The Canadian Alzheimer - STA HealthCare · PDF fileThe Alzheimer Society of Canada ......

Editorial 3Peter McCracken, MD, FRCPC

Traumatic Brain Injury and Dementia 4Mark Rapoport, MD, FRCPC, Nicolaas Paul L.G. Verhoeff, MD, PhD, FRCPC

and Robert van Reekum, MD, FRCPC

The Emerging Spectrum of Parkinsonian Dementias (Part 2) 9Inge Loy-English, MD, FRCPC and Howard Feldman, MD, FRCPC

The ACADIE Study:Does Donepezil Meet the Expectations of Treatment? 13

Kenneth Rockwood, MD, FRCPC

Personal Revelations, Experiences and Reflections of an AD Caregiver 20

Roberta Bedard

First Link: Your Link to a Community of Learning,Services and Support 22The Alzheimer Society of Canada

The Canadian

Disease ReviewVolume 7, Number 2 September 2004

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tin M

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Alzheimer

CHAIRMANPeter N. McCracken, MD, FRCPCGeriatric Medicine Staff,Glenrose Rehabilitation Hospital Part Director, Division of Geriatric Medicine and Professor of Medicine, University of Alberta Edmonton, Alberta

Paul J. Coolican, MD, CCFP, FCFP Family Physician, St. Lawrence Medical ClinicMorrisburg, Ontario Active Staff,Winchester District Memorial HospitalWinchester, Ontario

Shannon Daly, RN, MNClinical Nurse Specialist in GeriatricsGrey Nuns Community Hospital & Health CentreEdmonton, Alberta

Howard Feldman, MD, FRCPCProfessor of Medicine,Division of Neurology,University of British Columbia (UBC)Director, UBC Alzheimer Clinical Trials UnitVancouver, British Columbia

Steve Rudin, MEd, MSPHNational Executive DirectorAlzheimer Society of CanadaToronto, Ontario

Serge Gauthier, MD, CM, FRCPCProfessor of Neurology and Neurosurgery,Psychiatry and Medicine, McGill UniversityMcGill Centre for Studies in AgingMontreal, Quebec

Bernard Groulx, MD, CM, FRCPC Chief Psychiatrist, Ste-Anne-de-Bellevue HospitalAssociate Professor, McGill UniversityMcGill Centre for Studies in AgingMontreal, Quebec

Nathan Herrmann, MD, FRCPCAssociate Professor, University of TorontoHead of the Division of Geriatric Psychiatry,Sunnybrook Health Science CentreToronto, Ontario

Peter Lin, MD, CCFPMedical Director, University of TorontoHealth & Wellness Centre at ScarboroughScarborough, Ontario

Kenneth J. Rockwood, MD, MPA, FRCPCProfessor of Medicine, Dalhousie UniversityGeriatrician,Capital District Health AuthorityHalifax, Nova Scotia

Copyright 2004 STA HealthCare Communications Inc.All rights reserved.The Canadian Alzheimer Disease Review is published by STA Communications Inc.The opin-ions 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 con-dition and consult officially approved product monographs before making any diagnosis or treatment, or following any procedure based on suggestions made in thisdocument. Publications Agreement Number 40063348.

Publishing Staff

EDITORIAL BOARD

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

We’d Like to Hear From You!The Canadian Alzheimer Disease Review welcomes letters from its readers. Address all correspondences to Letters, The Canadian Alzheimer Disease Review, 955 Boul. St. Jean, Suite 306, Pointe Claire, Quebec, H9R 5K3. The Reviewalso accepts letters by fax or electronic mail. Letters can be faxed to 514-695-8554 and address electronic mail [email protected]. Please include a daytime telephone number. Letters may be edited for length or clarity.

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ON THE COVERUncertainty, by Martin MaAlthough the deteriorating effects of AD are centred around the affected individual, the impact of AD is much morewidespread and can often have a profound effect on friends and family. This is particularly true for the children ofindividuals afflicted with AD, who must face the uncertainty of the disease’s hereditary component.

In this painting, I attempt to explore the impact of AD on an afflicted individual’s children. Here, a physician tells aconcerned son that his father’s strange behavior in recent months is the result of AD. The son listens and hears thephysician’s words of explanation. However, as the explanation continues, the doctor’s words are interrupted andquickly dominated by the son’s own thoughts and worries, as he attempts to grasp the meaning of what the doctor hassaid. In the end, the son is left with the uncertainty that his father’s AD diagnosis brings to his own future.

2 • The Canadian Alzheimer Disease Review • September 2004

E D I T O R I A L

This issue of the Canadian Alzheimer DiseaseReview appears in timely fashion. Many readers

have taken notice of the “backlash” against the use ofcholinesterase inhibitors (ChEIs) for Alzheimer’s dis-ease (AD). I allude to the well-known article in theNew York Times which questioned whether “naming11 animals in a minute instead of 10” was worth theexpense of this class of medications. A further “coldshower” has been the report in the June 25 edition ofthe Lancet, which describes the results of courses oftreatment with donepezil in 565 community-dwellingresidents with mild to moderate AD. These subjectstaking donepezil fared only slightly better on cogni-tion and function and did not experience delays ininstitutionalization or progression of disability. Theauthors raised the sober question of the drug’s cost-effectiveness. Although the methodology of this studyinitially appears sound, by the trial's completion, itbecomes apparent that it is flawed. Only a small per-centage of the target enrollment sample is reached, alarge drop-out of subjects transpires, and the serialwashouts of donepezil (six- week and four-week) donot parallel the model of good clinical practice.Readers should not suddenly discount the numerousclinical trials that have demonstrated improvements incognition, function, and behavior with these agents inplacebo-controlled trials.

Furthermore, Dr. Rockwood’s article (page 13)points out that the outcome measures in clinical trialsare simply not applicable to clinical practice. Do statis-tically significant differences manifested in these stud-ies translate into truly positive results recognized by ADpatients and caregivers in the real world? To answer thisquestion, Rockwood designed a trial using GoalAttainment Scaling (GAS), a formal method by whichpatients, caregivers and the treating physician would settheir own goals and expectations of treatment. Ratherthan using outcome measures designed by an individ-ual geographically and culturally remote from anyindividual patient, GAS puts this process in the handsof the patient, the caregiver and the primary care physi-cian. The results indicated that the priorities of patientsand caregivers were indeed distinct from those of the

treating clinician. Their goals were more numerous andmore oriented to leisure and social interactions thanwere those of the family physician. Their evaluation ofthe treatment effect was more optimistic than thephysician’s. The results clearly showed the viewpointof patients and caregivers differed considerably fromthe standard outcomes of Phase III trials; it also servesas a rebuttal to the backlash mentioned above.

Drs. Loy-English and Feldman complete theirarticle from last month, focusing on parkinsoniandementias (page 9). Akin to its predecessor, thisarticle has a clinical focus and deals with the prac-tical approach to problem-solving within thisgroup of diseases. Accordingly, the differing char-acteristics of these perplexing conditions are elu-cidated. The clinical indications for ChEIs andatypical neuroleptics is documented.

In their article, Drs. Rapoport et al clarify themuddy waters surrounding the connection betweentraumatic brain injury and dementia (page 4).Physicians understand that cognitive impairment anddementia put the senior driver at risk for car crashes, aswell as the known relationship between traumatic headinjury and subsequent dementia. This article covers thedriving issue in useful detail. The literature is reviewedto illustrate how dementia is a risk factor for traumaticencephalopathy and how dementia is one of the cog-nitive sequelae of head injury. Evidence reviewed indi-cates that the association between the two has not beenfound consistently in the various studies.

Roberta Bedard describes with sensitivity the expe-rience of interacting with her husband, declining fur-ther into the tangled web of advancing AD (page 20).Relating to the Reisberg theory of retrogenesis, shedescribes her own adjustments that facilitate continu-ing personal interaction with her failing spouse.

A contribution from the Alzheimer Society ofCanada describes the process of establishing the FirstLink program, which has spread throughout the coun-try (page 22). The value of an experienced AD caregiv-er offering guidance and moral support is emphasized.The spin-off is increased linkages between physicians,community support providers and their organizations.

