throughout Life (National Retired Teachers Association et al. 321–322 Kraepelin. 219 augmentation of antidepressants. 33–34 psychotherapy for depression and. 12 Lifestyle modifications. 147 of frontotemporal dementia. 181 Late onset. Education cognition in normal aging and. 110 Lewy bodies. 161 List-learning tasks. 26 evaluation of Alzheimer’s disease and. 363–365 undue influence and. 179. See also Medical evaluation of Alzheimer’s disease. Emil. 15 Korsakoff ’s syndrome. 360–362 competency and. 115 Laboratory evaluation. needed for effective work with elderly patients. 79 Lewis. Sir Aubrey. 216.

204 and other dementias. 72 Longitudinal view. 263. 80. and depression. 234 vascular dementia. in partial remission. 190–191. 92 Management. 258 dementia and. 217 anxiety disorders and. 138 Marriage. 257. 249–254 depression due to. 252 dementia with Lewy bodies. 303 Loss. and social context of aging. See also Bereavement MacArthur Competence Assessment Tool—Treatment. 264 insomnia and. 110–117 psychosis and. Neurological disorders anxiety and. 71–72 diagnosis of. 129 insomnia and. 315 mania due to. of bipolar disorder. 331–332 Medical evaluation. 245 Maintenance treatment. 156 Major depression. 290. Neurological examination . 111. 45–47 Masked depression. 22 Long-term management. and acetaminophen. 336–337 sexual dysfunction and. of aging. 350. 85–87 Massachusetts Male Aging Study. 330 MCMI-III (Millon Clinical Multiaxial Inventory–III). 165 Long-term memory. 318 psychosis and. 70–76 diagnosis and treatment of depression and.406 Clinical Manual of Geriatric Psychiatry Lithium (continued) bipolar depression and. Health care. 163–166 Liver damage. 363 Longitudinal Aging Study Amsterdam. 298 treatment of. 338 Mania. 128 psychotic disorder due to. 203. 157– 159 Major depressive disorder. See also Health. 334–337 psychotherapy for depression and. 327 Living will. 98 Medical conditions. 162 MAOIs. 108. 112–113 psychiatric illness due to. 30 Lorazepam Alzheimer’s disease and. See Monoamine oxidase inhibitors Maprotiline. See also Laboratory evaluation. 277 delirium and. 291 delirium and. 358 Magnetic resonance imaging (MRI) and Alzheimer’s disease. 80–91 electroconvulsive therapy for. See also Depression chronic illness and. of chronic pain. with antidepressants. 157 bipolar disorder and. See also Bipolar disorder diagnosis of. 237 frontotemporal dementia.

183 Memory Prescription. 177. 78–79 diagnosis and treatment of depression and. 55– 61 insomnia and. and cognition in normal aging. 370–371 dementia induced by. 209 Mental activity. Working memory aging effects on cognitive performance and. See also Age of onset. 330 sexual dysfunction and. 247 Memory. See also Anticonvulsants. 332 signs and symptoms of mental disorder induced by. 165–166 vascular dementia and. Comorbidity. 159 psychotherapy for depression and. Psychopharmacotherapy. 30–32 Alzheimer’s disease and. 9 prevalence of for minority groups. 315 prescription of potentially addictive substances and. 129 guidelines for older adults and. 128 Memory and Behavior Problems Checklist. 37 electroconvulsive therapy and. 233 lithium therapy for bipolar disorder and. 212 Memory Impairment Screen (MIS). 329 Medications. 213– 214. 56 overview of in older adults. Treatment influence of aging on disorders of early onset. Antihypertensive agents. The (Small 2004). for Alzheimer’s disease. 33 competency to drive and.Index 407 dementia with Lewy bodies and. 5. See also Cognitive impairment. 277 cognitive changes of aging and monitoring of. 239 frontotemporal dementia and. 26–27. Psychiatric illness related to a general medical condition. Steroids. 29 Mental disorders. 79 Memantine Alzheimer’s disease and. 243–244 Medicare. 6–8. Antihistamines. 215 vascular dementia and. 56 Mefloquine. 11. Diagnosis. Antiepileptic agents. 339–341 medication-induced signs and symptoms of. 230– 231. 191 depression symptoms induced by. 202 clinical presentation of loss in old age. Withdrawal anxiety symptoms produced by. Treatment. 10 . 13–14 underrecognition of in older adults. Antiparkinsonian agents. 31 Memory training. Overdose. 208. 28.

