The Canadian Alzheimer - STA Communications...vation Screening Scale,20 the NEECHAM confusion scale,21 and the Confusion Assessment Method (CAM).22 The CAM can achieve better than

Editorial 3Serge Gauthier, MD, CM, FRCPC

Diagnosis and Prevention of Delirium in Elderly People 4Susan Freter, BSc, MSc, MD, FRCPC and Kenneth Rockwood, MD, MPA, FRCPC

Screaming and Wailing in Dementia Patients (Part 1) 11Bernard Groulx, MD, CM, FRCPC

Reporting from the Second Canadian Colloquium on Dementia 15Ron Keren, MD, FRCPC and John Wherrett, MD, PhD, FRCPC

Personal Revelations, Experiences andReflections of an AD Caregiver 20

Roberta Bedard

2004 Awareness Campaign:Addressing the Myths of Alzheimer Disease 22

The Alzheimer Society of Canada

The Canadian

Disease ReviewVolume 6, Number 2 January 2004

Art

by

Mic

hael

Cur

ley

The Review is online! You can find us at:

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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 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, FRCPCClinical Associate Professor 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,Queen Elizabeth II Health Sciences CentreHalifax, Nova Scotia

Copyright 2004 STA HealthCare Communications Inc.All rights reserved.The Canadian Alzheimer Disease Review is published by STA Communications Inc., throughan educational grant provided by Pfizer Canada Inc.The opinions expressed herein are those of the authors and do not necessarily reflect the views of the publisher orthe sponsor. 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.

Publishing Staff

EDITORIAL BOARD

The editorial board has complete independence in reviewing the articles appearing in this publication and is responsible for their accuracy.Pfizer Canada exerts 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.

Paul F. BrandExecutive Editor

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Robert E. PassarettiPublisher

ON THE COVERIn the Middle of the Room (Oil on canvas), by Michael Curley

Perhaps the best way to explain my painting is to explore what each individual component means to me. Theblackness around the person in the painting represents the world of a patient affected by Alzheimer’s. Theswirling colors represent the chaos and confusion that insidiously invade the patient’s life. In contrast to theobscured world of the Alzheimer’s patient, the real world is represented by a circular tunnel, illuminated bythe glowing white light of hope. Three people are shown—a doctor, a woman, and a child. The woman sym-bolizes the patient’s loved ones, including family, relatives and friends. It is often these people who bring themost light into their lives. The doctor represents medical services and the compassionate search for a cure.The child is a symbol of the future—and the hope it promises.

2 • The Canadian Alzheimer Disease Review • January 2004

E D I T O R I A L

This issue of the Canadian Alzheimer DiseaseReview is of special importance since it coin-

cides with the January 2004 Awareness Campaignof the Alzheimer Society of Canada. The range oftopics is quite broad. The review on the diagnosisand management of delirium by Drs. Freter andRockwood (page 4) is state-of-the-art. The evi-dence is compelling that a preoperative baselinecognitive status should be done on all elderly per-sons; for those already diagnosed with Alzheimer’sdisease (AD), local or regional anesthesia shouldbe preferred over general anesthesia, if possible.

Dr. Groulx shares with us his wisdom andexpertise in dealing with late-disease neuro-psychiatric symptoms, of which screaming is oneof the most difficult to understand; his systematicapproach will prove to be very useful (page 11).

The highlights of the second Canadian Col-loquium on Dementia are well summarized byDrs. Keren and Wherrett (page 15) and focus onour understanding of risk and preventive factorsfor AD, the heterogeneity of mild cognitiveimpairment (MCI) and the hope for additionalsymptomatic and disease-modifying therapies.

The personal experiences of Roberta Bedard,whose husband has AD, offer a unique view ofhow to adjust to life changes caused by AD(page 20).

The 10 myths discussed by the AlzheimerSociety of Canada (page 22) are among the mostfrequently asked questions in public lectures andtarget important issues about the genetic risks,early symptoms and management of AD.

What will happen in 2004 in the field of ADand related dementias? There are currently threeinternational scientific meetings scheduled: Mont-

real, Quebec (April 14-17), Philadelphia, Penn-sylvania (July 18-22) and Kyoto, Japan (October15-17). These meetings will present the results ofmany clinical trials involving persons with amnes-tic MCI, potentially leading to very early diagno-sis and treatment of AD.

Multiple clinical trials are underway, or willsoon start, for persons with AD. Many of these tri-als are aimed at modifying disease progression; ofnote is the Canadian-made AlzhemedTM, whichtargets amyloid fragment deposition into neuriticplaques. The N-methyl-D-aspartate (NMDA)-antagonist, memantine, is being tested acrossCanada for moderate to severe stages of AD,while the Therapeutic Products Directorate iscompleting its assessment of the safety and effi-cacy of this medication. Memantine’s mode ofaction is different from the acetylcholinesteraseinhibitors (i.e., donepezil, rivastigmine, galanta-mine) currently being used in the treatment ofAD. The combination of these two classes ofmedications may stabilize the progression ofsymptoms for extended periods of time.

The next level of clinical research will be todetermine individuals’ levels of risk for AD, beforeany symptoms emerge, based on genetic and vas-cular factors, followed by evidence-based advicetowards prevention. Until then, enjoy red wine(preferably from Bordeaux, France), fish and freshgreen vegetables, and watch your blood pressure.

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

Awareness by Serge Gauthier, MD, CM, FRCPC

The Canadian Alzheimer Disease Review • January 2004 • 3


Diagnosis and Prevention of Delirium in Elderly People

Delirium is a common, often unrecognized condition that is associated with considerablemorbidity and mortality. Several tools are available to help define and screen for delirium,but diagnosis ultimately relies upon the recognition of risk factors and keen observation ofsymptoms. A variety of management strategies, including supportive measures andpharmacotherapy, are available, as are simple preventive interventions.

by Susan Freter, BSc, MSc, MD, FRCPC, and Kenneth Rockwood, MD, MPA, FRCPC

Each of us knows that whenwe are ill, it is harder to con-

centrate and carry out mentaltasks. For many older people,however, especially those who arefrail, the change in mental statethat comes with acute illness iscatastrophic. This acute change,in the face of an external cause, isdelirium. Delirium is not justquantitatively different from thedecreased ability to concentrate: italso differs qualitatively, by im-pacting on memory and judge-ment and even giving rise to hal-lucinations and delusions.