The Canadian Alzheimer Disease Review • September 2004 • 3

Rebutting Bad Press for ChEIsby Peter N. McCracken, MD, FRCPC


Traumatic Brain Injury and DementiaAs Canada’s population ages, the incidence of traumatic brain injury (TBI) and theprevalence of dementia will certainly increase. Dementia is a significant risk factor for thetwo most common causes of brain injury, namely falls and motor vehicle accidents. TBI isassociated with a variety of cognitive deficits and may lead to the development of dementia.There is now compelling data to suggest that TBI causes AD.

by Mark Rapoport, MD, FRCPC, Nicolaas Paul L.G. Verhoeff, MD, PhD, FRCPC andRobert van Reekum, MD, FRCPC

While traumatic brain injury(TBI) is most commonly

seen in adolescents and youngadults, there is a bimodal distri-bution with a second peak inincidence after the age of 65years.1 In Canada, unintentionalinjuries were the sixth-leadingcause of death (22.8 deaths per100,000 population) amongadults aged 65 years and older in1996/1997.2 Among the causesof these injuries, falls and motorvehicle collisions were the mostcommon causes of death and

hospitalization.2 TBI is the third-most common injury leading tohospitalization in older adults.3

In Canada, an estimated 8% ofthe population has dementia and afurther 16.8% have cognitiveimpairment without dementia.4

Alzheimer’s Disease (AD) is themost common cause of dementiain older adults.5,6 As of 1992,364,000 Canadians over the ageof 65 years had AD and relateddementias, and it has been esti-mated that, by 2021, this figurewill reach 592,000.7 As personsover the age of 65 years representthe fastest-growing segment of theCanadian population, and areexpected to comprise 25% of thetotal population by the year2030,7 it will become increasinglyimportant to prevent TBI and ADwhenever possible.

For the purposes of this paper,we will first explore dementia as arisk factor for TBI and then dis-cuss evidence that suggests thatTBI may cause dementia. Thispaper will discuss the relationshipbetween TBI and dementia, usingSir Bradford Hill’s criteria8 forthe establishment of an argument

of causation. As reviewed by Dr. van Reekum,9 the most impor-tant of these criteria require that:a) the causal agent and the pur-ported outcome be associated; b)the causal agent should comefirst; and c) it should be biologi-cally plausible that the putativecausative agent might cause thepurported outcome.

Dementia as a Risk Factor for TBIThe two most common causes ofTBI in the elderly are motorvehicle accidents and falls.Dementia is an important risk fac-tor for both of these.

Driving. An estimated 4% ofmale drivers aged 75 years andolder have dementia,10 althoughin an older study of a retirementcommunity, 18% of drivers aged60 years and older were found tohave “senility.”11 While incidentdementia is a common reason fordriving cessation, between 22%and 68%10,12,13 of dementiapatients continue to drive, andabout one third of patients withdementia have at least one motorvehicle collision before ceasing to

Dr. Rapoport is on staff in theDepartment of Psychiatry and theTraumatic Brain Injury Clinic,Sunnybrook and Women’s CollegeHealth Sciences Centre,University of Toronto.

Dr. Verhoeff is on staff in theDepartment of Psychiatry and theKunin-Lunenfeld Applied ResearchUnit, Baycrest Centre for GeriatricCare and the Department ofPsychiatry, University of Toronto.

Dr. van Reekum is on staff in theDepartment of Psychiatry and aresearch scientist in the Kunin-Lunenfeld Applied Research Unit,Baycrest Centre for Geriatric Careand the Department of Psychiatry,University of Toronto.

drive.12-14 Crash rates in dementiaare increased two to eight timesrelative to age-matched con-trols.14,15 Research generally sup-ports the notion that patients withdementia have higher crash ratesand perform more poorly duringon-road or simulator assessments,but there are many excep-tions.16,17 Cognition itself, how-ever, only captures some elementsof driving risk. Cognitive screen-ing tests, such as the Mini-MentalStatus Examination (MMSE),have limited utility in predictingdriving performance in milddementia.17-19 Furthermore, moredetailed neuropsychological tests,which are not readily available inthe community, predict only 19% ofthe variance of collisions.20 Otherfactors, such as comorbid healthproblems and medication use,may play a significant role.

Falls. In a cross-sectional sur-vey of emergency-room patientspresenting with falls, dementiawas seen as a strong risk factor forfalls in the previous 12 monthswith an odds ratio of 3.80.21

Similarly, a recent prospectivecohort study in a chronic-care set-ting found dementia to be a strongpredictor of the risk of falls. Therisk of falling is double for thosewith dementia compared to thosewithout.22 Analogous results werefound in a cross-sectional analysisof patients discharged from med-ical inpatient services.23

The studies above describe anassociation between a causativeagent (i.e., dementia) and an out-come (i.e., falls or motor vehiclecollisions) in which the causativeagent comes first. Decline inattention, visuospatial skills, and

psychomotor speed associatedwith dementia provide a feasiblebiological mechanism that putssuch patients at risk of injury.While clearly not all falls or colli-sions lead to TBI, they are themost common causes of TBI andrepresent a means by which TBImay be prevented in the dementiapopulation. Clearer institutionaland governmental policies areneeded to provide guidance onwhich patients with dementiashould not be allowed to drive and

measures must be put in place toprevent falls in chronic-care orambulatory patients with dementia.

TBI as a Cause of DementiaCognitive sequelae of TBI.Cognitive sequelae are among themost disabling of post-concussionsymptoms following TBI24 andtypically contribute more to per-sisting disability than physicalimpairment.25 Following TBI,deficits are consistently demon-strated in the domains of atten-tion,26 memory27,28 and executivefunctioning.29,30 To date, thereare few studies of cognitive out-come following TBI in the elder-ly, and these have generally hadsmall sample sizes or have lackeda control group.31 A recent reportindicated that patients with mildTBI were similar in terms of cog-nition to matched controls in thefirst months after injury, and thatonly patients with moderate TBI

demonstrated deficits.32 Anotherstudy showed no difference incognition six weeks post-injurybetween older patients with TBIand orthopedic controls.33

Longer-term studies with largersample sizes are needed to furtherelucidate the effects of TBI oncognition in the elderly.

Dementia. Results of a recentmeta-analysis34 of 15 of theavailable and methodologicallyrigorous case-control studiesshow that TBI is associated with

AD, at least in males (odds ratioof 2.3 for males, and of 0.9 forfemales). The absence of an asso-ciation in females may relate toprotective effects of estrogen, orto other differences in female vs.male neuroanatomy/physiology,or may relate to differences inthe nature of the accidentswhich cause TBI in males vs.females, or perhaps to other fac-tors not yet understood. Asreviewed by Dr. Rapoport,31 theassociation between TBI and ADhas not been found consistentlybetween studies, with, for exam-ple, a relative risk of 4.1 foundin one prospective cohortstudy35 and an absence ofincreased relative risk found inanother.36 An historical cohortstudy37 found an associationbetween TBI and AD, not interms of increased frequency ofAD but rather in terms of earlieronset of AD (median 10 years


TBI is the third-most common injury leading tohospitalization in older adults. In Canada, an estimated8% of the population has dementia and a further 16.8%

have cognitive impairment without dementia.


from the date of the TBI vs. anexpected 18 years based on ageof onset distributions). Finally,evidence of an associationbetween AD and TBI exists atthe pathological level as well.38

Of 58 consecutive autopsies per-formed on individuals (mean age77.0 years), who had suffered asevere TBI, 22.4% had definite orprobable AD based on Braak stag-ing of Alzheimer’s pathology vs.14% in the general populationolder than age 70 years. Note thatthere is evidence that even mildTBI (or concussions) may beassociated with AD.34,39,40

Common pathologies. Thetemporal sequence frequentlyappears to be correct31,34,35,37,38

in that both the case-control and

cohort studies examined cases inwhich the TBI preceded thedementing illness. As discussedabove, it is clear that the temporalsequence will sometimes occur inthe opposite direction (with someindividuals with AD having aTBI). In terms of biologic plausi-bility, TBI has been found to:i) affect hippocampal synaptic

plasticity41 in a number ofanimal studies;

ii) cause accumulation of amyloidprecursor protein in injuredaxons42 with subsequent cleav-age to Aß-peptide in rats;

iii) cause persistent increase in

cerebrospinal Aß-peptide lev-els in humans who have suf-fered a severe TBI;43

iv) cause mild atrophy of thehippocampus40 in mice whohave had a single mild TBI(the atrophy is severe inapo-E-deficient mice, sug-gesting an interaction withapo-E); and

v) cause glial protein immunore-activity40 in these same mice(which is also worse in apo-E-deficient mice).

