The Canadian Review of

Volume 11, Number 3 • September 2008

FOCUS ON AD and Concomitant Conditions Osteoporosis in the AD Patient

4

Brian Wirzba, MD, FRCPC

Will the Real Pseudodementia Please Stand Up! Art by Josef, 1920-2007 Tel-Aviv, Israel

11

Ron Keren, MD, FRCPC

Hip Fractures and AD

15

Susan Freter, MSc, MD, FRCPC; and Kata Koller, MD, FRCPC

Pain in Severe Dementia: How to Assess

21

Maryse Savoie, RN, MSc

Safely Home® The Alzheimer Society of Canada

The Review is online! You can find us at: www.stacommunications.com/adreview.html

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The Canadian Review of

On the Cover…

Photograph by Dalia Gottlieb-Tanaka, PhD Chair of The Society for the Arts in Dementia Care

Josef (1920-2007), the artist of this month’s cover artwork, was a professor of philosophy who had never painted until he came to the day care-center at the Ichilov Medical Center in Tel Aviv, Israel. He loved working with colors and being involved in the process of painting—he was proud of his work. Dr. Dalia Gottlieb-Tanaka collected Josef’s watercolor on her visit to this care-center. The center specializes in evaluation, treatment and research (through the Psycho-geriatric Center) and includes day care for seniors with dementia. Staff members believe in providing a safe, supportive and encouraging environment that strengthens the identity and quality of life of their clients. Rivka Magen, a certified art rehabilitation instructor, developed many techniques to help her clients create artwork. “Painting touches the soul of an artist and helps them express their feelings,” she said.

Editorial Board CHAIRMAN Peter N. McCracken, MD, FRCPC Professor Emeritus of Medicine, Division of Geriatric Medicine University of Alberta Edmonton, Alberta Paul J. Coolican, MD, CCFP, FCFP Family Physician, St. Lawrence Medical Clinic Morrisburg, Ontario Active Staff, Winchester District Memorial Hospital Winchester, Ontario Shannon Daly, RN, MN Clinical Nurse Specialist in Geriatrics Grey Nuns Community Hospital & Health Centre Edmonton, Alberta Howard Feldman, MD, FRCPC Professor of Medicine, Division of Neurology, University of British Columbia (UBC) Director, UBC Alzheimer Clinical Trials Unit Vancouver, British Columbia

Serge Gauthier, MD, CM, FRCPC Professor of Neurology and Neurosurgery, Psychiatry and Medicine, McGill University McGill Centre for Studies in Aging Montreal, Quebec Bernard Groulx, MD, CM, FRCPC Chief Psychiatrist, Ste-Anne-de-Bellevue Hospital Associate Professor, McGill University McGill Centre for Studies in Aging Montreal, Quebec Nathan Herrmann, MD, FRCPC Professor, University of Toronto Head of the Division of Geriatric Psychiatry, Sunnybrook Health Science Centre Toronto, Ontario

Peter J. Lin, MD, CCFP Past Medical Director, University of Toronto Health & Wellness Centre at Scarborough Director, Primary Care Initiatives, Canadian Heart Research Centre Medical Director, LinCorp Medical Inc. Toronto, Ontario Kenneth Rockwood, MD, MPA, FRCPC Professor of Geriatric and Neurology Medicine, Kathryn Allen Weldon Chair Professor in Alzheimer Research, Dalhousie University Director, Canadian Dementia Knowledge Translation Network Halifax, Nova Scotia

The editorial board has complete independence in reviewing the articles appearing in this publication and is responsible for their accuracy. The advertisers exert no influence on the selection or the content of material published.

Publishing Staff Paul F. Brand Executive Editor

Mandi Watson Managing Editor

Donna Graham Production Manager

Jennifer Brennan Financial Services

Russell Krackovitch Editorial Director, Custom Division

Nathalie Ebata Editor-proofreader, French

Dan Oldfield Design Director

Sherri Tobin Administrative Assistant

Robert E. Passaretti Publisher

Copyright 2008 STA HealthCare Communications Inc. All rights reserved. The Canadian Review of Alzheimer’s Disease and Other Dementias is published by STA Communications Inc. The opinions expressed herein are those of the authors and do not necessarily reflect the views of the publisher. Physicians should take into account the patient’s individual condition and consult officially approved product monographs before making any diagnosis or treatment, or following any procedure based on suggestions made in this document. Publications Agreement Number 40063348. 2 • The Canadian Review of Alzheimer’s Disease and Other Dementias

E D I T O R I A L

Addressing Concomitant Conditions in Patients with Alzheimer’s Disease By Paul J. Coolican

T

his issue of The Canadian Review of Alzheimer’s Disease and Other Dementias deals with a number of interrelated topics relevant to most family physicians. The topics discussed include osteoporosis, pseudodementia, hip fractures, and pain. I remember as a young physician I had an elderly patient who had fallen and had been seen in the emergency department. An x-ray of her hip was reported as negative, surprisingly, as she could/would not bear weight on it. When her family tried to get her up and moving—worried she might develop a blood clot—she became increasingly agitated and was still unwilling to put any weight on her hip. By the time I saw her, her previously undisplaced hip fracture had slipped and she now had significant leg-length shortening and pain with any movement. A repeat x-ray confirmed the diagnosis: hip fracture. She underwent surgical

repair, had a prolonged hospital stay related to her mental status, and eventually was placed in a nursing home. After several months at the nursing home, her mental state improved. At the time, I remember we thought she had pseudodementia. Shortly after moving her to a nursing home, she was prescribed doxepin (an older antidepressant). In retrospect, I think she likely had mild dementia that was complicated by an episode of delirium. After a period of having her in a stable health environment, she improved back to her premorbid state. The article in this issue on pseudodementia is a balanced review of the relationship between dementia and depression, as well as an interesting review of pseudodementia. It is an excellent read. The remaining articles are complementary, with a lot of useful information to family doctors, addressing osteoporosis, hip fractures and pain, as they relate to dementia.

The Canadian Review of Alzheimer’s Disease and Other Dementias • 3

AD and Concomitant Conditions

Osteoporosis in the AD Patient Osteoporosis (OP) is a common disease that is characterized by low bone mass and microarchitectural disruption, which together lead to skeletal fragility, resulting in increased risk of fracture. Once a patient has fractured, their future risk of fracture is increased approximately four fold. Although adverse effects occur across the broad range of patients that suffer OP-related fractures, patients with Alzheimer’s disease may be even more susceptible to some of the adverse outcomes. By Brian Wirzba, MD, FRCPC

O

steoporosis (OP) is a common condition that affects approximately 1.4 million Canadians. It has been termed “the silent thief” as it remains completely asymptomatic until the patient suffers a fracture, at which point it can have a major impact on morbidity and mortality. Despite this, its importance in the elderly is often minimized as some patients and even healthcare providers still consider it a “natural” part of the aging process. Although it is certainly true that declines in bone density and the associated increased risk of fractures progress with age, our current knowledge of OP and how to effectively treat it allows us to reduce the risk of fractures in the Brian Wirzba, MD, FRCPC Specialist in General Internal Medicine and Medical Director of the Grey Nuns Hospital, Osteporosis Program, Edmonton, Alberta.

same way we reduce the risk of other age-related conditions such as cardiac events, cognitive decline and cancer (to name a few). Of course, fracture elimination is not possible, but by treating those at highest risk and by reducing their risk we can significantly improve their quality of life. In recent years, the trend to utilize Fracture Assessment Tools to estimate the five- or 10-year risk of fracture has allowed primary-care physicians to assess their patients’ risk in a manner very similar to using the Framingham study data to estimate 10-year risk of a cardiac event. This not only allows physicians to reassure younger patients with few risk factors of their low-risk status (where lifestyle interventions alone may be adequate) but has also emphasized just how high the risk is in the frail elderly population. There is no clear link between OP and Alzheimer’s disease (AD)

4 • The Canadian Review of Alzheimer’s Disease and Other Dementias

yet the two conditions often coexist. The understanding of the assessment and management of the OP patient is therefore essential for the physician caring for the AD patient. This article answers some of the most common questions asked about OP assessment and management of the elderly patient, and why patients with AD need their fracture risk assessed.

Why is Osteoporosis Something That Needs to be Considered in my AD Patients? Like many other disease states, we are often aware that the patient in our clinic may have some risk factors for OP but are not certain whether or not to be concerned about the likelihood of them eventually “suffering” from the condition. This is particularly true for asymptomatic conditions such as OP when the patient is not currently

Osteoporosis

being “bothered” by their disease and when they may have other conditions that are actively hindering their daily physical, mental or emotional wellbeing. However, the reality of the situation is that it is not the thinning of bones themselves that is the problem for the patient, rather it is the fact that thin bones fracture and these fractures can have a major impact on quantity and quality of life. Once a patient has fractured, their future risk of fracture is increased approximately four fold. We also know that 20% of patients die within one year after a hip fracture while only 50% return to their pre-fracture functional status— 20% require institutionalization.1 In an elderly patient with other comorbities their ability to recover is further hindered. Delirium may develop following fractures related to the pain associated with fractures, pain medication use, changes in environment (such as hospitalization) or altered functional capacity. Pulmonary and gastrointestinal compromise has also been described with progressive vertebral fractures and its associated kyphosis. Although these adverse effects occur across the broad range of patients that suffer OP-related fractures, patients with AD are not immune and may be more susceptible to some of the adverse outcomes, such as delirium.