Delirium is a common andimportant condition, frequently

unrecognized but associated withconsiderable morbidity and mor-tality. Prevalence estimates rangebetween 15% and 60%, depend-ing on the population studied andspecific methodology used.1-5

There is strong evidence thatdelirium predicts—and likelycontributes to—poor patient out-comes.3,6-10 Delirium has beenassociated with prolonged lengthof hospital stay and an increasedrisk of nosocomial complications.Decline in level of functioningand accelerated cognitive declineare routinely seen and associatedwith a greatly increased risk ofnursing-home placement. Delir-ium has been associated with anincreased risk of death in hospitaland at 12-month follow-up.10

These associations hold true evenafter controlling for illness severi-ty, age and baseline functional andcognitive status.6 Delirium maypersist for weeks to months in asubstantial proportion of elderlypatients.3,6-10

Numerous studies have delin-eated the risk factors associatedwith delirium. These risk factorscan be grouped into baseline (orpredisposing) factors and acute (orprecipitating) factors. Baseline fac-tors include advanced age, pre-existing cognitive or functionalimpairment, sensory impairment,and medical comorbidity.11-16

Male gender and history of ethanolabuse also have been reported insome studies. Medications are themost common iatrogenic cause ofdelirium,1 implicated in up to 40%of cases.17 Commonly offendingdrugs include benzodiazepines,narcotics and medications withanticholinergic properties. Drugwithdrawal must be considered, aswell. Other precipitating factorsinclude infections, cardiac decom-pensation, hypoxemia and meta-bolic abnormalities (particularlydehydration). Associated factorsinclude low hemoglobin, uncon-trolled pain and physical restraints.Delirium is quite common follow-

Dr. Freter is Assistant Professor inthe Division of GeriatricMedicine, Department ofMedicine, Dalhousie University,Halifax, Nova Scotia.

Dr. Rockwood is a Professor ofMedicine, Department ofMedicine (Geriatric Medicine &Neurology), Dalhousie University,Halifax, Nova Scotia.

ing anesthesia and surgery. Thefrail elderly with multiple predis-posing risk factors require the pres-ence of fewer precipitating factorsto tip them into delirium.

DiagnosisDelirium commonly is definedusing the Diagnostic and StatisticalManual of Mental Disorders,Fourth Edition (DSM-IV) criteria(Table 1).18 There are several toolsavailable to screen for delirium,including the Delirium SymptomInterview,19 the Delirium Obser-

vation Screening Scale,20 theNEECHAM confusion scale,21

and the Confusion AssessmentMethod (CAM).22 The CAM canachieve better than 95% sensitivityand specificity and does not takelong to administer (Table 2).

Delirium is commonly under-recognized by nurses and physi-cians.5,23-26 This is due in part tothe misconception that all deliri-ous patients are agitated, when infact the hyperactive form of delir-ium represents only a minority ofcases (Table 3). Delirious patients

who are hypoactive or somnolentoften go undetected, or are misdi-agnosed as demented.17,26 How-ever, hypoactive delirium may beassociated with poorer out-comes.17,23,27 The likelihood thatnurses will detect delirium duringroutine clinical care is lowest inthe presence of dementia, highbaseline delirium risk, and thehypoactive form of delirium.26

Severe delirium is associated withworse outcomes than is milddelirium, and patients who do notmeet the full criteria, but have


Table 1

DSM-IV Criteria for Delirium

• Disturbance of consciousness (reduced clarity of awareness of the environment) with reduced ability to focus, sustain or shift attention

• Change in cognition (such as memory deficit, distortion, language disturbance) or development of a perceptualdisturbance that is not better accounted for by a pre-existing established or evolving dementia

• Disturbance develops over a short period (usually hours to days) and tends to fluctuate during the course of the day

• Evidence from the history, physical examination or laboratory findings suggests that disturbance is caused by amedical condition, substance intoxication or medication side effects

Table 2

The Confusion Assessment Method (CAM)22

The diagnosis of delirium requires the presence of features 1 and 2 and either 3 or 4.

1. Acute change in mental status and fluctuating course

• Is there evidence of an acute change in cognition from the patient’s baseline?

• Does the abnormal behavior fluctuate during the day (i.e., tend to come and go, or increase and decrease in severity)?

2. Inattention

• Does the patient have difficulty focusing his/her attention (i.e., easily distractible or has difficulty keeping track ofwhat is being said)?

3.Disorganized thinking

• Is the patient’s thinking disorganized or incoherent (i.e., rambling or irrelevant conversation, unclear or illogicalflow of ideas, or unpredictable switching from subject to subject)?

4.Altered level of consciousness

• Is the patient’s mental status anything besides alert (i.e., vigilant or hyperalert, lethargic or drowsy/easily aroused,stuporous or difficult to arouse, comatose or unarousable)?


some symptoms, of delirium haveworse outcomes than if they hadno or few symptoms.28 Detectioncould be improved by documenta-tion of baseline cognitive status,incorporating cognitive screeninginto routine clinical practice,1,17

educational programs,23 and clini-cal pathways.1

There is good evidence thatdelirium can be better detectedwhen information on risk factorsis ascertained on admission. Thisfacilitates diagnosis and allowstargeting of patients for interven-tion. However, most protocolsemployed in funded studies arenot practically feasible to theextent that they can be applied inusual clinical settings.12 Nursesare in a critical position to detectmental status changes and alertphysicians to the development ofdelirium to allow for promptwork-up and management. Edu-cation of frontline nurses is desir-able, although recommendationsmay not be fully incorporated,

spontaneously, into the process ofnursing care.29

ManagementDetection. Management beginswith recognition, and this is facil-itated by routine cognitive assess-ment as a part of standard care forolder patients.1 Preoperative cog-nitive impairment, as measured bythe Mini-Mental State Exam(MMSE),4,30,31 or the Clock-Drawing Test (CDT),32 appears to be a useful predictor of postop-erative delirium. Detection also isfacilitated by examining the pat-ient’s history. Families commonlyfind delirium in a loved one to bevery alarming, and are keen totalk to a physician who realizesthat “mom is not always like this.”

Identification of underlyingcauses. Once delirium has beenidentified, appropriate investiga-tions must be carried out to detectunderlying causes. Investigationsare guided by comprehensiveassessment of the patient and

include careful review of pre-scribed medications (with particu-lar attention given to recent addi-tions and/or dosage changes).Laboratory testing should include,at the minimum, a complete bloodcount, electrolytes and renal func-tion tests, oxygen saturation, elec-trocardiogram, urinalysis andchest X-ray. Correction of elec-trolyte imbalance is associatedwith significant shortening in theduration of delirium.33 Frailpatients with delirium risk factorsor mild delirium may not be ableto feed themselves, and will there-fore benefit from attention toensure adequate hydration andnutrition.