Another theory is that TBIdoes not cause AD but rather that,by destroying neurons, TBIreduces the critical reserve of neu-rons and hence hastens the onsetof AD.44 Finally, a review45 oflimited data has suggested that

TBI causes cognitive impairmentswhich are similar to AD, andwhich interact with the effects ofaging to essentially mimic—rather than cause—AD.

Factors Mediating theRelationship Between TBIand Dementia.Various factors may mediate therelationship between TBI anddementia, as follows:i) Major depression has been sig-

nificantly associated with exec-utive dysfunction46 and, insome studies, with deficits inattention46 and memory.47 As

major depression is commonfollowing TBI,48-50 it may inter-act with the TBI itself to perpet-uate the cognitive disturbance.

ii) The epsilon 4 allele of apolipo-protein E (apoE-ε4) has beenestablished as a genetic riskfactor for AD, but may also pre-dict poor functional51,52 out-come following TBI. Whileone short-term study found thatthe presence of apoE-ε4 wasassociated with memorydeficits post TBI,53 a recentstudy with long-term neuropsy-chological data failed todemonstrate a relationshipbetween apoE-ε4 and cogni-tion.54 Nonetheless, apoE-ε4appears to interact with the TBIin predicting the developmentof AD.31 In about 30% of severeTBI patients, beta-amyloid pro-tein deposits were observedpost-mortem in one or morebrain areas.55 The beta-amyloidprotein deposition post-TBI isstrongly, and probably synergis-tically, enhanced by the pres-ence of the apoE-ε4 allele.56-59

The beta-amyloid protein is, atleast initially, mainly depositedas diffuse rather than dense coreplaques.55,60-62

iii) The elderly are commonlyaffected by an array of med-ical illnesses and medica-tions, which can affect theircognition. Following a TBIitself, particularly whenassociated with orthopedictrauma, elderly patients arecommonly treated with anumber of medicationswhich can lead not only tocognitive impairment, butalso to acute delirium.

Between 22% and 68% of dementia patients continueto drive, and about one third of patients with dementiahave at least one motor vehicle collision before ceasingto drive. Crash rates in dementia are increased two toeight times relative to age-matched controls.


ConclusionsWith the aging of the population,the incidence of TBI and theprevalence of dementia will cer-tainly increase in the years tocome. Dementia is a significantrisk factor for the two most com-mon causes of brain injury, name-ly falls and motor vehicle acci-dents. TBI itself is associated witha variety of cognitive deficits and,over time, may lead to the devel-opment of dementia. There is nowcompelling data to suggest thatTBI causes AD, as TBI is associat-ed with an increased risk of devel-oping AD, the temporal sequenceis generally correct (with under-standable exceptions) and finallybecause TBI causes changes in thebrain that are typical of the patho-logical changes of AD.

There is now increasing evi-dence that AD may be prevented,

or at least its onset delayed.63

Clearly, individuals at greater riskare more likely to consider ADprevention and the risks/costsinherent in some of the possiblepreventive strategies. The TBIpopulation deserves to be madeaware of the increase in theirlevel of risk and to be made awareof some of the possible preven-tion strategies available to them.While further research is requiredto establish their role, such strate-gies may include the use of nonsteroidal anti-inflammatories(NSAIDs), vitamin E (and perhapsother antioxidants), control ofother risk factors (such as bloodpressure and cholesterol/triglyc-erides) and prevention of furtherinsult to the brain. Maintainingcognitive activities, especially newlearning, may also play a preven-tive role. In the future, there may

well be other, perhaps riskier/cost-lier, strategies. Public healthefforts aimed at preventing colli-sions in younger adults have thusfar targeted alcohol, drunk driving,seatbelts and helmets in their cam-paigns, while research and policyhas lagged behind in investigatinghealth conditions and medicationsthat put older adults at high risk ofcollision. Falls in older peopleare multi-factorial and yet amultidisciplinary assessment andtreatment program involving exer-cise and, potentially, home modifi-cations can often prevent thesequite effectively.64, 65 In thedecades to come, it will beincreasingly critical to preventfalls and motor vehicle collisionsin older adults (and their youngercounterparts) as TBI represents acommon and preventable cause ofcognitive deficits and dementia.

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55. Roberts GW, Gentleman SM, Lynch A,et al. Beta amyloid protein depositionin the brain after severe head injury:implications for the pathogenesis ofAlzheimer’s disease. J NeurolNeurosurg Psychiatry 1994; 57:419-25.

56. Nicoll JA, Roberts GW, Graham DI.Apolipoprotein E epsilon 4 allele isassociated with deposition of amyloidbeta-protein following head injury. NatMed 1995; 1:135-7.

57. Mayeux R, Ottman R, Maestre G, et al.Synergistic effects of traumatic headinjury and apolipoprotein-epsilon 4 inpatients with Alzheimer’s disease.Neurology 1995; 45:555-7.

58. Katzman R, Galasko DR, Saitoh T, etal. Apolipoprotein-epsilon4 and headtrauma: Synergistic or additive risks?Neurology 1996; 46:889-91.

59. Hartman RE, Laurer H, Longhi L, et al.Apolipoprotein E4 influences amyloiddeposition but not cell loss after trau-matic brain injury in a mouse model ofAlzheimer’s disease. J Neurosci 2002;22:10083-7.

60. Horsburgh K, Cole GM, Yang F, et al.beta-amyloid (Abeta)42(43), abeta42,abeta40 and apoE immunostaining ofplaques in fatal head injury.Neuropathol Appl Neurobiol 2000;26:124-32.

61. Graham DI, Gentleman SM, Lynch A,et al. Distribution of beta-amyloid pro-tein in the brain following severe headinjury. Neuropathol Appl Neurobiol1995; 21:27-34.

62. Roberts GW, Gentleman SM, Lynch A,et al. Beta A4 amyloid protein deposi-tion in brain after head trauma. Lancet1991; 338:1422-3.

63. Sano M. Current concepts in the pre-vention of Alzheimer’s disease. CNSSpectr 2003; 8:846-53.

64. Skelton DA, Beyer N. Exercise andinjury prevention in older people.Scand J Med Sci Sports 2003; 13:77-85.

65. Cumming RG. Intervention strategiesand risk-factor modification for fallsprevention. A review of recent inter-vention studies. Clin Geriatr Med2002; 18:175-89.



Dementia with Lewy BodiesThe treatment of DLB can bechallenging. The mainstays ofpharmacologic treatment includethe acetylcholinesterase inhibitors(AChEIs) and judicious use of theatypical neuroleptics and lev-odopa (l-dopa).

AChEIs have recently beenshown to have efficacy in thetreatment of DLB. Given the pro-found cholinergic deficit of DLB,which is greater than that in AD,these medications are pharmaco-logically rational therapy.

Rivastigmine has been report-ed to have both efficacy and safe-

ty in the treatment of DLB. A dou-ble-blind, randomized, placebo-controlled trial (RCT)1 demon-strated improvements in neuro-psychiatric symptoms, includinghallucinations and delusions. Aswell, there were benefits on cog-nitive outcomes, including aseries of computerized attentionaltests. There was a striking loss ofclinical benefit with short with-drawal of the medication.

Donepezil has also beenreported to show efficacy in thetreatment of DLB, however thereare not yet any RCTs with thisagent. The available observationalstudies have reported thatdonepezil also has an effect oncognition (increasing or stabiliz-ing scores on tests of cognition)and on neuropsychiatric symp-toms, including hallucinationsand delusions.2-5

There are no published reportson the use of galantamine in thetreatment of DLB.

