Levels of evidence and grades of recommendation · PDF file1 Levels of evidence and grades of...
91
MOH Clinical Practice Guidelines 3/2007
Transcript of Levels of evidence and grades of recommendation · PDF file1 Levels of evidence and grades of...
MOH Clinical Practice Guidelines 3/2007
1
Levels of evidence and grades of recommendation
Levels of evidence Level Type of Evidence
1+ + High quality meta-analyses, systematic reviews of randomised controlled trials (RCTs), or RCTs with a very low risk of bias.
1+ Well conducted meta-analyses, systematic reviews of RCTs, or RCTs with a low risk of bias.
1- Meta-analyses, systematic reviews of RCTs, or RCTs with a high risk of bias
2+ + High quality systematic reviews of case control or cohort studies. High quality case control or cohort studies with a very low risk of confounding or bias and a high probability that the relationship is causal
2+ Well conducted case control or cohort studies with a low risk of confounding or bias and a moderate probability that the relationship is causal
2- Case control or cohort studies with a high risk of confounding or bias and a significant risk that the relationship is not causal
3 Non-analytic studies, e.g. case reports, case series
4 Expert opinion
Grades of recommendation
Grade Recommendation
A At least one meta-analysis, systematic review of RCTs, or RCT rated as 1++
and directly applicable to the target population; or A body of evidence consisting principally of studies rated as 1+, directly applicable to the target population, and demonstrating overall consistency of results
B A body of evidence including studies rated as 2++, directly applicable to the target population, and demonstrating overall consistency of results; or Extrapolated evidence from studies rated as 1++ or 1+
C A body of evidence including studies rated as 2+, directly applicable to the target population and demonstrating overall consistency of results; or Extrapolated evidence from studies rated as 2++
D Evidence level 3 or 4; or Extrapolated evidence from studies rated as 2+
GPP (good practice
points)
Recommended best practice based on the clinical experience of the guideline development group.
Levels of evidence and grades of recommendation
Type of EvidenceLevel
RecommendationGrade
2
CLINICAL PRACTICE GUIDELINES
Dementia
MOH Clinical Practice Guidelines 3/2007
3
Published by Ministry of Health, Singapore16 College Road,College of Medicine BuildingSingapore 169854
Printed by Golden City Colour Printing Co. (Pte.) Ltd.
Copyright © 2007 by Ministry of Health, Singapore
ISBN 978-981-05-8095-7
Available on the MOH website: http://www.moh.gov.sg/cpg
Statement of Intent
These guidelines are not intended to serve as a standard of medical care.Standards of medical care are determined on the basis of all clinical dataavailable for an individual case and are subject to change as scientificknowledge advances and patterns of care evolve.
The contents of this publication are guidelines to clinical practice, basedon the best available evidence at the time of development. Adherence tothese guidelines may not ensure a successful outcome in every case, norshould they be construed as including all proper methods of care orexcluding other acceptable methods of care. Each physician is ultimatelyresponsible for the management of his/her unique patient in the light of theclinical data presented by the patient and the diagnostic and treatmentoptions available.
Statement of Intent
4
Foreword
Dementia is the progressive decline in cognitive function due to damage ordisease in the brain. Essentially, dementia is a problem that makes it hard for aperson to remember, learn and communicate. With progression, it becomesdifficult for the person to take care of himself or herself. The disease extractsits toll not only on its victims but also on the family and caregivers in terms ofphysical, emotional and economic cost that translates into caregiver’s stress. Itis estimated that 44% of the total cost of dementia is due to informal care.*
According to the WHO data, nearly five million DALYs are lost each yeardue to dementia in the Asia-Pacific Region. In Singapore, neuropsychiatricillnesses are the leading cause of DALYs loss and dementia ranks 4th amongall neuropsychiatric illnesses. Dementia accounts for approximately 26,000DALYs lost each year in Singapore.* As Singapore’s population is ageingrapidly, it is projected that the prevalence (22,000 in 2005) of dementia woulddouble by 2020.*
The Ministry of Health released its first guidelines on Dementia in 2001 withthe aim of upgrading the skills of practitioners to conduct proper clinical,functional and social assessment of the patients with and/or suspected ofhaving dementia. Since then, further evidence have emerged in the area oftherapeutics namely the role of cholinesterase in the treatment of dementia;non-pharmacological methods for the management of behavioral andpsychological symptoms of dementia. It is thus timely to update this set ofguidelines.
Apart from updating the guidelines in the area of management, the guidelinealso addresses ethical issues involved in the care of patients suffering fromdementia and the utility of genetic tests.
I hope this set of guidelines will assist all doctors involved in the care ofpatients with dementia.
PROFESSOR K SATKUDIRECTOR OF MEDICAL SERVICES______________________*Asia Pacific Members of Alzeimer's Disease International. Dementia in the Asia Pacific Region:The epidemic is here. Alzeimer's Disease International 2006. Available at:http://www.accesseconomics.com.au/publicationsreports/search.php?searchby=year&searchfor=2006
�5
Contents
Page
Executive summary of recommendations 1
1 Guideline development and objective 7
2 Introduction and epidemiology of dementia 8
3 Screening and assessment of dementia 11
4 Pharmacological management of dementia 25
5 Management of behavioural and psychological symptomsof dementia
37
6 Social and caregiver management of dementia andcommunity resources
44
7 Ethical issues in dementia 47
8 Cost-effectiveness 54
9 Clinical quality improvement 55
Annex 1 56
References 60
Self-assessment (MCQs) 77
Workgroup members 81
�1
Executive summary of recommendations
Details of recommendations can be found in the main text at the pages indicated.
Screening and assessment of dementia
C There is currently insufficient evidence for routine screening fordementia in older adults. Individuals who should be evaluated for dementiainclude those with progressive cognitive or behavioural complaintssuggestive of dementia, as well as patients who arouse the physician’s orcaregiver’s suspicion of cognitive impairment despite absence ofcomplaints (pg 11).
Grade C, Level 2+
GPP Assessment of dementia should be done via a comprehensiveevaluation. This approach will aim to diagnose dementia early, assess forcomplications of dementia and establish the cause of the dementia (pg 11).
GPP
B In individuals with suspected cognitive impairment, diagnosis can bemade using the DSM-IV criteria for dementia with history from a reliableinformant. This can be supplemented by an objective approach withcognitive tests (ECAQ/AMT/CMMSE) and/or neuropsychologicalassessment (pg 12).
Grade B, Level 2++
B The complications of dementia can be broadly divided into behaviouraland psychological symptoms, functional problems and social problems.These should be evaluated in all patients with dementia as these issues arethe major causes of stress on the caregiver and assessment would enable theclinician to target subsequent management effectively (pg 15).
Grade B, Level 2++
D The aim of determining dementia aetiology is to rule out potentiallyreversible causes of dementia and selecting appropriate treatment strategiesfor the irreversible dementias. This is done via clinical history and physicalexamination, followed by laboratory investigations and neuroimaging(pg 18).
Grade D, Level 4
Executive summary of recommendations
C
GPP
B
D
B
� �2
B A number of well-validated clinical criteria for the two most commontypes of dementia (Alzheimer’s disease and Vascular dementia) have beendeveloped over the years. These can be used in the specialized dementiaclinics for the definition of Alzheimer’s disease and Vascular dementia(pg 20).
Grade B, Level 2++
Pharmacological management of dementia
GPP Pharmacotherapy should be part of a multi-pronged strategy todementia management that encompasses a well-established diagnosis,education of patient and caregiver, non-pharmacological measures andcomprehensive caregiver psychosocial intervention (pg 25).
GPP
B Although high dose vitamin E (2000 IU per day) may have a modesteffect in delaying disease progression in moderately severe Alzheimer’sdisease, doses of vitamin E in excess of 400 IU a day should be avoided forthe treatment of Alzheimer’s disease until there is further data on its safety,especially in patients with cardiovascular disease (pg 26).
Grade B, Level 1+
A Anti-inflammatory agents (such as non-steroidal anti-inflammatoryagents and cyclo-oxygenase 2 inhibitors) are not recommended for theprevention of cognitive decline in Alzheimer’s disease (pg 27).
Grade A, Level 1++
B Prednisolone is not recommended for the prevention of cognitive declinein Alzheimer’s disease (pg 27).
Grade B, Level 1+
A Oestrogen is not recommended for the prevention of cognitive decline inwomen with dementia (pg 27).
Grade A, Level 1++
A Acetylcholinesterase inhibitors should be considered for the managementof all patients with mild to moderate Alzheimer’s disease (pg 27).
Grade A, Level 1++
B
GPP
B
B
A
A
A
� �3
A Acetylcholinesterase inhibitors can be considered for the management ofmoderate to severe Alzheimer’s disease (pg 28).
Grade B, Level 1+
A Acetylcholinesterase inhibitors have been shown to be of clinical benefitand may be considered for use in the management of mild to moderatevascular dementia (pg 28).
Grade A, Level 1+
B Acetylcholinesterase inhibitors can be considered for the management ofdementia with Lewy bodies and Parkinson’s disease dementia (pg 29).
Grade B, Level 1+
B All three available acetylcholinesterase inhibitors (donepezil,rivastigmine and galantamine) can be considered for the pharmacologicalmanagement of dementia, since there is no definite evidence to support adifference in clinical efficacy between them (pg 30).
Grade B, Level 1+
A Where tolerated, acetylcholinesterase inhibitors should be titrated torecommended doses (5-10 mg/day donepezil; 6-12 mg/day rivastigmine;16-24 mg/day galantamine), which have been shown to confer greaterbenefit compared with lower doses (pg 30).
Grade A, Level 1++
B N-methyl D-aspartate antagonists such as memantine can be consideredfor the management of moderate to severe Alzheimer’s disease, either aloneor in combination with acetylcholinesterase inhibitors (pg 31).
Grade B, Level 1+
B N-methyl D-aspartate antagonists such as memantine may be a treatmentoption for mild to moderate Alzheimer’s disease, if acetylcholinesteraseinhibitor therapy is contra-indicated, not tolerated or if there is diseaseprogression despite an adequate trial of acetylcholinesterase inhibitor(pg 31).
Grade B, Level 1+
A N-methyl D-aspartate (NMDA) antagonists have been shown to be ofclinical benefit and may be considered for use in the management of mild tomoderate vascular dementia (pg 32).
Grade A, Level 1+
A
B
B
A
A
B
B
B
� �4
B Practitioners who prescribe ginkgo for the treatment of dementia shouldbe aware of the unestablished benefit, variability of active ingredient amongpreparations, and potential for drug interactions (pg 32).
Grade B, Level 1+
A Selegiline is not recommended for the treatment of core or associatedsymptoms in Alzheimer’s disease (pg 33).
Grade A, Level 1++
GPP Appropriate treatment of vascular risk factors is recommended for allpatients. However, it should be noted that whilst promising observationaldata exists, it remains to be shown in a randomised controlled clinical trialif any prevention strategy such as blood pressure reduction or antiplatelettreatment for the secondary prevention of stroke, will reduce the incidenceof vascular dementia (pg 33).
GPP
GPP The decision to initiate costly symptomatic dementia treatment, suchas acetylcholinesterase inhibitors or N-methyl D-aspartate antagonists,should always be made in consultation with the patient and family aftercareful consideration of the expected magnitude of benefit, side effects, co-morbidities and costs of treatment (pg 33).
GPP
GPP Patients who are started on acetylcholinesterase inhibitors or N-methyl D-aspartate antagonists, should be carefully monitored for sideeffects and response to treatment (pg 34).
GPP
Management of behavioural and psychologicalsymptoms of dementia (BPSD)
GPP Non-pharmacological methods to manage behavioural andpsychological symptoms of dementia should be instituted, prior toconsideration of pharmacological measures (pg 37).
GPP
GPP Antidepressants may be used for the treatment of comorbiddepression in dementia provided their use has been evaluated carefully foreach patient (pg 39).
GPP
A
B
GPP
GPP
GPP
GPP
GPP
� �5
A Conventional and atypical antipsychotics may be used with caution,given their side effect profile, to treat neuropsychiatric symptoms ofdementia (pg 39).
Grade A, Level 1+
B Trazodone may be considered for patients with depressive symptoms anddementia associated agitation (pg 40).
Grade B, Level 1+
A Routine use of mood stabilizers, such as carbamazepine and sodiumvalproate, is not recommended for treatment of behavioural symptomsassociated with dementia (pg 41).
Grade A, Level 1+
GPP An individualized approach to managing behavioural problems indementia patients is required (pg 41).
GPP
GPP Cholinesterase inhibitor therapy may be considered in treatment ofpatients with behavioural problems if antipsychotics are inappropriate(pg 41).
GPP
GPP The decision to start antipsychotic therapy to control behaviouralproblems in dementia patients should be made in consultation with thepatient and family, after careful consideration of the benefit, adverse-effectsand co-morbidities (pg 41).
GPP
B For patients with dementia with Lewy Body and behavioural problems,acetylcholinesterase inhibitors should be considered first for management ofthe behavioural problems (pg 42).
Grade B, Level 1+
GPP In all patients started on antipsychotic medication, they should bemonitored carefully for side effects and response to treatment. In patientswho are stable, antipsychotic withdrawal should be considered (pg 42).
GPP
A
B
GPP
A
GPP
GPP
GPP
B
� �6
Social and caregiver management of dementia andcommunity resources
A Caregiver interventions via a multifaceted approach should be consideredin the total management of the person with dementia (pg 44).
Grade A, Level 1+
GPP Where appropriate, respite care can be offered to relieve the burdenof caregiving on the family caregiver (pg 45).
GPP
GPP Referral to community resources to meet the care needs of the personwith dementia and his/her carer should always be considered (pg 46).
GPP
GPP
A
GPP
� �7
1 Guideline Development and Objectives
1.1 Guideline development
The guidelines have been produced by a committee of psychiatrists,neurologists, geriatricians and primary care physicians appointed bythe Ministry of Health. They were developed by the adaptation ofexisting guidelines, by the review of relevant literature and by expertclinical consensus with consideration of local practice.
1.2 Objectives
The main aim of these guidelines is to provide an approach forhealthcare professionals to assess, evaluate and manage dementia(using local evidence where possible).
1.3 Target group
These guidelines are mainly developed for all healthcareprofessionals involved in the care of patients with dementia.
1.4 What’s new in the revised guidelines?
Since the last MOH Clinical Practice Guidelines on Dementia in2001, new research findings and developments have emerged. Thesehave culminated in updated recommendations in the area oftherapeutics, namely the benefit of cholinesterase inhibitors invascular dementia and dementia with Lewy Body; the revision ofrecommendations for the use of selegiline and vitamin E forAlzheimer’s disease; the management of behavioral andpsychological symptoms of dementia and ethical issues in dementia.
1.5 Review of guidelines
Evidence-based clinical practice guidelines are only as current as theevidence that supports them. Users must keep in mind that newevidence could supercede recommendations in these guidelines. Theworkgroup advises that these guidelines be scheduled for review 5years after publication, or if new evidence appears that requiressubstantive changes to the recommendations.