Supportive measures includemaintaining a consistent, com-fortable and familiar environ-ment. Involving the family, ifpossible, may foster a sense ofsecurity. If family members areable to spend time at the bedside,they can be encouraged to pro-vide reorientation and/or distrac-tion, and to assist with feeding,finding sensory aids, and access-ing help for toileting. Consist-ency in staff—particularly ofnursing staff—is desirable. At-tempts should be made to providea quiet, well-lit room which,preferably, includes an easily vis-ible clock, a calendar and familiaritems from home. Identifyingsensory impairment, and ensuringthat glasses and hearing aids arein place, need to be part of routinecare. Whenever possible, medi-

Table 3

Phenotypes of Delirium

Delirium with psychomotor agitation

• Paradymitic case: delirium tremens

• Hypervigilance, but distractibility

• Autonomic overactivity

• Psychomotor agitation, from restlessness to violence

Delirium with psychomotor retardation

• Paradymitic case: the patient between stupor and coma

• Decreased attention and arousal (you find yourself talking loudly to suchpatients, or vigorously rubbing their arms to stimulate them)

Mixed presentation (alternating psychomotor agitation and retardation)


cation schedules should allowuninterrupted sleep overnight.Restraints, both physical andchemical, are not only inhumanebut are associated with increasedseverity of delirium. Ambulatorypatients should be mobilized atleast daily. Family members ben-efit from education and reassur-ance, as well. Unfortunately, suchenvironmental strategies freq-uently are overlooked.34

Pharmacologic management.In some cases of hyperactivedelirium, agitation, aggression, orpsychotic symptoms are so dis-turbing they pose a danger to thepatient or others, and thus meritpharmacologic treatment. As themedications used to alleviatethese symptoms can worsen con-fusion on their own, it is impor-tant to exercise caution in dosing.Empiric data on pharmacologicmanagement of delirium is limit-ed.5 Haloperidol has been shownto be more useful than narcotics35

and than lorazepam,36 althoughbenzodiazepines are used whendelirium results from withdrawalfrom alcohol or from benzodi-azepines themselves. Haloperidolmay be used in combination witha benzodiazepine in order toreduce the doses and, thus, theadverse effects associated witheach.37 Haloperidol generally isconsidered the drug of choicebecause of its minimal anticholin-ergic effects, and should be pre-scribed in low doses, regularly, fora limited time period (i.e., 0.5 mg

every six hours for three days).Case reports of the atypical neu-roleptics are promising.38 Therehas been some interest in mian-serin,39,40 a relatively selective 5-HT2 receptor blocker, but therealso are case reports of deliriumbeing caused by this drug.41

Multifactorial intervention.Delirium is a multifactorial syn-drome, and frail patients withmore predisposing factors are atgreater risk of developing deliri-um with minor insults. As such,the most effective interventionstrategies will be multifactorial innature and will be applied proac-tively. The principles of preven-tion and comprehensive manage-ment are similar and should beincorporated into routine standardof care.

A number of studies have eval-uated the effectiveness of a varietyof interventions to prevent deliri-um, with inconsistent results.2,42

A nursing intervention in hip-fracture patients with no priorcognitive impairment, which incl-uded attention to sensory impair-

ment and a nurse visitor who pro-vided reorientation and consist-ency, resulted in a significantreduction in incident postopera-tive delirium.16 Another nurse-ledstudy demonstrated the beneficialeffects of an intervention programwhich focused on early recogni-tion and treatment of delirium inhip-fracture patients.43 This studyemphasized education of nursingstaff, systematic cognitive screen-ing and regularly scheduled painmedications, and resulted in dec-reased severity and shorter dura-tion of delirium.43 Proactive geri-atric consultations, with attentionto environmental issues, medica-tions and metabolic abnormali-ties, reduced the postoperativeincidence of delirium by over onethird (severe cases of deliriumreduced by one half) in elderlyhip-fracture patients.44 A com-bined geriatric-anesthesiologicintervention program focusing onintra- and postoperative medicalcomplications in hip-fracturepatients resulted in a lower inci-dence and shorter duration of

Table 4

Delirium Prevention Interventions

• Routine cognitive screening on admission and during hospital stay

• Medication review to minimize use of deliriogenic medications

• Ensuring sensory aids (glasses, hearing aids) are in place

• Ensuring adequate intake of fluids and nutrition by providing assistance ifnecessary

• Early identification and treatment of dehydration

• Early mobilization

• Avoiding restraints (chemical and physical)

• Involving family members or employing sitters to calm and reorient

delirium, fewer postoperativecomplications and a shorter lengthof stay on the orthopedic unit.45

Earlier delirium intervention trials in elderly medical inpatientshave yielded inconsistent res-ults2,46 but were plagued by limita-tions, such as small sample sizesand a very low incidence of deliri-um47 or a very high prevalence of

delirium.48 An important study byInouye et al12 used a speciallytrained interdisciplinary team con-sisting of a geriatrician, nurses,therapists and volunteers on a gen-eral medicine service. Standard-ized intervention protocols wereapplied to targeted risk factors,including cognitive impairment,sleep deprivation, immobility, sen-

sory impairment and dehydration.The intervention was successful inreducing the incidence and totalnumber of days of delirium, com-pared to usual hospital care.

ConclusionDelirium is a common and seriouscondition with important prognos-tic implications. Unfortunately, it

commonly is underdiagnosed andsuboptimally managed. Appropr-iate diagnosis and management ofdelirium will require raising gen-eral awareness and education offrontline staff. Simple preventiveinterventions (Table 4) are avail-able and can result in substantialcost savings, as well as raising thestandard of care of the hospital-

ized elderly. As noted, delirium isvery stressful to patients and theirfamilies. We find it is worthwhileto explain to patients that they are“a bit mixed up now, but will getbetter” and to reassure them inthat regard. Most patients who re-cover from delirium appear not toremember much about it, butthose who do remember typicallyrecall it as a very frightening exp-erience. It also is useful to talk tofamilies about what is going on.We usually cover several points insuch a discussion (Table 5).

Treating patients with deliriumis a challenge to physicians, par-ticularly since one of our chieftools (the patient history) often isnot available to us. It is a condi-tion that can cause great anxietyand in which good care is critical.As such, it is an important test ofour skills as physicians.

References1. Inouye SK, Schlesinger MJ, Lydon TJ.

Delirium: a symptom of how hospitalcare is failing older persons and a win-dow to improve quality of hospital care.Am J Med 1999; 106:565-73.


Supportive measures include maintaining a consistent,comfortable and familiar environment. Involving thefamily, if possible, may foster a sense of security. Iffamily members are able to spend time at the bedside,they can be encouraged to provide reorientationand/or distraction, and to assist with feeding, findingsensory aids, and accessing help for toileting.

Table 5

Advice for Families of a Patient Who is Delirious

What is delirium? Delirium is a sign that your family member is quite ill. At present, he/she has only limited control over what he/she does.

Will it get better? Most patients with delirium show some degree of recovery. Many people recovercompletely, but many have persistent problems in some thought-process areas (especiallymemory). Time is the best test.

How long will it take A rule of thumb is that, in someone who has had no memory problems before, to get better? recovery time is two to four times longer than the time interval between the delirium being

apparent and treatment being started.

What can I do to help? Reassure the patient. Especially if the patient is restless, evening visits (things usually getworse as it gets dark) are very helpful.

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11. Marcantonio ER, Flacker JM, MichaelsM, et al. Delirium is independently asso-ciated with poor functional recovery afterhip fracture. JAGS 2000; 48:618-24.

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32. Fisher BW, Flowerdew G. A simplemodel for predicting postoperative deliri-um in older patients undergoing electiveorthopedic surgery. JAGS 1995; 43:175-8.