Atypical neuroleptics.Neuroleptics are used in thetreatment of DLB because of thefrequency and severity of neu-ropsychiatric symptoms. Whilemany of these symptoms canoften be ameliorated by the useof AChEIs, they often stillrequire adjunct treatment. This isespecially true if the patientrequires dopaminergic agents forhis or her parkinsonian symp-toms. DLB patients have anexceptional sensitivity to neu-roleptics, especially the older,atypical neuroleptics. Thissupersensitivity can result notonly in a worsening of theirparkinsonian features, but also insedation, falls, neurolepticmalignant syndrome anddeath.6,7 Because of this sensi-tivity, treatment of hallucina-tions and other psychotic symp-toms with neuroleptics is gener-ally limited to situations wheresuch symptoms are interfering

The Emerging Spectrumof Parkinsonian Dementias (Part 2)This is the second in a two-part article examining the emerging spectrum of parkinsoniandementias. The first part looked at pathology and neurochemistry, the clinical features andthe differences between dementia with Lewy bodies (DLB), the dementia of Parkinson’sdisease (PDD) and the advanced stages of Alzheimer’s disease (AD). This secondinstallment will examine the treatment of these conditions.

by Inge Loy-English, MD, FRCPC and Howard Feldman MD, FRCPC

Dr. Loy-English is an AssistantProfessor in the Division ofNeurology, Department ofMedicine, University of Ottawa.

Dr. Feldman is a Professor ofMedicine, Division of Neurology,University of British Columbia(UBC) Director, UBC AlzheimerClinical Trials Unit, Vancouver,British Columbia.


with the care or well-being of thepatient. Even then, treatment isapproached cautiously. The cur-rent preferred atypical neurolep-tic for this situation is quetiap-ine, though hard evidence forthis preference is still limited.Fernandez et al8 studied 11patients with DLB using a retro-spective chart review.Quetiapine was well tolerated,with a 90% response rate forpsychosis. Motor decline wasnoted in 27% of subjects.

There have been two studiesevaluating olanzapine in the

treatment of DLB, with conflict-ing results. Walker et al9 foundthat the majority of their patientswere either unable to tolerateeven minimal doses of olanzap-ine, or experienced no benefitwith the medication. Cummingset al,10 with a slightly largerstudy group in a placebo-con-trolled study, found benefit forolanzapine. The best dose wasfound to be 5 mg/day.

Risperidone has also hadmixed results in the treatment ofDLB. While some investigatorshave found it useful in control-ling psychotic and behavioralsymptoms,11 others have foundthat the adverse effects outweighthe benefits.12-14

L-Dopa. There have been noformal studies evaluating theeffects of l-dopa in patients with

DLB, however it is used clinical-ly to treat the parkinsoniansymptoms of this disease.Caution must be exercised in itsuse to not exacerbate psychoticsymptoms. However, in manyinstances, it can be safely insti-tuted with the target symptomsbeing motor parkinsonism andnot the associated dementia.

Combination therapy. Therehave been a few case reportsdetailing successes with combi-nation therapy in DLB. The com-binations include risperidoneand donepezil,15 and l-dopa and

risperidone.16 Both were foundto be safe. Consequent to thisemerging evidence, mostpatients are now placed on anAChEI at the time of diagnosisand l-dopa or atypical neurolep-tics are added as necessary tocontrol symptoms.

Parkinson’s Disease DementiaAChEIs. There are currently nolarge-scale double-blind RCTspublished evaluating the effect ofAChEIs in PDD. There have, how-ever, been a number of small trialsand case series that suggest a pos-itive response.17-21 These havebeen conducted with all three ofthe AChEIs. All three appear, atleast in this preliminary work, tobe effective in improving cognitiveand behavioral symptoms withoutworsening motor symptoms.

There are a number of RCTs withplacebo control being performed.

Atypical neuroleptics. Thereare no large-scale, blinded,placebo-controlled studies usingatypical neuroleptics in PDD.Again, as in DLB, caution must beexercised when using theseagents, as PDD patients areextremely sensitive to theextrapyramidal side effects ofthese medications.

Alzheimer’s Disease withParkinsonism. There are currently no reports inthe literature looking at the phar-macologic treatment of parkin-sonism in Alzheimer’s disease,however recent study reports haveindicated that AchEIs are safe andwell tolerated in more advancedAD including in patients withmotor parkinsonism

ConclusionsThe Parkinsonian dementias area challenging therapeutic prob-lem, however recent researchfindings have informed clini-cians of new treatment options.DLB has deep cholinergicdeficits for which symptomaticbenefits can be obtained withacetylcholinestere inhibitors.The utility of AchEIs for PDD isnot yet determined but prelimi-nary reports are encouraging.For more advanced AD whereParkinsonian features areencountered AchEIs can still beefficacious therapy and are gen-erally well tolerated withoutincreasing motor Parkinsonism.The use of neuroleptics in theParkinsonian dementias must bevery judicious.

AChEIs have recently been shown to have efficacy inthe treatment of DLB. Given the profound cholinergicdeficit of DLB, which is greater than that in AD, thesemedications are pharmacologically rational therapy.

References1. McKeith IJ, Del Ser T, Spano P, et al.

Efficacy of rivastigmine in dementiawith lewy bodies: a randomized dou-ble blind placebo-controlled interna-tional study. Lancet 2000; 356:2031-6.

2. Aarsland D, Bronnick K. Donepezil fordementia with lewy bodies, a casestudy, Int J Geriatr Psychiatry 1999;14:69-74.

3. Lancetot K, Herrman N. Donepezil forbehavioral disorders associated withlewy bodies: A case series. Int J GeriatrPsychiatry 2000; 15:338-45

4. Rojas-Fernandez C. Successful use ofDonepezil for the treatment of demen-tia with lewy bodies. Ann pharma-cother 2001; 25:202-5.

5. Skejerve A, Nygaard H. Improvementin sundowning in dementia with lewybodies after treatment with donepezil.Int J Geriatr Psychiatry 2000; 15:1147-51.

6. Feldman H, Solomons K, Cooney T, etal. Neuroleptic malignant syndromeand dementia with lewy bodies: A casestudy. In Fisher et al. (eds.) Progress inAlzheimer’s and Parkinson’s Diseases.Plenum Press, New York. 1998.

7. Sechi G, Agnetti V, Masuri R, et al.Risperidone, neuroleptic malignantsyndrome, and probable dementia withlewy bodies. Progress in neuropsy-chopharmacology and biological psy-chiatry 2000; 24:1043-51.

8. Fernandez. Quetiapine for psychosis in

Parkinson’s disease versus DLB. J ClinPsychiatry 2002; 63(6):513-5.

9. Walker Z, Grace J, Overshot, et al.Olanzapine in dementia with lewybodies: A clinical study. Int J GeriatrPsychiatry.1999; 14:459-66.

10. Cummings J, Street J, Masterman D, etal. Efficacy of olanzapine in the treat-ment of dementia with lewy bodies.Dement geriatr cogn disord 2002;13(2):67-73.

11. Allen RL, Walker Z, D’ath P, et al.Risperidone for psychotic and behav-ioural symptoms in Lewy body demen-tia. Lancet 1995; 346(8968):185.

12. McKeith IG, Ballard CG, Harrison RWSNeuroleptic sensitivity to risperidone inlewy body dementia. Lancet 1995;346(8976):699.

13. Sechi G, Agnetti V, Masuri R, et al.Risperidone, neuroleptic malignantsyndrome, and probable dementia withlewy bodies. Progress in neuropsy-chopharmacology and biological psy-chiatry 2000; 24:1043-51.

14. Morikawa M, Kishimoto T. Probabledementia with lewy bodies and risperi-done induced delirium. Can J psychia-try 2002; 47(10):976.

15. Geizer M, Ancill RJ. Combination ofrisperidone and donepezil in dementiawith lewy bodies. Can J Psychiatry1998; 43(4):421-2.

16. Kato K, Wada T, Kawakatsu S, et al.Improvement of both psychotic symp-toms and parkinsonism in a case of

DLB by the combination therapy ofrisperidone and L-dopa. ProgressNeuropsycopharmacol Biol Psychiatry2002; 26(1):201-3.

17. Aarsland D, Larsen J, Janvin C, et al.Donepezil treatment in Parkinson’s dis-ease with dementia: A double blindplacebo controlled crossover study.Neurology 2001; 56(Suppl 3):A128.

18. Giladi N, Shabtai H, Benbunan B, et al.The effect of treatment with rivastigmine(Exelon) on cognitve functions ofpatients with dementia and Parkinson’sdisease. Neurology 2001; 56(Suppl3):A128.