Why Are the Elderly More Susceptible to Fracture? OP is a common disease that is characterized by low bone mass

and microarchitectural disruption, which together lead to skeletal fragility and resulting increased risk of fracture.2 Unfortunately the only test readily available to assess for OP is a Bone Density Scan (DEXA) which can estimate bone mass (or bone quantity) reasonably well. Despite significant interest and research into other radiologic or laboratory modalities, to date, no clinically useful test for the microarchitectural changes (or bone quality) has been identified. With age, the

estrogen deficiency-related postmenopausal OP which primarily affects trabecular bone (such as that found in vertebrae), and senile OP which more frequently affects cortical bone, predisposing older women and men to hip fractures.4 Although the former mechanism may lead to increased rapid bone loss for female patients in the early postmenopausal years, the latter process leads to a 0.5% per year bone density loss well into the elderly years. This loss occurs due to periosteal apposition from the out-

Changes in bone quality occur for a variety of reasons beginning at a young age when the skeleton is still maturing. Peak bone density and its optimal “strength” generally occur in the third and fourth decades of life, after which a gradual decline in quantity and quality occurs. rates of fracture increase exponentially, certainly more than would be expected based upon loss of bone mass alone. Changes in bone quality occur for a variety of reasons, beginning at a young age when the skeleton is still maturing. Peak bone density and its optimal “strength” generally occur in the third and fourth decades of life, after which a gradual decline in quantity and quality occurs. In their recent review of the mechanisms of senile OP, Duque and Troen3 describe the two main pathophysiological processes that generate bone loss. There is the more commonly recognized

side of bones (more pronounced in women compared to men) and endosteal bone resorption on the inside of the bone, both of which lead to a mechanically more fragile macroarchitecture. It has also been noted that senile OP involves the accumulation of bone marrow fat at the expense of osteoblastogenesis5 thereby negatively affecting the microarchitecture. One potentially preventable risk factor for microarchitectual changes that affects all ages but is particularly important in the frail or institutionalized elderly patient is vitamin D insufficiency. Despite being readily treatable, this condi-

The Canadian Review of Alzheimer’s Disease and Other Dementias • 5

AD and Concomitant Conditions tion remains extremely common,6 particularly in the elderly who generally have decreased intake of vitamin D-rich foods, lower levels of sunlight exposure and, even if sunlight exposure does occur, suffer from the age-related reduced ability to metabolize vitamin D in

in risk of vertebral and non-vertebral fractures.10 At the same time, primary-care physicians have become very familiar with the use multifactorial risk assessment tools such as those based upon Framingham data to estimate a patient’s risk of a cardiac event.

One potentially preventable risk factor for microarchitectual changes that affects all ages but is particularly important in the frail or institutionalized elderly patient is vitamin D insufficiency. the skin.7 This hypovitaminosis D often leads to secondary hyperparathyroidism and its subsequent enhanced osteoclastic bone resorption.8

How Can a Patient’s Risk of Fracture Be Assessed? Despite all we know about OP and the risk factors of fracture, we do not have a crystal ball that tells us exactly who will fracture and when. Like every other area of medicine, we deal with risk and risk reduction (not elimination). With more than 80% of low trauma fractures occuring in people who do not have a T-score below -2.5 (the definition of “osteoporosis” utilized in bone mineral density [BMD] reports)9 it is very apparent that we need more than just BMD to estimate fracture risk. In addition, changes in bone density in people taking antiresorptive drugs explains only 4% to 30% of the reduction

Such tools allow for a more realistic estimate of what the individual patient’s risk really is if they do not undergo therapeutic interventions. Although a number of such tools are available for OP, including one that is suggested for use when reporting (dual-energy x-ray absorptiometry (DXA) results,11 perhaps one of the most robust tools has recently been published by the World Health Organization12 and is available online at www.shef.ac.uk/FRAX. This FRAXTM fracture assessment tool is based upon international data and, after entering some basic clinical risk factors (Table 1) and the femoral neck bone density (T-score or Z-score) a 10-year risk of hip fracture and major osteoporotic fracture (clinical spine, forearm, hip, or shoulder) is provided. Although this tool may have some drawbacks (such as the use of femoral neck BMD rather than potentially lower BMD sites, underestimation in patients with particularly strong per-

6 • The Canadian Review of Alzheimer’s Disease and Other Dementias

sonal or family fracture histories, and the absence of a specific Canadian calculation tool), it is very simple to use and relatively intuitive, yet robust and well validated. The resulting 10-year fracture risk assessment can then be used to discuss with the patient or family member the magnitude of risk, with a value of approximately 15% risk of hip fracture being considered by many to be an appropriate treatment intervention threshold. The use of antiresorptive therapy would be expected to reduce the risk of fracture by 40% to 50% over the first three years (the duration of most randomized control trials). Their effect over 10 years (compared to placebo) is unknown and unstudied but they are thought to remain effective with such long-term use. As a result it is also important to note that once a patient is taking an antiresorptive agent their risk of fracture is reduced (assuming the medication is taken appropriately and appropriately absorbed), although the exact degree of reduction is unknown. By utilizing this method of assessment, one can avoid the overtreatment of the low-risk patient (10-year fracture risk < 10%) as well as the undertreatment of those at highest risk (10-year fracture risk > 20%)— two problems that are unfortunately all too common and propagated by an over-reliance on BMD values alone.

Osteoporosis What Are The Treatment Options for Osteoporosis? Exercise. Fracture risk-reduction treatment options include lifestyle measures as well as pharmacologic means. Bone density is known to be higher in physically active people and exercise does reduce the rate of age-related bone loss.13 Despite several studies in elderly patients that have shown surrogate endpoint benefit (BMD, bone turnover markers, balance, leg strength), none have been large enough or designed to demonstrated fracture reduction. Given that the strongest single risk of a fracture is falling and not bone density,14,15 it is unfortunate that larger studies looking at various exercise programs or balance improvement interventions have not been performed. Regardless, it is recommended that patients who have difficulty performing a simple sit-to-stand test or take longer than 13 seconds to complete a simple “up-and-go” test be referred for further assessment and management of their fall risk including an environmental assessment and strength and balance training.16,17 Calcium and vitamin D. Elderly patients demonstrate diminished absorption of calcium and reduced serum levels of vitamin D typically resulting in high parathyroid hormone (PTH) levels and subsequent bone loss. Despite this, the numerous trials that have looked at whether or not replacement is able to prevent fractures

have demonstrated varying results. Many of these studies were small, underpowered or involved lower-risk populations. In general however, studies in the highest-risk individuals do demonstrate benefit—the fact that supplementation was used in the treatment and placebo groups of all the randomized controlled trials testing antriresorptive agents makes supplementation important to recommend to all patients. The total daily intake of elemental calcium should be 1500 mg with most diets including 500 mg to 1000 mg per day depending on dairy product intake. As such, 500 mg to 1000 mg of supplemental calcium is recommended. Dietary vitamin D intake, however, is very low (often < 100 IU per day) and as such, 1000 IU as a single daily dose supplement is recommended for most patients. Patients with malabsorp-

Table 1

Clinical Risk Factors for FRAXTM Fracture Risk Assessment Tool • Age • Sex • Height and weight (for BMI) • Previous fracture • Paternal hip fracture • Current smoking • Glucocorticoid use • Rheumatoid arthritis • Secondary osteoporosis

the sunlight-deprived group having an increased risk of fracture at one year (odds ratio 3.7).18 Pharmacologic therapy. Antiresorptive therapies remain the mainstay of OP pharmacologic therapy. These agents reduce osteoclast-associated bone breakdown relative to the normal osteoblast-associated bone buildup. As we age the rate of breakdown

Antiresorptive therapies remain the mainstay of OP pharmacologic therapy. These agents reduce osteoclast-associated bone breakdown relative to the normal osteoblast-associated bone buildup. As we age the rate of breakdown overtakes buildup, leading to the gradual BMD decline associated with senile OP. tion syndromes should have serum vitamin D levels tested to ensure they are within the normal range of supplements. In one novel study, institutionalized patients with AD were randomized to regular sunlight exposure or deprivation for one year with

overtakes buildup, leading to the gradual BMD decline associated with senile OP. Some breakdown and buildup is desirable in order for the bone to repair damaged areas and microfractures. By slightly reducing the breakdown however, the overall BMD will

The Canadian Review of Alzheimer’s Disease and Other Dementias • 7

AD and Concomitant Conditions stabilize and ideally increase while still preserving the bone’s self-repairing abilities. Bisphosphonates, such as cyclical etidronate, alendronate, risedronate, ibadronate (not available in Canada), and more recently intravenous zoledronate, regu-

such, it is essential that the tablets be taken on an empty stomach (> 2 hours after the last meal at minimum) and that no food or pills (other than water) be taken for at least 30 minutes (although our clinic recommends one hour) after the tablet.