33. Koizumi J, Shiraishi H, Ofuku K, et al.Duration of delirium shortened by thecorrection of electrolyte imbalance. JpnJ Psychiatry Neurol 1988; 42:81-8.

34. Meagher DJ, O’Hanlon D, O’MahoneyE, et al. The use of environmental

strategies and psychotropic medicationin the management of delirium. Brit JPsychiatry 1996; 168:512-5.

35. Sanders K, Stern T, O’Hara P, et al.Delirium during intra-aortic balloonpump therapy: incidence and manage-ment. Psychosomatics 1992; 33(1):35-44.

36. Breitbart W, Marotta R, Platt M et al. Adouble-blind trial of haloperidol, chlor-promazine, and lorazepam in the treat-ment of delirium in hospitalized AIDSpatients. Am J Psychiatry 1996;153:231-7.

37. Menza MA, Murray GB, Holms VF, etal. Controlled study of extrapyramidalreactions in the management of deliri-ous, medically ill patients: intravenoushaloperidol versus intravenous halo-peridol plus benzodiazepines. HeartLung 1988; 17:238-41.

38. Sipahimalani A, Masand PS. Use ofrisperidone in delirium: case reports.Ann Clin Psychiatry 1997; 9:105-7.

39. Ikeguchi K, Kuroda A. Mianserin treat-ment of patients with psychosisinduced by antiparkinsonian drugs. EurArch Psychiatry Clin Neurosci 1995;244(6):320-4.

40. Cole MG, Primeau FJ, Elie LM.Delirium: prevention, treatment andoutcome studies. J Geriatr PsychiatrNeurol 1998; 11:126-37.

41. Bonne O, Shalev AY, Bloch M. Deliriumassociated with mianserin. Eur Neuro-psychopharmacol 1995; 5(2):147-9.

42. Britton A, Russell R. Multidisciplinaryteam interventions for delirium inpatients with chronic cognitive impair-ment (Cochrane Review). In: TheCochrane Library, Issue 1, 2003.Oxford: Update Software.

43. Milisen K, Foreman MD, Abraham IL, etal. A nurse-led interdisciplinary interven-tion program for delirium in elderly hip-fracture patients. JAGS 2001; 49:523-32.

44. Marcantonio ER, Flacker JM, Wright J,et al. Reducing delirium after hip frac-ture: a randomized trial. JAGS 2001;49:516-22.

45. Gustafson Y, Brännström B, BerggrenD, et al. A geriatric-anesthesiologicprogram to reduce acute confusionalstates in elderly patients treated forfemoral neck fractures. JAGS 1991;39:655-62.

46. Cole M. Delirium: effectiveness of sys-tematic interventions. Dement GeriatrCogn Disord 1999; 10:406-11.

47. Nagley SJ. Predicting and preventingconfusion in your patients. J GerontolNursing 1986; 12:27-31.

48. Wanich CK, Sullivan-Marx EM,Gottlieb GL, et al. Functional statusoutcomes of a nursing intervention inhospitalized elderly. Image J Nurs Sch1992; 24:201-7.



Screaming patients, especiallythose in the late stages of

dementia (i.e., totally or almosttotally aphasic), comprise one ofthe most puzzling clinical para-doxes in clinical geriatrics. Everynurse and orderly who has had totake care of a “screamer,” espe-

cially at night, will tell you thatthis behaviour affects the well-being and quality of life of every-one around the patient.

It is surprising that such a diffi-cult entity has not been exploredon all facets and that more reliefmeasures have not been found.And herein lies the paradox.While screaming is a major con-cern for everyone working in thefield of dementia, there have beenvery few studies on this behaviourspecifically, and even less atten-tion has been given to the topic inacademic literature. For example,the academic book I consider tobe the best resource on Alzhei-mer’s disease (AD) and recom-mend for everyone in the field ofAD management, entitled Clini-cal Diagnosis and Management of Alzheimer’s Disease, has only a little over 30 words on the sub-ject of screaming.

Everyone knows how difficultit is to manage screaming pat-ients. Yet, many approaches, plansof treatment or medications havebeen tried with little or no suc-cess; this, I am sure, has created asense that nothing, or very little,can be done.

I must admit that, at times, apart of me shares this pessimism.To combat this sense of despair, Iwill review my approach to thedifficult clinical problem ofscreaming, with the hope of stim-ulating some thoughts from ourreaders and being the catalyst foran exchange of information onthis subject, including any inter-ventions or approaches whichhave been successful for others.

Many people working in thefield of AD have seen a number ofscreamers who are not very ad-vanced in their dementia, who canspeak readily with their care-

Dr. Groulx is Chief Psychiatrist,Ste-Anne-de-Bellevue Hospitaland Associate Professor, McGillUniversity, Montreal, Quebec.

Screaming and Wailing in Dementia Patients (Part 1)Screaming is a behavioural problem that can be extremely overwhelming and createenormous stress, not only on other patients, but on staff as well. Despite the commonconcerns and frustrations with this behaviour, there is a scarcity of information availableaddressing this issue. Therefore, the purpose of Part 1 of this article is to address the issueof screaming, discuss possible causes for the behaviour and, perhaps, inspirethoughts/feedback from our readers on this subject.

by Bernard Groulx, MD, CM, FRCPC


givers, yet still cannot explain whythey scream. In these cases, withtime and patience and the real pos-sibility of communicating withthese patients, it usually is mucheasier to determine the causes ofthe behaviour and eventually cor-rect the problem. The purpose ofthis article, therefore, is to focuson those patients who cannot read-ily offer us information.

This article will be completedin two parts. Part 1 discusses ap-proaches to evaluating behaviour-al and psychologic symptoms ofdementia and contemplates thepossible causes for screamingbehaviour. Intervention (whichwill be covered in Part 2 of thisarticle to be published in the nextissue of the Review) cannot bepossible without this knowledge.

Exploring the CausesThere are two basic approaches forevaluating behavioural and psycho-logic symptoms of dementia. Theseapproaches evaluate the circum-stances surrounding the episode.a) The temporal approach. What

seems to trigger the behaviour?What seems to help relieve it or

make it less acute? Whatmakes it stop completely?

b) The five “Ws.” Who is withthe patient or, conversely, whois absent? What helps, makesit worse and/or accompaniesthe behaviour? Where does itoccur (e.g., is there a particu-lar milieu or event associatedwith it?) When does it occur(e.g., is it limited to specific

times, such as bathtime, dur-ing hygiene care, bedtime,when the patient has to bephysically moved, daytime,evening)?The answer to these “Ws” and

to the questions asked in the afore-mentioned temporal approach willcertainly help in understanding theproblem and in subsequent inter-ventions. Unfortunately, some-times no information can be gath-ered from these questions and weare left with the last terrible “W”:why?

Why?There are possibly as many caus-es for screaming as there are indi-viduals who scream. However, itstill is possible to get answers to

“why” by exploring the “basics”in terms of what could be goingwrong either inside or outside thepatient.