1 Guideline Development and Objectives
� �8
2 Introduction and Epidemiology of Dementia
2.1 Introduction and epidemiology
Rapidly graying demographics characterize many economicallydeveloped, as well as developing countries and from this perspective,dementia and its attendant problems are on the agendas of manygovernments. An estimated 25 million persons in the world haveAlzheimer’s disease (AD) – generally considered to be thecommonest subtype of dementia - and these numbers are expected toincrease to 63 million in 2030, and by 2050, an estimated 114 millionwill be afflicted with the illness.1
The number of those with dementia will increase in Asia-Pacificregion from 13.7 million people in 2005 to 64.6 million people in2050.2 Singapore has one of the fastest ageing populations in theAsia-Pacific region with 15-20% of total population consisting ofpersons aged 65 and above by the year 2030.3 The prevalence ofdementia is expected to increase from 22,000 in 2005 to almost53,000 in 2020 and 187,000 in 2050.2
The prevalence of dementia or cognitive impairment in localepidemiological studies using various screening instruments rangesfrom 2% to 14%,4-7 with age-related increases in prevalence ofcognitive impairment from 0.8% in those aged between 60-64 yearsto 32.2% among those aged 85 years and older.7 These prevalencerates are comparable with other populations in the world in evidence-based estimates generated by Delphi Consensus Study8 (See Table 1)and other comparison studies.9
2 Introduction and Epidemiology of Dementia
� �9
Table 1 Dementia prevalence in WHO worldregions8,9
Consensus dementiaprevalence (%) (60+)
Western Europe – EURO A 5.4Eastern Europe low adult mortality –EURO B
3.8
Eastern Europe high adult mortality –EURO C
3.9
North America – AMRO A 6.4Latin America – AMRO B/D 4.6North Africa & Middle East EMROB/D
3.6
Developed Western Pacific –WPRO A
4.3
China and developing Western Pacific– WPRO B
4.0
Indonesia, Thailand and Sri Lanka –SEARO B
2.7
India and S Asia – SEARO D 1.9Africa – AFRO D/E 1.6
(Sources: Ferri CP et al, 2005; Kua EH, 1996)
Subgroups based on patterns of child and adult mortality from A (lowest) toE (highest).WPRO = Western Pacific RegionWPRO A = Australia, Japan, Brunei Darussalam, New Zealand, SingaporeWPRO B = Cambodia, China, Lao People’s Democratic Republic, Malaysia,Mongolia, Philippines, Republic of Korea, Vietnam, Cook Islands, Fiji,Kiribati, Marshall Islands, Micronesia (Federated States of), Nauru, Niue,Palau, Papua New Guinea, Samoa, Solomon Islands, Tonga, Tuvalu andVanuatu.SEARO = Southeast Asian regionSEARO D = Bangladesh, Bhutan, Democratic People’s Republic of Korea,India, Maldives, Myanmar and Nepal
�0 ��10
Ethnic variations in dementia prevalence have also beendemonstrated with higher dementia prevalences among the Malays(9.4%) and Indians (8.8%) as compared to the Chinese elderlypopulation (4.2%).7 With regards to dementia aetiology, Alzheimer’sdisease was found to be more common in Indians and Eurasianswhile vascular dementia more common in Chinese and Malays.10 Aseparate study found that among the elderly Malays, the prevalenceof vascular dementia was higher in women than men.11
With this rising trend, the evaluation of dementia, especially at theearly stage, becomes increasingly important because with earlydiagnosis, the affected patients are more amenable to treatmentadvances. Interventions to slow down the progression of cognitivedecline (both pharmacological and non-pharmacological measures)can translate into prolongation of functioning in the community,delay in institutionalisation and lower healthcare expenditure.12-14
This may help reduce the heavy cost and burden of the illness, both tofamily and society, especially in the light of our rapidly ageingpopulation.
�0 ��11
3 Screening and Assessment of Dementia
3.1 Screening
C There is currently insufficient evidence for routine screening fordementia in older adults. Individuals who should be evaluated fordementia include those with progressive cognitive or behaviouralcomplaints suggestive of dementia, as well as patients who arousethe physician’s or caregiver’s suspicion of cognitive impairmentdespite absence of complaints.
Grade C, Level 2+
The evaluation of dementia should be targeted at patients in whomthere is some suspicion of cognitive impairment. They include:
- subjects with memory and other cognitive complaints, eitherreported by the patient himself or a significant other15
- progressive forgetfulness16
- subjects who arouse the physician’s suspicion of cognitiveimpairment during interview despite absence of memory orcognitive complaints
- those who are at increased risk for dementia (such as those witha strong family history of dementia)
- elderly patients who need to make important decisions (such asthe sale of a house or making a will) and in whom mentalcompetency is questionable.
3.2 Assessment of dementia
GPP Assessment of dementia should be done via a comprehensiveevaluation. This approach will aim to diagnose dementia early, assessfor complications of dementia and establish the cause of thedementia.
GPP
3 Screening and Assessment of Dementia
GPP
C
�� ��12
In evaluation patients who present with forgetfulness or confusion, itis important to exclude delirium (acute confusional state) if this is ofan acute nature. If the forgetfulness or confusion is of a subacutenature (weeks to few months), potentially reversible neurologicalconditions and depression have to be excluded.
(I) Diagnosis of dementia
B In individuals with suspected cognitive impairment, diagnosis canbe made using the DSM-IV criteria for dementia with history from areliable informant. This can be supplemented by an objectiveapproach with cognitive tests (ECAQ/AMT/CMMSE) and/orneuropsychological assessment.
Grade B, Level 2++
Subjective approach
a) The Diagnostic and Statistical Manual of Mental Disorders -IV (DSM-IV) criteria17 are very often used as the gold standardfor the clinical diagnosis of dementia.18-20 The criteria requirememory impairment to be present, as well as deficits in one othercognitive domain (aphasia, apraxia, agnosia and executivedysfunctioning). Moreover, these cognitive declines must be ofsufficient severity to cause perceptible impairment in social oroccupational functioning (Table 2).
B
�� ��13
Table 2 DSM-IV clinical criteria for diagnosis ofdementia17
Cognitive domain QuestionsAmnesia Any forgetfulness? Did it start
gradually or suddenly? Is it progressivelyworse? And if so, is it smoothly decliningor showing a step-wise/ fluctuatingdecline? Is it over short-term or long-termmatters?
AND declines in one of the following domains:Aphasia Any word-finding difficulty or
other difficulties with communication?Apraxia Any problems with buttoning or dressing?
Any difficulties with using utensils duringmealtimes?
Agnosia Any problems recognising familiar facesor familiar items?
Executivedysfunctioning
Any problems handling money (loosechange)? Any change in general problem-solving abilities? Is one’s work getting tobe more disorganised?
OF sufficient severity tocause significantimpairment in social oroccupational functioning
AS a result of the above, is he becomingless independent in the- community?- home-care?- self-care level?
(Source: American Psychiatric Association. Diagnostic and Statistical Manual of MentalDisorders, 1994).
b) The Informant Questionnaire on Cognitive Decline in theElderly (IQCODE)21,22 is a 26-item test that enquires about thesubject’s memory, cognition and language ability for the last 10years (see Appendix 1).
There is recent evidence of the Brief Informant Screening Test15
consisting of a single-item informant report of memory problem anda 4-item Instrumental Activities of Daily Living, as a usefulscreening instrument for patients with early cognitive impairment.
�� ��14
Objective approach
This is an observer-based approach using either performance-basedinstruments, such as mental status test (brief screening instruments),or a more detailed neuropsychological tests, which is usuallyadministered by clinical psychologists.
a) The Elderly Cognitive Assessment Questionnaire (ECAQ)23,24
is a 10-item test screening for cognitive impairment assessingmemory and information-orientation (Appendix 2).
b) The 10-item Abbreviated Mental Test (AMT) and
c) 28-item Chinese Mini Mental State Examination (CMMSE)(Appendix 3 and 4) have also been validated locally with age andeducation-adjusted cut-off values available.25 The CMMSE ismore useful in those with higher educational attainment as theAMT may not be as sensitive.
d) Neuropsychological testing is usually administered by clinicalpsychologists. It is useful in detecting subtle cognitive difficultieswhich are not picked up by the brief screening instruments. Theyshould be performed on subjects:• who have memory complaints but do not yet satisfy criteria
for dementia;• depressed subjects who present with memory complaints to
help in determining whether the memory complaints are duesolely to the depression or whether they have concomitantdementia;
• Subjects in whom decision-making capacity is beingassessed.
Psychometric testing can be a useful adjunct in the latter scenario.They are also useful in aetiologic differentiation of dementia.
Neuropsychometric batteries have been validated locally in theelderly Chinese26 and the Vascular Dementia Battery test has alsobeen validated in the Singapore population.27
Neuropsychological tests are also useful in individuals in whom thediagnosis of dementia is inconclusive and serial monitoring forperformance decline over time may be useful in establishing thediagnosis.
�� ��15
(II) Assessing complications of dementia
B The complications of dementia can be broadly divided intobehavioural and psychological symptoms, functional problems andsocial problems. These should be evaluated in all patients withdementia as these issues are the major causes of stress on thecaregiver and assessment would enable the clinician to targetsubsequent management effectively.
Grade B, Level 2++
a) Behavioural problems
Behavioural problems occur frequently in dementia patients; theyaffect 10% to 75% of all patients at some stage of their dementia.28
They can present severe problems to all who interact with them,leading to premature institutionalization, increased costs of care andsignificant loss in quality of life for the patient and family. Most ofthe major behavioural problems are amenable to treatment and arecapable of reducing the suffering of the patients and their caregivers.
Different behavioural problems present at the different stages of thedementia process; anxiety and depression being common in earlystages while abberant motor behaviour is more common during thelater stages of illness.29 In the clinic setting, the physician shouldroutinely ask about depression, anxiety, agitation, paranoia,hallucinations and sleep problems, as these are potentially amenableto treatment, by way of either psychosocial interventions orpharmacologic agents.
These behavioural problems can also be rated objectively usingbehaviour scales which may be either self-rated, caregiver-based orobserver reports. The Behavioural Pathology in Alzheimer’s DiseaseRating Scale (BEHAVE-AD)30 and Neuropsychiatric Inventory(NPI)31 are examples of behaviour scales, but they are often usedonly in research settings.
Depression in the elderly may not show the classical featuresindicated in the DSM-IV and, in this regard, clinicians may find thebrief depression scales useful in practice. Locally, the single-questiontest for depression, Geriatric Depression Scale (GDS) and EvenBriefer Assessment Scale for Depression (EBAS-DEP) have beenvalidated in cognitively intact, community-dwelling Chineseelderly.32 The Cornell Depression Scale in Dementia specifically
B
�� ��16
assesses depression in dementia33 and has been shown to be a usefulscreening instrument in our local population.34
b) Functional difficulties
Functional difficulties can be assessed at three levels: communityfunctioning, home functioning and self-care (See Appendix 5)35.They are generally affected with the progression of dementia in adescending order and also allow these functional deficits to serve asmarkers of dementia severity. It is also important to make sure thatthese difficulties result from cognitive difficulties and not physicaldisabilities. The severity of dementia can be staged using theDiagnostic and Statistical Manual of Mental Disorders - 3rd revisededition (DSM-III-R)36 or other formal functional assessment scaleswhich include Clinical Dementia Rating Scale (CDR)37,38, FunctionalAssessment Staging (FAST), Barthel Index and Blessed DementiaScale (BDS).
c) Social problems
As a result of dementia, there is also loss of social role of the patientas a parent, spouse, friend and member of the larger society and theseoften result in caregivers’ coping difficulties. Identification ofcaregiver’s stress can allow targeted family education andcounselling at tertiary dementia care centres, or even dementia day-care centres, and this has been shown to reduce institutionalisation.14
Elder abuse may also occur when the frustrated caregiver directs hisor her stress at the vulnerable patient whose care is proving to bedifficult.39 Likewise, financial difficulties should be asked for and ifproblems are identified, families can be referred to a social worker.
(III) Determining the aetiology of Dementia
Having determined the cognitive impairment to be chronic andhaving met clinical criteria for dementia, as well as assessing for thecomplications of dementia, the final step of the clinical evaluationinvolves determining the dementia aetiology. The types of dementiacan be broadly divided into 2 categories – irreversible and reversiblecauses.
The more common causes of dementia can be classified intoirreversible and potentially reversible causes.
�� ��17
• The irreversible causes include degenerative causes(Alzheimer’s disease, fronto-temporal dementia and dementiawith Lewy body), cerebrovascular disease (Vascular dementia),prion-associated disorders (Creutzfeld-Jakob disease) andneurogenetic disorders.
• The potentially reversible causes include infectious disorders(meningitis and encephalitis), toxic or metabolicencephalopathies (hypothyroidism, vitamin B12 deficiency, andalcohol-related syndromes), neoplastic causes andhydrocephalus (obstructive or normal pressure hydrocephalus).
Alzheimer’s disease
Studies in many countries have shown that Alzheimer’s disease isthe most common cause of dementia. Familial cases are rare andusually present as early onset dementia (less than 60 years). Sporadiccases usually present after the age of 60 with insidious, gradualdeterioration of cognitive function. Short-term memory loss is themost common early symptom. However, other aspects of highercognitive function may become affected over the course of time.Thus, patients may experience increasing difficulty with activities ofdaily living, changes in personality, behavioural and psychiatricproblems, language dysfunction, loss of visuo-spatial and executivefunction.
Vascular dementia
Vascular dementia remains a controversial entity as there aredisagreements over the validity of clinical criteria. Nevertheless,cognitive impairment and dementia is common in patients withcerebrovascular disease and it is often reported as the second mostcommon cause of dementia in many studies.
Vascular dementia can be suspected in patients who have an abruptonset of symptoms, stepwise deterioration, focal neurological signsand symptoms or a history of stroke. However, neuropathologicalstudies have shown that many patients diagnosed with vasculardementia have Alzheimer’s disease pathology in addition tocerebrovascular lesions giving rise to doubts whether “pure”Vascular dementia exists. Due to the high variability ofcerebrovascular pathology and its causative factors, no validatedneuropathological criteria exist for vascular dementia. Nevertheless,in a large unselected, community-based neuropathology study of an
�� ��18
elderly population with prospectively evaluated dementia status,Alzheimer’s disease-type and vascular pathology were the majorpathological correlates of cognitive decline but most patients hadmixed disease40, emphasising the important role of vascularpathology in dementia.
Dementia with Lewy Body (DLB)
DLB has been found in some studies to be the second most commonform of degenerative dementia, accounting for up to 20% cases in theelderly. It is characterized by fluctuating cognitive impairment,spontaneous parkinsonism and recurrent visual hallucinations.Recognition of DLB is clinically important in view of the highincidence (60%) of adverse and life-threatening reaction toantipsychotics.
Fronto-temporal dementia
Fronto-temporal lobar degeneration produces 3 clinical syndromes:• The most common is fronto-temporal dementia, characterized by
personality change and profound alteration in social conduct andassociated with bilateral atrophy of the frontal and anteriortemporal lobes.
• Progressive non-fluent aphasia characterized by difficulty inverbal expression in the presence of relative preservation ofcomprehension, and
• Semantic dementia where there is fluent speech with semanticerrors and severely impaired comprehension and naming,together with a visual associative agnosia.
D The aim of determining dementia aetiology is to rule outpotentially reversible causes of dementia and selecting appropriatetreatment strategies for the irreversible dementias. This is done viaclinical history and physical examination, followed by laboratoryinvestigations and neuroimaging.41-44
Grade D, Level 4
HistoryIt is important to ask for the nature of the cognitive decline (suddenor gradual), progression – either gradually progressive (moresuggestive of Alzheimer’s disease) or stepwise/fluctuating course(suggestive of Vascular dementia). A history of significant alcohol
D
�� ��19
ingestion and medication use (such as antipsychotics,antidepressants, anticholinergic agents and sedative-hypnotic agents)and history of medical, neurological and psychiatric illness isimportant.
Physical examination and mental state examination
A targeted physical examination should be performed, looking forevidence of depression, focal neurological deficits (such as visualfield defects, hemiparesis, hemisensory loss, asymmetric deep tendonreflexes or unilateral extensor plantar responses). It is also importantto examine for extrapyramidal signs such as rigidity andbradykinesia, movement disorders and gait abnormalities as thesemay point to certain aetiologic diagnosis.