The newest agent (zoledronate) is administered via 10- to 15-minute infusion yearly and may prove particularly useful in this patient population. This class of therapy is considered by many to be the first line of pharmacologic therapy for elderly patients at high risk for fracture. late bone resorption by reducing bone breakdown by the induction of osteoclasts apoptosis. Although commonly utilized in Canada, cyclical etidronate was developed prior to the medical field’s desire for RCT trials that demonstrate fracture reduction and, as such, we are not as certain of its benefits, while the newer nitrogen-containing bisphosphonates have all demonstrated fracture reduction for vertebral, hip and other clinical fractures. The most common side effect of the oral bisphosphonates is upper GI irritation, which can be managed in some patients by ensuring administration of the agents with a large glass of water and remaining upright after ingestion. Bioavailability of oral bisphosphonates is, however, very poor; approximately 2% under ideal circumstances. As

Although several agents are available with weekly or even monthly dosing, the precise method of ingestion that is required may still present a significant challenge for elderly patients who may already have a complex medication regimen. Use of dosettes, blister-packaged medications and even institution-based nursing distribution practices for medications are just a few examples where the very specific timing of administration may be problematic and potentially make the use of this class ineffective. The newest agent (zoledronate) is administered via 10- to 15-minute infusion yearly and may prove particularly useful in this patient population. This class of therapy is considered by many to be the first line of pharmacologic therapy for elderly patients at high risk for fracture.

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Selective Estrogen Receptor Modulators (SERMs), such as raloxifene or tamoxifene (not utilized for OP) stimulate or inhibit the various organ estrogen receptors in varying manners. By specifically stimulating the bonebased estrogen receptors, raloxifene can provide the proven estrogen bone-building and fracturereduction benefits. Compared to estrogen alone, there is no increase in uterine or breast cancer and no difference with regard to venous thromboembolic risk and an increased risk of vasomotor symptoms. Raloxifene does have proven vertebral fracture reduction data, but because it was studied in a younger population than other agents, there was a lower risk for hip fracture and no significant fracture benefit was observed. In the absence of other significant thromboembolic risk however, this agent remains a good and relatively underutilized treatment for patients with osteoporosis and, in particular, those intolerant to oral bisphosphonates. Anabolic treatments increase the amount of bone laid down in each remodeling unit by enhancing osteoblastogenesis, decreasing adipogenesis, or protecting osteoblasts against apoptosis. Currently, an analog of teriparatide, the recombinant 1-34 fragment of human parathyroid hormone, is the only approved anabolic treatment for OP in Canada. By intermittent daily dosing of PTH, anabolic effects

Osteoporosis

Table 2

Agents Approved for the Treatment of Osteoporosis in Canada Treatment

Pros

Cons

Bisphosphonates

Alendronate 10 mg po qd

Well proven fracture reduction data for most agents (including vertebral, non-vertebral and hip fracture reduction)

Oral agents MUST be taken on an empty stomach (including no other pills) due to poor bioavailability

Alendronate 70 mg po weekly

Reasonable cost

Poor adherence to therapy

Risedronate 5 mg po qd

Long-term safety record (> 15 years for some agents)

GI irritation (relatively common)

Simple administration with very few drug interations

No hip fracture data

Cyclical etidronate 400 mg po qd for two weeks every three months

Risedronate 35 mg po weekly Risedronate 75 mg po qd for two days each month

Very rare risk of osteonecrosis of the jaw (approximately 1/100,000 in OP patients)

Zoledronate 5 mg IV yearly SERMs Raloxifene 60 mg po qd

Does not require empty stomach Reasonable cost Cardiac-disease neutral

Increased risk of venous thromboembolic disease (the same as estrogen) Increased vasomotor symptoms in patients close to the age of menopause Not for male patients

Hormone Replacement Therapy Estrogen

Proven fracture reduction

Numerous other pros and cons involving other organs make use of hormone replacement therapy for OP alone, not advisable

Simple administration

Weaker quality data supporting fracture reduction

Calcitonin Nasal calcitonin 200 IU qd

Nasal irritation Well tolerated Anabolic Agents Teriparatide (rPTH 1-34) 20 µg sc qd for 18 months

are observed—rather than the marked bone resorption seen with continuous PTH exposure (such as primary hyperparathyroidism). Daily subcutaneous injection for 18 months has been shown to reduce vertebral and nonvertebral fractures—its cost, however, is prohibitive for many patients and the

Only anabolic agent available

Very high cost

Well proven fracture-reduction data

Requires subcutaneous injection

patient or caregiver must be able to administer the treatment. It is also imperative to ensure that the patient is not taking a bisphosphonate while receiving therapy and that an antiresorptive agent is initiated immediately upon stopping this treatment if optimal benefit is expected.

Summary Osteoporosis is common in elderly patients, including those with AD. The resultant fractures can have a major adverse effect on morbidity and mortality. By recognizing this risk and estimating its severity using a simple fracture risk assessment tool, the clinician can

The Canadian Review of Alzheimer’s Disease and Other Dementias • 9

AD and Concomitant Conditions make an informed decision about which patients require pharmacologic therapy in addition to lifestyle management (with exercise, calcium and vitamin D) alone. Given the current treatment options that

have demonstrated excellent fracture-reduction capabilities available in a variety of administration methods, and with various pros and cons (Table 2), there is at least one agent that should suit every at-risk

patient. The future is also bright with newer agents and classes on the horizon (not discussed in this article), and with our understanding of aspects of bone quality ever improving.

References 1. Chrischilles EA, Butler CD, Davis CS, et al. A model of lifetime osteoporosis impact. Arch Intern Med 1991; 151(10):2026-32. 2. Kanis JA, Melton LJ 3rd, Christiansen C, et al. The diagnosis of osteoporosis. J Bone Miner Res 1994; 9(8):1137-41. 3. Understanding the Mechanisms of Senile Osteoporosis: New Facts for a Major Geriatric Syndrome. J Am Geriatr Soc 2008; 56(5):935-41. 4. Chan GK, Duque G. Age-related bone loss: Old bone, new facts. Gerontology 2002; 48(2):62-71. 5. Rosen CJ, Bouxsein ML. Mechanisms of disease: Is osteoporosis the obesity of bone? Nat Clin Pract Rheumatol 2006; 2(1):35-43. 6. Lips P. Vitamin D status and nutrition in Europe and Asia. J Steroid Biochem Mol Biol 2007; 103(3-5):620–5. 7. Kira M, Kobayashi T, Yoshikawa K. Vitamin D and the skin. J Dermatol 2003; 30(6):429–37. 8. Lips P. Vitamin D deficiency and secondary hyperparathyroidism in the eld

erly: Consequences for bone loss and fractures and therapeutic implications. Endocr Rev 2001; 22(4):477-501. 9. Stone KL, Seeley DG, Lui LY, et al. BMD at multiple sites and risk of fracture of multiple types: long-term results from the study of osteoporotic fractures. J Bone Miner Res 2003; 18(11):1947-54. 10. Seeman E. Is a change in bone mineral density a sensitive and specific surrogate of anti-fracture efficacy? Bone 2007; 41(3): 308-17. 11. K. Siminoski, et al. Recommendations for Bone Mineral Density Reporting in Canada. Can Assoc Radiol J 2005; 56(3):178-88. 12. J. Kanis, et al. FRAX and the assessment of fracture probability in men and women from the UK, Osteoporos Int 2008;19(4):385-97. 13. Szulc P, Beck TJ, Marchand F et al. Low skeletal muscle mass is associated with poor structural parameters of bone and impaired balance in elderly men— the MINOS study. J Bone Miner Res

2005; 20(5):721–9. 14. Kannus P, Niemi S, Parkkari J, et al. Why is the age-standardized incidence of low-trauma fractures rising in many elderly populations? J Bone Miner Res 2002;17(8):1363-7. 15. Kannus P, Sievanen H, Palvanen M, et al. Prevention of falls and consequent injuries in elderly people. Lancet 2005; 366(9500):1885-93. 16. Whitney JC, Lord SR, Close JC. Streamlining assessment and intervention in a falls clinic using the timed up and go test and physiological profile assessments. Age and Ageing 2005; 34(6):567-71 17. Järvinen TL, Sievänen H, Khan KM, et al. BMJ 2008; 336(7636):124-6. 18. Sato Y, Iwamoto J, Kanoko T, et al. Amelioration of Osteoporosis and Hypovitaminosis D by Sunlight Exposure in Hospitalized, Elderly Women With Alzheimer's Disease: A Randomized Controlled Trial, Journal of Bone and Mineral Research 2005; 20(8):1327-33.

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Will the Real Pseudodementia Please Stand Up? “Your reality, sir, is lies and balderdash and I'm delighted to say that I have no grasp of it whatsoever” Baron Munchausen

By Ron Keren, MD, FRCPC

P

seudodementia is a term that has been widely adopted in clinical practice, yet vastly misunderstood. As its name suggests, pseudodementia infers a “functional artifact” rather than a “true dementia” that is based on neuropathological disease. Wernicke1 first coined the term in the 1880s to describe “chronic hysterical states mimicking mental weakness.” It was not widely used until it was reintroduced by Madden2 in 1952 to describe patients with signs and symptoms of dementia that disappeared with successful treatment of an underlying psychotic illness. In 1961 Kiloh3 described 10 cases that mimicked irre-

Ron Keren, MD, FRCPC, Clinical Director, University Health Network and Whitby Mental Health Centre Memory Clinics Physician Leader, Toronto Rehabilitation Institute, Psycho-geriatric Service Toronto, Ontario

versible dementia which resolved with treatment and time. Kiloh asserted that endogenous depression was the most frequent cause of pseudodementia and cautioned against misdiagnosing it as irreversible dementia. He argued that pseudodementia should be used as a descriptive term and not a diagnosis. In 1979, Wells,4 while reporting 10 patients with psychiatric disorders as examples of pseudodementia, was the first to refer to pseudodementia as a diagnosis. In 1981, Caine proposed diagnostic criteria for pseudodementia (Table 1). With an increasing awareness of cognitive changes in late-life depression, the concept of pseudodementia was further narrowed to describe cognitive impairment caused by depression, commonly in the elderly, that mimics dementia and resolves when the depression is successfully treated. Estimates on the prevalence of pseudodementia as it relates to depression were reported to be between 10% and 20%.5,6 This

underscored the risk of misdiagnosing dementia in individuals with a potentially reversible disorder. However, over time, it became apparent that all the socalled reversible dementias, especially the “pseudodementia of depression,” were much less prevalent than previously thought. A meta-analysis of 39 studies from 1987 to 20027 identified potentially reversible dementias in 9% of patients but only 0.6% actually reversed and only 0.31% Table 1

Proposed Diagnostic Criteria for Pseudodementia 1. Intellectual impairment in a patient with a primary psychiatric disorder 2. Features of impairment are similar to those seen in central nervous system disorders 3. The cognitive deficits are reversible 4. There is no known neurological condition to account for the presentation Caine ED. Arch Gen Psychiatry 1981; 38(12):1359-64.