Inside. When trying to deter-mine what is happening within apatient that makes him/her wail orscream, it is important to start byfocusing on the most commoncauses of distress in patients withdementia:1) Is the patient in pain? A patient

in stage 6 of AD (unable totalk, unable to express pain)often shouts or screams.

2) Is the patient constipated? Dec-reased physical activity alongwith side effects from multiplemedications are conducive toconstipation. The constipationmay cause discomfort or evenpain and, therefore, result inscreaming from the patient.Another cause for discomfortis a wet or soiled diaper; it goeswithout saying that this shouldbe looked into right away.

3) Is the patient undernourished?Hunger is a surprisingly com-mon cause of physical discom-fort and, therefore, a potentialsource of wailing. It is difficultto ask aphasic patients if theyare hungry, let alone what isappealing or appetizing tothem. An inquiry made with thespouse, family or friends willhelp in this regard. Attentionalso must be given to the envi-ronment in which the patient

While screaming is a major concern for everyoneworking in the field of dementia, there have been veryfew studies on this behaviour specifically,and even less attention has been given to the topic in academic literature.


eats, as well as what he/shelikes. Healthy snacks betweenmeals also may be part of thesolution in these cases.

4) Finally, there often is a mult-itude of medical or physiolog-ic factors which combine andlead to a patient’s discomfortand eventual screaming be-haviour. A standard “medicalcheckup” should always be a part, if not the beginning,of an evaluation for any be-havioural problem, includingscreaming. Outside. Causes for a patient’s

wailing or screaming also mayinvolve the patient’s external envi-ronment. Therefore, it is impor-tant to consider common externalstressors:1) Does the patient feel secure or

unsafe?2) Are the schedules of the care

unit made to accomodate thepatient’s rhythms? In otherwords, are the patient’s routineactivities (hygiene, meals,treatments, tests, etc.) des-igned, where possible, to fit thepatient’s schedule or only thestaff’s schedule?

3) Is the patient in an environ-ment that overstimulates him/her? Considering the patient’sdiminished cognitive capaci-ties and the stresses inherent todementia, are too many dem-ands being made on thepatient, or do certain demands

correspond to capacities thathe/she has lost?

4) On the contrary, is the patientunderstimulated? Is his/herscreaming or wailing a way tocreate sounds and stimulationsthat decrease anxieties? Forthat matter, is the patient expe-riencing sensory deficits thatnobody around him/her hasnoticed? I have seen patientsalmost lose their vision orhearing without anybody notic-ing, simply because the patientcould not speak. These patients

started making certain loudnoises as a way to compensatefor their sensory losses andinability to speak.

5) Has there been a recent changein the patient’s environment(e.g., change of rooms orchange of nursing homes)? Forpatients with advanced demen-tia, having lost the capacity tomake new memories, a suddenintense disorientation can be sofrightening that it may triggerscreaming behavior.

6) Has the patient been restrainedin some form? The debate sur-rounding restraints could—andshould—be the subject of awhole other article; in short,

study after study has shownthat restraints rapidly increasethe risk of delirium and worsenbehavioural problems, etc.Sometimes restraints are per-ceived (by professional care-givers) as true security mea-sures—ways to protect thepatient. But how can a severelydemented patient be anythingbut totally mystified, stressedand scared by these restraints?Restraints are a significantsource of stress conducive towailing and screaming.

The nature of dementia. Thenature of dementia is, itself, acause for periods of wailing, shout-ing or screaming. Consider that, asnondemented individuals, we areuncomfortable when we are disori-ented even for short periods oftime, or when we have to face peo-ple who may have a connection tous but who we don’t recognize.Imagine living this way not just fora moment or two, but for weeksand months at a time. This is whatpatients with advanced dementiaexperience upon exposure to a newenvironment.

Imagine entering a confusionalor delirious state (history ofdementia is the most common

A standard “medical checkup” should always be apart, if not the beginning, of an evaluation for any

behavioural problem, including screaming.


cause of delirium) and nobodynotices or can do anything aboutit. Imagine a cloud of confusioncoming over you, day after day,culminating with Sundowner’sSyndrome. These considerationscan help us understand the fearsand psychic pains plaguing somescreamers.

Psychiatric causes. At the riskof sounding too philosophical, itis said that the most basic humanneed is the need to love and beloved. The most difficult cases ofwailing or screaming patients thatI have seen may be attributed tothis “philosophy.” Nothing seemsto relieve or soothe these patients.Right or wrong, I have the impres-sion that, at a deep and mysteriouslevel, these patients feel theirbasic needs for love will never benourished again. There is also,perhaps, a deep sense of loneli-ness and/or abandonment, com-bined with a lack of the intellectu-al capacity to make sense of it.Even in these cases, there are cer-

tain interventions that can be ap-proached. Beforehand, however,we must always make sure there isnot a bona fide psychiatric illnessbehind the behavior.

Psychosis, with its accompany-ing psychic pain and symptoms(e.g., delusions, hallucinations), iscertainly enough to make any-

body, moreso someone sufferingfrom severe dementia, want toscream. But, for reasons I havenever understood, people general-ly dismiss the possibility of a clin-ical depression. However, aftereliminating any possible “inside”and “outside” causes, I alwaysconsider the possibility of clinicaldepression. It makes more sense,to me, that wailing or screamingbecomes, in such situations, theonly way for patients to expressthe despair caused by a majoraffective disorder.

SummaryAs noted at the beginning of thisarticle, there might be as many rea-

sons for screaming in dementia asthere are individuals who scream.This article was not meant to be anexhaustive list of possible reasons,but a simple attempt at organizingmy thoughts, and perhaps yours,on the subject. In Part 2 of this arti-cle, we will explore interventionsfor screaming—both pharmaco-logic and nonpharmacologic.

Further reading:1. Cohen-Mansfield J, Billig N. Agitated

behaviors in the elderly: a conceptualreview. J Am Geriatr Soc 1986;34:711-21.

2. Cohen-Mansfield J, Marx MS,Rosenthal AS. A description of agita-tion in a nursing home. J Gerontol1989; 44(3):M77-84.

3. Burgio L. Interventions for thebehavioral complications ofAlzheimer’s disease: behavioralapproaches. Int Psychogeriatr 1996;8 (Suppl. 1):45-52.

4. Whall A, Black M, Groh C, et al. Theeffect of natural environments uponagitation and aggression in late statedementia patients. Amer J Alzheimer’sDis 1997; 12:216-20.

5. Cohen-Mansfield J, Werner P, MarxMS. Screaming in nursing-home resi-dents. J Am Geriatr Soc 1990;38:785-92.

6. Inouye SK. The dilemma of delirium:clinical and research controversiesregarding diagnosis and evaluation ofdelirium in hospitalized elderly med-ical patients. Am J Med 1994;97:278-88.

For patients with advanced dementia, having lost thecapacity to make new memories, a sudden intensedisorientation can be so frightening that it may triggerscreaming behavior.