19. Mori S. Responses to domepezil inAlzheimer’s disease and Parkinson’sdisease. Ann N.Y. Acad. Sci. 2002;977:493-500.

20. Reading PJ, Luce AK, McKeith IG.Rivastigmine in the treatment ofparkinsonian psychosis and cognitiveimpairment: Preliminary findings froman open trial. Movement Disorders2001; 16(6):1171-95.

21. Aarsland D, Hutchinson M, LarsenJP. Cognitive, psychiatric, and motorresponse to galantamine inParkinson’s disease with dementia.Int J Geriatr Psychiatry 2003;18(10):937-41.

22. Feldman H, Gauthier S, Hecker J et al.A 24 week randomized double-blindstudy of donepezil in moderate tosevere Alzheimer’s disease. Neurology2001; 57(2):613-620.



Knowing whether or notAlzheimer’s disease (AD)

has been successfully treatedremains difficult, due in part to alack of understanding of how totranslate the results of pivotalstudies into clinical practice.1 Asmany of the measures employedin these pivotal trials are rarelyused in practice, and because thecourse of treatment is long, thereis uncertainty about what treatmenteffects to look for, how long to lookfor them, or whether a given bene-fit is worthwhile. For example, arecent article in the New York Timesraised the question of whether“naming 11 animals in one minuteinstead of 10” was worth it.2 Thatfrustration can perhaps be bettersummarized like this: are treatmentresults clinically important?

At present, while we have nostandard criteria for understanding

whether a given effect is likely to beclinically important, some featuresmake it more likely.3 For example,the strategy of cholinesterase inhibi-tion appears to be biologically plau-sible.4-6 An overview of thecholinesterase inhibitor trials showsa reproducible dose response effectand that the outcome measures con-verge.7 As reviewed elsewhere, clin-ically detectable patterns seem tohold in interviews8 using theClinician’s Interview-based Im-pression of Change (CIBIC).9 Still,the essential question of whether allthese statistically significant differ-ences translate into clinically evidenttreatment success recognized bynon-experts remains a troublingone.10 This is what the AtlanticCanada Alzheimer’s DiseaseInvestigation of Expectations(ACADIE) study sought to address.

ACADIE: The ObjectivesThe results of ACADIE have beenpublished elsewhere.11 ACADIEsought to add to the existing bodyof information about cholinesteraseinhibition in general, and donepezil

in particular, in two ways. First, wesought to understand whethertreatment met the expectations ofpatients, caregivers and theirphysicians. Next, we wanted toknow whether the treatmenteffects observed in highly selectedclinical trial patients might also beseen in patients who more closelyconformed to those seen in usualclinical practice. The latter weattempted to achieve by situatingthe study in Atlantic Canada, byusing sites (with the exception ofHalifax and Saint John) that hadnot been part of earlier trials, andby using liberal enrolment criteria.That we enrolled 108 patients,brought 100 to their baseline visit,and had 88 complete all 12 monthsof the trial suggests that this objec-tive was achieved.

The objective of understandingwhether treatment met expecta-tions was tested using GoalAttainment Scaling (GAS).11

GAS is a formal method of settingindividualized treatment goals,and was reviewed in TheCanadian Alzheimer Disease

The ACADIE Study: Does DonepezilMeet the Expectations of Treatment? The Atlantic Canada Alzheimer Disease Investigation of Expectations (ACADIE) study was a12-month phase IV trial, in which patients with mild to moderate Alzheimer’s disease (AD),their primary caregivers and treating physicians set treatment goals, divided into fivedomains: cognition, function, behavior, leisure activities and social interactions. Patients andcaregivers described consistent goal attainment, whereas physicians observed variable effects,such as decline in cognition, but improved social interaction and behavior.

by Kenneth Rockwood, MD, FRCPC

Dr. Rockwood is a Professor ofMedicine at Dalhousie Universityand a Geriatrician, Capital DistrictHealth Authority in Halifax, Nova Scotia


Review last year.13 Using GAS,goals are defined prior to the initi-ation of treatment. Over thecourse of the ACADIE trial, theywere monitored every threemonths. Although the goals areindividualized, so they varybetween one patient and the next,the extent to which goals are

achieved can be standardized. Weused a formula which takes intoaccount the number of goals set,the importance of one goal com-pared to the others for a givenpatient, the proportion of goalsattained, and the extent, over anine-point scale of “much worsethan expected” to “much better thanexpected,” to which goals were met.Because their perspectives differ,and because each has importantinsights into expectations andtheir attainment, we elicited goals

separately from patients, fromtheir caregivers and from treatingphysicians. In addition, becauseour intent was to understand howthese patient-centred accountsmight help us interpret the usualclinical trials accounts from stan-dard clinical trials measures, sever-al of the latter were also incorpo-

rated in the ACADIE study as sec-ondary measures. These secondarymeasures included the Alzheimer’sDisease Assessment Scale-Cognitive (ADAS-cog),14 and theClinician’s Interview-based Im-pression of Change, Plus CaregiverInterview (CIBIC-Plus).9

ACADIE: The MethodsACADIE was conducted like manyphase IV trials, in that all patientswere evaluated for participation andgave written, informed consent.

Patients were treated with 5 mg/daydonepezil for the first 12 weeks,after which they could eitherreceive 10 mg/day (this was done in 82%) or stay with 5 mg/day. At baseline and at each ofthe quarterly follow-up interviews,patients and caregivers underwent abattery of standard clinical assess-ments. In contrast to other phase IVtrials, they participated in an open-ended, home-based interview con-ducted by trained field researchers.Clinicians’ findings were blindedfrom those of the field researchersand vice versa.

Having used GAS in an earlydementia drug study,15 we requiredthat inquiries about goal areas bemade in at least four generaldomains: cognition, function,behavior and leisure. Within each ofthese domains, patients/caregiversand physicians could choose to setas many goals or as few (includingnone) as they wished. As wereviewed these goal areas, as part ofour planned qualitative researchprogram, each of the goals that hadbeen recorded was classified in oneof these domains. However, itquickly became apparent, particu-larly for the patient/caregiver goalsset in their own homes, that a fifthdomain (social interaction) wasneeded and was added.

Sometimes, a single goal couldbe classified into more than onedomain. For example, considerthe goal of being able to use thetelephone. This could be classi-fied as an aspect of function,under the subdomain of instru-mental activities of daily living(IADLs). In some cases, it mightalso reflect cognition, asimproved telephone use might be

We wanted to know whether the treatment effects observedin highly selected clinical trials patients might also be seenin patients who more closely conformed to those seen inusual clinical practice.

Figure 1

Mean Change From Baseline by Domain for Patient/Caregiver GAS

Cognition Function Social Behavior Leisure

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JNNP 2002; 73:500-7, Figure 4 by Rockwood et al.Reproduced with permission from the BMJ Publishing Group.


an instance of better languageabilities. In other cases, it mightreflect better visuospatial func-tion. Better use of the telephonemight reflect recovery of lost ini-tiative, or reflect improved social-ization or be key to less caregiverstress. The point is that, in theabsence of knowing what suc-cessful treatment means, ourstrategy was to listen closely towhat patients, caregivers andphysicians observed, and then toevaluate which patterns emerged.

In addition to GAS, the ADAS-Cog and the CIBIC-Plus, we alsostudied treatment responseregarding performance on theMini-Mental State Examination(MMSE)16 and measures of func-tion17,18 and depression,19 includ-ing caregiver depression.20,21

ACADIE: The Results Most ACADIE patients (71%)were elderly women (mean age 76years) and most had mild AD.Eighty-two patients had treatmentincreased from 5 mg/day to 10 mg/day for at least one dose.Most caregivers were women (66%),spouses (48%) and younger than thepatients (mean age 61 years). Wewere interested to observe thatpatients and caregivers set moregoals (855; or 9 ± 3 per patient) thandid clinicians (342; or 3 ± 1 perpatient). While patients/caregiversand clinicians set cognition goalsin the great majority of cases (83%and 85%, respectively) and behav-ior goals (58% and 57%) therewere intriguing differences in otherdomains. For example,patients/caregivers set functiongoals most often (86%, compared to68% of cases for physician goals).