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AD and Concomitant Conditions fully reversed. Better and longer follow-up in studies of patients presenting with depression and cognitive impairment was thought

independent risk factor and it may also be the result of brain abnormalities in patients with AD. Caregivers have been shown to

Loss of interest/apathy, loss of confidence, difficulties in making decisions, agitation, irritability and changes in sleep and appetite are common in patients with dementia, independent of whether or not they are depressed. to be the primary reason for this dramatic shift in the prevalence of reversible dementias.

The Association Between Depression and Dementia The relationship between depression and dementia is complicated for many reasons. The two syndromes have significant symptomatic overlap, cognitive impairment is common in late-life depression, and depression is a common neuropsychiatric feature of dementia. Depression may contribute to the etiology of AD as an

over-report depression in patients with AD8 and, lastly, numerous diagnostic criteria for depression in dementia have been utilized with poor agreement between them. Hence, it is not surprising that estimates of the prevalence of depression in AD are highly variable, ranging from 0%9 to 87%.10

Symptom Overlap Many of the symptoms listed in the DSM-IV criteria for major depression are frequently seen in patients with dementia (Table 2). Loss of interest/apathy, loss of confidence,

Table 2

DSM-IV Diagnostic Criteria: Neuropsychiatric Features of Dementia 1. Depressed mood or loss of interest (apathy) 2. Poor concentration/indecisiveness (poor memory and impaired judgement)

difficulties in making decisions, agitation, irritability and changes in sleep and appetite are common in patients with dementia, independent of whether or not they are depressed. Therefore, diagnosing depression in individuals with dementia based on these criteria alone would likely lead to an overestimation on the prevalence of depression in dementia. A number of different sets of diagnostic criteria for depressive syndromes have been used to estimate the prevalence of depression in AD. Depending on the symptoms included in the diagnostic criteria, the number of patients identified with depression in the same cohort of patients can be highly variable, and there is a low rate of agreement between the various diagnostic criteria, that is, different patients are identified by different criteria. For example, in the same patient cohort, the prevalence of depression using ICD-10 criteria was 4.9%. It was 27.4% when using the proposed diagnostic criteria for depression in AD and 43.7% when using the screening question from the Neuropsychiatric Inventory (NPI). The inclusion of irritability alone as a symptom of depression significantly increases the prevalence of depression in AD.11

3. Decreased energy (lack of initiation, avolition) 4. Changes in sleep (impairments in diurnal sleep patterns) 5. Changes in appetite (weight loss/gain) 6. Psychomotor agitation (aberrant motor activity) Symptoms need to coexist in the same two-week period and not be due to a general medical condition Adapted from the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV).

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Is Depression a Risk Factor or a Prodrome? Is depression a cause or an effect of dementia? Depression as an independent risk factor for AD is debatable. It is difficult to know whether depression in itself con-

Pseudodementia

tributes pathophysiologically to the development of AD, whether it is a prodrome of AD, or both. Prospective follow-up of elderly patients presenting with cognitive impairment to a memory disorders clinic showed that many of these patients had symptoms of depression. When followed over time, most of them developed AD12 despite successful treatment of their depression and initial improvements in cognition. Also, depression, similar to other medical conditions, such as renal or cardiac disease, may bring forward the expression of dementia in patients with AD pathology. The more distant the depressive episode is from the onset of dementia, the more likely that it is a contributor to the cause of the dementia as opposed to being a prodrome or part of the dementia syndrome. Taking this into consideration, a systematic evidence review concluded that a history of depression is likely an independent risk factor for dementia in general, and for AD specifically.13 This concept is supported by the glucocorticoid cascade hypothesis which postulates that prolonged adrenal glucocorticoid secretion in patients with depression has toxic effects on the hippocampus,14 leading to hippocampal atrophy, which is also an early hallmark of AD. The debate on depression as an independent risk factor is unresolved, however, given the complexities in the relationships between depression and dementia and the

misperceptions regarding the potential reversibility of dementia in elderly patients with depression, it is increasingly apparent that the concept of depressive pseudodementia, as a common cause of reversible dementia, should be abandoned.

A Return to Wernicke and the Concept of Conversion Pseudodementia In examining the evolution of pseudodementia, one has to wonder whether Wernicke was correct in conceptualizing this condition in terms of a conversion disorder. Traditionally, conversion disorders have been used to describe the unconscious conversion of anxiety into physical symptoms. Little has

ria for “Cogniform Disorder” and “Cogniform Condition.” They claim that excessive symptomatology involving cognitive complaints is a pervasive problem that has been extensively documented in peer-reviewed neuropsychological journals. Cognitive symptoms can be produced or exaggerated in an intentional, voluntary manner for an external incentive as in malingering, to adopt a “sick role” as in factitious disorder, or unintentionally, as in conversion disorder. As opposed to conversion disorder and malingering, where the feigned or exaggerated symptoms are either completely unconscious (conversion disorder) or completely conscious (malingering), the authors

The more distant the depressive episode is from the onset of dementia, the more likely that it is a contributor to the cause of the dementia as opposed to being a prodrome or part of the dementia syndrome. been written about the potential of converting anxiety into cognitive symptoms. In a case series, Hepple15 described 10 older individuals with “conversion pseudodementia.” He reported that the core features of this disorder are: apparent cognitive impairment, regression and increasing physical dependency beginning in latemiddle or early-old age, without evidence for an organic dementia from investigations or from taking into account the course of the illness. More recently, Delis and Wetter16 proposed diagnostic crite-

argue against the dichotomous approach of the DSM-IV for a continuum, from completely unconscious at one end of the spectrum, to partial and then full consciousness at the other end, whether or not in the presence of an external incentive (e.g., litigation, disability) or an adoption of the “sick role” (factitious disorder). The terms disorder and condition differentiate the degree to which the individual exhibits cognitive dysfunction in widespread areas of everyday life. It is likely that cases of exaggerated cognitive symptoms are under-

The Canadian Review of Alzheimer’s Disease and Other Dementias • 13

AD and Concomitant Conditions

reported as it is challenging for physicians to make judgments about their patients as possibly exaggerating their symptoms, whether intentionally or unintentionally. They are unlikely to know whether an external incentive is present or whether the patient has adopted a “sick role.” Furthermore, few patients assessed for cognitive impairment undergo rigorous neuropsychological evaluations with validity testing, and even if they do, today’s patients have a wealth of information at their disposal from the internet, media, or coaching from experienced litigation lawyers which may fool even the experienced examiner.

Conclusion In summary, depressive pseudodementia evolved from a concern about the improper labeling of elderly patients with depression as having irreversible dementia. Recent data on the prevalence of reversible dementia has shown that this condition is extremely rare. Subsequently, depression is less often an imitator of dementia than a predictor of dementia or a symptom of dementia. Treating depression remains important. While it may not cure the cognitive disorder or reverse the dementia, it will likely improve the patient’s quality of life.

In today’s era of diseasemodifying clinical drug trials for AD, mild depressive symptoms in patients with dementia should not delay their diagnosis nor should it exclude them from participating in AD research. Lastly, cases of feigned or exaggerated cognitive complaints or symptoms are likely underappreciated. Clinicians should be urged to consider this as a possibility when assessing patients whose cognitive complaints or symptoms are not substantiated by the clinical interview or cognitive assessment, especially when reinforced by an external incentive or the adoption of a “sick role.”