Diagnostic tests to rule out metabolic and structural causes ofdementia
Dementias which are related to metabolic abnormalities are thoughtto be reversible. The haematological tests include full blood count,urea and electrolytes, serum calcium, serum glucose, thyroidfunction tests and vitamin B12 levels.
Routine testing for neurosyphilis is problematic given the difficultiesin interpretation of test results. It is best done when patients exhibitclinical features of neurosyphilis.
Other biomarkers which can help in establishing dementia diagnosisinclude apolipoprotein-E 4 allele, CSF-tau and -amyloid forAlzheimer’s disease, CSF 14-3-3, neuron-specific enolase andelectroencephalogram for Creutzfeld-Jakob disease. However, theseare not performed routinely.
Neuroimaging
Neuroimaging is useful in the differential diagnosis of dementia andalso necessary in the diagnostic criteria in Alzheimer’s disease andvascular dementia. It is also useful in detection of very earlydementia as the functional and structural brain changes takes placebefore clinical manifestation of cognitive deficits. It consists of either
• Structural imaging techniques (computed tomography (CT) scanof head and magnetic resonance imaging (MRI)), or
�0 ��20
• Functional neuroimaging techniques (Positron emissiontomography and single-photon emission tomography).
Whether all patients with dementia require a structural imaging is animportant clinical question, for which there is no consensus. Thevalue of neuroimaging is in the identification of cerebral infarcts andclinically important surgical brain lesions (SBLs) such as subduralhaematomas, cerebral tumors and normal pressure hydrocephalus.The Canadian Consensus Conference on the Assessment of Dementia(CCCAD)45 (Appendix 6) has outlined the criteria for undertaking aCT scan of the head, only if certain clinical conditions are met. In apatient with advanced dementia of a long duration (>2 years based onCCCAD’s recommendations), we believe a brain scan is notwarranted to detect potentially reversible SBLs. Conversely, if thepatient’s dementia is only mild to moderate (even after 2 years), it isstill advisable to request for an initial CT scan of the brain.46 If theclinician is not inclined to perform a brain scan, there is immensevalue in discussing the matter with the caregivers and in securingtheir agreement not to order a neuroimaging procedure.
Neuroimaging is also useful for aetiologic differentiation of thedifferent dementias.
B A number of well-validated clinical criteria for the two mostcommon types of dementia (Alzheimer’s disease and Vasculardementia) have been developed over the years. These can be used inthe specialized dementia clinics for the definition of Alzheimer’sdisease and Vascular dementia.
Grade B, Level 2++
In Alzheimer’s disease, the common clinical criteria used includeDSM-IV criteria for DAT, National Institute of Neurologic,Communicative Disorders and Stroke-Alzheimer’s disease andRelated Disorders Association (NINCDS-ADRDA).47 In VD, thecommon clinical criteria used include DSM-IIIR, National Instituteof Neurologic Disorder and Stroke and the Association Internationalepour la Recherche et l’Enseignment en Neurosciences (NINDS-AIREN)48, State of California AD Diagnostic and Treatment Centerscriteria (ADDTC)49, Hachinski Ischemic Score (HIS)50, modifiedRosen scale51 (the latter two being clinical scales).
Clinical Criteria for dementia with Lewy bodies52 and fronto-temporal dementia53 have been developed.
B
�0 ��21
Appendix 1 Informant Questionnaire on Cognitive Declinein the Elderly (IQCODE)21,22
Rated on 5-point scale from 1. Much improved, A bit improved, Not much change, A bit worse, Much worse [1 5]
1. Recognising the faces of family and friends2. Remembering the names of family and friends3. Remembering things about family and friends e.g.occupations,
birthdays, addresses4. Remembering things that have happened recently5. Recalling conversations a few days later6. Forgetting what he/she wanted to say in the middle of a conversation7. Remembering his/her address and telephone number8. Remembering what day and month it is9. Remembering where things are usually kept10. Remembering where to find things which have been put in a different place from usual11. Adjusting to any change in his/her day-to-day routine12. Knowing how to work familiar machines around the house13. Learning to use a new gadget or machine around the house14. Learning new things in general15. Remembering things that happened to him/her when
he/she was young16. Remembering things he/she learned when he/she was young17. Understanding the meaning of unusual words18. Understanding magazine or newspaper article19. Following a story in a book or on TV20. Composing a letter to friends or for business purposes21. Knowing about important historical events of the past22. Making decisions on everyday matters23. Handling money for shopping24. Handling financial matters, e.g. pension, dealing with bank25. Handling other everyday arithmetic problems e.g. knowing how much
food to buy, knowing how long between visits form family or friends26. Using his/her intelligence to understand what’s going on and to reason
things through.
(Source: Jorm AF et al, 1991; Lim HJ et al, 2003)
�� ��22
Appendix 2 Elderly Cognitive Assessment Questionnaire (ECAQ)23
Items Score
Memory1. I want you to remember this number.
Can you repeat after me (4517). I shall test youagain in 15 min.
1
2. How old are you? 13. When is your birthday? OR in what year were you
born?
Orientation and information4. What is the year? 15. date? 16. day? 17. month? 18. What is this place called? Hospital/Clinic 19. What is his/her job? (e.g. nurse/doctor) 1
Memory Recall10. Can you recall the number again? 1
Total
(Source: Kua EH & Ko SM, 1992)
Appendix 3 Abbreviated Mental Test (AMT)25
Items Score
What is the year? 1What is the time? (within 1 hour) 1What is your age? 1What is your date of birth? 1What is your home address? 1Where are we now? 1Who is our country’s Prime Minister? 1What is his/her job? (show picture) 1Memory phrase “37 Bukit Timah Road” 1Count backwards from 20 to 1 1Recall memory phase 1
Total score
(Source: Sahadevan S et al, 2000)
�� ��23
Appendix 4 Chinese Mini Mental State Examination(CMMSE)25
Items Score
What day of the week is it? 1What is the date today? 1What is the month? 1What is the year? 1Where are we now? 1What floor are we now? 1In which estate are we? 1In which country are we? 1Repeat the following words: “Lemon, Key, Balloon” 3Substract $7 from $100 and make 5 subtractions 5Can you recall the three wods 3What is this? (show a pencil) 1What is this? (show a watch) 1Repeat the following:a) “No ifs, ands or buts” (English) 1b) “Forty-four stone lions” (Chinese)Follow 1 3-stage command:“Take this piece of paper, fold it in half, and put it on thefloor
3
Say a sentence of your choice 1Read and obey what is written on this piece of paper“Raise your hands” 1Copy this drawing on a piece of paper 1
Total score
(Source: Sahadevan S et al, 2000)
�� ��24
Appendix 5 Functional complications of dementia35
Variable QuestionsCommunityfunctioning
Can patient find his way around in unfamiliarsurroundings, manage his finances, do shoppingor marketing?
Home-care functioning Can he prepare his own food, help in houseworkand cooking? Is he able to choose proper attire todress himself? Is he safe to be left at home alone?
Self-care functioning Is he able to bathe, dress himself? Is he able to goto toilet, transfer or feed himself? Is he continentof bladder and bowels?
(Source: MS Chong et al, 2003)
Appendix 6 Canadian Consensus Conference on theAssessment of Dementia (CCCAD) forperforming Cranial CT in patients withdementia45
Criteria:
• < 60 years old• Rapid (e.g., over 1-2 months), unexplained decline in cognition or
function• Dementia of relatively short duration (<2 years)• Recent, significant head trauma• Unexplained neurologic symptoms (e.g., new onset of severe headache
or seizures)• History of cancer, especially of a type or at a site associated with
metastasis to the brain• Use of anticoagulants or history of bleeding disorder• History of urinary incontinence and gait disturbance early in the disease
(suggestive of normal pressure hydrocephalus)• Presence of any new localising signs on physical examination
(hemiparesis, Babinski’s sign)• Unusual or atypical cognitive symptoms or presentation (e.g.,
progressive aphasia)• Gait disturbance• CT is recommended if one or more of these criteria are present.
(Source: Patterson CJ et al, 1999)CT: computed tomography
�� ��25
4 Pharmacological Management of Dementia
4.1 Overview
GPP Pharmacotherapy should be part of a multi-pronged strategy todementia management that encompasses a well-establisheddiagnosis, education of patient and caregiver, non-pharmacologicalmeasures and comprehensive caregiver psychosocial intervention.
GPP
All dementia patients should be evaluated for suitability ofpharmacological strategies to:• Reverse or stabilize the underlying disease• Improve cognitive symptomatology• Treat behavioural, mood or psychiatric symptoms associated
with dementia
4.2 Pharmacological interventions to reverse or stabilizethe underlying disease
Pharmacological strategies to address the underlying disease includetreating identifiable reversible causes, reduction of established riskfactors, and disease modifying measures to slow the rate of diseaseprogression (Table 3).54
Table 3 Possible pharmacological strategies to addressunderlying disease
1. Treating identifiable reversible causes• Replace deficiency states (e.g. B12 deficiency, hypothyroidism)• Correct metabolic abnormalities (e.g. hypercalcemia,
hypoglycemia)• Treat infections (e.g. neurosyphilis)
2. Reduction of vascular risk factors• Treatment of hyperlipidemia, hypertension, diabetes mellitus, and
smoking cessation• Anti-platelet agents for secondary stroke prevention• Anti-coagulation for atrial fibrillation and cardioembolic strokes
3. Slowing rate of disease progression (disease modifying)
4 Pharmacological Management of Dementia
GPP
�� ��26
When significant neuronal damage has occurred, treatment ofpotentially reversible causes often arrests the underlyingpathophysiology but may not reverse the dementia. Only a smallpercentage of potentially reversible abnormalities are completelyreversible, and the more common of such conditions arehypothyroidism and vitamin B12 deficiency.55 An increasing body ofevidence suggests that vascular risk factors are putative not only invascular dementia (VaD), but also in Alzheimer’s disease (AD)56,thus, vascular risk factors (such as hyperlipidemia, hypertension,diabetes mellitus, atrial fibrillation, smoking) should be sought forand managed in all dementia cases.
4.2.1 Disease-modifying strategies
B Although high dose vitamin E (2000 IU per day) may have amodest effect in delaying disease progression in moderately severeAlzheimer’s disease, doses of vitamin E in excess of 400 IU a dayshould be avoided for the treatment of Alzheimer’s disease untilthere is further data on its safety, especially in patients withcardiovascular disease.
Grade B, Level 1+
The reported (and as yet unreplicated) benefit of high dose vitamin E(2000 IU per day) is at best a modest benefit in retarding progressionin moderately severe Alzheimer’s disease.57 A recent meta-analysisexamined vitamin E supplementation (alone and in combination withother vitamins and minerals) in doses up to 2000 IU a day, andreported a slight but significant risk for all-cause mortality withvitamin E dosage ≥ 400 IU a day (risk ratio 1.04, 95% CI 1.01-1.07).58 Of note, seven of the eight high-dosage studies in the meta-analysis that showed harmful effects of vitamin E involveparticipants with vascular risk factors or established cardiovasculardisease.59 However, interpretation of the results of the meta-analysisis mitigated by methodologic concerns, including a possible type Ierror as the meta-analysis excluded vitamin E trials that reportedfewer than 10 deaths and did not adjust for mortality over differentfollow-up periods.59
B
�� ��27
A Anti-inflammatory agents (such as non-steroidal anti-inflammatory agents and cyclo-oxygenase 2 inhibitors) are notrecommended for the prevention of cognitive decline in Alzheimer’sdisease.60, 61
Grade A, Level 1++
B Prednisolone is not recommended for the prevention of cognitivedecline in Alzheimer’s disease.62
Grade B, Level 1+
A Oestrogen is not recommended for the prevention of cognitivedecline in women with dementia.
Grade A, Level 1++
Contrary to evidence from epidemiological studies which suggests aprotective role of oestrogens in Alzheimer’s disease, evidence fromrandomized controlled trials supports the ineffectiveness of estrogenfor the treatment of Alzheimer’s disease.63-65 In addition, there areconcerns about increased risk for heart attacks, strokes, breast cancerand thromboembolism with combination (oestrogen plus progestin)therapy.66
There is insufficient evidence to support the use of other agents suchas supplemental omega 3 polyunsaturated fatty acid,67 folatesupplementation with or without B12 (in the absence of a deficiencystate),68 and statins69 for the prevention of cognitive decline indementia.
4.3 Pharmacological interventions to improve cognitivesymptomatology
4.3.1 Acetylcholinesterase inhibitors
A Acetylcholinesterase inhibitors should be considered for themanagement of all patients with mild to moderate Alzheimer’sdisease.
Grade A, Level 1++
There are currently three acetylcholinesterase inhibitors (AchEI)regularly used for the symptomatic treatment of dementia: donepezil,rivastigmine and galantamine (Table 4). Clinical trials (the majority
B
A
A
A
�� ��28
lasting one year or less in duration) involving the use of donepezil,rivastigmine or galantamine that are conducted in patients with mildto moderate Alzheimer’s disease consistently demonstrate modestimprovement in (1) cognition and global functioning (on average, a3-point difference on the 70-point Alzheimer’s disease assessmentscale over a 6-month period), (2) activities of daily living and (3)neuropsychiatric symptoms (delay in emergence of symptoms,improvement in apathy, and variable patterns of improvement formilder degrees of anxiety, depression and hallucination).70-72 It isunclear whether AchEI therapy confers benefit in terms of reducingtime to institutionalisation.73 The duration of benefit may persist aslong as three years in some patients.74
Patients in whom the start of AchEI treatment is delayed maydemonstrate slightly reduced benefits as compared with those startedon AchEI early in the course of disease.75 Although the placebogroup did show improvement when switched to AchEI during open-label extensions of double-blind pivotal trials, they did not “catchup” with the group that received AchEI since trial inception.76 Thissuggests that AchEI may provide greater benefit when started as soonas dementia is diagnosed, rather than waiting until symptomsdeteriorate further and become more prominent. In addition, drugholidays should be discouraged as they can be associated withclinical deterioration that may not revert to baseline even onresumption of therapy.
A Acetylcholinesterase inhibitors can be considered for themanagement of moderate to severe Alzheimer’s disease.
Grade B, Level 1+
There is evidence to suggest that the cognitive, functional andbehavioural benefit of AchEI may extend to the more severe stagesof Alzheimer’s disease.77,78 A recent Swedish study found thatdonepezil improves cognition and preserves function in individualswith severe Alzheimer’s disease (Mini Mental State examinationscore 1-10) who were living in assisted care nursing homes.79
A Acetylcholinesterase inhibitors have been shown to be of clinicalbenefit and may be considered for use in the management of mild tomoderate vascular dementia.
Grade A, Level 1+
A
B
�� ��29
Deficient cholinergic neurotransmission has been postulated tocontribute to the cognitive impairment of vascular dementia. Tworandomized, double-blind, parallel-group, placebo-controlled trialswith a total of 1,219 people suffering from mild to moderateprobable or possible vascular dementia have been published.80,81
Donepezil, at doses of 5 or 10 mg a day was compared with placebofor 24 weeks. A meta-analysis that includes these studies showedthat the donepezil treated patients had a statistically significantlyimprovement in cognitive outcome compared to placebo treatedpatients on the cognitive subscale of the Alzheimer's DiseaseAssessment Scale (ADAS-Cog) as well as on the Mini-Mental StateExamination (MMSE) at 12 and 24 weeks at both doses. However,in terms of global function and activities of daily living, patientsshowed a less uniform dose response.82
Donepezil was well tolerated; most of the side effects were transientand were resolved by stopping the medication.