34 delirium and. 248–249 Mixed episode. 174. 92–95 Mirtazapine advantages and disadvantages of. 179 schizophrenia and. and mania. 174. 31 Moclobemide depression and. 144 receptor affinities of. barriers to geriatric. 152. 155 frontotemporal dementia and. and depression. 11 working effectively with older adults. 138. See Mini-Mental State Examination MMPI-2 (Minnesota Multiphasic Personality Inventory–2). 323–324 Mild cognitive impairment. 79 Metronidazole. 235 Modafinil Alzheimer’s disease and. 117 MMSE. 339 Minnesota Multiphasic Personality Inventory–2 (MMPI-2). of hypomania and mania. 25 Millon Clinical Multiaxial Inventory– III (MCMI-III). 151. 35–38 Mild decline. 78 Methylphenidate advantages and disadvantages of. 112 Methyldopa. 152 Metabolic disturbances. 15–16 Mentally disabled persons. 177. 117 Mixed mood disorder. 153 . 78. 150. 175–177 vascular dementia and. 357 depression and. 88 frontotemporal dementia and. 175. 134 Mixed dementia. 257–259 dementia of unspecified cause and. 173–174. 98 Mini-Cog. 79 Meyer. See also Psychiatrists barriers to geriatric mental health care and. Adolf. 98 Mnemonic training. 136 depression and. 352 Mental status examination. See also Mini-Mental State Examination (MMSE) Alzheimer’s disease and. 137 Alzheimer’s disease and.408 Clinical Manual of Geriatric Psychiatry Mental health care. 153 Methylsergide. 110 Michigan Alcoholism Screening Test— Geriatric Version. 219 depression and. 182 Mini-Mental State Examination (MMSE) cognitive impairment and. 98 Minor depression. 8–12 Mental health professionals. 219 depression and. 79 Methyprylon. 178–181. 202 caution in interpretation of. 243 Meperidine. 318 Metoclopramide. 74. 232 sample items from. and competency.

73 Musculoskeletal system. and emotional changes in aging. 195. 371–372 National Household Survey on Drug Abuse. 149–153. 175 Neurobiochemistry. 112 Nervous system. 372 NEO Five-Factor Inventory (NEOFFI). 196 National Institute of Neurological and Communicative Disorders and Stroke (NINCDS). and depression. 325 Narcotic analgesics medication-induced mental disorders and. 352 National Center on Elder Abuse. 283. 78 Monoamine oxidase inhibitors (MAOIs) advantages and disadvantages of. See also Lithium Alzheimer’s disease and. 166 Morale. 219 bipolar disorder and. 328 symptoms of depression induced by. 72 Naltrexone. 154 drug-drug interactions and. 198– 199. Fatality rate delirium and rates of posthospitalization. See also Bipolar disorder. 263 poststroke depression and. and mania. 248 Mood stabilizers. 54 Myocardial infarction. 203 National Institutes of Health. Depression. and biological aging. Mixed mood disorder influence of aging on early-onset. 53 Neurobehavioral Cognitive Status Examination (NCSE). 207–208. 332 Mood disorders. See also Death. 98 Neoplasms. 25 Modified Ischemic Score. 78 National Bioethics Advisory Commission. of Alzheimer’s disease. 155 sexual dysfunction and. 109 Neglect. and elder abuse. for Alzheimer’s disease. 152–153. 244 Molindone. 339 mood disorder with anxiety and.Index 409 Moderate decline. 157 depression and. See also Neurotransmitters . and vascular dementia. 56 substance abuse and. 41 Mortality. and biological aging. 285 treatment of vascular dementia and. 174. 137 bipolar depression and. 139. 326 National Institute on Aging and Ronald and Nancy Reagan Institute of the Alzheimer’s Association criteria. 373 National Elder Abuse Incidence Study.