References: 1. Berrios GE. Depressive pseudodementia or melancholic dementia: A 19th century view. J Neurol Neurosurg Psychiatry 1985;48(5): 393-400. 2. Madden JJ, Luhanet JA, Kaplan LA, et al. Non-dementng psychoses in older persons. JAMA 1952; 150: 1567-70. 3. Kiloh, LG. Pseudo-dementia. Acta Psychiatrica Scandinavica 1961; 37:336-51 4. Wells C. Pseudodementia. Am J Psychiatry 1979; 136(7):895-900. 5. Garcia CA, Reding MJ, Blass JP, et al. Overdiagnosis of dementia. J Am Geriatr Soc 1981; 29(9):407-10. 6. Jeste, DV et al. Pseudodementia: Myths and realities. Psychiatric Annals 1990; 20:71-9. 7. Clarfield AM. The Decreasing Prevalence of Reversible Dementias: An

Updated Meta-analysis. Arch Intern Med 2003; 163(18):2219. 8. Burke WJ, Roccaforte WH, Wengel SP, et al. Disagreement in the Reporting of Depressive Symptoms Between Patients With Dementia of the Alzheimer Type and their Collateral Sources. Am J Geriatr Psychiatry 1998; 6(4):308-19. 9. Knesevich JW, Martin RL, Berg L, et al. Preliminary report on affective symptoms in early stages of senile dementia of the Alzheimer type. Am J Psychiatry 1983; 140(2):233-5. 10. Merriam AE, Aronson MK, Gaston P, et al: The psychiatric symptoms of Alzheimer’s disease. J Am Geriatr Soc 1988; 36(1):7-12. 11. Vilalta-Franch J, Garre-Olmo J, LópezPousa S, et al. Comparison of different clinical diagnostic citeria for depression in Alzheimer’s disease, Am J Geriatr

Psychiatry 2006; 14(7):589-97. 12. Visser PJ, Verhey FR, Ponds RW, et al, Distinction Between Peclinical AD and Depression. J Am Geriatr Soc 2000; 48(5):479-84. 13. Jorm AF. History of depression as a risk factor for dementia: an updated review. Aust N Z J Psychiatry 2001; 35(6):776-81. 14. Sapolsky RM, Krey LC, McEwen BS. The neuroendocrinolgy of stress and aging: the glucorticoid cascade hypothesis. Endocr Rev 1986; 7(3):284-301. 15. Hepple J. Conversion pseudodementia in older people: a descriptive case series. Int J Geriatr Psychiatry 2004; 19(10):961-7. 16. Delis DC, Wetter SR. Cogniform disorder and Cogniform condition: Proposed diagnoses for excessive cognitive symptoms. Arch Clin Neuropsychol 2007; 22(5):589-604.

14 • The Canadian Review of Alzheimer’s Disease and Other Dementias

Hip Fractures and Alzheimer’s Disease People with Alzheimer’s disease have a higher incidence of hip fractures than other elderly people. Unfortunately, patients with dementia are also less likely to recover their previous functional status following a hip fracture, are more likely to require institutionalization, and have a higher mortality rate. By Susan Freter, MSc, MD, FRCPC; and Kata Koller, MD, FRCPC

H

ip fractures are common and often devastating in the elderly population. Annually, there are more than 35,000 hip fractures in Canada and more than 270,000 in the United States, and most occur in individuals older than 60 years. Overall incidence is anticipated to double by the year 2040.1,2 In Canada alone, the current annual cost of hip fractures has been estimated at $650 million and is expected to increase to $2.4 billion by 2041. Lifetime incidence of hip fracture at age 50 is 17% to 22% for women, and 6% to 11% for men.3 Amongst Caucasian women, one in six will suffer a hip fracture in her lifetime.4

Susan Freter, MSc, MD, FRCPC Attending Geriatrician, Queen Elizabeth II Health Sciences Centre Associate Professor of Medicine, Dalhousie University Halifax, Nova Scotia Kata Koller, MD, FRCPC Fellow in Geriatric Medicine, Dalhousie University, Special interest in Palliative Care Halifax, Nova Scotia

Classification of Hip Fractures Hip fractures can be classified by the location of the fracture line along the femur, into intracapsular or extracapsular. Intracapsular fractures include femoral head and neck fractures, and extracapsular fractures can be subdivided into intertrochanteric or subtrochanteric. The femoral neck is the most common location for a hip fracture, accounting for 45% to 53%. Approximately 38% to 49% of hip fractures are intertrochanteric, and 5% to 15% are subtrochanteric.7 Most of the blood supply to the femoral head is supplied by the posteromedial and lateral femoral circumflex arteries, which wrap around the neck of the femur. Intracapsular fractures can cause disruption of this arterial system, potentially resulting in avascular necrosis of the femoral head and/or nonunion.5,6 One large study followed more than 900 elderly inpatients with hip fractures and found that patients with intertrochanteric fractures tended to be older and had

a poorer health status. They had decreased functional recovery at two and six months, as well as longer hospital stays.8

Outcomes After Hip Fracture Hip fractures in older adults have potentially serious consequences, resulting in increased morbidity, mortality, functional impairment, and healthcare costs.3 By global estimates, there were 1.31 million new hip fractures in 1990 and the prevalence of individuals with hipfracture-related disability was 4.48 million with 1.75 million disabilityadjusted life-years (DALYs) lost.9 The mortality rate associated with hip fracture is estimated at 10% at one month, 20% at four months, and 30% one year after.10 Complications relating to restricted mobility, such as pneumonia, deep vein thrombosis, pulmonary embolism, deconditioning and poor rehabilitation outcomes correlate with increased mortality rates postoperatively.2 Functional decline commonly follows hip fracture, with rates of

The Canadian Review of Alzheimer’s Disease and Other Dementias • 15

AD and Concomitant Conditions increased dependence in activities of daily living (ADLs) approaching 50%.10 By six months postfracture, only 50% of patients will have recovered their prefracture walking ability. By one year postfracture, less than 50% of patients can walk without aids and only 40% are independent in all ADLs. Hip fractures are associated with subsequent institutionalization in 10% to 20% of individuals.11 Several studies have shown that delay in surgery is correlated with higher mortality, longer hospital stays and a higher complication rate.12 In one large study, a signif-

one-year mortality following a second hip fracture is 24%.14

Risk Factors The two principle determinants of hip-fracture risk are low bone mineral density (BMD) and falls.15 It is generally accepted that the vast majority of hip fractures in the geriatric population are “fragility fractures,” occurring in the setting of underlying bone weakness stressed to a breaking point.3 History of either vertebral compression fracture or distal radial fracture doubles the risk of hip fracture. History of previous hip fracture increases the

Falls are the causal mechanism for 95% of all hip fractures. One in every three individuals older than 65 sustains a fall each year. icant increase in short-term and one-year mortality was seen in patients who waited for surgery more than four days, when compared to those who had surgery within two days.13 For those patients who survive their hip fracture and regain some independence in ambulation, there is an increased risk of suffering a second hip fracture. Older age and a low body mass index (BMI) are predictive of a second hip fracture, as is having regained a higher functional status after the first hip fracture, presumably because of increased opportunities for suffering a second devastating fall. Whereas the risk of death following an initial hip fracture is around 16%, the

risk for second hip fracture by sixfold.16 There is an exponential risk increase with age, particularly after age 70.17 This likely relates to the age-associated decline in BMD, as well as an increase in number of comorbid conditions and risk of falls.4 Falls are the causal mechanism for 95% of all hip fractures. One in every three individuals older than 65 sustains a fall each year. Individuals in residential and longterm care facilities have a threefold risk of hip fracture, as compared to the general population. Having sustained one fall increases the probability of having another fall by three-fold.3 In elderly women, approximately 1% of falls will result in hip fracture.

16 • The Canadian Review of Alzheimer’s Disease and Other Dementias

Aside from bone quality, the likelihood that a fall will result in fracture depends on the point of impact and the energy of the fall. Elderly individuals tend to fall with relatively low velocity, but directly onto their hips and without putting their arms out to slow their fall.4 The multifactorial nature of hip-fracture risk is reflective of general frailty, fall risk and bone fragility.5,18 Table 1 organizes risk factors for hip fracture by factors associated with osteoporosis and those raising the risk of falls.

Hip Fractures and Alzheimer’s Disease (AD) People with AD have a higher incidence of hip fractures than other elderly people. Unfortunately, patients with dementia are also less likely to recover their previous functional status following a hip fracture, and are more likely to require institutionalization, and have a higher mortality rate. One study found that institutionalized patients with AD were approximately twice as likely to have sustained a hip fracture over a 12 month period as nursing-home residents without dementia.19 There may be a number of reasons for this association, including a higher rate of falls and osteoporosis in patients with AD. Weller et al found that there is a relationship between AD and fractures which is independent of falls and osteoporosis. They suggest that low BMI, weight loss, decreased muscle mass, nutritional deficien-

Hip Fractures

cies, and sideways direction of falling may be more common in patients with AD and might help explain the increased risk of sustaining a hip fracture.19 Community-dwelling people with dementia who are prescribed antipsychotic drugs are at an increased risk of having a hip fracture, and this association holds for atypical and conventional antipsychotics.20 Interestingly, apolipoprotein E4, which is associated with a higher risk of developing AD, may also be a marker for hip-fracture risk.21 The relationship between AD and hip fracture needs further exploration, as in some instances the onset of AD follows the hip fracture, implying that either the hip fracture brought the patient’s cognitive deficits to medical attention or that the hip fracture and surgery may have precipitated the cognitive decline. Hospitalization for hip fracture is costly, and the cost goes up with longer length of stay and comor-

bidities. Average cost increases with the number of comorbid illnesses, but the specific type of associated illness has also been found to be important, with dementia topping the list by adding the largest amount to total costs.22 Cost-containment solutions could include efforts at reducing length of stay, by reducing wait times before surgery, and further exploring how dementia contributes to length of stay and cost. Concerns about quality of hospital care for patients with AD and hip fractures have been raised, in part because of the greater odds of death during index hospitalization, compared to individuals without AD.23 The situation is more complex in patients from chronic-care facilities. Although patients from chronic-care settings generally have lower prefracture function, the decline in level of functioning and mobility after a hip fracture is much greater than in their community-dwelling

counterparts.24 It is concerning that this post-fracture decline in ambulation and functioning is actually associated with a shorter length of hospital stay, reflecting a tendency to send these patients back to their nursing homes as soon as they are medically stable, rather than having access to inpatient rehabilitation. Individuals with dementia are at greater risk of developing delirium during hospitalization for hip fracture, with published incidences ranging from 15% to 60%, depending on the specific criteria used. Hip-fracture patients with delirium have worse outcomes, including longer hospitalizations, decreased recovery of functional abilities and ambulation, and increased risk of institutionalization and death. Cognitive impairment and dementia have been cited as the best predictors of post-orthopedic surgery delirium.25-27 As delirium can potentially be prevented and treated,28,29 this may be an important starting point for improving the care