Moreover, galantamine showed statistically significant improvementsin cognition (ADAS-cog), global functioning (CIBIC-plus), activitiesof daily living (DAD) and behaviour (NPI) in patients with vasculardementia diagnosed according to recognised criteria combined with apopulation of patients with Alzheimer's disease and coincidentalradiographic findings of cerebrovascular disease.83
Thus, AchEI have been shown to be effective and safe for thetreatment of cognitive symptoms in vascular dementia. However, noAchEI has been licensed for the treatment of vascular dementia dueto concerns as to the aetiological heterogeneity of patients includedin the trials as well as lack of consistent effects on domains otherthan cognition.
B Acetylcholinesterase inhibitors can be considered for themanagement of dementia with Lewy bodies and Parkinson’s diseasedementia.
Grade B, Level 1+
There is growing appreciation that dementia with Lewy bodies(DLB) and Parkinson’s disease dementia (PDD) may actuallyrepresent different clinical manifestations of the spectrum of Lewybody synucleinopathies: the initial presentation is predominantlyneuropsychiatric in DLB and motor in PDD.
B
�0 ��30
Consistent with the neurobiochemical profile of cholinergic deficit inDLB, a study of 120 DLB patients reported that rivastigminesignificantly reduced the core psychiatric symptoms of apathy,anxiety, delusions and hallucinations while enhancing cognitiveperformance in tasks with a substantial attentional component,without worsening the motor symptoms of Parkinsonism.84,85
Similarly, in Parkinson’s disease dementia, a rivastigmine study of541 patients reported modest improvements in cognition mirroringthe degree seen in Alzheimer’s disease, as well as benefits inactivities of daily living and neuropsychiatric features.86 Althoughgenerally well tolerated, there were significantly more cholinergic-mediated adverse events such as nausea, vomiting and tremors in thetreated group.86
Clinical experience suggests that similar benefits in DLB and PDDmay be observed with other AchEI, although more robust data areneeded.87-89
B All three available acetylcholinesterase inhibitors (donepezil,rivastigmine and galantamine) can be considered for thepharmacological management of dementia, since there is no definiteevidence to support a difference in clinical efficacy between them.
Grade B, Level 1+
With regards to the three currently used AchEI (donepezil,rivastigmine and galantamine), there is very little to choose betweenthem in practice in terms of core efficacy. The few head-to-headcomparative studies are all industry sponsored, small, inconsistent inresults, and offer little basis to make a clinical choice.78,90 The choiceof AchEI therapy depends on the experience of the clinician,tolerance to side effects, ease of use, and the clinical profile of theindividual to be treated (such as weight, co-morbid diseases and druginteractions). For instance, where medication compliance is an issue,once-daily formulations would be helpful. For patients who requiremedications to be crushed due to swallowing difficulties, the capsuleformulations should be avoided (Table 4).
A Where tolerated, acetylcholinesterase inhibitors should be titratedto recommended doses (5-10 mg/day donepezil; 6-12 mg/dayrivastigmine; 16-24 mg/day galantamine), which have been shown toconfer greater benefit compared with lower doses.
Grade A, Level 1++
B
A
�0 ��31
To reduce intolerability to gastrointestinal adverse effects, AchEI areoften started at lower doses (donepezil 2.5 mg/day; rivastigmine 1.5mg twice daily; galantamine 8 mg/day) (Table 4). Studies haveconsistently shown that patients who received recommended doses ofAchEI exhibited better outcomes than those who received placebo orlower doses.70-72 Thus, where tolerated, AchEI should be graduallytitrated to recommended doses (5-10 mg/day donepezil; 6-12 mg/dayrivastigmine; 16-24 mg/day galantamine) over 4-8 weeks.
4.3.2 N-methyl D-aspartate (NMDA) antagonists
B N-methyl D-aspartate antagonists such as memantine can beconsidered for the management of moderate to severe Alzheimer’sdisease, either alone or in combination with acetylcholinesteraseinhibitors.
Grade B, Level 1+
Memantine appears to be beneficial alone or in combination withdonepezil for moderately advanced Alzheimer’s disease.91-93 A studyof moderate to severe Alzheimer’s disease patients on stable doses ofdonepezil (5-10 mg a day) reported that the addition of memantine20 mg a day slightly improved cognitive, functional and globalscores in comparison with patients taking placebo.92 Further analysisof the same study revealed that memantine reducedagitation/aggression in patients who were agitated at baseline anddelayed its emergence in those who were free of agitation atbaseline.93
B N-methyl D-aspartate antagonists such as memantine may be atreatment option for mild to moderate Alzheimer’s disease, ifacetylcholinesterase inhibitor therapy is contra-indicated, nottolerated or if there is disease progression despite an adequate trial ofacetylcholinesterase inhibitor.
Grade B, Level 1+
The efficacy of memantine in mild-to-moderate Alzheimer’s disease(alone or in combination with AchEI) has yet to be firmlyestablished.94 A recent study of memantine use in mild-to-moderateAD reported a small beneficial effect on cognition and behaviour, butnot function.95 Taken together, memantine may provide a treatmentoption if AchEI treatment is contra-indicated, not tolerated, or ifthere is disease progression despite an adequate trial of AchEI.
B
B
�� ��32
The initial dose of memantine is 5 mg once a day, with 5mgincrements at intervals of at least one week until a maximum of 10mg twice a day is achieved (Table 4). It should be used with cautionin patients with epilepsy and renal impairment, and the clinicianshould be aware of interactions involving commonly prescribedmedications such as dextromethorphan and L-dopa.
A N-methyl D-aspartate (NMDA) antagonists have been shown to beof clinical benefit and may be considered for use in the managementof mild to moderate vascular dementia.
Grade A, Level 1+
There have been 2 clinical trials of memantine in mild to moderatevascular dementia.96,97 A Cochrane review98 of these 6-month studiesshowed that whilst memantine improved cognition and behaviour theclinical global measures did not show a significant difference. Therewas no difference in drop-out or adverse event rates betweentreatment and placebo groups.
Thus, memantine has been shown to be effective and safe for thetreatment of cognitive symptoms in vascular dementia. However,memantine has not been licensed for the treatment of vasculardementia due to concerns as to the aetiological heterogeneity ofpatients included in the trials as well as lack of consistent effects ondomains other than cognition.
4.3.3 Other treatment modalities
B Practitioners who prescribe ginkgo for the treatment of dementiashould be aware of the unestablished benefit, variability of activeingredient among preparations, and potential for drug interactions.
Grade B, Level 1+
There is insufficient evidence to support that there is positive benefitof Ginkgo biloba on cognition and function in the treatment ofdementia.99 There are two negative studies100,101 and the magnitude ofbenefit is less potent compared with AchEI.102 Practitioners need tobe mindful that the dose of the active ingredient is not standardisedand may differ among the different preparations. There are alsoclinically relevant drug interactions involving ginkgo, such asincreased bleeding risk when combined with warfarin and antiplatelet
B
A
�� ��33
agents, and the antagonism of thiazides and anticonvulsants(valproate and carbamazepine).103
A Selegiline is not recommended for the treatment of core orassociated symptoms in Alzheimer’s disease.104
Grade A, Level 1++
GPP Appropriate treatment of vascular risk factors is recommendedfor all patients. However, it should be noted that whilst promisingobservational data exists, it remains to be shown in a randomisedcontrolled clinical trial if any prevention strategy such as bloodpressure reduction or antiplatelet treatment for the secondaryprevention of stroke, will reduce the incidence of vascular dementia.
GPP
4.3.4 Treatment considerations
GPP The decision to initiate costly symptomatic dementiatreatment, such as acetylcholinesterase inhibitors or N-methyl D-aspartate antagonists, should always be made in consultation with thepatient and family after careful consideration of the expectedmagnitude of benefit, side effects, co-morbidities and costs oftreatment.
GPP
Despite the evidence of efficacy from clinical studies, there is debateover whether AchEI and NMDA-antagonist therapy are costeffective, because the treatment effects are small and not alwaysapparent in practice.73,94,105,106 Cost-effectiveness issues becomeincreasingly relevant in the advanced stages of dementia, since themagnitude of treatment benefit becomes less obvious and there areoften competing demands on the available financial resources withregards to provision of care and placement. Until definitive findingsare available, practitioners should continue to individualise treatmentdecisions for each patient.54 For instance, where financial resourcesare limited, the opportunity cost of employing a maid to look after apatient requiring help with activities of daily living may override themodest benefits of symptomatic therapy.
GPP
A
GPP
�� ��34
For many, the diagnosis of dementia can be devastating and thus,individuals with dementia and their family may have high,sometimes unrealistic, expectations of any treatments offered. It istherefore important to communicate with the patient and hiscaregiver/family from the onset that54,106:
- The medications are not a cure.
- The medications may not work for everyone.
- Although there may be a response in terms of modestimprovement or stabilization of symptoms, symptomatic therapyultimately does not prevent progression of disease and cognitivedecline will continue even with treatment.
- The medication may be discontinued if the patient does notrespond after an adequate trial of 3-6 months.
GPP Patients who are started on acetylcholinesterase inhibitors orN-methyl D-aspartate antagonists, should be carefully monitored forside effects and response to treatment.
GPP
Although generally well tolerated, dose-related gastrointestinal sideeffects (nausea, vomiting, diarrhea, anorexia) are common withAchEI use. These are transient and often circumvented to a largeextent by a slower titration and taking the medication with food.Great caution should be exercised in those with bradycardia, sicksinus syndrome or cardiac conduction disturbances, in view ofpossible adverse effects of symptomatic bradycardia and syncope.Other less common side effects that have been reported includemuscle cramps, insomnia, vivid dreams and weight loss. DLB andPDD patients commenced on AchEI should be carefully monitoredfor worsening of motor symptoms. Compared with AchEI,gastrointestinal-related side effects are uncommon with memantineuse. Common adverse events of memantine include dizziness,headache, fatigue, hallucinations and confusion, but these tend to betransient.
GPP
�� ��35
Stabilisation or modest improvement above baseline may beobserved in the first 6-9 months, which can be monitored by the useof106,107:
(i) clinical methods, via assessment of cognitive, functional andbehavioural domains through interview with the patient andcaregiver; and/or
(ii) standardized rating scales, which involves either:
a. brief mental status tests such as the Chinese Mini MentalState Examination (CMMSE), Abbreviated Mental Test(AMT) and Elderly Assessment Cognitive Questionnaire(ECAQ), or
b. more detailed psychometric testing. After 6-9 months, alesser decline can be observed, which can be documented bypatient and caregiver interview for cognitive, functional andbehavioural (emergence of neuropsychiatric symptoms)features.107
A trial of withdrawal of symptomatic treatment should be consideredwhen the harm outweighs the benefit, and should be undertaken onlyafter careful discussion with the patient and caregiver.54 Examplesinclude intolerable or serious side effects, and progression of diseaseto the severe stages despite optimising treatment. When attemptingwithdrawal, it is important to monitor closely for any deterioration sothat therapy can be quickly reinstated to regain the same level ofsymptomatic effect.90
�� ��
36
Table 4 Dosing information of dementia drugs inclinical use
Medication Forms Dosinginterval
Startingdose
Recommendeddosing
(1) Cholinesterase inhibitorsDonepezil(Aricept®)
Tablet (5 mg, 10mg)
Once daily 2.5-5 mgonce daily
5-10 mg/day
Rivastigmine(Exelon®)
Capsule (1.5mg, 3 mg, 4.5mg, 6 mg)
Twice daily 1.5 mg bidafter meals
6-12 mg/day
Galantamine(Reminyl®)
PR Capsule (8mg, 16 mg and24 mg)*Solution (4mg/ml; 100 mlbottle)†
PR capsules:Once dailyOralsolutions:twice daily
8 mg oncedaily aftermeals
16-24mg/day
(2) NMDA antagonistsMemantine(Ebixa®)
Tablet (10 mg)Solution (10mg/g oraldrops)‡
Twice daily 5 mg oncedaily
CCT >60:20 mg/dayCCT 40-60:10 mg/day
(Source: British National Formulary; Geriatric Dosage Handbook, 11th Ed)
* PR: prolonged release once-a-day formulation. The immediate-releaseformulation has been phased out.
† Solution can be mixed with non-alcoholic beverage, but must be consumedimmediately.
‡ 10 drops = 5 mgCCT: Creatinine clearance
�� ��37
5 Management of Behavioural and PsychologicalSymptoms of Dementia (BPSD)
5.1 Non-pharmacological therapies (NPT)
GPP Non-pharmacological methods to manage behavioural andpsychological symptoms of dementia should be instituted, prior toconsideration of pharmacological measures.
GPP
Behavioural problems are a major cause of caregiver stress and oftenlead to premature institutionalisation of the patient. Factors such aspain or environmental triggers can be identified or manipulated anduse of other non-pharmacological methods to manage behaviouralproblems prior to as well as in conjunction with pharmacologicalmethods.
Problematic behaviours may respond to non-pharmacologicaltherapies (NPT). NPTs are based on theoretical frameworks thatconceptualize these behaviours, and four frameworks are particularlyrelevant.
First, the direct impact model whereby the behaviours are seen to bethe direct result of brain pathology. Second, the unmet needsmodel108, where unmet physical, emotional, spiritual andidiosyncratic needs underlie challenging behaviours. Behaviour isseen as a means of communication, a “cry for help” to fulfill a basichuman need. Third, the behavioural model109,110 assumesconnection between Antecedent, Behaviour and Consequence of thebehaviour (ABC model), where antecedents operate through stimuluscontrol, and the consequences reinforce behaviour. Modification ofthe behaviour would thus entail changing the antecedents and/or theconsequences. Last, the concept of progressively lowered stressthreshold111 (PLST) holds that dementia results in greatervulnerability to the environment, where minor stressors canprecipitate anxiety, agitation and even a catastrophic reactionbecause the person with dementia is more susceptible and less able tocope with stressors or triggers in the environment compared tocognitively normal elderly individuals. Often, more than one modelis needed to explain the problematic behaviour in question.
5 Management of Behavioural and Psychological Symptoms of Dementia (BPSD)
GPP
�� ��38
NPT are multifaceted and varied, and one form of intervention canbring about a broad range of effects. The appropriate NPTs areinstituted when a good understanding of the issues behind thebehaviour is procured. The following categories of NPT arenoteworthy but this list is not exhaustive:
1) Medical/nursing care interventions, e.g. pain management, reliefof fecal impaction and urinary retention, removal of restrainers,enhanced care methods such as person-centred showering andtowel bath.
2) Environmental interventions, e.g. dementia safe and friendlyenvironments, wandering paths, natural or enhancedenvironments, merry-walker.
3) Activities, e.g. structured activity programmes, physicalrehabilitation and physical exercises.
4) Social contact, e.g. one-on-one interaction, pet therapy,simulated presence.
5) Timalation (interaction in which the senses are the main focusfor engagement rather than interactions which involve anintellectual or emotional component), e.g. music, aromatherapy,massage, dance and movement, multi-sensory approaches suchas snozelen.
6) Standard psychological therapies, e.g. behavioural therapy,validation, resolution, reality orientation, reminiscence.
7) Alternative therapies, e.g. art therapy, bright-light therapy.
8) Staff training.
Although the research evidence for these therapies is varied, someinterventions being more evidenced-based than others, the reason forconsidering NPT first and as an enduring endeavour in addressingdifficult behaviour is two-fold. First, NPTs guided by anunderstanding of behaviour in the frameworks elaborated above,address the underlying reasons for the behaviour. Second,medications carry adverse side-effects and often mask and suppressthe behaviour that actually serves to communicate the need of theperson with dementia. Therefore, the appropriate approach mustentail trying to understand the etiology of the behaviour andaddressing the problem at its root cause.
�� ��39
5.2 Pharmacological interventions to manage BPSD
5.2.1 Antidepressants
GPP Antidepressants may be used for the treatment of comorbiddepression in dementia provided their use has been evaluated carefullyfor each patient.