See also Neurobiological theories. 368–369 Neuropsychological tests. 116 depression and. 233– 234. 333 Nonbenzodiazepine hypnotics. Neuropsychological tests. 186. 109–110 New Jersey. 110 Neurotransmitters. 74. 286–288 of bipolar disorder. See also Neuropsychology. 243–244 Neuropathology. 239 for vascular dementia. 244–245 Neuropsychology. and depression. 214 caution with lithium and. and anxiety disorders.410 Clinical Manual of Geriatric Psychiatry Neurobiological theories. 24–25. 388 Neuropsychological Assessment Battery. to antidepressants. 315 Nonamnestic mild cognitive impairment. 299–300 Neurofibrillary tangles. 338 competency to drive and. See also Analgesics Alzheimer’s disease and. 165–166 chronic pain and. 193–194. 351– 352 Nocturnal myoclonus. Neurobiological theories anxiety disorders and. Neurotransmitters of anxiety disorders. and In re Conroy case. 202–203 for dementia with Lewy bodies. See also Neuropsychology. 36 Nonarteritic anterior ischemic optic neuropathy (NAION). See also Neuropathology dementia and. 67 . 206 Neuroleptics. 113 Neurological examination for dementia with Lewy bodies. 233. 371 substance abuse and. 296–297 for vascular dementia. 116 of depression. 328 symptoms of depression induced by. See Antipsychotics. Atypical antipsychotics Neurological disorders. of Alzheimer’s disease. and cognitive changes in aging. 184–185. See also Neurobiochemistry. 190 secondary mania and. 319– 320 Nonresponse. 195–197. 109–110 of psychosis. 154 Nonsteroidal anti-inflammatory agents (NSAIDs). 286–287 Normative fallacy. 239–240 for dementia of unspecified cause. 212. 187–189 for frontotemporal dementia. 286–288 bipolar disorder and. 236 for psychosis. 78 Noradrenergic system. and Alzheimer’s disease. Neurotransmitters Neuroticism. 206–207 Neuropsychiatric Inventory (NPI). Rating scales for Alzheimer’s disease.

183. 282 prevalence of. 3 Object Memory Evaluation. and medication guidelines for older adults. 21–22 health and functioning of. and symptoms of depression. 237. 289–290. 382 Overdose. 248 Older adults. Very old people barriers to mental health care for. 291 insomnia and. 1–2 mental disorders in later life and. in older adults. 174. 76 Paroxetine depression and. 4–5 substance abuse and. 177. 61 Oxazepam anxiety disorders and. 290. 220 bipolar disorder and. 61 Oral contraceptives. 52–54 Orientation-Memory-Concentration Test (OMCT). 253 depression and. 134 NSAIDs. 329 Nutritional disorders. 9 health care for older adults and. 9 working effectively with. 273 treatment of. 251. 281. 79 Orbitofrontal syndrome. 163 delirium and. 273 treatment of. 292. 139. 335–336 Organ systems. 235 receptor affinities of. 264 psychosis and. 148 receptor affinities of. 293 Olanzapine Alzheimer’s disease and. 302–303. 338 Optimistic and supportive attitude. and dementia with Lewy bodies. 304 vascular dementia and. See Nonsteroidal antiinflammatory agents Nursing homes barriers to geriatric mental health care and. 8– 12 definition of. 279–281. and treatment of older adults. 275 diagnosis of. 134 . 8 Opioids. See also Age and aging. and biological aging. 188 Obsessive-compulsive disorder diagnosis of.Index 411 Nortriptyline depression and. and chronic pain. and dementia. 328 Pain. 142 frontotemporal dementia and. 238. 318 Oxycodone. 15–16 Omnibus Budget Reconciliation Act (1987). See Chronic pain Panic disorder and panic attack autonomic and psychomotor features of. 239 Parkinson’s disease dementia and. 3–6 increase in population of. 190–191 Obesity. 145–146. 216. 292–293 Parkinsonism. 217. 6– 8. 283 prevalence of.