Reporting from the Second CanadianColloquium on DementiaThe second Canadian Colloquium on Dementia (CCD) was held in Montreal, Quebecbetween October 16-18, 2003 and featured many internationally renowned speakers fromacross Canada and the United States. Although this conference is only a new development,it’s rapid growth over the past couple of years has confirmed the need for a nationalconference on dementia. Drs. Ron Keren and John Wherrett attended the conference andherein present it’s background and the highlights of the program.

by Ron Keren, MD, FRCPC and John Wherrett, MD, PhD, FRCPC

Background The second Canadian Colloqu-ium on Dementia (CCD) washeld at the Marriott ChateauChamplain in Montreal, Quebecbetween October 16-18, 2003.The first CCD was held inToronto, Ontario in October of2001. A broad range of healthcare

workers and clinicians with aninterest in Alzheimer’s disease(AD) and related disorders at-tended the second CCD. The pri-mary audience was comprised ofspecialists involved in the diagno-sis and management of individu-als with dementing disorders.

The idea of a national confer-ence on dementia came from the recognition that, while Canadais disproportionately endowedwith internationally acclaimedexperts in dementia, there was nonational forum that allowed forthe exchange of knowledge bet-ween these experts and the spe-cialists caring for their patients.The rapid growth of the CCD overthe past two years has confirmedthe strong need for a national con-ference on dementia, geared pri-marily towards medical special-ists in this field.

The composition of the secondCCD’s organizing committee ref-lected a broad representation ofspecialists and their national organizations, including the Can-adian Academy of Geriatric Psy-chiatry (CAGP), the CanadianGeriatric Society (CGS), the Can-adian Neurological Society (CNS)and the Consortium of Canadian

Dr. Wherrett is Professor Emeritusof Neurology, University ofToronto and Consultant inNeurology, Toronto WesternHospital, Toronto, Ontario.

Dr. Keren is a GeriatricPsychiatrist and AssistantProfessor, University of Toronto,Toronto, Ontario.


Centres for Clinical CognitiveResearch (C5R), as well as repre-sentatives for neuropsychologyand family medicine. The orga-nizing committee tailored the pro-gram for the second CCD to theguidelines of the Royal College of Physicians and Surgeons foraccredited group learning. An im-portant component of these guide-lines is interactive learning. In thesecond CCD, this was accom-plished through small groupworkshops as well as a debate and

a town-hall meeting. The contentof the program was driven by aneeds assessment completed atthe end of the first CCD.

Program HighlightsThe second CCD was fortunate tohave a large number of interna-tionally renowned speakers fromacross Canada and the UnitedStates. Some of the highlights areas follows:

The Nun Study. One of thekeynote presentations of the

CCD was by Dr. Suzanne Tyas, agraduate in epidemiology andbiostatistics from the Universityof Western Ontario and an inves-tigator in the Nun Study, headedby Dr. David Snowden at theUniversity of Kentucky. Dr. Tyasspoke on “Early and Late-lifePredictors of Alzheimer’s Dis-ease,” based on findings from theNun Study. She reported find-ings from the Nun Study sug-gesting that AD is a consequenceof a long chain of events span-

ning the life experience, in-cluding genetics, lifestyle andenvironment, brain developmentand reserve, AD severity in thebrain, atrophy, other medical dis-eases, age at symptom onset andseverity of symptoms. For exam-ple, early-life autobiographiesfrom the convent archives haveshown a strong relationshipbetween low linguistic ability inearly life and a high risk of ADin late life. Late-life events, suchas stroke, can increase the risk as

well as the severity of AD. Dr.Tyas also suggested that folatedeficiency might be an importantrisk factor in the development ofAD.

In describing a group of cogni-tively intact nuns referred to as the“Magnificent Seven,” Dr. Tyasshowed how the prevalence of ADincreases linearly with age, from65 years until 90 years, afterwhich there appears to be a dropin prevalence.

MCI debate. In the true natureof a Canadian debate, there wasmore consensus than differencebetween the two internationallyacclaimed debaters on mild cogni-tive impairment (MCI): Dr. JohnMorris from the Washington University School of Medicineand Dr. Howard Chertkow from McGill University. The resolutionwas “MCI is the earliest stage of Alzheimer’s disease,” with Dr. Morris debating in the affir-mative and Dr. Chertkow debatingin the negative. Dr. Morris empha-sized the importance of a reliableinformant in detecting dementia.He claimed that change in every-day function due to cognitiveimpairment predicts the develop-ment of dementia and that thequality of clinical informationfrom the informants and the label-ing threshold of the cliniciandetermine the diagnosis. Whileagreeing that not all MCI predicts

The idea of a national conference on dementia camefrom the recognition that, while Canada isdisproportionately endowed with internationally acclaimed experts in dementia, there was no nationalforum that allowed for the exchange of knowledge between these experts and the specialists caring fortheir patients.


AD, he argued that all AD patientsgo through a MCI stage. In addi-tion, Dr. Morris argued that allpatients with plaques and tangleswill develop AD if they live longenough.

Dr. Chertkow pointed out thatthe high degree of variabilityamong definitions of MCI couldalter, by up to four-fold, the num-ber of subjects meeting MCI crite-ria. He also pointed out that therate of progression of MCI todementia varies substantially a-cross different centres and referralsources, from 100% in St. Louis,France (tertiary referral) down to0%-18% in Montpellier, France(population study). In a McGillstudy, 27 of 90 patients still hadMCI after a mean of 11 years ofmemory complaints. Dr. Chert-kow stressed the importance ofdifferentiating between thoseindividuals who progress fromMCI to dementia and nonprogres-sors. It is possible that some ofthose who do not progress todementia may have age-relatedmemory loss, unrelated to ADpathology. Dr. Chertkow gaveexamples of pathological studieswhere patients with clinicallydiagnosed AD had no AD pathol-ogy, and where patients meetingthe pathological definition of ADhad no dementia. Dr. Chertkowargued that AD should be regard-ed as a clinical disease and not as

a neuropathology. Because somepatients with MCI will notprogress to AD, Dr. Chertkow sawa message of hope in the diagno-sis of MCI.

From the onset of the debate,there was consensus that not allMCI patients develop AD. At theend of the debate, the audiencewas left with the impression that,while there is uncertainty aboutthe definition of MCI and the abil-ity to predict its progression toAD, it remains an important diag-nostic concept to researchers andclinicians alike.

Vascular dementia. Dr. Vladi-mir Hachinski of the University ofWestern Ontario and editor forStroke, brought his considerableperspective and wisdom to anentertaining appraisal of the roleof vascular disease in dementia,entitled “Vascular Dementia:Sorting Through the Confusion.”Although there are criteria of highspecificity for dementia of prima-ry vascular origin, Dr. Hachinskiexplained that sensitivity is poor.