The biggest differences were in thedomains of leisure and social inter-actions. In 76% of cases, patientsand caregivers set leisure goals,compared to only 20% of cases forclinician goals. Similarly, socialinteraction goals were set in twice asmany cases by patients/caregivers(49%) as by clinicians (24%).

In general, patient/caregivergoal attainment scores gave amore optimistic account of theextent to which treatment metexpectations than did physicianaccounts. Statistically significantimprovements in the totalpatient/caregiver GAS scoreswere seen to week 36 (meanchange = 3.19, p = 0.03; treatmenteffect size = 0.28). However, byweek 52, there was no significantdifference from baseline (meanchange = 1.62, p = 0.74; treatmenteffect size = 0.15).

The total GAS score for clinician-identified goals improved signifi-cantly from baseline to week 24(mean change = 2.39, p = 0.04;treatment effect size = 0.26), butwas not significantly differentfrom baseline thereafter (week 52

mean change = 0.43, p = 1.00;treatment effect size = 0.03).

Clearly, the perspective ofpatients and caregivers, whetherelicited from detailed interviews intheir own homes or by clinician-driven inquiries in physicians’offices, offer a different perspectiveon disease treatment success than dothe standard measures. For example,despite improved overall perform-ance, including improved cognition(see Figures 1 and 2), the standardcognitive measures showed signifi-cant improvements only at week 12(MMSE mean change = 0.86 andADAS-Cog mean change = -1.17).Decline from baseline was observedfor both measures thereafter (e.g., week 52: mean change = -1.04and mean change = 3.07, respec-tively). Similarly, the functionalassessments showed patterns of ini-tial maintenance of functional per-formance, followed by later decline,chiefly in IADLs. In general, thecorrelations between GAS totalscores, GAS domain scores and thestandard measures were low, savefor moderate correlations betweenclinician-assessed GAS cognition

Figure 2

Mean Change From Baseline by Domain for Clinician GAS

Cognition Function Social Behavior Leisure

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JNNP 2002; 73:500-7, Figure 5 by Rockwood et al.Reproduced with permission from the BMJ Publishing Group.


goals and the MMSE (r = 0.51) andthe ADAS-cog (r = -0.43) at week52, each of which reflected wors-ening. However, there was no sig-nificant worsening from baselinein the patient/caregiver cognitiongoals (Figure 1).

However, there were interestingdifferences between patient/care-giver goal areas and cliniciangoals. Briefly, patients and care-givers generally observed improve-ment and each domain tended to gowith the others, and with the global

GAS score (Figure 1). The largesttreatment effects were observed inbehavior. The physician profiles ofpatient goal attainment are less read-ily summarized. Of note, similar tothe standard cognitive measures,clinician-identified cognition andfunction goals had been met atweek 12, but these initial gainswere not maintained. Few leisuregoals were set, resulting in particu-larly wide confidence intervals.Clinicians recorded behavior andsocial-interaction goals above base-line at each time-point (Figure 2)but in contrast to the patient/care-giver goals, goal attainment wasnot consistent across domains.

Almost all patients (104/108)experienced at least one adverseevent, usually pain (n = 46,including 19 with headache) orvarious gastrointestinal problems,such as diarrhea (n = 24), nausea(n = 23) and dyspepsia (n = 15).Twenty-two serious adverse events

were reported in 16 patients, oneof whom died as the result ofmyocardial infarction. No seriousadverse events occurred more thanonce and none had a clear relationto the study drug. Ten patientswere obliged to discontinue due toadverse events, which includedanxiety (n = 2), weight loss (n = 2), diarrhea (n = 1), pacing (n = 1), transient ischemic attack(n = 1), confusion (n = 1), agitat-ed depression (n = 1) and footpain (n = 1).

ACADIE: Points for DiscussionThe ACADIE study found that, forat least the first six months of treat-ment, a patient-centred accountgave an optimistic profile of expec-tations being met, whether judgedby patients/caregivers or by physi-cians. After six months, the picturebecame murkier, with patients/care-givers continuing to see overall goalattainment for another three monthsand persistently beneficial effectsin behavior throughout the study.While physician-set goals were alsomet in behavior and in social inter-actions, their account showeddecline in some areas by 12 months.

Like any study, ACADIE is sub-ject to important caveats. Note that itis not a controlled trial, so we cannotanswer the question (nor did we seekto) about whether donepezil is moreeffective than placebo. The reasonwe did not test this question is that itappears to have been satisfactorily

answered in placebo-controlled dou-ble-blind conditions.22-26 Our ques-tion was whether treatment of ADmeets a priori expectations. This isan important question because thedebate has now moved to whetherthe treatment effects demonstrated inearlier studies are clinically mean-ingful. As detailed in the mainreport,11 the ACADIE patientsappear to be comparable to those indouble-blind studies, and haveADAS-Cog responses comparableto other published reports.

Perhaps the most striking featureof the ACADIE study is the widerange of expectations patients andcaregivers bring to the table when itcomes to dementia treatment.Reflecting our training and concep-tualization of the disease, physi-cians tend to focus on cognition,behavior and, to a lesser extent,function. But our patients have abroader range of concerns. We canlearn from this not just clinically, interms of what we talk to ourpatients about, but also scientifical-ly. In as many ways as they can,patients and caregivers are telling usthat impaired executive function isan essential aspect of dementia. Yet,in comparison with memoryimpairment, it has received scantformal attention. Although somerelatively brief (in the sense of sev-eral minutes) tests exist,27-29 thislack of attention reflects that execu-tive function is an area that is lessstandardized than other aspects ofcognitive testing—there is nothingabout it on the MMSE, for example.In addition, many of the standarditems that purport to test executivefunction seem quite removed fromknowing how someone’s judgmentwill actually hold up in practice.

The ACADIE study found that, for at least the first six monthsof treatment, a patient-centred account gave an optimisticprofile of expectations being met, whether judged bypatients/caregivers or by physicians.


Clinical ConsequencesWhat should we look for in patientinterviews? The experience ofstudying formal goal setting andattainment in patients with demen-tia has changed my practice in thisway: I now routinely inquire aboutso-called target symptoms as partof my clinical interview. I do sobecause I know from ACADIEthat, despite their broad range ofexpectations, patients and care-givers largely set goals that reflecta realistic understanding of whatmight be possible. In ACADIE,only about 1% of goals werejudged to be unrealistic. It is alsoimportant to recognize that some-times maintenance is explicitlyunderstood as the desired goal:“we’ll be fine if things stay as theyare.” That realization, and theobservation that setting goals canbe problematic for some patientsand caregivers, has led me to focuson particular symptoms. These tar-get symptoms, like goals, need tobe observable and measurable, butthey do not require people to antic-ipate how they will react to afuture change. For example, a com-mon target symptom is repetitive

questioning and it often respondsto treatment. Another commonlyreported symptom is misplacingobjects, which responds far lessfrequently, so I find it to be of lit-tle value as a target. The same istrue for forgetting names. Otherresponsive symptoms include get-ting lost in familiar neighborhoodenvironments, irritability, lackinginitiative (especially for socialevents), not answering the tele-phone, and needing assistancewith tasks that require sequencing,such as housework and mealpreparation.

In my clinical practice, I alsorecognize that, even in successfullytreated patients, not everything willbe improved. More often, especial-ly after nine to 12 months, patientsare more likely to exhibit new com-binations of symptoms and signs,as some that were present at base-line improve, while others worsen,and still others stay the same.1,8

ACADIE’s Legacy The ACADIE study has allowedus to learn how to listen topatients with dementia. GAS isnow being used in another anti-

dementia drug study. In NovaScotia and New Brunswick, theexperience with GAS hasinformed the way in which theprovincial formularies approveand monitor anti-dementia drugs:instead of specified changes onthe MMSE, the standard is thattarget symptoms be set and moni-tored. The ACADIE data havealso shown that we must developbetter ways to measure executivedysfunction if we are to under-stand clinical meaningfulness indementia. They also producedresults compatible with the propos-al for a prefrontal compensatorynetwork in AD and one that mightbe enhanced by cholinesterase inhi-bition. In addition, they haveinspired us to also considercholinesterase-inhibitor studies asunique ways in which we canunderstand human cholinergicneurotransmission. Given that somuch of what we uniquely value asa species depends on our abilitiesof abstract reasoning, this perspec-tive gives us a means of communi-cating the vital importance ofcholinesterase inhibition as both aclinical and scientific stratagem.