334 Penn State Worry Questionnaire. 250 and dementia. 328 Phenylpropanolamine. 240 frontotemporal dementia. 298–300 vascular dementia and. 237 and Parkinson’s disease. and depression. 234–235 psychosis and. 105 Patient history Alzheimer’s disease and. 231 general dementia and. 328 Phobias diagnosis of. 199–202 delirium and. 185 and dementia with Lewy bodies. 243 Pathogenesis and pathology. 203. 115–116 delirium and. 273 Phosphodiesterase-5 inhibitors. 57–58 Phencyclidine. 278–279 prevalence of. 251 Poststroke depression. increase of older adults as percentage of. for effective work with elderly patients. 16 Pharmacokinetic and psychodynamic changes. and delirium. 204. 173 vascular dementia and. 286–288 bipolar disorder and. 242 Patient Self-Determination Act of 1990. 264 Pick’s disease. 333 Physical examination. in normal aging. 201. 318 Perceptual changes. 257 dementia with Lewy bodies and. 102. of cognitive deficits in vascular dementia. 45 Pentobarbital. and psychosis. 300 Phenelzine. 252 Pittsburgh Compound-B (PIB). and insomnia.412 Clinical Manual of Geriatric Psychiatry Patchiness. influence of aging on early-onset forms of. 150. and dementia. 246–247 Patient Health Questionnaire (PHQ9). 334–336 Personality disorders. See also Etiology anxiety disorders and. 238 frontotemporal dementia and. 152 Phenothiazines. See Primary care physicians Physostigmine. and medications for older adults. 78 Phenylephrine. 276 Pension programs. 340–341 Personal qualities. 24 Perphenazine. 73 . 38–43 cognition in normal aging and. 1–2 Positron emission tomography (PET) and Alzheimer’s disease. 204 Population. 263. and financial status. 29 psychiatric illness related to a general medical condition and. 304 Personality changes of in normal aging. 262 dementia with Lewy bodies and. 349–350 Penile prosthesis. See Medical evaluation Physicians.

247 Primary aging. 348 Pretreatment evaluation. 198–199. 16 Prognosis. 231 Propentofylline. among elderly. 78 Prospective memory. 320–321 of Alzheimer’s disease. 165–166 Prevalence. 363. 192–195 for suicidality. See also Health care alcohol abuse and. 369. 128 Problem Solving Treatment in Primary Care (PST-PC). 115 of depression. 350–351 Pseudodelirium. 131 Processing speed. 15–16 Psychodynamic theories of anxiety disorders. 11 working effectively with older adults. 203 Probate. 363–365 Problem-solving therapy. 52–54 Primary care physicians. for geriatric depression. 7. for elderly patients with delirium.Index 413 Posttraumatic stress disorder (PTSD). 30 Protective factors for Alzheimer’s disease. 281–283. for lithium therapy. 328 Propranolol. 91 Primary insomnia. 106 barriers to geriatric mental health care and. See also Epidemiology of age-associated memory impairment. 23. 286 of bipolar disorder. 50. 49. 256–257 of frontotemporal dementia. 298–299 . 229 of major depression. 193 of anxiety disorders. 315. 316 Probable Alzheimer’s disease. 284–285 Poverty. 350. 273 of delirium. of vascular dementia. See also Mental health professionals barriers to geriatric mental health care and. 371 elder abuse and. 372–373 Primary dysthymia. 325 assessment of suicidality and. and vascular dementia. 45 Power of attorney. 365 Prednisone. 10–11 competency to drive and. 80 Prevention. and surrogate decision-makers. 264 Progressive nonfluent aphasia. 107 Proxy directives. and cognitive abilities. 247–248 Propoxyphene. 334–337 Psychiatrists. 108 of psychosis. 35 of alcohol abuse and dependency. 79 President’s Commission for the Study of Ethical Problems in Medicine and Biomedical and Behavioral Research (1982). for effective work with elderly patients. 27 Professional approaches. 262 Psychiatric illness related to a general medical condition.