GPP
The use of antidepressants for patients with dementia and depressivesymptoms is common, however, their efficacy on depression andcognitive function is weak.112,113
Evidence for use of older tricyclic antidepressants (clomipramine andimipramine) is weak.112 Selective serotonin reuptake inhibitor(SSRIs) which are commonly used to treat depression in the elderlydoes not appear effective in the treatment of neuropsychiatricsymptoms of dementia other than depression.112,113 No currentevidence is available on the newer antidepressants for treatment indementia (e.g. newer classes of antidepressants such as selectivenoradrenergic reuptake inhibitors).
5.2.2 Antipsychotics
A Conventional and atypical antipsychotics may be used withcaution, given their side effect profile, to treat neuropsychiatricsymptoms of dementia.
Grade A, Level 1+
Conventional antipsychoticsConventional antipsychotics have been used to treat behaviouralproblems associated with dementia. There is evidence for slightbenefit of haloperidol over placebo for treatment of aggression.However, adverse events of extrapyramidal side effects andsomnolence may limit its routine use.113 Low-potency antipsychoticslike chlorpromazine should be used with caution in view of posturalhypotension and anticholinergic side-effects.
Atypical antipsychoticsThe atypical antipsychotics, olanzapine and risperidone have beenshown to be modestly effective in the management of behavioural
GPP
A
�0 ��40
problems in patients with moderate to severe dementia at doses ofolanzepine at 5-10 mg/day and risperidone 1.0 mg/day.113-115 Thereis some evidence of quetiapine at doses of 25-100 mg/day showingimprovement in agitation scores.115,116 In frail elderly patients,titration of dosage should be based on individual responses, startingat the lowest possible dose with gradual increments.
However, adverse effects of somnolence (5-8 times greater) and gaitdisturbance is 7.5-11 times more common in olanzepine-treatedgroup compared to placebo.117 Serious adverse events occurred in16.8% of risperidone versus 8.8% of placebo group, including 5strokes and 1 transient ischaemic attacks, all in Risperidone group.118
Meta-analysis of adverse events performed showed 3-foldstatistically increased risk of cerebrovascular adverse events withRisperidone and Olanzepine (no statistically significant increase inmortality)119 while another meta-analysis comparing risk of deathwith atypical antipsychotics (Aripiprazole, Olanzepine, Risperidoneand Quetiapine) with placebo showed increase risk of death (OR1.54, 95% CI 1.06-2.23) with number need to harm = 100 (95% CI50-250).120 Other serious adverse events reported includedsomnolence and metabolic complications of hyperglycemia andweight gain.
Comparison between typical and atypical antipsychoticsComparing the efficacy of typical and atypical antipsychotics, thereis little good quality evidence to suggest one group is superior.
A recent retrospective cohort study had shown increased mortalityamong subjects using conventional antipsychotics compared toatypical antipsychotics.121
Thus, despite the risks of atypical antipsychotics, there is currentlyno evidence to suggest that typical antipsychotics are better.
5.2.3 Trazodone
B Trazodone may be considered for patients with depressivesymptoms and dementia associated agitation.
Grade B, Level 1+
B
�0 ��41
One small randomised controlled trial showed reduction in agitationwhen accompanied by depressive symptoms in patients withdementia.122
5.2.4 Mood stabilisers
A Routine use of mood stabilizers, such as carbamazepine andsodium valproate, is not recommended for treatment of behaviouralsymptoms associated with dementia.
Grade A, Level 1+
There is no improvement in behavioural symptoms with moodstabilizers (carbamazepine and sodium valproate).113
5.2.5 Benzodiazepines
There is no evidence of the efficacy of benzodiazepines in thetreatment of behavioural problems associated with dementia.
There are no systematic reviews or randomised controlled trials ofthe use of benzodiazepines in the management of behaviouralsymptoms of dementia.
5.2.6 Treatment considerations
GPP An individualized approach to managing behaviouralproblems in dementia patients is required.
GPP
GPP Cholinesterase inhibitor therapy may be considered intreatment of patients with behavioural problems if antipsychotics areinappropriate.
GPP
GPP The decision to start antipsychotic therapy to controlbehavioural problems in dementia patients should be made inconsultation with the patient and family, after careful considerationof the benefit, adverse-effects and co-morbidities.
GPP
GPP
A
GPP
GPP
�� ��42
In view of the potential adverse effects associated with antipsychotictherapy, non-pharmacological interventions and identification of painand other environmental factors should be assessed and managedaccordingly.
If the above fails and the behavioural problems are assessed to besignificant causing difficulty in caring process (medically andfunctionally) with significant amount of caregiver distress, there hasto be a discussion with the family members with regards toantipsychotic therapy, with the attendant risks of adverse effects(extrapyramidal side effects, somnolence, stroke, metaboliccomplications), especially in those patients with risk factors forcerebrovascular disease.
A recommended algorithm for management of neuropsychiatricsymptoms of dementia is available (see Figure 1).
B For patients with dementia with Lewy Body and behaviouralproblems, acetylcholinesterase inhibitors should be considered firstfor management of the behavioural problems.
Grade B, level 1+
Antipsychotic medication should be used cautiously in patientssuspected to have dementia with Lewy Body as these patients havemarked sensitivity to neuroleptic agents, including life-threateningneuroleptic malignant syndrome.123
There is evidence of improvement of neuropsychiatric symptomswith Rivastigmine therapy in dementia with Lewy Body patients (seeearlier section on acetylcholinesterase inhibitors treatment ondementia with Lewy Body).
GPP In all patients started on antipsychotic medication, they shouldbe monitored carefully for side effects and response to treatment. Inpatients who are stable, antipsychotic withdrawal should beconsidered.
GPP
B
GPP
�� ��43
Figure 1 Algorithm for management ofneuropsychiatric symptoms of dementia
Yes
YesNo
Yes
Yes
Yes
No
No
No
No
No
Patient with dementia and a behaviour problem
Evaluate for and manage delirium, pain, other medical and environmental causes of behaviour
Monitor for recurrence and adverse drug events
Begin non-pharmacological management directed at specific behaviour.Caregiver education
Does patient have symptoms of depression or anxiety? Monitor for recurrence
Is patient receiving a cholinesterase inhibitor? Begin antidepressant (e.g. SSRI)
Begin trial of cholinesterase inhibitor with orwithout Memantine
Behaviour problem improved?
Evaluate the behaviour problem (Antecedent, Behaviour and Consequence of Behaviour)
Begin trial of atypical antipsychotic medication
Behaviour problem improved?
Behaviour problem improved?
Monitor for extrapyramidal symptoms and sedation.Attempt to taper medication every 6 months
Begin trial of SSRI
Consider trial of mood stabilizers (valproate/carbamazepine). If still uncontrolled, consider
referral to specialist.
Monitor for recurrence andadverse effects
SSRI = selective serotonin reuptake inhibitorAdapted with permission from KM Sink et al. JAMA 2005;293; 596-608. Recommendedalgorithm for management of neuropsychiatric symptoms of dementia.
Behaviour problem improved?
Yes
�� ��44
6 Social and Caregiver Management of Dementiaand Community Resources
Psychosocial interventions are targeted at both the person withdementia as well as the family caregiver. The goal is to enableappropriate care to be given according to the needs of the person withdementia and his caregiver, and these needs vary depending on thetype and stage of dementia, as well as the systems in their ecologicalspace. As the person with dementia is, by nature of the disease,largely unable to help himself, most interventions are directed at thefamily caregiver to indirectly help the person with dementia. Theseinterventions are largely provided for by the community.
6.1 Family caregivers – rationale and role in dementiamanagement
Most patients with dementia are cared for in their own homes byfamily members. Caregiver management is important for thefollowing reasons:1) Family caregivers need to be empowered with the necessary
knowledge and skills, and psychosocial support to facilitate themin their task.
2) Family caregivers who face much negative consequences as aresult of long-term caregiving need to be helped and supported.
Caregiver intervention can take several forms and they include:1) Education sessions to impart knowledge on dementia and
caregiving skills such as communication and behaviouraltechniques
2) Individual and family counselling3) Regular caregiver support group meetings4) Continuous availability of health care professionals and
counsellors to provide support and help with crises and thechanging nature of the patient’s symptoms
5) Respite care6) Technology-based interventions
A Caregiver interventions via a multifaceted approach should beconsidered in the total management of the person with dementia.
Grade A, Level 1+
6 Social and Caregiver Management of Dementia and Community Resources
A
�� ��45
Several caregiver interventions have yielded promising results, theNYU spouse-caregiver intervention14,124,125 and the REACH126
(Resources for Enhancing Alzheimer’s Caregiver Health) initiativeare noteworthy. They have been shown to reduce caregiver burdenand depression, ease caregiver reaction to behavioural problems anddelay nursing home placement. A meta-analysis127 also found thatcounselling and training caregivers in how best to care hadmoderate, statistically significant results. Multi-componentinterventions have a greater effect than narrowly focused ones. Asupport system that can meet the individual needs of differentcaregivers, and be able to provide on-going support that isresponsive and continuous is most beneficial.
In addition, technology-based interventions such as web-basedlearning, on-line discussions and support groups, andtelecommunications systems have burgeoned in recent years.Improvements in caregiver outcomes like depression and strain havebeen demonstrated in interventions involving technology.128,129
Caregivers also report they find the on-line resources useful andappreciate the ability to communicate with each other and health careprofessionals.130 Given the rapid advancement and easy availabilityof technology, it should be harnessed more fully to make helpavailable to more family caregivers in a continuous, timely andeconomical way.
GPP Where appropriate, respite care can be offered to relieve theburden of caregiving on the family caregiver.
GPP
Respite care can take place in the home of the person with dementiaor a daycare centre. It may also vary in terms of who provides care;trained staff, relatives of the patient or volunteers. The care providedcan also differ in duration, ranging from a couple of hours to weeks.Caregivers often express the need for respite to allow them sometimeto rest, rejuvenate and have some moment to themselves. Althoughthe few trials performed have not shown improvements in caregiverburden, improved caregiver satisfaction is reported.131,132 Asystematic review133 failed to show any benefit in caregiver outcomesbut as the review was only based on 3 studies that met inclusioncriteria, this reflects the lack of high quality research rather than anactual lack of benefit.
GPP
�� ��46
6.2 Community resources
GPP Referral to community resources to meet the care needs of theperson with dementia and his/her carer should always be considered.
GPP
Integral to a comprehensive management plan is the referral ofpeople with dementia to appropriate community resources. Thisassists in providing care and improving quality of life of both thepatient and the caregiver. Generic eldercare services such as mealservices, home help, befriender services, case management, homemedical, home nursing and social day care services have alreadybeen established and some agencies are able to accommodate peoplewith dementia on an ad hoc basis. However, referrals to specialiseddementia services may be more suitable as such facilities havetrained staff and special programmes for dementia. At present,dementia day care centres and nursing homes form the core ofdementia services locally. It has been shown that the structured,social and modestly stimulating environment provided by a dementiaprogramme, often offered in dementia day care centres and somenursing homes, can improve the well-being of people withdementia.134 The benefits of caregiver intervention and respite havebeen elucidated above. Other services such as home based dementiacare and home respite care are still not well developed. Finally,organisations providing dementia care can also act as a resourcecentre that provides information, support, training and education forcaregivers. The range of dementia services currently available areshown in Annex 1.
GPP
�� ��47
7 Ethical Issues in Dementia
7.1 Preamble
Dementia is a clinical syndrome characterized by global cognitivedecline and impairments, which result in a loss of a patient’sindividuality and autonomy. At different stages, the disease causesdifferent extents of functional decline, and different severities inbehavioural and psychiatric symptoms. The disease also results invarying extents of impairments in decision-making capacity, and atsome point, a patient becomes mentally incompetent and ceases to bean autonomous agent.
Nevertheless, the dignity of the patient should be respected at allstages irrespective of the patient’s functional status. Therapeuticgoals and treatment options that are coherent and appropriate topatient’s functional status should be individually tailored andadjusted at different stages of dementia, with an emphasis on qualityfor life of the patient, as well as the caregiver. The importantquestion to ask for each individual patient is therefore what value oflife holds for the patient, and directed at how life is experienced bythe patient under the contextual circumstances specific to the patient.It is important to distinguish such evaluations from morallyinappropriate social-worth evaluations, which base treatmentdecisions on an individual’s ability to contribute to society.135 Thegeneral ethical imperative must be to delay, prevent, stabilisedementia, but not to protract life and morbidity artificially in thesevere stages of the disease.136
7.2 Decision-making
1. Respect for autonomous decision making is a fundamentalethical and legal right of a mentally competent individual. Thisright of self-determination should be respected to the fullestpossible extent, even in dementia or conditions associated withcognitive impairment.
2. When affected by dementia, the key to a patient’s right ofautonomy is the presence of adequate decision-making capacity.As a patient’s cognition and hence functional abilities fordecision making is impaired in dementia, a patient may or may
7 Ethical Issues in Dementia
�� ��48
not possess adequate decision making capacity to make aninformed choice.
3. A diagnosis of dementia per se, however, does not automaticallyimply a loss of decision making capacity, which is specific toeach patient and to each medical decision. Therefore, those whocannot comprehend complex situations may still possess thecapacity to make simple decisions, or to convey their opinionsregarding the burdens and benefits of ongoing treatments.
4. In deciding if a patient with dementia possesses adequatecapacity with respect to making a particular decision, a clinicalevaluation of the following functional abilities should bemade137:a. Ability to express a choiceb. Ability to understand information providedc. Ability to appreciate significance of information and
relevance to selfd. Ability to manipulate information rationally before arriving
at a decision5. If the patient lacks adequate decision making capacity, the
ethical imperative switches to one that aims to protect the patientfrom his or her own harmful decisions or actions. Patients mustnot be under-treated nor forced to receive inappropriatetreatment just because they lack decision making capacity orlegally appointed guardian(s). Consideration of the patient’sfunctional status and quality of life is vital in making treatmentdecisions for the patient.
6. In Singapore, treatment decisions for a patient who is incapableof giving a valid consent will be made:a. in immediate, life threatening emergencies by doctors, based
on the principle of medical necessityb. in less emergent situations, by:
i. legal guardian (Committee of Person) appointed under theMental Disorder and Treatment Act (Cap 178, 1985 RevEd)138
ii. the doctor, in accordance to principle of best interests (inthe absence of any legally appointed guardian).Nevertheless, this does not exempt the doctor fromcommunicating with patient’s family members andcaregivers, so as to incorporate patient’s known valuesand established preferences in the determination ofpatient’s best interests. The opinions and sentiments of
�� ��49
the patient’s family ought to be sought, but they are notlegally binding.139
7. For patients adjudged clinically to have permanent and globaldecisional incapacity as a result of dementia, decisions abouthealth care will be recurrent over their remaining lifetime.Therefore, when such issues arise, the attending physician maywish to consider a formal application should be made to theHigh Court for the declaration of mental incompetence and forthe formal appointment of guardianship (committee of person(s)and committee of estate) under the provision of the MentalDisorder and Treatment Act (MDTA).
7.3 Genetic testing
1. As with any medical test, the decision regarding the utility of agenetic test should take into consideration the benefits to theindividual patient and the ways that a test result would modifythe care that the patient would receive.