This is shown not only by variablevascular pathologies and the high-ly variable clinical expression ofvascular disease, but by more rec-ently recognized interactions ofcerebrovascular disease and neu-rodegenerative pathology, such asAD. Clinically apparent strokeposes a major risk for later dem-entia. Experimental infarction inmice bearing a familial AD geneleft these animals with larger res-idual lesions than those seen inanimals without the AD gene. Al-though a precise diagnostic defin-ition of the vascular contribution

to dementia is problematic, thevalue of therapy directed to riskfactors, including hypertensionand hypercholesterolemia, to pre-vent or retard development ofdementia is becoming established.

Amyloid cascade theory.Dr. Peter St. George-Hyslop, dir-ector of the Centre for Neurode-generative Diseases at the Univ-ersity of Toronto, reviewed theevidence for the “amyloid cas-cade” theory of AD and the ratio-

… findings from the Nun Study … suggest that AD isa consequence of a long chain of events spanning the

life experience, including genetics, lifestyle andenvironment, brain development and reserve, AD

severity in the brain, atrophy, other medical diseases,age at symptom onset and severity of symptoms.


nale for therapy with injections ofAß proteins—the so-called vac-cination therapy. The pioneerhuman trial of Aß40 injections hadbeen stopped because of theoccurrence of a sterile enceph-alitis. The clinical and pathologi-cal data currently available fromthe human trial suggests a fav-ourable effect on cognitive func-tion and a reduction in amyloidburden in the brain. Transgenicanimals developed by Dr. Hyslop

and his colleagues at the Centrefor Research in Neurodegen-erative Diseases are making itpossible to pursue a variety ofstrategies to circumvent the in-flammatory reaction observed inthe human study. These strategiesinclude modification of the inject-ed Aß peptide to remove the seq-uences triggering inflammationand passive immunizations. Thevaccination approach remains anexciting research priority.

Other program highlights.There were many other superb presentations, including an excel-lent update on dementia with Lewybodies by Dr. Bradley Boeve from

the Mayo Clinic. Dr. Boeve dis-cussed the relationship betweenrapid-eye-movement (REM) be-havioural sleep disorder and Lewy-body disease using graphic videoclips of patients undergoing sleepstudies who violently enacted theirdreams.

Dr. Serge Gauthier discussedthe design of clinical trials in ADand Dr. Howard Feldman rev-iewed the data on current andforthcoming treatments for AD,

including the new (to NorthAmerica) drug, memantine.

Drs. David Conn and DmytroRewilak reviewed the pharmaco-logic and nonpharmacologic ap-proaches to the treatment of behav-ioural symptoms of dementia.

Dr. Michael Gordon talkedabout ethical issues in dementiaand Dr. Gary Naglie presented hisresearch on the rating of quality oflife in individuals with AD.

Dr. Morris Freedman present-ed on frontotemporal dementia(FTD) while introducing theaudience to the Theory of Mindand its potential use in diagnosingFTD.

The use of neuroimaging in the diagnosis of dementia wasreviewed by Dr. Piero Antuonofrom the Medical College ofWisconsin.

Dr. Chris MacKnight discussedthe value of case-finding versusscreening for dementia in primarycare.

While still savouring the suc-cess of the second CCD, the orga-nizing committee is already work-ing hard on the program for thethird CCD, to be held in Ottawa,Ontario between October 27-29,2005. We look forward to seeingyou there!

Relationships with IndustryIn this era of increased vigilanceover relationships between thepharmaceutical industry and phy-sicians, it was extremely imp-ortant to the organizers of thesecond CCD that clear bound-aries exist between the pharma-ceutical companies providingfinancial support and the pro-gram development. As a result,the pharmaceutical companiessponsoring the second CCD gen-erously provided their supportthrough unrestricted educationalgrants. These were grants-in-aidethat allowed the organizing com-mittee to develop the programindependent of any influencefrom the industry.

Dr. Chertkow argued that AD should be regarded as aclinical disease and not as a neuropathology. Becausesome patients with MCI will not progress to AD,Dr. Chertkow saw a message of hope in the diagnosisof MCI.

ValidationRay tells me today that when he islying in bed, all alone, he getsdepressed, his thoughts go in cir-cles. He says he needs to feel thathe has a purpose, that there iswork for him to do, that he canhelp the “organization,” that heneeds a niche. When I tell himthat he has a niche with me, “doesthat count?,” he is comforted.

This set me to thinking aboutwhat I have been told abouthelping persons with AD by val-idating the things they havedone in their past lives. Bygoing over who they were, thevalue of their contributions—in

short, what good things theyhave done.

And I wonder.When we are reminding them

of how valuable they were, are wenot, to some degree, confirmingthat they are not valuable now?When I tell my husband that he isessential to my well being now,as he is at this moment, I sensethe depth of comfort this affordshim. His face relaxes, his eyesglint, he smiles and says, “I’mglad I talked to you.” He can stillexpress himself, but I plan toremember these moments for thefuture when he can’t tell me howhe feels.

I plan, in language he willunderstand, to continue to let himknow how important he is, at thatvery moment. Not how importanthe has been in the past, but howvaluable a human being he is inthe present.

If we can love a “useless”child, just because he or sheexists and is ours, and if we canlove a cat, for heaven’s sake, whodoes nothing but accept our feed-ing and our cleaning of it’s litterpan, then we should be able toconvince persons with AD thatthey matter in the present. Thatthey do not need to feel onlydependence, but can know that

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 “Validation,” Roberta emphasizes the value and importance of a person asa human being—in sickness or in health. We have also included “Cranky vs.Dusty”—Roberta’s endearing description of an event that leads her to soul-search and consequently adjust her priorities. P

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Chapter 3by Roberta Bedard

Personal Revelations, Experiencesand Reflections of an AD Caregiver


they are, and will be, valued asthey are now.

I believe this process of valida-tion must start early, before feel-ings of worthlessness becomeentrenched. It behooves us, whenconsidering the whole person, togive the present person equalimportance.

Cranky vs. DustyI’ve finally found a solution to myembarrassment and guilt over myinability to maintain my house-keeping standards while being aloving wife, mother, companion,nurse, chef, physiotherapist andall-around caregiver to my hus-band. While staying relativelysane and maintaining some kindof life for myself.

I’ve given up. Trying to main-tain my standards, that is. What arelief!

I came to my decision when Iheard myself snapping at Ray,“I’ve just cleaned that!!!” when heput a dirty spoon down right onthe counter. The poor man stoodthere, looking ashamed of him-self, thinking he had just commit-ted a terrible deed. He shuffleddejectedly out of the kitchen, satdown on the couch, stared aheadand stayed out of trouble.

And my heart broke.This is not what I want for us.

Neither for him nor for me. “But Ican’t do it all!” I told myself, andproceeded to have a severe attackof the “poor-me” syndrome. Iwept in guilt and frustration. “Ican’t do this.”

Luckily, I am a practical per-son, even when I’m feeling terri-ble. What was it I couldn’t do,exactly? I was happy and contentdoing everything that needed to bedone to be a good wife to Ray. Ienjoyed my volunteer work, andthe occasional Rotary meeting. Iloved having lunch and gigglingwith a girlfriend. I could manageall these things as well as nappingevery day. The only thing that gotin the way was the housework.