96– 97. 208–210 Psychosocial therapy for anxiety disorders. 290–293 for bipolar depression. 248 Psychosocial theory. 298–300 risk factors for. 293–294 medications for agitation in Alzheimer’s disease and. 163–166 for delirium. See also Antidepressants. 277 depression and. Benzodiazepines. 294. Beta-blockers. 220 neuropsychological tests for. Drug-drug interactions. 317–320 for late-onset psychosis. 296 differential diagnosis of. 56 research on for depression. Anxiolytic agents. Augmentation. 298. and depression. 156 Psychosis. 248. Medications. 157 for bipolar disorder. 213–220 for anxiety disorders. 127–130 guidelines for treatment of older adults and. 300–302 Psychostimulants advantages and disadvantages of. Psychotic disorder due to a general medical condition. Schizophrenia clinical presentation of. of Alzheimer’s disease. Family therapy. 210–213 for geriatric depression. 337 epidemiology of. 158 for geriatric depression. 156 . 34–35 for alcohol abuse or dependency. 162–163 for late-onset psychosis. 93 treatment of. 288–290 for bipolar disorder. 325 for Alzheimer’s disease. Dosage. Antipsychotics. Supportive therapy. Monoamine oxidase inhibitors.414 Clinical Manual of Geriatric Psychiatry Psychological tests. 137 Alzheimer’s disease and. 132–156 for insomnia. 210 for dementia caregivers. 294 subsyndromal depression and. 325–326 for Alzheimer’s disease. 300–306 vascular dementia and. 83–85. See also Psychotic depression. Treatment age-related cognitive changes and. 219 anxiety symptoms induced by. 153 Psychotherapy. Treatment for alcohol abuse or dependency. See also Neuropsychological tests Psychopharmacotherapy. 130–132 Psychotic depression. Psychosocial therapy. Sedativehypnotics. Psychostimulants. See also Cognitivebehavioral therapy. 296– 297 pathogenesis of. Side effects. 263–264 electroconvulsive therapy and. Maintenance treatment. Group therapy. 302–306 for psychotic depression. Selective serotonin reuptake inhibitors. Mood stabilizers.

184 for anxiety disorders. 10 Relaxation training. 232– 233 Recent memory. 241 psychosis and. for geriatric mental health care. 12–14. 174–183 for depression. 255–256 Revised Memory and Behavior Problems Checklist. 78 Resources for Enhancing Alzheimer’s Caregiver health (REACH). Hispanic Americans Ranitidine hydrochloride. 69 Referrals. of bereavement. 79 Rating scales. See also Neuropsychological tests. 284–285 Public health. 48 Reminiscence therapy for Alzheimer’s disease. 274 Quetiapine Alzheimer’s disease and. 217. 98 Risk factors for alcohol abuse or dependency. 30. 192–195 for major depression. 304 Race. and anxiety disorders. 353 on psychotherapy for geriatric depression. 67 Quality of life. 130 Remote memory. 321 for Alzheimer’s disease. 353–354 Reversible dementia. 211. and diversity in patterns of health and aging. 386–387 Revised NEO Personality Inventory (NEO-PI-R). 336–337 PTSD (posttraumatic stress disorder). Contracts 2d (American Law Institute 1981). and social context of aging.Index 415 Psychotic disorder due to a general medical condition. 107 for vascular dementia. 97–105 for frontotemporal dementia. See also Black Americans. 303. 357–358 Repetitive transcranial magnetic stimulation (rTMS). and depression in later life. 29. and biological aging. Standardized tests for activities of daily living. 159 Research competency to enroll in studies. 242 . 212 Respiratory system. 80 for suicidality. and depression. 30 Recovery phase. 106. 352. 281–283. 209 for geriatric depression. 52 Restatement of the Law Second. 220 dementia with Lewy bodies and. 216. 130–132 Reserpine. 274 for cognitive impairment. 290 Religion. for obsessivecompulsive disorder.

293 bipolar depression and. 100. for depression. 28 . 206 Sensory changes. 220 anxiety disorders and. and pathogenesis of anxiety disorders. 318 Secondary aging. 157 geriatric depression and. 292 bipolar disorder and. 58–59 Sexual dysfunction. 232– 233. 339 anxiety and. 326. 318 substance abuse and. 49 Secondary dysthymia. See also Hypnotic agents insomnia and. 304 vascular dementia and. 151. See also Psychosis aging and early-onset. 248 Rivastigmine Alzheimer’s disease and. 161 memory function in old age and. 295 Screening instruments. and depression. for frontotemporal dementia. 24. 288 Sertraline anxiety disorders and. 247 Rorschach Inkblot Test. and Alzheimer’s disease. 54 treatment of depression and.416 Clinical Manual of Geriatric Psychiatry Risperidone Alzheimer’s disease and. 219 anxiety disorders and. 139. 231 Senile plaques. 218 dementia with Lewy bodies and. 292–293 depression and. 214 depression and. and secondary mania. 241 frontotemporal dementia and. 128 Serotonin system. 328 symptoms of depression induced by. See also Visual acuity normal aging and. 142. 99. 31–32 Self-report scales. John’s wort. 329–334 Short-term memory. See also Rating scales Seattle Longitudinal Study. 235 vascular dementia and. 161 Schizoid disorder. 150. 285–286 St. 91 Sedative-hypnotics. 72 sexual dysfunction and. 215. 216. 285–286 diagnostic criteria for. 136. for treatment of older adults. 22 Secobarbital. 112 Selective serotonin reuptake inhibitors (SSRIs) Alzheimer’s disease and. 217. 148 receptor affinities of. 163 psychosis and. 340–341 Schizophrenia. 152 Self-help materials Alzheimer’s disease and. 302. 148 heart disease and. 332 Selegiline Alzheimer’s disease and. 78 Seizure disorders. 133. 138–145. 134 Setting. 213 depression and. 104–105 Semantic dementia.