References:1. Rockwood K, Wallack M, Tallis R.

Alzheimer’s disease: understandingtreatment success short of a cure.Lancet Neurol 2003; 2:630-3.

2. Grady D. Minimal benefit is seen indrugs for Alzheimer’s. New YorkTimes; National Desk, April 7, 2004.

3. Rockwood K, MacKnight C.Assessing the clinical importanceof statistically significant

improvement in anti-dementiadrug trials. Neuroepidemiology2001; 20:51-6.

4. Francis PT, Palmer AM, Snape M, etal. The cholinergic hypothesis ofAlzheimer’s disease: a review ofprogress. J Neuro NeurosurgPsychiatry 1999; 66:137-47.

5. Rockwood K, Darvesh S. Cholinergicdrugs for Alzheimer’s disease. In:Gray J (ed.) Drug Advances Volume

One. Remedica Publishing Limited,London, 2003.

6. Grady CL, McIntosh AR, Beig S, etal. Evidence from functional neu-roimaging of a compensatory pre-frontal network in Alzheimer’s dis-ease. J Neurosci 2003; 23:986-93.

7. Rockwood, K. Size of the treatmenteffects on cognition of cholinesteraseinhibition in Alzheimer’s disease. JNeurol Neurosurg Psychiatry 2004;


75:677-85.8. Rockwood K, Joffres C. Improving clin-

ical descriptions to understand theeffects of dementia treatment: consen-sus recommendations. Int J GeriatrPsychiatry 2002; 17:1006-11.

9. Schneider LS, Olin JT. Clinical GlobalImpressions in Alzheimer’s ClinicalTrials. Int Psychogeriatr 1996; 8:277-86.

10. Winblad B, Brodaty H, Gauthier S, etal. Pharmacotherapy of Alzheimer’sdisease: is there a need to redefinetreatment success? Int J GeriatrPsychiatry 2001; 16:653-66.

11. Rockwood K, Graham JE, Fay S. Goalsetting and attainment in Alzheimer’sdisease patients treated with donepezil.J Neurol Neurosurg Psychiatry 2002;73:500-7.

12. Kiresuk, TJ, Smith RE, Cardillo JE. GoalAttainment Scaling: ApplicationsTheory and Measurement. LawrenceErlbaum Associates Publishers, Hillside,NJ, 1994.

13. Rockwood K, Gorman M. Setting treat-ment goals using cholinesterase inhibitorsin AD. Can Alz Dis Rev 2003; 5(3):5-8.

14, Rosen WG, Mohs RC, Davis KL. A newrating scale for Alzheimer’s disease.Amer J Psychiatry 1984; 141:1356-64.

15. Rockwood K, Stolee P, Howard K, et al.Use of goal attainment scaling to measure

treatment effects in an anti-dementia drugtrial. Neuroepidemiology 1996; 15:330-8.

16. Folstein MF, Folstein SE, McHugh PR.Mini-mental-state: a practical methodfor grading the cognitive state ofpatients for the clinician. J PsychiatricRes 1975; 12:189-98.

17. Lawton MP, Brody EM. Assessment ofolder people: Self-maintaining andinstrumental activities of daily living.Gerontologist 1969; 9:179-86.

18. Pfeffer RI, Kurosaki TT, Harrah CH, etal. Measurement of functional activitiesin older adults in the community. JGerontol 1982; 37:323-9.

19. Abrams A, Young S. Cornell scale fordepression in dementia. Biol Psychiatry1988; 23:271-84.

20. Lyness JM, Noel TK, Cox C, et al.Screening for depression in elderly pri-mary care patients. Arch Intern Med1997; 157:449-54.

21. Radloff, LS. The CES-D scale: A self-reportdepression scale for research in the gener-al population. Appl PsychologicalMeasurement 1977; 1:385-401.

22. Rogers SL, Friedhoff LT, the DonepezilStudy Group. The efficacy and safety ofDonepezil in patients with Alzheimer’sdisease: results of a US multicentre, ran-domized, double-blind, placebo-con-trolled trial. Dementia 1996; 7:293-303.

23. Rogers SL, Farlow MR, Doody RS, etal. A 24-week double-blind, placebo-controlled trial of donepezil in patientswith Alzheimer’s disease. Neurology1998; 50:136-45.

24. Burns A, Rossor M, Hecker J, et al. Theeffects of donepezil in Alzheimer’s dis-ease - results from a multinational trial.Dement Geriatr Cogn Disord 1999;10:237-44.

25. Winblad B, Engedal K, Soininen H, etal. A 1-year, randomized, placebo-con-trolled study of donepezil in patientswith mild to moderate AD. Neurology2001; 57:489-95.

26. Mohs RC, Doody RS, Morris JC, et al. A1-year placebo-controlled preservationof function survival study of donepezilin AD patients. Neurology 2001;54:481-8.

27. Royall DR, Rauch R, Roman GC, et al.Frontal MRI findings associated withimpairment on the Executive Interview(EXIT25). Exp Aging Res 2001;27(4):293-308.

28. Royall DR, Cordes JA, Polk M. CLOX:an executive clock drawing task. JNeurol Neurosurg Psychiatry 1998;64:588–94.

29. Dubois B, Slachevsky A, Litvan I, et al.The FAB: a Frontal Assessment Batteryat bedside. Neurology 2000; 55:1621-6.

Acknowledgements:ACADIE was funded by a grant from Pfizer Canada. Janice Graham was co-Principal Investigator.Study sites included Antigonish, NS (Mary Gorman), Charlottetown, PEI (Ronald Hutchings),Fredericton, NB (Roger McKelvey), Halifax, NS (Dan Carver), Saint John, NB (Peter Bailey) andYarmouth, NS (Julie Chandler).Dr. Rockwood is supported by an Investigator Award from the Canadian Institute of Health Research andthe Dalhousie Medical Research Foundation as the Kathryn Allen Weldon Professor of AlzheimerResearch.


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New Stage“Looking at you right now, I’mnot quite sure who you are.”

This addressed to me by thequiet, gentle man who is my hus-band, as he sits up in bed.

He has just explained to meseriously that, “… we have tomake sure that the windows areopen, because Roberta needs herfresh air.”

“I’m Roberta. I’m your wife andI love you more than anything.”

“Oh, good.”This confirms what I have

been suspecting for a fewmonths now. The Alzheimer’ssymptoms are becoming worse.This after four years of a morato-rium on symptoms imposed bydonepezil.

Lately, even an overnight stayat a hotel has left him disorientedfor about a week afterward. I haveawakened to find him packingbecause, “It’s really too bad that

we have to move every month.There should be a way that we canstay in the same place for longerthan that. Oh, we have purchasedthis home? We can stay? That’sgood,” he says as he snugglesunder the covers and drifts off.He’s also been asking me whereJuliette, his long-dead sister, is. Ihave to accept the reality. He isslipping.

Oddly, I am not terribly upsetby this. I have had four years to

Roberta Bedard is a caregiver for her husband who has Alzheimer’s disease(AD). She has written many humorous and touching vignettes about herpersonal experiences in dealing with the development of the disease, and hasgraciously agreed to feature these vignettes as a series in the CanadianAlzheimer Disease Review. Roberta’s writings enable readers to share in herjourney with AD caregiving, provide valuable insight on the human aspect ofdisease and stimulate contemplation on the deeper meanings of life and love.

In this feature...In “New Stage,” Roberta talks about how the Reisberg theory is a source ofcomfort and confidence as she and her husband must accept that, as she putsit, “he is slipping.”P

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Chapter 5by Roberta Bedard

Personal Revelations, Experiencesand Reflections of an AD Caregiver



prepare for this time, and theknowledge I have gained, espe-cially understanding theReisberg theory, has given methe confidence that I will knowwhat to do.

My biggest fear when I under-took this journey was that Iwould not be able to cope; thatRay would not have good carefrom me.

But now I have a road map.What I must establish is whereRay is now in terms of AD andthen correlate this to a develop-mental stage in a child. I amalready, without much thought,relating to him at a different level.