2. As in any genetic testing, especially in pre-symptomaticsusceptibility testing, individuals must be clearly informedregarding140:a. potential for severe psychological complications of testing
positive for an incurable, devastating illnessb. potential ramifications in the area of employment and
medical insurancec. probabilistic implications of a positive test on genetically
related family members, who may not have participated inany counselling or consented to testing
APOE ε43. There is a body of evidence that APOE ε4 is strongly associated
with late-onset Alzheimer’s Disease (AD) and that when presentmay represent an important risk factor for the disease. However,at the present time, it is not recommended for use in routineclinical diagnosis nor should it be used for predictive testing.a. APOE genotyping does not provide sufficient sensitivity or
specificity to be used alone as a diagnostic test for AD.141 Itis therefore not recommended as a diagnostic tool in routineclinical evaluation of patients for sporadic early- and late-onset AD.136,141-147
b. Based on presently available data, APOE genotyping is notestablished as a predictive marker of AD. Furthermore,
�0 ��50
APOE testing does not provide any medically usefulinformation linked to treatments that are effective inpreventing or delaying the onset of disease. Therefore,susceptibility testing in asymptomatic individuals is notrecommended and may be associated with potentialpsychological harm.136,142-144
7.4 Driving
1. Driving a motor vehicle is a complex task that requires thesimultaneous and coordinated application of different cognitiveabilities including ability to recall and apply traffic rules, soundjudgement, attention span, and quick responses. A person’sability to drive safely can therefore be affected in dementia,148,149
with consequently higher risk of accidents.150,151
2. Driving also represents independence, freedom and mobility.The issue of driving in dementia requires therefore the balancingof individual freedom and patient confidentiality on one sideversus public and patient safety on the other.152
3. Dementia adversely affects driving performance even in its mildstages, although some persons with late-onset Alzheimer’sdisease DAT appear capable of driving safely for some timeafter disease onset.148 A diagnosis of dementia therefore does notautomatically mean that a person is incapable of driving.148,153,154
The decision should be based on dementia severity or ademonstration of impaired driving competence.148
4. Longitudinal data suggests that driving performance deterioratesas the severity of dementia progresses over time,155 primarily inearly dementia. In one study, drivers with AD at a severity ofCDR 1 were found to pose a significant traffic safety problemboth from crashes and from driving performancemeasurements.148
5. In patients with mild to moderate dementia, physicians find itdifficult to identify which individuals should not drive.Performance-based measures of driving skills, such as on-roaddriving tests, are recommended as a means of assessing drivingcompetency.156,157 A traffic-interactive, performance-based roadtest that examines cognitive behaviours provides an accurate andreliable functional assessment of driving ability.148
6. Even if a driver with early dementia passes a road test,progression of the disease is expected to lead to deterioration indriving skills.155 Therefore, repeat road testing at regular
�0 ��51
intervals, usually 6 to 12 months, or earlier if suggested bysignificant cognitive decline, is important.
7. For patients who are assessed to be unsafe for driving, doctorsshould enlist the help of family members to persuade patient tostop driving. To encourage such patients to surrender theirdriving licences, alternative forms of transport should bearranged, where possible.158 If the patient is absolutely inflexibleand insists on driving, thereby creating a reasonable risk topublic safety, it is then ethically and professionally permissiblefor the doctor to breach doctor-patient confidentiality and file areport to the relevant licensing authorities.136 Other measuresdeemed to be ethical include hiding the patient’s car keys orimmobilising the car if necessary.159
7.5 Truth-telling of diagnosis to patient
1. Although patients generally would like to know the truth abouttheir own medical condition, the rights of those who do not wantto know should also be respected. Health care professionalsshould therefore seek to understand their patients' preferenceswith respect to the diagnosis of dementia and act appropriatelyaccording to their choice.160
2. Studies have shown that the vast majority of patients with milddementia wish to be fully informed.161,162 Therefore, unless apatient suffering from dementia explicitly declines to beinformed of the diagnosis, the default mode should be to informtruthfully as it will enable the patient to:a. plan for optimal life experiences in remaining years of intact
capacitiesb. designate and appoint a surrogate decision maker to take
over the making of treatment decision upon eventualincompetence
c. settle personal financial and legal mattersd. participate in treatment decisionse. consider possible enrolment in research programmes and
participate in informed consent process3. When informing the diagnosis, the doctor needs to take into
account the patient and family’s prior knowledge and theirperception of the problems. The doctor should also be mindfulof the impact the diagnosis can have on the patient’s life andfamily relationships. The communication should therefore beconducted sensitively and empathically, and should include a
�� ��52
discussion on treatment options and available support servicesboth in the hospital and the community.
4. After the diagnosis has been communicated, the patient andfamily should be given time to process the information and tocome to terms with it. They should be given ample opportunityto ask questions and seek clarification from the doctor.
5. The objectives of truthful disclosure of diagnosis to patientswith dementia are to empower the patient with: the courage torequest for information, the cognition to understandinformation and the strength and resources to cope with theburden of information.
7.6 Restraints
1. Restraints, whether environmental, physical orpharmacological, are used in the management of patients withdementia to restrict or control the patient’s movement orbehaviour that may compromise the safety of the patient and/orothers.
2. However, the use of restraints is not without potentialproblems:a. Risk of harm and injuryb. Decrease in ability to perform cognitive and physical
activities, thereby resulting in cognitive and functionaldecline, and ultimately loss of independence
c. Loss of freedom, leading to loss of confidence and self-esteem
3. The preferred choice should therefore be to avoid the use ofrestraints. Restraints should not be a substitute for a proactivesearch for reversible precipitating factors for patient’sbehavioural problems, or for good communication with thepatient.
4. If restraints have to be used on a patient, it should be seen as atemporary means and should be stopped as soon as theindication is no longer present. Excessive use of restraintsshould be avoided - any restraint should therefore be institutedfor the minimal period of time and at the minimal strength ordegree needed to achieve the intended outcome for the patient.The patient should also be carefully monitored while onrestraints.
�� ��53
7.7 Living alone
1. Many patients diagnosed to have dementia continue to insist onliving alone. In some of these patients, cognitive decline arisingfrom dementia leads to poor compliance with medical treatment,lack of safety awareness and poor judgement. All these can posea risk to the safety and well-being of the patient. The patientmay also be exposed, as a result, to mistreatment, fraud andexploitation by others.
2. A diagnosis of dementia does not automatically mean that thepatient is incapable of living alone. This decision should bebased on an assessment of the patient’s decision making capacitywith respect to placement, and ability to continue living alone inthe community without posing too much risk to self and toneighbours. Considerations should also be given to the potentialnegative social and physical impact of moving from a familiarenvironment to institutional care.
3. If the patient is assessed to have adequate decision makingcapacity and insists on living alone, the health care professionalsshould then support the decision by simplifying the daily tasks athome and using available community resources. The patientshould also be reassessed as the dementia progresses and erodesboth his decisional capacity and ability for self-care.
4. If the patient has doubtful decisional capacity, then there shouldbe an assessment, preferably with the occupational therapist, onthe following: safety to self and to neighbours when carrying outactivities of daily living and tasks such as food preparation,handling of monies, laundry and compliance to medication.
5. The final objective is to provide the patient with dementia with asafe, familiar and comfortable living environment, and to avoidpremature institutionalisation.
�� ��54
8 Cost-effectiveness
There are currently no local data on cost effectiveness ofpharmacological agents, non-pharmacological methods andcomplex caregiver intervention programmes in dementia.
Due to the different healthcare funding mechanisms in othercountries, we are thus unable to extrapolate from cost-effectivenessstudies from overseas countries.
8 Cost-effectiveness
�� ��55
9 Clinical Quality Improvement
The following clinical audit parameters, based on recommendationsin these guidelines are proposed:
1. Percentage of patients whose caregiver report subjectivememory complaints underwent cognitive evaluation withsubsequent appropriate management.
2. Percentage of patients newly diagnosed with dementia who hadsubsequent multi-pronged strategy to dementia managementthat encompasses education of patient and caregiver, non-pharmacological measures and comprehensive caregiverpsychosocial intervention.
3. Percentage of patients newly diagnosed with dementia,institution of cognitive enhancers such as acetylcholinesteraseinhibitors or N-methyl D-aspartate antagonists, was made inconsultation with the patient and family after carefulconsideration of the expected magnitude of benefit, sideeffects, co-morbidities and costs of treatment.
4. Percentage of patients newly diagnosed with dementia withsignificant behavioural problems, appropriate non-pharmacological management was instituted prior toconsideration of pharmacological agents.
5. Percentage of patients newly diagnosed with dementia withsignificant behavioural problems despite non-pharmacologicalmanagement, institution of antipsychotic therapy was made inconsultation with the patient and family, after carefulconsideration of the benefit, adverse-effects and co-morbidities.
6. Percentage of patients newly diagnosed with dementia who hada referral to community resources to meet the care needs of theperson with dementia and his caregivers.
9 Clinical Quality Improvement
�� ��56
Annex 1
Diagnosis and treatment
1 Alexandra HospitalGeriatric MedicineClinic
378 Alexandra RoadSingapore 159964
Tel. 64768828 (Appointment) 63793420 (M Clinic)Fax: 63793880
2 Changi General HospitalMemory Clinic
2 Simei Street 3Singapore 529889
Tel. 68503333Fax: 67872141
3 Institute of MentalHealthPsychogeriatric Clinic
10 Buangkok ViewSingapore 539747
Tel. 63892200Fax: 63851075
4 National UniversityHospitalNeuroscience Clinic
5 Lower Kent RidgeRoadSingapore 119074
Tel. 67795555Fax: 67795678
5 Singapore GeneralHospitalDept of Neurology
Geriatric Medicine UnitClinic
Outram RoadSingapore 169036
Tel. 63214377(Central Appt)Fax: 62203321Fax:62243655
6 Tan Tock Seng HospitalGeriatric MedicineClinic
11 Jalan Tan TockSengSingapore 308433
Tel: 63578013Fax: 63578682
57
Dementia day care centres
1 Alzheimer’s DiseaseAssociation(New Horizon Centre –Toa Payoh)(Has an Early DementiaProgramme)
Blk 157, Toa PayohLor 1 #01-1195Singapore 310157
Tel: 63538734Fax: 63538518
2 Alzheimer’s DiseaseAssociation(New Horizon Centre –Bukit Batok)(Has an Early DementiaProgramme)
Blk 511, Bukit BatokSt. 52 #01-211Singapore 650511
Tel: 65659958Fax: 65652257
3 Alzheimer's DiseaseAssociation - (NewHorizon Centre-Tampines)
Tampines Polyclinic(Level 3)1 Tampines Street 41Singapore 529203
Te. 67865373Fax: 67849587
4 Apex Harmony Lodge 10 Pasir Ris Walk Singapore 518240
Tel: 65852265Fax: 65852982
5 Sunlove Dementia DayCare Centre
70 Buangkok ViewSingapore 534190
Tel: 63873593Fax: 63863716
6 Sunshine WelfareAction Mission(SWAMI) DementiaDay Care Centre
5 Sembawang WalkSingapore 757717
Tel: 62576117Fax: 67548443
7 Thong Teck Home forSenior Citizens (DayCare Centre)
91 Geylang EastAvenue 2Singapore 389759
Tel: 68460069Fax: 68460396
8 Yong-en DementiaDay Care Service
Blk 335A Smith Street,#03-57Singapore 051335
Tel: 62251002Fax:62255218
Annex 1
�� ��57
Dementia day care centres
1 Alzheimer’s DiseaseAssociation(New Horizon Centre –Toa Payoh)(Has an Early DementiaProgramme)
Blk 157, Toa PayohLor 1 #01-1195Singapore 310157
Tel: 63538734Fax: 63538518
2 Alzheimer’s DiseaseAssociation(New Horizon Centre –Bukit Batok)(Has an Early DementiaProgramme)
Blk 511, Bukit BatokSt. 52 #01-211Singapore 650511
Tel: 65659958Fax: 65652257
3 Alzheimer's DiseaseAssociation - (NewHorizon Centre-Tampines)
Tampines Polyclinic(Level 3)1 Tampines Street 41Singapore 529203
Te. 67865373Fax: 67849587
4 Apex Harmony Lodge 10 Pasir Ris Walk Singapore 518240
Tel: 65852265Fax: 65852982
5 Sunlove Dementia DayCare Centre
70 Buangkok ViewSingapore 534190
Tel: 63873593Fax: 63863716
6 Sunshine WelfareAction Mission(SWAMI) DementiaDay Care Centre
5 Sembawang WalkSingapore 757717
Tel: 62576117Fax: 67548443
7 Thong Teck Home forSenior Citizens (DayCare Centre)
91 Geylang EastAvenue 2Singapore 389759
Tel: 68460069Fax: 68460396
8 Yong-en DementiaDay Care Service
Blk 335A Smith Street,#03-57Singapore 051335
Tel: 62251002Fax:62255218
�� ��58
Nursing homes with dementia facilities
Carers support groups
1 Alexandra HospitalGeriatric Centre(Support Group inEnglish)
378 Alexandra RoadSingapore 159964
Tel: 63793420Fax: 64714508
2 Alzheimer’s DiseaseAssociation(Support Groups inEnglish, Mandarin andMalay)
Blk 157, Lorong 1,Toa Payoh#01-1195Singapore 310157
Tel: 63538734Fax: 63538518
3 O’Joy Care Services(Support Group inMandarin)
701 Geylang RoadTeambuild Centre#03-03Singapore 389687
Tel: 67490190
1 Apex Harmony Lodge 10, Pasir Ris WalkSingapore 518240
Tel. 65852265Fax:65852982
2 Ju Eng Home for SeniorCitizens
205 Jalan KayuSingapore 799436
Tel. 64846891Fax: 64846892
3 Ling Kwang Home forSenior Citizens
156 Serangoon GardenWaySingapore 556055
Tel. 62875466Fax: 62843567
4 Lions Home for theElders
41 Toa Payoh RiseSingapore 298101
Tel. 62529900Fax: 63535725
5 Peacehaven NursingHome for the Aged
9, Upper Changi RdNorthSingapore 507706
Tel. 65465678Fax: 65461831
6 Sunshine WelfareAction Mission(SWAMI) Home
5 Sembawang WalkSingapore 757717
Tel. 62576117Fax: 67548443
59
Training in dementia
1 Alzheimer’s DiseaseAssociation ( includingdomestic helpers)
Blk 157, Lorong 1, ToaPayoh#01-1195Singapore 310157
Tel: 63538734Fax: 63538518
2 TSAO FoundationSingapore
5, Temasek Boulevard, #12-06 Suntec TowerFiveSingapore 038985
Tel: 64332740
Home-based care
1 Aged PsychiatryCommunity Assessmentand Treatment ServiceInstitute of MentalHealthDepartment of GeriatricPsychiatry
10 Buangkok ViewSingapore 539747
Tel. 63892175Fax: 63851051
�� ��59
Training in dementia
1 Alzheimer’s DiseaseAssociation ( includingdomestic helpers)
Blk 157, Lorong 1, ToaPayoh#01-1195Singapore 310157
Tel: 63538734Fax: 63538518
2 TSAO FoundationSingapore
5, Temasek Boulevard, #12-06 Suntec TowerFiveSingapore 038985
Tel: 64332740
Home-based care
1 Aged PsychiatryCommunity Assessmentand Treatment ServiceInstitute of MentalHealthDepartment of GeriatricPsychiatry
10 Buangkok ViewSingapore 539747
Tel. 63892175Fax: 63851051
�0 ��60
References
1. Wimo A, Winbald B, Aguero-Torres H, von Strauss E. Themagnitude of dementia occurrence in the world. Alz Dis AssocDisord 2003; 17(2):63-7.
2. Asia Pacific Members of Alzeimer's Disease International. Dementiain the Asia Pacific Region: The epidemic is here. Alzeimer's DiseaseInternational 2006. Available at:http://www.accesseconomics.com.au/publicationsreports/search.php?searchby=year&searchfor=2006
3. Inter-Ministerial Committee on Health Care for the Elderly 1999.
4. Kua EH. The prevalence of dementia in elderly Chinese. ActaPsychiatr Scand 1991;83:350-2.
5. Kua EH, Ko SM. Prevalence of dementia among elderly Chinese andMalay residents of Singapore. Int Psychogeriatr 1995; 7:439-46.