Table 1

Risk Factors for Hip Fractures Osteoporosis-associated

Increased Risk of Falls

Low bone mineral density (BMD)

Polypharmacy

Diabetes

Age

High bone turnover

Sedative medication use

Peripheral neuropathy

Frailty

Calcium deficiency

Orthostatic hypotension

Sensory impairment

Previous falls/fractures

Low body mass index (BMI)

Deconditioning

Balance problems

Vitamin D deficiency

Weight loss

Dementia

Foot disorders

Physical inactivity

European or Asian ancestry

Parkinson’s disease

Urinary urgency

Anticonvulsant use

Female gender

Stroke

Environmental hazards

Thyroid disorders

Caffeine intake

Arthritis

Cigarette smoking

Both

Alcohol intake Certain medications

Family history

The Canadian Review of Alzheimer’s Disease and Other Dementias • 17

AD and Concomitant Conditions of elderly dementia patients with hip fractures. Targeting patients who are at greatest risk of developing postoperative delirium with deliriumprevention strategies may help to improve quality of care and postoperative outcomes, and reduce costs. More research on delirium prevention and management is needed in this population, as many research trials have excluded patients with dementia.

Improving Care of Hip Fracture In Patients with Dementia (Table 2) Delirium Prevention and Management. Having sustained a hip fracture is an independent risk factor for developing delirium and this risk is increased several-fold in patients with pre-existing dementia.27 There may be ways to improve the perioperative care of frail elderly hip-fracture patients, with the goal of decreasing the incidence of delirium. Work by Marcantonio28 has demonstrated that combined medical and nursing interventions, augmented by proactive geriatric consultation, can potentially reduce the incidence and severity of delirium complicating postoperative hip-fracture care. Another intervention study, involving systematic cognitive screening, regularly scheduled pain medications, and education of nursing staff, resulted in decreased severity and shorter duration of delirium in hip-fracture patients.36 Routine cognitive screening on admission can be helpful in establishing baseline cognitive function-

ing, against which later cognitive changes can be compared. Uncontrolled pain is itself a risk factor for developing delirium, in addition to being inhumane. Pain medications are frequently prescribed on an as-needed basis, but patients with cognitive impairment may not be able to effectively communicate their needs. This increases the likelihood of relatively severe postoperative hip pain, which may then result in the administration of higher opioid doses. Regular administration of non-narcotic analgesics, such as acetaminophen, may help to reduce uncontrolled severe pain and the total amount of opioid that is needed.5,28 Unfortunately, environmental strategies, such as limiting changes in staff and involving relatives in reorientation, are frequently overlooked.31 Delirium-prevention studies have, by and large, been fully funded research studies in tertiary referral centres and it is unclear whether their results can be replicated in everyday practice. A challenge in delirium research is to discover ways in which good practice can be disseminated widely, so that permanent improvements in quality of care for vulnerable elderly people can be achieved and appropriate interventions become part of routine care. Nutrition. Malnutrition is common amongst elderly hip-fracture patients. This, in addition to the catabolic response to surgery, can contribute to muscle wasting and weakness and may contribute to

18 • The Canadian Review of Alzheimer’s Disease and Other Dementias

poor rehabilitation outcomes. Undernutrition may also contribute to delayed wound healing and impaired functioning of the immune system. Early medical complications and dementia have been shown to be major risk factors for inadequate postoperative nutritional intake.32 Strategies to improve nutrition in high risk groups may include reducing fasting time preoperatively, reducing opioid load, and nutritional supports. Patients with dementia who are at increased risk of complications may benefit from further intensification of nutritional support.32 Another innovative approach may include providing one-on-one attention from dietary assistants, in high-risk patients, to help with meal choices and actual food consumption, if needed.33 Rehabilitation. A multidisciplinary approach to rehabilitation after hip fracture can help to optimize recovery of mobility and functional capacity.34,35 Rehabilitation in patients with dementia can be more challenging and may require specialized geriatric rehabilitation teams. However, research has shown that pre-morbid ambulatory status is more important than the presence or absence of dementia at predicting who will reach motor independence and safe gait, following rehabilitation efforts.36,37 Functional status at discharge from rehabilitation after hip fracture does depend, to some extent, on pre-operative cognitive status and functional ability, but nonetheless, the ability to perform functional activities is

Hip Fractures

Table 2

Improving Care of Hip Fracture Patients with Dementia Perioperative Care Multidisciplinary team approach Education of healthcare team Routine cognitive screening Delirium prevention strategies Regularly scheduled non-opioid analgesia Nutritional support Geriatric rehabilitation Prevention Strategies Fall prevention Exercise programs in the community and nursing home Osteoporosis treatments

improved by the rehabilitation process in cognitively impaired patients.38,39 Indeed, the greatest benefit by specialized geriatric rehabilitation programs may be derived by hip-fracture patients with mildto-moderate dementia.40,41 Taking this one step further, it may be beneficial to introduce a multidisciplinary approach even earlier in the postoperative course. In one study, a multidisciplinary, multi-factorial intervention program was implemented in the acute-care and rehabilitation phases of hip-fracture patients, resulting in a significant reduction in falls during the inpatient stay, related at least in part to a reduction in postoperative delirium in the intervention group. Dementia patients, who are at highest risk of delirium and further falls after hip-fracture surgery, seemed to benefit the most from this intervention program.42 Future directions in hip fracture rehabilitation may include home-

based rehabilitation programs,43 and body-weight-supported treadmill techniques, which may be useful in more severe dementia.44 Prevention. Hip-fracture prevention starts with efforts at fall prevention, for which multifactorial programs in certain settings may be effective. Not all falls, of course, can be prevented. There has been some interest in hip-protector use to prevent fractures resulting from falls. Meta-analysis on this question is inconclusive, but there may be a small reduction in rates of hip fracture in care homes with the use of hip protectors.45 There is good evidence for the pharmacologic treatment of osteoporosis, with outcomes including fracture reduction in postmenopausal women, including those with a previous fracture history.3,46,47 Risedronate has been found to reduce the risk of hip fracture in elderly women with AD.48 Dietary intake of calcium

and sun exposure are unpredictable in nursing-home populations. A number of studies have found that oral calcium and vitamin D supplementation reduced falls and fractures in nursinghome patients.45 However, a subsequent study failed to replicate these findings,49 so the jury is still out on this issue. Patients with dementia may be less likely to engage in regular exercise, which can contribute to muscle weakness from deconditioning, and may increase their risk of falls and fractures. Rolland et al50 implemented a twice-weekly exercise program in nursing-home patients with dementia. Over the course of a year, they noted an increase in walking speed and significantly less decline in ADLs in the exercise group. There were too few fractures in either group to allow any insight into fracture prevention, but it is thought-provoking that it was possible to implement a regular exercise program in this population. Preliminary work in people with dementia living in the community showed that it is possible to successfully train caregivers to implement a home exercise program, which may have a persistent effect on physical health and functioning .51

Conclusions As the population ages, the prevalence of Alzheimer’s disease and other dementias, as well as the incidence of hip fractures, will continue to rise. Outcomes after hip fracture

The Canadian Review of Alzheimer’s Disease and Other Dementias • 19

AD and Concomitant Conditions tend to be poor in patients with dementia, and much can be done to improve the care of this group. Health care providers from all disci-

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20 • The Canadian Review of Alzheimer’s Disease and Other Dementias

period, which will include delirium recognition and management, as well as a multifactorial approach to optimizing outcomes.

and functional gain in elderly patients operated on for intracapsular hip fracture. Arch Orthop Trauma Surg 2001; 121(5):257-60. 37. Rozzini R, Frisoni GB, Barbisoni P, et al. Dementia does not prevent the restoration of safe gait after hip fracture. J Am Geriatr Soc 1997; 45(11):1406-07. 38. Ruchinskas RA, Singer HK, Repetz NK. Cognitive status and ambulation in geriatric rehabilitation: walking without thinking? Arch Phys Med Rehabil 2000; 81(9):1224-28. 39. Heruti RJ, Lusky A, Barell V, et al. Cognitive status at admission: does it affect the rehabilitation outcome of elderly patients with hip fracture? Arch Phys Med Rehabil 1999;80(4):432-6. 40. Huusko TM, Karppi P, Avikainen V, et al. Randomized, clinically controlled trial of intensive geriatric rehabilitation in patients with hip fracture: subgroup analysis of patients with dementia. BMJ 2000; 321(7269):1107-11. 41. Toussant EM, Kohia M. A critical review of literature regarding effectiveness of physical therapy management of hip fracture in elderly persons. J Gerontol A Biol Sci Med Sci 2005; 60(10):1285-91. 42. Stenvall M, Olofsson B, Lundström M, et al. A multidisciplinary, multifactorial intervention program reduces postoperative falls and injuries after femoral neck fracture. Osteoporos Int 2007; 18:167-75. 43. Giusti A, Barone A, Pioli G. Rehabilitation after hip fracture in patients with dementia. J Am Geriatr Soc 2007; 55(8):1309-10. 44. Bellelli G, Guerini F, Trabucchi M. Body weight-supported treadmill in the physical rehabilitation of severely demented subjects after hip fracture: A case report. J Am Geriatr Soc 2006; 54(4):717-78. 45. Oliver D, Connelly JB, Victor CR, et al. Strategies to prevent falls and fractures in hospitals and care homes and effect of cognitive impairment: systematic review and meta-analyses. BMJ 2007; 334(7584):82. 46. Reginster J, Minne HW, Worensen OH et al. Randomized trial of the effects of risedronate on vertebral fractures in women with established postmenopausal osteoporosis. Osteoporos Int 2000; 11:83-91. 47. McClung MR, Geusens P, Miller PD, et al. Effect of risedronate on the risk of hip fracture in elderly women. N Engl J Med 2001; 344:333-40. 48. Sato Y, Kanoko T, Satoh K, Iwamoto J. The prevention of hip fracture with risedronate and ergocalciferol plus calcium supplementation in elderly women with Alzheimer Disease. Arch Int Med 2005; 165:1737-42. 49. Law M, Withers H, Morris J, Anderson F. Vitamin D supplementation and the prevention of fractures and falls: results of a randomized trial in elderly people in residential accommodation. Age Ageing 2006;35:482-6. 50. Rolland Y, Pillard F, Klapouszczak A, et al. Exercise program for nursing home residents with Alzheimer’s disease: a 1-year randomized, controlled trial. J Am Geriatr Soc 2007; 55(2):158-65. 51. Teri L, Gibbons LE, McCurry SM, et al. Exercise plus behavioral management in patients with Alzheimer disease: A randomized controlled trial. JAMA 2003; 290(15):2015-22.