“So,” I asked myself, “whycan’t I give up most of the house-work?” Other than what theneighbours would think, did itreally matter if my windowssparkled? All I really needed to dowas lower my standards to justabove what was needed to keepthe Board of Health away; whichonly means sanitary and safe;which doesn’t even attempt per-fect; which doesn’t even care,really, about neat. The clutter onlyneeds to be kept within reasonablebounds. I don’t need always to be“ready for company.”

This decision came hard. I hadthe sort of mother who could spota thread on the carpet at 20 paces,who insisted that not only mustwork be done well, it must be seento be done well. I’m the type ofperson who schedules housekeep-ing chores into my MicrosoftOutlook® computer program, withreminders for daily, weekly,monthly and yearly duties. If thesechores are done regularly andwell, keeping a small condomini-um “up to snuff” is relatively easy.

But … I don’t like housework.I like a shiny house, but I wasborn to have maids (notice theplural—it would take at least two)who would do the work for me.Housework makes me snappy andcranky, which is not a good thingto be when your beloved has AD.Hence, my decision.

Now we hold hands and watchtelevision while a pile of unsorted,unironed clothes are piled on achair. Now my carpet keeps itsspots. Forget writing my name inthe dust—I could build little forts.But I now have time to cook greatdinners, searching through mycookbooks for variety. I don’t rushthrough eyecare and footcare dut-ies. I have the time to just sit andlisten to and appreciate the terrificguy I’m married to—Alzheimer’sor no Alzheimer’s. My husband issmiling more, as am I. I even havetime for a belly laugh.

The ghost of my mother looksdisapprovingly over my shoulder. Istill cringe internally when thedoorbell rings unexpectedly. I amnot able to get over my upbringingenough not to be embarrassed, orfeel occasionally like a failure atwifehood because I can’t do every-thing. But I’ve made my choice.

Cranky? Dusty? If that’s thechoice—and for me it is—then itmakes itself. Life is too short to keepchasing dirt as my main mission.

Please look for Chapter 4: Youand Me and Spook in the nextissue of the Canadian AlzheimerDisease Review.



Do your patients think that cooking with aluminumpots and pans can cause Alzheimer Disease (AD)?Do they believe that AD can be prevented by exer-cising and taking vitamin supplements? Sur-prisingly, many other Canadians think the sameway, judging from the questions the AlzheimerSociety receives on a daily basis. As increasingnumbers of Canadians are expected to develop ADand related dementias in the coming years—750,000 by the year 2031—the importance of teach-ing Canadians some basic facts about the diseasebecomes crucial.

January is Alzheimer Awareness Month inCanada and the 2004 Awareness Campaign aims todispel the myths surrounding AD. Below are 10 common misconceptions about AD.

Myth 1: Because someone in my family has AD, I’m goingto get it.

Reality:Although genetics play a role in the disease, only5% to 10% of AD cases derive from genes thatcause the disease. The majority of cases have nosingle identifiable cause. The role of genetics con-tinues to be studied.

Myth 2: AD is only an old person’s disease.

Reality:While age is the most significant known risk factorfor AD, not everyone will develop the disease asthey age. People at the ages of 40 years and 50 years

can also be affected. What is most important forpeople to understand is that AD is not a normal partof aging.

Myth 3: There is a cure for AD.

Reality:There is no cure for AD, but there are medicationsand other approaches that can manage some of thesymptoms in some people. The good news is thatAD researchers have made great strides and areoptimistic about finding a cure.

Myth 4: Memory loss means AD.

Reality:Many people have trouble with their memory, but thisby itself does not mean they have AD. When memo-ry loss affects day-to-day function and is coupledwith lack of judgment and reasoning, or there arechanges in communication abilities, it is best to visita doctor to determine the cause of the symptoms.

Myth 5: Aluminum causes AD.

Reality:Although there has been a lot of research into theconnection between aluminum and AD, there is noconclusive evidence to show a link. The diseasemay develop from a combination of many risk fac-tors, including genetics, lifestyle and environmentalfactors.

2004 Awareness Campaign: Addressing theMyths of Alzheimer Disease

News from the Alzheimer Society of Canada


Myth 6: AD is preventable.

Reality:Because there is no known cause for AD, there is noconclusive evidence that the disease can be prevent-ed. There is, however, a growing amount of evi-dence that lifestyle choices directed at keeping themind and body fit may help reduce the risk. Thesechoices include physical exercise, a healthy dietincluding fresh fruits, vegetables, and fish, as wellas keeping your brain active.

Myth 7: Vitamins, supplements and memory boosters canprevent AD.

Reality:Many studies have been done to test the effectivenessof products such as vitamin E, vitamin B, and Ginkgobiloba in preventing AD. The findings are inconclu-sive, however research in this area is ongoing.

Myth 8: If I’m diagnosed with AD, my life is over.

Reality:Many people with the disease live meaningful,active lives. They have a sense of purpose and donot feel their lives are over. Earlier diagnosis andmedications are helping. It is also important to pro-vide appropriate surroundings, services, supportand activities to people with the disease, to helpenrich their quality of life throughout the progres-sion of disease.

Myth 9: All people who have AD become violent andaggressive.

Reality:AD affects each person differently. For a personwith AD, the loss of memory and the resulting con-fusion is often frustrating or even frightening. Bylearning about the disease, adapting the person’ssurroundings and changing the way we communi-cate with the person, aggressive responses may bepreventable.

Myth 10: People with AD cannot understand what is going onaround them.

Reality:Some people with AD do understand what is goingon around them; others have difficulty. AD doesaffect a person’s ability to communicate and makesense of the world around them. When we assumesomeone does not understand, feelings can be hurtunintentionally. The fact is a person with AD is stillthe same person as before, and needs to be treatedwith dignity and respect.

The Alzheimer Society’s Awareness Campaignkicks off January 5, 2004 with the release of its newbrochure Dispelling the myths (available in Englishand French).

Update: Safely Home—Alzheimer WanderingRegistry. On October 8, 2003 the Society’sWandering Registry program was given a new nameto more accurately reflect the goal of the program:to return a person safely home. Safely Home is anationwide program designed to help find a personwith AD who is lost and assist him/her in a safereturn home. Vital information about registrants isstored confidentially on a police database accessibleby police anywhere in Canada and the UnitedStates. Safely Home is available to those living athome or in a long-term care facility.

Also, thanks to foundation and corporate sup-port, Safely Home is undergoing a number ofenhancement initiatives to further improve the pro-gram in 2004.

The Alzheimer Society of Canada is a not-for-profithealth organization dedicated to helping those affectedby Alzheimer Disease. The Society provides supportand educational programs for people with AlzheimerDisease and their caregivers. The Society also fundsresearch into finding the causes and cure of the disease, and into improved methods of caregiving.

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

Documents

The Canadian Alzheimer - STA Communications...vation Screening Scale,20 the NEECHAM confusion scale,21 and the Confusion Assessment Method (CAM).22 The CAM can achieve better than