6. Lim HJ, Lim JP, Anthony P, Yeo DH, Sahadevan S. Prevalence ofcognitive impairment amongst Singapore’s elderly Chinese: acommunity-based study using the ECAQ and the IQCODE. Int JGeriatr Psychiatry 2003; 18:142-8.
7. Chiam PC, Ng TP, Tan LL, Ong PS, Ang A, Kua EH. Prevalence ofdementia in Singapore – Results of the National Mental HealthSurvey of the Elderly 2003.Ann Acad Med Singapore 2004; 33(5Suppl): S14-5.
8. Ferri CP, Prince M, Brayne C, Brodaty H, Fratiglioni L, Ganguli M,Hall K, Hasegawa K, Hendrie H, Huang Y, Jorm A, Mathers C,Menezes PR, Rimmer E, Scazufca M; Alzheimer's DiseaseInternational. Global prevalence of dementia: a Delphi consensusstudy. Lancet. 2005;366(9503):2112-7.
9. Kua EH, Shen YC. Epidemiology of dementia in elderly Chinese – across national comparison of Singapore and Beijing. Neurobiology ofAging, 17 (1996) : 39-40.
References
�0 ��61
10. Ampil ER, Fook-Chong S, Sodagar SN, Chen CP, Auchus AP.Ethnic variability in dementia: results from Singapore. AlzheimerDis Assoc Disord. 2005;19(4):184-5.
11. Kua EH, Ko SM. Prevalence of dementia among elderly Chinese andMalay residents in Singapore. International Psychogeriatrics;(1995):439-446
12. Kua EH, Tan SL. Stress of caregivers of dementia patients in theSingapore Chinese Family. International Journal of GeriatricPsychiatry 1997, 12: 466-469.
13. Lim PP, Sahadevan S, Choo GK, Anthony P. Burden of caregiving inmild to moderate dementia: an Asian experience. Int Psychogeriatr1999;11:411-20.
14. Mittelman MS, Ferris SH, Shulman E, Steinberg G, Levin B. Afamily intervention to delay nursing home placement of patients withAlzheimer’s disease.A randomized controlled trial. JAMA 1996;276:1725-31.
15. Li M, Ng TP, Kua EH, Ko SM. Brief Informant Screening Test forMild Cognitive Impairment and Early Alzheimer Disease. DementGeriatr Cogn Disord 2006; 21:392-402.
16. Chong MS, Chin JJ, Saw SM, Chan SP, Venketasubramanian N, TanLC, Hong CY, Sahadevan S. Screening for dementia in the olderChinese with a single question test on progressive forgetfulness. Int JGeriatr Psychiatry. 2006;21(5):442-448.
17. American Psychiatric Association. Diagnostic and Statistical Manualof Mental Disorders. Fourth ed. Washington, DC: 1994:142-3.
18. Holmes C, Cairns N, Lantos P, Mann A. Validity of current clinicalcriteria for Alzheimer’s disease, vascular dementia and dementiawith Lewy bodies. Br J Psychiatry 1999; 174:45-50.
19. Jobst KA, Barnetson LP, Shepstone BJ. Accurate prediction ofhistologically confirmed Alzheimer’s disease and the differentialdiagnosis of dementia: the use of NINCDS-ADRDA and DSM-III-Rcriteria, SPECT, X-ray CT, and ApoE 4 in medial temporal lobe
�� ��62
dementias. Oxford Project to Investigate Memory and Aging. IntPsychogeriatr 1998; 10:271-302.
20. Lim A, Tsuang D, Kukull W, Nochlin D, Levernz J, McCormick W,et al. Clinico-neuropathological correlation of Alzheimer’s disease ina community-based case series. J Am Geriatr Soc 1999; 47:564-9.
21. Jorm AF, Scott R, Cullen JS, MacKinnon AJ. Performance of theInformant Questionnaire on Cognitive Decline in the Elderly(IQCODE) as a screening test for dementia. Psychol Med 1991;21:785-90.
22. Lim HJ, Lim JP, Anthony P, Yeo DH, Sahadevan S. Prevalence ofcognitive impairment amongst Singapore’s elderly Chinese : acommunity-based study using the ECAQ and the IQCODE. Int JGeriatr Psychiatry 2003; 18:142-8.
23. Kua EH, Ko SM. A questionnaire to screen for cognitive impairmentamong elderly people in developing countries. Acta Psychiatr Scand1992 Feb; 85:119-22.
24. Kua EH, Ko SM. Prevalence of dementia among elderly Chinese andMalay residents of Singapore. Int Psychogeriatr 1995; 7:439-46.
25. Sahadevan S, Lim PP, Tan NJ, Chan SP. Diagnostic performance oftwo mental status tests in the older Chinese: influence of educationand age on cut-off values. Int J Geriatr Psychiatry 2000; 15:234-41 .
26. Sahadevan S, Lim JP, Tan NJ, Chan SP. Psychometric identificationof early Alzheimer disease in an elderly Chinese population withdiffering educational levels. Alzheimer Dis Assoc Disord 2002;16:65-72.
27. Tham W, Auchus AP, Thong M, Goh ML, Chang HM, Wong MC, etal. Progression of cognitive impairment after stroke: one year resultsfrom a longitudinal study of Singaporean stroke patients. J NeurolSci 2002; 203:49-52.
28. Eastwood MR. Abnormal behavior associated with dementia. IntPsychiatry Today 1994; 4:8-10.
�� ��63
29. Mega MS, Cummings JL, Fiorello T et al. The spectrum ofbehavioral changes in Alzheimer’s disease. Neurology 1996; 46:130-5.
30. Reisberg B, Borenstein J, Salob SP, Ferris SH, Franssen E,Georgotas A. Behavioral symptoms in Alzheimer’s disease:phenomenology and treatment. J Clin Psychiatry 1987; 48:9-15.
31. Cummings JL, Mega M, Gray K, Rosenberg-Thompson S, CarusiDA, Gornbein J. The Neuropsychiatric Inventory: comprehensiveassessment of psychopathology in dementia. Neurology 1994;44:2308-14.
32. Lim PP, Ng LL, Chiam PC, Ong PS, Ngui FT, Sahadevan S.Validation and comparison of three brief depression scales in anelderly Chinese population. Int J Geriatr Psychiatry 2000; 15:824-30.
33. Alexopoulos GS, Abrams RC, Young RC , Shamoian CA. Cornellscale for depression in dementia. Biol Psychiatry 1988; 23:271-84.
34. Lam CK, Lim PP, Low BL, Ng LL, Chiam PC, Sahadevan S.Depression in dementia: a comparative and validation study of fourbrief scales in the elderly Chinese. Int J Geriatr Psychiatry2004;19(5):422-8.
35. MS Chong, S Sahadevan. An Evidence-Based Clinical Approach tothe Diagnosis of Dementia. Ann Acad Med Singapore 2003; 32:40-8.
36. American Psychiatric Association. Diagnostic and Statistical Manualof Mental Disorders. Third ed. Washington, DC,1987.
37. Morris J C. The Clinical Dementia Rating (CDR): current versionand scoring rules. Neurology 1993 ; 43:2412-4.
38. Lim WS, Chin JJ, Lam CK, Lim PP, Sahadevan S. Clinical dementiarating: experience of a multi-racial Asian population. Alzheimer DisAssoc Disord 2005;19(3):135-42.
39. Cham GW, Seow E. The pattern of elderly abuse presenting to anemergency department. Singapore Med J 2000; 12:571-4.
�� ��64
40. Neuropathology Group, Medical Research Council CognitiveFunction and Aging Study. Pathological correlates of late-onsetdementia in a multicentre, community-based population in Englandand Wales. Neuropathology Group of the Medical Research CouncilCognitive Function and Ageing Study (MRC CFAS). Lancet 2001;357(9251):169-75.
41. Larson EB, Reifer BV, Sumi SM et al. Diagnostic tests in thevaluation of dementia. A prospective study of 200 elderlyoutpatients. Arch Intern Med 1986;146: 1917-20.
42. Clarfield AM. The reversible dementia: do they reverse? Arch InternMed 1988; 109: 476-86.
43. Walstra GJ. Teuniesse S, Van Gool WA, et al. Reversible dementiain elderly patients referred to a memory clinic. J Neurol 1997; 224:17-22.
44. Siu AL. Screening for dementia and investigating its causes. AnnIntern Med 1991; 115: 122-32.
45. Patterson CJ, Gauthier S, Bergman H, Cohen CA, Freightner JW,Feldman H, et al. The recognition, assessment and management ofdementing disorders: conclusions from the Canadian ConsensusConference on Dementia. CMAJ 1999; 160:S1-15.
46. Sitoh YY, Kanagasabai K, Sitoh YY, Earnest A, Sahadevan S.Evaluation of Dementia: The Case for Neuroimaging All Mild toModerate Cases. Ann Acad Med Singapore 2006; 35:383-9.
47. McKhann G, Drachman D, Folstein M, Katzman R, Price D, StadlanEM. Clinical diagnosis of Alzheimer’s disease: report of theNINCDS-ADRDA Work Group under the auspices of Department ofHealth and Human Services Task Force on Alzheimer’s disease.Neurology 1984; 34:939-44.
48. Roman GC, Tatemichi TK, Erkinjuntti T, Cummings JL, Masden JC,Garcia JH, et al. Vascular dementia: diagnostic criteria for researchstudies. Report of the NINDS-AIREN International Workshop.Neurology 1993; 43:250-60.
�� ��65
49. Chui HC, Victoroff JI, Margolin D, Jagust W, Shankle R, KatzmanR. Criteria for the diagnosis of ischemic vascular dementia proposedby the State of California Alzheimer’s Disease Diagnostic andTreatment Centers. Neurology 1992; 42:473-80.
50. Hachinski VC, Lassen NA, Marshall J. Multi-infarct dementia. Acause of mental deterioration in the elderly. Lancet 1974; 2:207-10.
51. Rosen WG, Terry RD Fuld PA, Katzman R, Peck A. Pathologicalverification of ischemic score in differentiation of dementias. AnnNeurol 1980; 7:486-8.
52. McKeith IG, Dickson DW, Lowe J, et al; Consortium on DLB.Neurology 2005;65 :1863-72. Diagnosis and management ofdementia with Lewy bodies: third report of the DLBConsortium.
53. Neary D, Snowden JS, Gustafson L, et al. Frontotemporal lobardegeneration: a consensus on clinical diagnostic criteria. Neurology1998;51:1546-54.
54. Lim WS. Pharmacological treatment of dementia. Singapore FamPhysician 2006; 32: 20-24.
55. Larson EB, Reifler BV, Sumi SM, et al. Diagnostic tests in thevaluation of dementia. A prospective study of 200 elderlyoutpatients. Arch Intern Med 1986;146:1917-20.
56. Stewart R. Cardiovascular risk factors in Alzheimer’s disease. JNeurol Neurosurg Psychiatry 1998;65:143-7.
57. Sano M, Ernesto C, Thomas RG, et al. A controlled trial ofselegiline, alpha-tocopherol, or both as treatment for Alzheimer’sdisease. The Alzheimer’s Disease Cooperative Study. N Eng J Med1997; 336:1216-22.
58. Miller ER 3rd, Pastor-Barriuso R, Dalal D, et al. Meta-analysis: high-dosage vitamin E supplementation may increase all-cause mortality.Ann Intern Med 2005; 142:37-46.
�� ��66
59. Lim WS, Liscic RM, Xiong CJ, et al. Letter to the editor: A reply toMeta-Analysis: High-dosage vitamin E supplementation mayincrease all-cause mortality. Ann Intern Med 2005; 143:152.
60. Aisen PS, Scahfer KA, Grundman M, et al. Effects of rofecoxib ornaproxen vs placebo on Alzheimer disease progression: a randomisedcontrolled trial. JAMA 2003; 289:2819-26.
61. Reines SA, Block GA, Morris JC, et al. Rofecoxib: no effect toAlzheimer’s disease in a 1-year, randomized blinded, controlledstudy. Neurology 2004; 62:66-71.
62. Aisen PS, Davis KLM, Berg JDM et al. A randomised controlledtrial of prednisolone in Alzheimer’s disease. Neurology 2000;54:588-93.
63. Henderson VW, Paganini-Hill A, Miller BL ,et al. Estrogen forAlzheimer's disease in women: randomized, double-blind, placebo-controlled trial. Neurology 2000;54:295-301.
64. Mulnard RA, Cotman CW, Kawas C, et al. Estrogen replacementtherapy for treatment of mild to moderate Alzheimer disease: arandomized controlled trial. Alzheimer's Disease Cooperative Study.JAMA. 2000;283:1007-15.
65. Hogervorst E, Yaffe K, Richards M, et al. Hormone replacementtherapy to maintain cognitive function in women with dementia. In:The Cochrane Library, Issue 2, 2002. Oxford: Update Software.
66. Shumaker SA, Legault C, Rapp SR, et al. Oestrogen plus progestinand the incidence of dementia and mild cognitive impairment inpostmenopausal women. The Women’s Health Initiative MemoryStudy: a randomised controlled trial. JAMA 2003; 289:2651-62.
67. Lim WS, Gammack JK, Van Niekerk J, Dangour AD. Omega 3 fattyacid for the prevention of dementia. In: The Cochrane Library, Issue1, 2006. Oxford: Update Software.
68. Malouf R, Grimley Evans J, Areosa Sastre A. Folic acid with orwithout vitamin B12 for cognition and dementia. In: The CochraneLibrary, Issue 4, 2003. Oxford: Update Software.
�� ��67
69. Scott HD, Laake K. Statins for the prevention of Alzheimer's disease.In: The Cochrane Library, Issue 3, 2001. Oxford: Update Software.
70. Loy C, Schneider L. Galantamine for Alzheimer's disease and mildcognitive impairment. In: The Cochrane Library, Issue 1, 2006.Oxford: Update Software.
71. Birks J, Harvey RJ. Donepezil for dementia due to Alzheimer'sdisease. In: The Cochrane Library, Issue 1, 2006. Oxford: UpdateSoftware.
72. Birks J, Grimley Evans J, Iakovidou V, et al. Rivastigmine forAlzheimer’s disease (Cochrane Review). In: The Cochrane Library,Issue 3, 2005. Oxford: Update Software.
73. Courtney C, Farrell D, Gray R, et al. Long-term donepezil treatmentin 565 patients with Alzheimer’s disease (AD 2000): randomizeddouble-blind trial. Lancet 2004; 363:2105-15.
74. Raskind MA, Peskind ER, Truyen L, et al. The cognitive benefits ofgalantamine are sustained for at least 36 months; a long-termextension trial. Arch Neurol 2004; 61:252-6.
75. Winblad B, Wimo A, Engedal K. 3-year study of donepezil therapyin Alzheimer’s disease: effects of early and continuous therapy.Dement Geriatr Cogn Disord 2006;21:353-363.
76. Hake AM. The treatment of Alzheimer’s disease: the approach froma clinical specialist in the trenches. Sem Neurol 2002;22:71-74.
77. Feldman H, Gauthier S, Hecker J ,et al. A 24-week, randomized,double-blind study of donepezil in moderate to severe Alzheimer’sdisease. Neurology 2001;57:613-20.
78. Birks J. Cholinesterase inhibitors for Alzheimer's disease. (CochraneReview). In: The Cochrane Library, Issue 1, 2006. Oxford: UpdateSoftware.
79. Winblad B, Kilander L, Eriksson S, et al. Donepezil in patients withsevere Alzheimer’s disease: double-blind, parallel-group, placebo-controlled study. Lancet. 2006;367:1057-65.