Pain In Severe Dementia: How to Assess The International Association for the Study of Pain defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.” Pain is chronic when it persists or recurs beyond a reasonable healing period of three to six months. It is therefore a highly subjective personal experience, for which there is no objective biological marker. By Maryse Savoie, RN, MSc

A

lthough pain is not a normal consequence of aging, it is very common in elderly persons who require long-term care. According to the American Geriatrics Society, 45% to 80% of residents in long-term-care facilities suffer significant pain,1 most frequently identified as musculoskeletal and neuropathic pain.2 In the elderly, pain is associated with several negative consequences, such as a decline in mobility, the risk of falling, depression, insomnia, social isolation and malnutrition.3 Even though pain is a very common occurrence, it remains under-detected, under-evaluated

Maryse Savoie, RN, MSc Director of Research, Innovation and Learning St. Anne’s Hospital, Veterans Affairs Canada

and under-treated in long-term-care facilities.3 A study4 has shown that 25% of residents in such establishments who present with pain on a daily basis receive neither analgesics nor nonpharmacologic management for this condition. The problem is even greater with long-term-care patients with cognitive impairment. Since statistics show that approximately 50% of long-term care patients fall into this category, the detection and assessment of pain in this population represent a major challenge.5-7 Only one study has been able to determine the incidence of pain in long-term-care patients with cognitive impairment. In Ferrell’s study8 of 217 subjects, the incidence of pain was shown to be 62%. While it has been demonstrated that dementia has no impact on

the threshold of pain and tolerance to it, an increasing number of studies indicate that cognitively impaired residents receive a significantly lower proportion of analgesics than the non-impaired, even though their clinical pictures may be similar.7-9 Marzinski10 stated that the tragedy of dementia is the possibility that residents who are unable to express their pain may be exposed to undue suffering.

Pain Detection and Assessment The relief of pain depends upon its detection and subsequent rigorous assessment. Routine screening for pain is one of the recommendations made by the American Geriatrics Society, the American Medical Directors Association and the Registered

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Figure 1

a) Pain Scale

0

1

No pain

2

3

Slight pain

0

4

5

Moderate pain

2

Figure 2

Face Scale for Non-verbal Adults in the ICU16

4

6 Severe pain

6

Nurses’ Association of Ontario best practice guidelines on pain management. The concept of pain as the fifth vital sign developed in the United States during the 1990s, is an effective example of the systematic detection of pain. The detection and assessment of pain is incorporated into the routine taking of vital signs and their documentation. As pain is subjective and personal, patients are the only ones who can correctly assess their own level of pain. The golden rule, suggested by McCaffery,11 is that “Pain is whatever the experiencing person says it is, existing whenever the experiencing person say it does.” Several studies12-14 have compared patients’ and nurses’ assessment of pain, and have all reached the same conclusion: nurses tend to underestimate their patients’ pain. Choinière’s study14 in severe burn patients has shown that the more experienced the nurse (more than 15 years), the

22 • The Canadian Review of Alzheimer’s Disease and Other Dementias

7

8

9

10

Very severe pain

8

Intolerable pain

10

more he/she underestimates patients’ pain. Pain assessment poses a particular challenge in patients with cognitive impairment. However, studies have shown that it is possible for patients with mild-tomoderate dementia and MiniMental State Examination (MMSE) scores of 15 or more to use self-assessment pain intensity tools.15 The scales most commonly used are: verbally administered numerical rating scales from 0 to 10 with 0 representing no pain and 10 representing the worst pain—patient’s are asked “how much pain are you feeling now?” (this scale appeared easier for elderly men than for women);3 the visual analogue scale, like the colored scale and the thermometer; the verbal descriptor scale, the best known of which is the McGill Pain Scale; and the faces pain scale, like that of Wong-Baker (Figure 1). The use of the latter scale in geriatrics is, however,

Pain open to criticism, as it was developed for pediatric use: some of the faces with tears would mean less to an older population. The face scale developed by Céline Gélinas16 (Figure 2) for non-verbal adults in intensive care units, appears promising even though it has not yet been validated for use in cognitively impaired geriatric patients. A study conducted in 20007 compared the McGill Pain Scale, the Wong-Baker scale, a visual analogue scale and a verbal numeric rating scale in 37 dementia patients with scores of 15 or less on the MMSE. The study lasted for one year. Results showed that 73% of patients had been able to use the McGill Pain Scale, vs. 61% for the Wong-Baker Scale, 57% for the visual analogue scale and 51% for the verbal numeric rating scale. Ferrell et al8 carried out a similar study on 217 patients with an average MMSE score of 12.1 (standard error 7.9), and 65% of those subjects were able to use the McGill Pain Scale. In recent studies, patients with MMSE scores as low as 6/30 were able to use the verbal scale.15 This may be explained by the fact that verbal scales using words, like the McGill Pain Scale, require a lower level of abstraction. Based on clinical observation, the difficulty that cognitively impaired patients experience when using pain self-assessment tools is not only related to their cognitive limitations, but also to the sometimes awkward approach taken by caregivers. When a self-assessment tool is used in

Table 1

PQRST Method for Pain Assessment29 P = Provoke and Palliate Identify elements that provoke and worsen pain Ex.:

What causes pain? What makes it worse?

Identify elements that procure pain relief Ex.:

What makes your pain better?

Q = Quality Obtain a pain description in the patient’s own words Ex.:

Can you describe your pain? What does it feel like?

R = Region and Radiate Determine the location of the pain Ex.:

Can you show me, with your hand, where your pain is located? Where does the pain radiate? Does it go anywhere else?

S = Severity and Other Signs and Symptoms Determine the intensity of pain Ex.:

How severe is your pain on a scale from 0 to 10?

Identify other signs and symptoms Ex.:

Are there other unusual signs or sensations along with your pain (claudication, stiffness, spasms, etc.)?

T = Time Identify the occurrence and duration of pain Ex.:

Since when have you been in pain? When did the pain start? Are you always or sporadically in pain?

patients with cognitive impairment, it is recommended that instructions be given three times, with one minute between repetitions. When such patients are unable to communicate or use the self-assessment scales, the most acceptable alternative is behavioral observation using validated tools. Three recent meta-analyses17-19 have identified

the Pain Assessment Checklist for Seniors with Limited Ability to Communicate (PACSLAC)20 as the best tool currently available. A French-language version (PACSLAC-F),21 is also available. PACSLAC is a multidimensional scale developed for use in non-verbal, cognitively-impaired seniors in long-term care facilities. It contains

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Table 2

Myths About Pain in the Elderly30-33 • Complaining about pain is a sign of a weak character • Pain is a normal consequence of aging • Pain is a way to pay for one’s sins • Pain means that death is near • The use of morphine means that death is near • Pain is a pathway to heaven • Pain indicates a serious illness • Elderly people have a lower tolerance of pain • Pain is a way to attract attention and manipulate others • Elderly people are likely to become dependent on their medication • The use of narcotics is not recommended in the elderly • Elderly people have a higher risk of respiratory depression • Fear of administering the final dose

60 elements, divided into four categories: facial expressions, activity/body movement, social/personality/mood indicators and physiological indicators. PACSLAC is easy to use and takes about five minutes to administer. Among French pain behavior observational tools is the DOLOPLUS-2.22 This tool requires prolonged observation and is criticized for its small number of elements and the low specificity of some of these with respect to pain. The simplified behavioral scale (échelle comportementale simplifiée [ECS])23 and elderly behavioral scale (échelle comportementale de la personne âgée [ECPA])24 are also available, but have not been fully tested as yet.

The tools available in English include the Assessment of Discomfort in Dementia (ADD) and the Discomfort Scale for Dementia Alzheimer’s Type (DS-DAT), which assess the level of discomfort in elderly patients. They are not, however, recommended for pain assessment situations.25-26 The Checklist of Nonverbal Pain Indicators (CNPI)27 was developed for elderly patients requiring acute care following hip fracture. It is therefore not suitable for use in an long-term-care setting. Finally, Pain Assessment in the Communicatively Impaired Elderly (PACI)28 seems a promising tool for detecting pain in this population, although more testing is required.