280 Spielberger State-Trait Anxiety Inventory. 177. 254–255 . of aging. 111. 96 Social clock. and dementia. 328–329 Substance-induced insomnia. 201. 315 Sleep evaluation. 60 lithium and. 191 Specific phobia. 327 diagnostic criteria for. 333 Simple consent. 275 Stage theories. 56. 166 monoamine oxidase inhibitors and. 276 Six-Item Orientation-MemoryConcentration Test. and depression. See also Insomnia dementia with Lewy bodies and. 85 Somatization disorder. 112 Substance-induced mood disorder. 174. 21. 152 Sildenafil. 73 vascular dementia and. 83. 83 sleep apnea. 242 Substance abuse. 77 treatment of. 43–48 Social Security. 43–44. 79 Stroke depression following. and social context of aging. 39–40 Standardized tests. 323 distinguishing substance use from. 250 and dementia with Lewy bodies. 39 Social context. 349 Single photon emission computed tomography (SPECT) and Alzheimer’s disease. 47 Side effects. and major depression. 237 and frontotemporal dementia. of personality. 327–328 epidemiology of. 194–195 Steroids. 183.Index 417 Sibling relationships. 76– 80 Substance-induced persisting dementia. 86 Somnolent or hypoactive subtype. See also Alcohol and alcohol abuse common patterns of. See also Rating scales Statins. 45 Somatic complaints. 274. 304–305 guidelines for treatment of older adults and. 322. of delirium. 326–327 prescription of potentially addictive substances and. 148–149 antipsychotics and atypical antipsychotics. 382 Sleep disturbance. 237 major depression and. of decisional competency. of medications antidepressants for geriatric depression and. 330 substance-induced mood disorder and. and Alzheimer’s disease. and medication-induced mental disorders and. 258 Space-occupying lesions. 234 Situational anxiety. 203– 204. 315 Substance-induced mania. 358.

368 Tramadol. 134 sexual dysfunction and. 350 Subthreshold depression. 96 Time course. 263–264 of dementia with Lewy bodies. doctrine of. Psychopharmacotherapy.418 Clinical Manual of Geriatric Psychiatry Substitute decision makers. 240– 241 . 138. 107 Supportive therapy for Alzheimer’s disease. 372 Texas Medication Algorithm Project. 216. 210 for late-onset psychosis. of mental disorders in older adults. 304 Thiothixene. 350. 291 Testamentary capacity. 318 pharmacological properties of. 217. 338 Tranylcypromine. 354–356 Testosterone. 213 Tadalafil. 217. 99. 320 receptor affinities of. 332–333 Texas. 158 Thiazide diuretics. Psychotherapy. and elder abuse. and electroconvulsive therapy. 332 Treatment. 156 Thematic Apperception Test (TAT). and treatment of older adults. of normal grief. 191 Tacrine. 351– 352 Substituted judgment. and depression. 235 Telomeric shortening. Undertreatment of anxiety disorders. 333 Target symptoms. 285–286 Theophylline. 191 Trail Making Test (TMT). Compliance. and Alzheimer’s disease. 162–166 of delirium. 363–365 Sydenham’s chorea. 49–50 Temazepam insomnia and. 277 Systemic disorders. 304 Thyroid function. 152 Trazodone advantages and disadvantages of. and dementia. 235 insomnia and. 189. and depression. 274. 301–302 Surrogate decision-makers. 220 depression and. Combined treatment. 105–106. 150– 151. Medications. 78 Thioridazine. See also Clinical implications. 194 Toxins. 92–95 Suicide and suicidality anxiety disorders and. 59 Tau-positive pathology. 69 Tocopherol forms. of frontotemporal dementia. and dementia. and depression. 335 Sympathomimetics. and treatment of sexual dysfunction. and anxiety. 288–293 of bipolar disorder. 278 assessment of in elderly. 136 Alzheimer’s disease and. 146 frontotemporal dementia and.