I was right that joy can stillbe found. We are having manyhilarious moments. This isbecause I am also free toexpress my inner childishness.Ray is the one person withwhom I can be as silly andchildish as I want, and it’salright with him. So we sharestupid jokes at which no one butus would laugh. I can dancearound making monkey noisesand the fact that I am in mymid-sixties, and a large woman,does not appear to him to beincongruous. He just thinks it’sfunny and we laugh together.

At this point, his moments ofdisorientation are few. Most ofthe time, he is himself. He canstill think and has invaluableinsights that I am not willing tooverlook just because he doesn’talways know exactly what’s

going on at any particularmoment.

The man I married still lives.Because we have been honest andclear with each other from thestart of this illness, we can discusswhat is going on and the changeswe need to make.

He doesn’t have to pretend hedoes not get confused. He canacknowledge that I have to hide

the medications. If I don’t hidethem, he does, which leads topanic on my part when I can’tfind them. He accepts that driv-ing is not a good idea and that heshould not have the ignition keyto the car. This wonderful manlooked me straight in the eye andsaid, “We have to do what wehave to do. My ego’s notinvolved here.”

I have never lied to him. Neverpretended that things were differ-ent than they are. And he knowsat the core of his being that all hehas to do to be loved by me is tobreathe. I dare to hope that willhold. AD patients respond tofeelings and I don’t expect myfeelings to change.

Those who don’t agree withthe Reisberg theory are opposedto the whole idea of “treating

AD patients like children.” Theyfeel that AD patients are adultsand should be treated likeadults. My feeling is that it isthe height of disrespect to theindividual to refuse to respondto who they are, and ratherinsist on responding to them aswe wish they were.

Treating a person with digni-ty involves being truthful. I

believe the AD patient knows inthe core of his/her heart thatsomething is wrong. How frus-trating must it be to have thatinner truth denied by those whoare supposed to be loving themand caring for them.

As my husband changes, Iplan to continue to relate to himas he is at that moment. As anadult when he is an adult and asmy beloved child when that iswhere he is.

It’s working so far.

Please look for Chapter 6: I amLoved in the next issue of theCanadian Alzheimer DiseaseReview.


I have never lied to him. Never pretended that things were

different than they are. And he knows at the core of his

being that all he has to do to be loved by me is to breathe.


Communicating the Diagnosis of“The first steps in the Alzheimer journey are justlike the steps we would take when beginning anyother voyage: we need to plan early, anticipateany problems we may encounter along the way,talk to others who have already been there, learnabout where we are going and how best to getthere, and make sure we have a faithful compan-ion with whom to travel. First Link can helpwith those first steps and make your journey alittle bit smoother.”

These words, from the First Link brochure, describea pilot project led by the Alzheimer Society of Ottawa,in collaboration with the Dementia Network of Ottawa(www.alzheimerott.org/network/network1.htm). FirstLink is a direct referral system that links newly diag-nosed individuals with dementia and their families to acontinuum of care through a community of learning,services and support.

Once an individual has been diagnosed, theirphysician offers to refer the patient and their fami-ly to the First Link Coordinator. With the family’sconsent, their physician contacts the First LinkCoordinator with the information. This referralconnects the family directly to the AlzheimerSociety of Ottawa and the Dementia Network ofOttawa programs.

Within three to four weeks of the referral, fami-lies receive a phone call from the First LinkCoordinator. This initial call builds a connectionwith the family and the First Link program.Families are given the opportunity:• to ask questions about the new diagnosis; • to receive written information about the disease; • to learn of community supports as needed; and

• to participate in First Link learning series, the peersupport program and other appropriate supports pro-vided by Dementia Network of Ottawa organizations.“The idea for First Link was developed when we

recognized that there were many unmet needs in theareas of service delivery, education and researchrelated to dementia,” said Marg Eisner—Director,Family Support and Education, Alzheimer Societyof Ottawa. “First Link ensures support services arein place for families affected by dementia fromonset to end-stage.”

The peer support component of First Linkinvolves an experienced Alzheimer caregiver offer-ing guidance, a listening ear, understanding, encour-agement and moral support to a new caregiver. Thepeer volunteer acts as a mentor to the caregiver, byproviding support over the phone, through in-personmeetings, or by e-mail.

The First Link learning series covers every step ofthe Alzheimer journey. These sessions are progres-sive, building upon each other to provide participantswith a complete overview of dementia, information,skills and resources. Sessions are taught by staffwithin the Dementia Network of Ottawa, includinggeriatricians, social workers, nurses and occupation-al therapists. Learning series are offered in the spring,fall and winter, during the day and evening.

The learning series include:• First Steps: focusing on the early stages of the

disease;• Care Essentials: centering on the best ways to

provide care;• Options for Care: concentrating on the increas-

ing care needs and long-term options; and

First Link: Your Link to a Communityof Learning, Services and Support

News from the Alzheimer Society of Canada


• Quality of Life at the End of Life: focusing onthe later stages.Funding for the First Link pilot program was

provided by the Ontario Trillium Foundation fromApril 2002 to March 2004. Initially created as apilot project, First Link will continue to be offeredby the Alzheimer Society of Ottawa, and is beingexpanded to include the satellite regions ofRenfrew County.

An evaluation report of First Link was com-pleted in May 2004 demonstrating that the pro-gram is a success. More than 690 referrals werereceived by the First Link Coordinator from fam-ily physicians, community service providers andcommunity service organizations. Linkagesbetween physicians, community service providersand the Alzheimer Society of Ottawa werestrengthened, as all partners worked collabora-tively to develop a referral system, to design andimplement learning series, and to develop evalua-tion methodologies. More than 250 different fam-ilies participated in the First Link learning seriessince the project’s inception, improving theirunderstanding of Alzheimer disease, dementia andcoping skills.

“We know that after a diagnosis, families arefeeling overwhelmed,” said Inika Anderson, FirstLink Coordinator. “It can be extremely difficult forthem to pick up the phone and ask for help. WithFirst Link, we can reach out to families instead ofwaiting for them to call us. Families truly appreci-ate knowing that there is someone they can callwhen they need to.”

Evaluation results indicate that First Link hashelped people with dementia and their family mem-bers in several ways, including learning about thedisease, linking families to community services,increasing caregivers’ confidence in caring for theirfamily member, and helping caregivers to moreeffectively manage crises.

First Link also has benefits for community agencystaff and family physicians. Health care professionalsreported a stronger relationship with the AlzheimerSociety as a result of the First Link program. Family

physicians reported that their patients greatly bene-fited from First Link.

The program has worked so well that, in additionto First Link programs in Ottawa and RenfrewCounty, other provincial societies including BritishColumbia, Alberta, Saskatchewan and Nova Scotiaare exploring adapting the First Link program.

In addition, local Ontario Alzheimer Society chap-ters in Halton-Wentworth, Lanark County, LondonMiddlesex, and Kitchener-Waterloo have all discussedthe program with their respective dementia networks.The Alzheimer Society of Brant is moving ahead witha version of the program and Perth County is repro-ducing the First Link referral materials and activelyworking with local physicians while Toronto hasimplemented the program on a limited basis and isworking with one or two partners to receive referrals.

The Alzheimer Society of Ottawa has developeda First Link Toolkit as a how-to guide that discusseshow the program was implemented there and makessuggestions as to how it can be adapted to suit othercommunities. They are assisting other AlzheimerSocieties by providing resource materials, answeringquestions and offering consultation services.

For more information on First Link, or to obtain theToolkit, please visit the Alzheimer Society of Ottawa’sweb site at www.alzheimerottawa.org/first_link or con-tact Inika Anderson, First Link Coordinator by phone at 613-523-4004 or by e-mail [email protected].

The Alzheimer Society of Canada is a not-for-profit healthorganization dedicated to helping people affected byAlzheimer Disease. The Society provides support and edu-cational programs for people with Alzheimer Disease andtheir caregivers. The Society also funds research into find-ing the causes and cure of the disease, and into improvedmethods of caregiving. The Society consists of a nationaloffice, 10 provincial organizations and more than 140 localgroups across the country.

For more information on Alzheimer Disease andrelated dementias, Alzheimer Society programs and serv-ices, and how you can help, contact your local AlzheimerSociety or visit the Society’s website at www.alzheimer.caor call 1-800-616-8816.

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