To round out the assessment, the American Medical Directors Association recommends taking the patient’s pain history and performing a thorough physical examination. The PQRST Checklist29 (Table 1) can be used as a reference when collecting information on the patient’s history and documenting the patient’s chart.

Barriers to Pain Relief Apart from the difficulty in detecting and assessing pain in cognitively-impaired elderly patients, other factors can also hinder pain relief, such as a lack of knowledge on the part of professionals and persistent myths concerning pain in the elderly, some of which can be found in Table 2.

Conclusion Relieving pain in elderly cognitively impaired patients represents a considerable challenge. Despite the progress made over the past few years, further research is required in this area and innovative clinical projects must continue to be developed. The continuing education of health professionals should also be encouraged in order to improve clinical practice in this field and meet the ever-growing needs of this population. References on page 26

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References: 1. AGS Panel on Persistent Pain in Older Persons: The management of persistent pain in older persons. J Am Geriatr Soc 2002; 50(6):S205-24. 2. Stein WM. Pain in the nursing home. Clin Geriatr Med 2001; 17(3):575-94. 3. Hutt E, Buffun MD, Fink R, et al. Optimizing Pain Management in Longterm care residents. Geriatrics & Aging 2007; 10(8):523-7. 4. Won AB, Lapane KL, Vallow S, et al. Persistent non-malignant pain and analgesic prescribing patterns in elderly nursing home residents. J Am Geriatr Soc 2004; 52(6):867-74. 5. Epps CD. Recognizing pain in the institutionalized elder with dementia. Geriatr Nurs 2001; 22(2):71-9. 6. Kaasalainen S, Crook J. A comparison of pain assessment tools for use with elderly long-term care residents. Can J Nurs Res 2003; 35(4):58-71. 7. Wynne CF, Ling SM, Remsburg R. Comparison of pain assessment instruments in cognitively intact and cognitively impaired nursing home residents. Geriatr Nurs 2000; 21(1):20-3. 8. Ferrell BR, Ferrell BA, Rivera L. Pain in cognitively impaired nursing home patients. Journal of Pain Symptom Management 1995; 10:591-8. 9. Horgas AL, Tsai P. Analgesic drug prescription and use in cognitively impaired nursing home residents. Nursing Research 1998; 47: 235-242. 10. Marzinsky LR. The tragedy of dementia: Clinically assessing pain in the confused, non-verbal elderly. J Gerontol Nurs 1991; 17(6): 25-28. 11. McCaffery M. Nursing Management of the Patient with Pain (2nd edition). Philadelphia: Lippincott 1979. 12. Grossman SA, Sheidler VR, Swedeen K, Mucenski J, Piantadosi S. Correlation of patient and caregiver ratings of cancer pain. Journal of Pain and Symptom Management 1991; 6(2): 53-57.

13. Zalon ML. Nurses’ assessment of postoperative patients’ pain. Pain 1993; 54(3): 329-334. 14. Choinière M, Melzack R, Girard N, Rondeau J, Paquin M. Comparisons between patients’ and nurses’ assessment of pain and medication efficacy in severe burn injuries. Pain 1990; 40(2): 143-152. 15. Pautex S, Michon A, Guedira M. Pain in severe dementia : self-assessment or observational scales? Journal of the American Geriatric Society 2006; 54: 1040-1050. 16. Gélinas, C. Pain Intensity Thermometer. A new tool for adult critical care patients. Perspective infirmière 2007, 4(4),12-20. 17. Aubin M, Giguère A, Verreault R, Hadjistavropoulos T. Évaluation systématique des instruments pour mesurer la douleur chez les personnes âgées ayant des capacités réduites à communiquer. Pain and Research Management 2007; 12(3):195-203. 18. Herr K. State of the art review of tools for assessment of pain in non-verbal older adults. In City of Hope Pain/Palliative Care Resource Center website (www.cityofhope.org). 19. Zwakhalin SM, Hamers JP, Abu-Saad HH, Berger MP. Pain in elderly people with severe dementia: A systematic review of behavioral pain assessment tools. BMC Geriatric 2006; 6: 3-37. 20. Fuchs-Lacelle S, Hadjistavropoulos T. Development and preliminary validation of the pain assessment checklist for seniors with limited ability to communicate (PACSLAC). Pain Management Nursing 2004; 5: 37-49. 21. Aubin M, Verreault R, Savoie ML, Le May S, et coll. Validité et utilité d'une grille d'observation (PACSLAC-F) pour évaluer la douleur chez des aînés atteints de démence vivant en milieu de soins de longue durée. Canadian Journal of Aging 2008; 27(1): 45-55.

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22. Wary B. Doloplus-2, une échelle pour évaluer la douleur. Soins gérontologie 1999; 19: 25-27. 23. Le Quintrec JL, Baulon A, Maga A. L'échelle comportementale simplifiée, un nouvel outil d'évaluation de la douleur en long séjour gériatrique. Revue de gériatrie 1995; 20(6): 363-368. 24. Jean A. Évaluation de la douleur du sujet très âgé hospitalisé en long séjour. Revue de gériatrie 1998; 23: 253-256. 25. Closs SJ. Pain in elderly patients: A neglected phenomenon. Journal of Advanced Nursing 1994; 19: 10721081. 26. Miller J. The assessment of discomfort in elderly confused patients: A preliminary study. Journal of Neuroscience Nursing 1996; 28: 175-182. 27. Feldt KS. The checklist of nonverbal pain indicators (CNPI). Pain Management Nursing 2000; 1(1): 13-21. 28. Hadjistavropoulos T. et al. An interdisciplinary expert consensus statement on assessment of pain in older persons. The Clinical Journal of Pain 2007; 23 suppl: S1-S43. 29. Voyer P. Course notes (2007). 30. Savoie ML, Le May S. Les besoins d'apprentissage, les valeurs et les croyances des infirmières concernant la douleur chronique chez la personne âgée. Frontières 2005; 17: 59-65. 31. Jones KR, Fink R, Pepper G. Improving nursing home staff knowledge and attitudes about pain. Gerontologist 2004; 44: 469-478. 32. Jones KR, Fink R, Pepper G. Nursing home resident barriers to effective pain management: why nursing home residents in pain may not seek pain medication. Journal of the American Medical Directors Association 2005; 6: 10-17. 33. American Medical Directors Association (AMDA): Pain assessment in the longterm care setting. American Medical Directors Association; 2003.

News from the Alzheimer Society of Canada

Enhancements to Safely Home®: Helping to Save Lives P

eople with dementia are no different than anyone else. They want to be able to move about freely, and live as independently as possible. However, as people with the disease become increasingly confused and lost in even familiar places, this desire to remain independent can become dangerous. This is Where the Alzheimer Society Can Help New enhancements to its Safely Home® Program are helping to provide peace of mind for people living with dementia, their families and caregivers, as well as healthcare professionals and emergency search and rescue personnel. Aimed at saving lives, the Alzheimer Society is now offering two online interactive training courses, available to download free of charge from www.safelyhome.com “Preventing people with Alzheimer’s disease from becoming lost is our primary goal,” says Mary Schulz, Director of Information, Support Services and Education for the Alzheimer Society of Canada. “However, if they do become lost, we want to ensure that everyone responsible for their care, from family to healthcare workers, as well as police officers, have the training and resources to find them as quickly as possible.” The first course, “Plan to be Prepared! Bringing people with Alzheimer’s and related diseases Safely Home,” is targeted at healthcare professionals to help them better understand the characteristics of Alzheimer’s disease, concepts of emergency preparedness and how to plan for, and carry out, emergency search procedures. The second course, “Search is an Emergency: Bringing people with Alzheimer’s and related diseases Safely Home,” is targeted at police and emergency services. This course is designed to assist police and emergency services to learn about the distinguishing characteristics of persons with Alzheimer’s disease who may become lost, effective communication strategies, the Safely Home program and vital information to help reunite lost persons with their family members.

30 • The Canadian Review of Alzheimer’s Disease and Other Dementias

Online Registration People with Alzheimer’s disease and their caregivers now have the option to register for the Safely Home program online, and to manage their own record through the Society’s new and improved Safely Home website. Each person registered through Safely Home wears an identification bracelet that provides critical information to police and search and rescue personnel. The ID number on the bracelet is linked to a central database storing information such as addresses and physical characteristics that can be accessed by police and emergency services during a search emergency. “Keeping this information up to date is crucial and is now much easier to do,” adds Schulz. “With more people going online, we wanted to make our program more user-friendly, responsive and flexible.” Developed in 1995 in partnership with the RCMP, Safely Home is a nationwide program that assists police in finding people who become lost. Today there are approximately 30,000 people with Alzheimer’s disease in Canada registered. For more information about Safely Home or Alzheimer’s disease, please visit www.safelyhome.ca. The Alzheimer Society is the leading, nationwide health organization for people affected by dementia in Canada. The Society is a principal funder of Alzheimer research and training, provides enhanced care and support to people with the disease, their families and their caregivers, while acting as a prominent voice in the call for policy change within all levels of government. Active in more than 140 communities across Canada, the Alzheimer Society is also at the forefront of worldwide efforts to fight dementia as a founding member and affiliate of Alzheimer’s Disease International. For more information on Alzheimer’s or related diseases, Alzheimer Society programs or to support the Alzheimer’s Advocacy campaign, contact 1-800-616-8816 or visit the Society’s website at www.alzheimer.ca.