138. 245 neuropsychological tests and. and insomnia. and Alzheimer’s disease. 155 Trusts. 250 epidemiology of. 162 of insomnia. 10 Undertreatment. 358–360 Uniform Probate Code. 365 Twin studies. 368 Vagus nerve stimulation. 304 Triiodothyronine. 219 Vardenafil. 315–320 of late-onset psychosis. 335 of frontotemporal dementia. and augmentation of antidepressants. 335 of substance abuse. 333 Vascular dementia clinical presentation of. and dementia. and depression. 372 Useful Field of View (UFOV). 144. 133. 242 physical and neurological examinations for. 247–248 Treatment resistance. 109 Vascular disorders. 145–146. 73–74 diagnosis of. 220 Valproic acid. 332–334. 156 Trifluoperazine. 134 sexual dysfunction and. 160 Valproate. 148 receptor affinities of. 332 . 241 laboratory evaluation of. 247 treatment of. of mental health problems in older adults.S. mental health problems in older adults. 361 U. 138. 105. 136 bipolar depression and. 300–306 of psychotic disorder due to a medical condition. See also Antidepressants advantages and disadvantages of. 218. 149. 356. 247–248 Vascular depression. and Alzheimer’s disease. 243–244 prevention of. Preventive Services Task Force. 136 depression and. 246–247 patient history in. 157 geriatric depression and. of Alzheimer’s disease. 191 Vascular lesions. 337 of sexual dysfunction. 244– 245 pathogenesis of. 245–246. 60. 153–155 Triazolam. 74–76. 67–68 Undue influence. 154 psychotic depression and. 243 depression and. and mania. and question of voluntariness. and competency.Index 419 of erectile dysfunction. 235 guidelines for. 241–242. 55–61 of hypomania and mania. 243 differential diagnosis of. 208 Underrecognition. 317–318 Tricyclic antidepressants (TCAs). and antidepressants. 112 Venlafaxine advantages and disadvantages of. 328–329 of vascular dementia.

and Alzheimer’s disease. 354–356. and social context of aging. 277 delirium and. 294. 275 Xanthine derivatives. 296. for information on Alzheimer’s disease. and anxiety. 277 Zaleplon. 194. 44 personality changes during aging and. See also Age and aging definition of “old-old” and. 194 Word List Learning. 73 Visual acuity. 1 Veterans Affairs.420 Clinical Manual of Geriatric Psychiatry Very-late-onset schizophrenia-like psychosis (VLOSLP). 357 Wechsler Memory Scale. 358–360 Voluntary consent. and competency. 23–24. 189 Withdrawal. 274. 28. 318. 39 poststroke depression in. See also Living will Will substitution test. and normal aging. and aging effects on cognitive performance. 319–320 Ziprasidone bipolar disorder and. 359 Wisconsin Card Sorting Test. and undue influence. 294 widowhood and. 61 Women diversity in patterns of health and aging. 45 social context of aging and. 368 Visuospatial ability. from medications anxiety and. 187 Widowhood. and insomnia. 21 as percentage of population. 297. 45–47 Wills. and social context of aging. 43– 45 Working memory. 163 dementia with Lewy bodies and. 241 psychosis and. 319–320 . 75 very-late-onset schizophrenia-like psychosis and. 352 Web sites. 27 Vitamin B deficiency. and Alzheimer’s disease. 301. 73 poverty and. 373 Wechsler Adult Intelligence Scale. 214 Voluntariness. 45–47 Women’s Health Initiative Memory Study. and undue influence. 187. 28 Worry Scale. 298. 194 Vitamin E. 318. 304 Zolpidem. and insomnia. 203 Work. 256 Vitamin C. and dementia. 263 guidelines for treatment of older adults and. 213 on elder abuse. 24. 48 vascular depression and. 29 employment trends for. 303 Very old people (85 years and older). 303. 14–15. and Alzheimer’s disease.