�� ��68
80. Black S, RomanG, Geldmacher D, Salloway S, Hecker J, Burns A,Perdomo C, Kumar D, Pratt R, the Donepezil 307 VascularDementia Study Group. Efficacy and tolerability of donepezil invascular dementia positive results of a 24-week multicenterinternationl randomized placebo controlled trial. Stroke 2003;43:2323-32.
81. Wilkinson D, Doody R, Helme R, Taubman K, Mintzer J, Kertesz A,Pratt RD, Donepezil 308 study. Donepezil in vascular dementia arandomized placebo controlled study. Neurology 2003;61(4):479-86
82. Malouf, R; Birks, J Donepezil for vascular cognitive impairment.Cochrane Library 2005.
83. Erkinjuntti T, Kurz A, Gauthier S, Bullock R, Lilienfeld S, DamarajuCV. Efficacy of galantamine in probable vascular dementia andAlzheimer's disease combined with cerebrovascular disease: arandomised trial. Lancet 2002;359(9344):1283-90.
84. Wild R, Pettit T, Burns A. Cholinesterase inhibitors for dementiawith Lewy bodies (Cochrane Review). In: The Cochrane Library,Issue 3, 2003. Oxford: Update Software.
85. McKeith IG, Del Set T, Spano P, et al. Efficacy of rivastigmine indementia with Lewy bodies: a randomised, double-blind, placebo-controlled international study. Lancet 2000; 356:2031-6.
86. Emre M, Aarsland D, Albanese A, et al. Rivastigmine for dementiaassociated with Parkinson’s disease. N Engl J Med 2004; 351:2509-18.
87. Maidment I, Fox C, Boustani M. Cholinesterase inhibitors forParkinson's disease dementia. In: The Cochrane Library, Issue 1,2006. Oxford: Update Software.
88. Samuel W, Caliguri M, Galasko D, et al. Better cognitive andpsychopathologic response to donepezil in patients prospectivelydiagnosed as dementia with Lewy bodies: a preliminary study. Int JGeriatr Psychiatry 2000; 15:794-802.
�� ��69
89. Leroi I, Brandt J, Reich SG, et al. Randomised controlled trial ofdonepezil in cognitive impairment in Parkinson’s disease. Int JGeriatr Psychiatry 2004;19:1-8.
90. Overshott R, Burns A. Treatment of dementia. J Neurol NeurosurgPsychiatry 2005;76(S):v53-v59.
91. Reisberg B, Doody R, Stoffler A, et al. Memantine in moderate tosevere Alzheimer’s disease. N Engl J Med 2003; 348:1333-1341.
92. Tariot PN, Farlow MR, Grossberg GT, et al. Memantine treatment inpatients with moderate to severe Alzheimer disease already receivingdonepezil: A randomized controlled trial. JAMA 2004;291:317-24.
93. Cummings JL, Schneider E, Tariot PN, et al. Behavioural effects ofmemantine in Alzheimer Disease patients receiving donepeziltreatment. Neurology 2006;67:57-63.
94. McShane R, Areosa Sastre A, Minakaran N. Memantine for dementia(Cochrane Review). In: The Cochrane Library, Issue 2, 2006.Oxford: Update Software.
95. Peskind ER, Potkin SG, Pomara N, et al. Memantine treatment inmild to moderate Alzheimer’s disease: a 24-week randomized,controlled trial. Am J Geriatr Psychiatry 2006;14:704-15.
96. Orgogozo JM, Rigaud AS, Stoffler A, Mobius HJ, Forettte F.Efficacy and safety of memenatine in patients with mild to moderatevascular dementia. A randomised, placebo-controlled trial(MMM300 Trial Group). Stroke 2002
97. Wilcock G, Mobius HJ, Stoffler A on behalf of the MM 500 group.A double-blind, placebo-controlled multicentre study of memantinein mild to moderate vascular dementia. International ClinicalPsychopharmacology 2002;17:297-305
98. Areosa Sastre A, Sheriff F, McShane R. Memantine for dementiaCochrane Library 2005.
99. Birks J, Grimley Evans J. Ginkgo biloba for cognitive impairmentand dementia (Cochrane Review). In: The Cochrane Library, Issue 4,2002. Oxford: Update Software.
�0 ��
70
100. Solomon PR, Adams F, Silver A, et al. Ginkgo for memoryenhancement: a randomized controlled trial. JAMA 2002;288: 835-40.
101. Van Dongen M, Van Rossum E, Kessels AGH, et al. The efficacy ofginkgo for elderly people with dementia and age-associated memoryimpairment: New results of a randomized clinical trial. J Am GeriatrSoc 2000; 48:1183-94.
102. Kurz A, van Baelen B. Ginkgo biloba compared with cholinesteraseinhibitors in the treatment of dementia: a review based on meta-analyses by the Cochrane Collaboration. Dement Geriatr CognDisord 2004; 18:217-26.
103. Hu Z, Yang X, Ho PC, et al. Herb-drug interactions: a literaturereview. Drugs 2005; 65:1239-82.
104. Birks J, Flicker L. Selegiline for Alzheimer’s disease (CochraneReview). In: The Cochrane Library, Issue 1, 2003. Oxford: UpdateSoftware.
105. Garfield FB, Getsios D, Caro JJ, et al. Assessment of HealthEconomics in Alzheimer’s Disease (AHEAD). Treatment withGalantamine in Sweden. Pharmacoeconomics 2002;20:629-37.
106. National Institute for Health and Clinical Excellence. Appraisalconsultation document: donepezil, rivastigmine, galantamine(review) and memantine for the treatment of Alzheimer’s disease.London: NICE, 2006, http://www.nice.org.uk/page.aspx?0=245 098.
107. Lovestone S, Gauthier S. Management of dementia 2001; MartinDunitz, London.
108. Algase DL, Beck C, Kolanowski A et al. Need-driven dementia-compromised behaviour: An alternative view of disruptivebehaviour. Am J Alzheimer’s Disease Other Dementias 1996;11: 10-19.
�0 ��71
109. Teri L, Schmidt A. Understanding Alzheimer’s: A Guide forFamilies, Friends and Health Care Providers. University ofWashington, 1993.
110. Teri L, McCurry SM, Logsdon R,Gibbons LE. Training CommunityConsultants to Help Family Members Improve Dementia Care: ARandomized Controlled Trial. The Gerontologist 2005; 45: 802-811.
111. Hall GR, Buckwalter KC. Progressively lowered stress threshold: aconceptual model for care of adults with Alzheimer's disease. ArchPsychiatr Nurs 1987;1: 399-406.
112. Bains J, Birks JS, Dening TR. Antidepressants for treating depressionin dementia. Cochrane Database Syst Rev. 2006;(3).
113. KM Sink, KF Holden, K Yaffe. Pharmacological Treatment ofNeuropsychiatric Symptoms of Dementia. A Review of the evidence.JAMA 2005; 293; 596-608.
114. PE Lee, SS Gill, M Freedman, Bronskill SE, MP Hillmer, PARochon. Atypical antipsychotic drugs in the treatment of behaviouraland psychological symptoms of dementia: a systematic review. BMJ2004.
115. Schneider LS, Tariot PN, Dagerman KS, Davis SM, Hsiao JK et al.Effectiveness of Atypical Antipsychotic Drugs in Patients withAlzheimer’s Disease. N Engl J Med 2006 ; 355 :1525-38.
116. Tariot PN, Schneider L, Katz IR, Mintzer JE, Street J, CopenhaverM, Williams-Hughes C. Quetiapine treatment of psychosis associatedwith dementia: a double-blind, randomized, placebo-controlledclinical trial. Am J Geriatr Psychiatry. 2006 Sep;14(9):767-76.
117. Sreet JS, Clark WS, Gannon KS et al. Olanzepine treatment ofpsychotic and behavioral symptoms in patients with Alzhiemerdisease in nursing care facilities: a double-blind, randomized,placebo-controlled trial: the HGEU Study Group. Arch GenPsychiatry 2000; 57:968-76.
118. Brodaty H, Ames D, Snowdon J et al. A randomized placebo-controlled trial of risperidone for the treatment of aggression,
�� ��72
agitation and psychosis of dementia. J Clin Psychiatry 2003; 64:134-43.
119. UK Committee of Safety of Medicines (CSM) 9th March 2004.
120. Schneider LS, Dagerman KS, Insel P. Risk of death with atypicalantipsychotic drug treatment for dementia. Meta-analysis ofrandomized placebo-controlled trials. JAMA 2005; 294:1934-43.
121. PS Wang, S Schenneweiss, J Avorn, MA Fischre, H MOrgun, DHSolomon, MA Brookhart. Risk of death in elderly users ofconventional vs atypical antipsychotic medications. NEJM 2005;353: 2335-41.
122. Sultzer DL, Gray KF, Gunay I, Wheatly MV, Mahler ME. Doesbehavioral improvement with haloperidol or trazodone treatmentdepend on psychosis or mood symptoms in patients with dementia? JAm Geriatr Soc 2001; 49(10):1294-300.
123. Ballard C, Grace J, McKeith I, Holmes C. Neuroleptic sensitivity indementia with Lewy bodies and Alzheimer’s disease. Lancet 1998;351:1032-33.
124. Mittelman MS, Roth DL, Haley WE, Zarit SH. Effects of a caregiverintervention on negative caregiver appraisals of behaviour problemsin patients with Alzheimer’s disease: results of a randomised trial. JGerontolol B Psychol Sci Soc Sci 2004; 59B: 27-34.
125. Mittleman MS, Roth DL, Coon DW, Haley WE. Sustained benefitof supportive intervention for depressive symptoms in caregivers ofpatients with Alzheimer’s disease. Am J Psychiatry 2004; 161: 850-56.
126. Gitlin LN, Belle SH, Burgio LD et al; REACH Investigators. Effectof multicomponent interventions on caregiver burden and depression:the REACH multisite initiative at 6-month follow-up. PsycholAging. 2003; 18: 361-74.
127. Brodaty H, Green A, Koschera A. Meta-analysis of psychosocialintervention for caregivers of people with dementia. J Am GeriatrSoc 2003; 51: 657-64.
�� ��73
128. Beauchamp N, Irvine AB, Seeley J, Johnson B. Worksite-basedinternet multimedia programme for family caregivers of persons withdementia. Gerontologist 2005; 45: 793-801.
129. Eisdorfer C, Czaja SJ, Loewenstein DA et al. The effect of a familytherapy and technology-based intervention on caregiver depression.Gerontologist 2003; 43: 521-31.
130. Czaja SJ, Rubert MP. Telecommunications technology as an aid tofamily caregivers of persons with dementia. Psychosom Med 2002;64: 469-76.
131. Lawton MP, Brody EM, Saperstein AR. A controlled study of respiteservice for caregivers of Alzheimer's patients. Gerontologist1989;29(1):8-16.
132. Wishart L, Macerollo J, Loney P, King A, Beaumont L, Browne G,Roberts J. "Special Steps": an effective visiting/walking program forpersons with cognitive impairment. Canadian Journal of NursingResearch 2000;31(4):57-71.
133. Lee H, Cameron M. Respite care for people with dementia and theircarers. Cochrane Database Syst Rev 2004; 2: CD004396.
134. Spector A, Thorgrimsen L, Woods B, Royan L, Davies S,Butterworth M and Orrell M. Efficacy of an evidence-basedcognitive stimulation therapy programme for people with dementia:Randomised Controlled Trial. British Journal of Psychiatry 2003;183: 248-54.
135. Dresser R. Anatomy revisited: The limits of anticipatory choices. InDementia and Aging: ethics, values and policy choice. Ed: BinstockRH, Post SG, and Whitehouse PJ. Johns Hopkins University Press,Baltimore (1992).
136. Post SG. Key issues in the ethics of dementia care.Neurol Clin. 2000;18:1011-22.
137. Grisso T, Appelbaum PS. Assessing competence to consent totreatment: A Guide for Physicians and other Health Professionals.Oxford University Press 1998.
�� ��74
138. Mental Disorder and Treatment Act (Cap 178, 1985 Rev Ed).
139. Re LP [2006] SGHC 13.
140. Nussbaum RL, Ellis CE. Genomic Medicine: Alzheirmer’s diseaseand Parkinson’s disease. N Engl J Med 2003;348:1356-64.
141. Mayeux R, Saunders AM, Shea S et al. Utility of the apolipoproteinE genotype in the diagnosis of Alzheimer's disease. Alzheimer'sDisease Centers Consortium on Apolipoprotein E and Alzheimer'sDisease. N Engl J Med 1998;338:506-511.
142. The American Geriatrics Society Ethics Committee. Genetic testingfor late-onset Alzheimer’s disease. J Am Geriatr Soc 2001;49:225-226.
143. American College of Medical Genetics/American Society of HumanGenetics Working Group. Statement on use of apolipoprotein Etesting for Alzheimer disease. JAMA 1995; 274(20):1627-1629.
144. Post SG, Whitehouse PJ, Binstock RH, et al. The clinicalintroduction of genetic testing for Alzheimer's disease. JAMA 1997;277(10):832-836.
145. Connell LM, Koenig BA, Greely HT, et al and Alzheimer DiseaseWorking Group of the Standford Program in Genomics E&S.Genetic testing and Alzheimer disease: Has the time come? NatureMedicine 1998; 4:757-759.
146. Practice parameter: diagnosis of dementia (an evidence-basedreview). Report of the Quality Standards Subcommittee of theAmerican Academy of Neurology. Neurology. 2001 May8;56(9):1143-53
147. van der Cammen TJM, Croes EA, Dermaut B, et al. Genetic testinghas no place as a routine diagnostic test in sporadic and familial casesof Alzheimer’s disease. J Am Geriatr 2004; 52:2110-2113.
148. Hunt LA, Murphy CF, Carr D, et al. Reliability of the WashingtonUniversity Road Test. A performance-based assessment for driverswith dementia of the Alzheimer type. Arch Neurol 1997;54:707-712.
�� ��75
149. Dubinsky RM, Stein AC, Lyons K. Practice parameter: risk ofdriving and Alzheimer's disease (an evidence-based review): reportof the quality standards subcommittee of the American Academy ofNeurology. Neurology 2001;56:695.
150. Drachman DA, Swearer JM. Driving and Alzheimer's disease: therisk of crashes. Neurology 1993; 43: 2448-2456.
151. Freidland RP, Kos E, Kumar A, et al. Motor vehicle crashes indementia of the Alzheimer's type. Ann Neurol 1988; 24: 782-786.
152. Fox GK, Bashford GM. Driving and dementia: balancing personalindependence and public safety. Med J Aust 1997; 167:406-407.
153. Fox GK, Bowden SC, Bashford GM, Smith DS. Alzheimer's diseaseand driving: prediction and assessment of driving performance. J AmGeriatr Soc 1997; 45: 949-953.
154. Trobe JD, Waller PF, Cook-Flanagan CA, et al. Crashes andviolations among drivers with Alzheimer disease. Arch Neurol 1996;53: 411-416.
155. Duchek JM, Carr DB, Roe CM, et al. Longitudinal drivingperformance in early-stage dementia of the Alzheimer type. J AmGeriatr Soc 2003;51:1342-7.
156. Odenheimer GL, Beaudet M, Jette AM, et al. Performance-baseddriving evaluation of the elderly driver: safety, reliability andvalidity. J Gerontol 1994; 49: M153-M159.
157. Dobbs BM, Carr DB, Morris JC. Evaluation and management of thedriver with dementia. Neurologist. 2002; 8:61-70.
158. Driving and dementia: a cause for concern. Med J Aust 1997; 167:453-454.
159. Post SG. The moral challenge of Alzheimer’s disease: Ethical issuesfrom diagnosis to dying,ed 2 revised. Baltimore, The Johns HopkinsUniversity Press, 2000.
�� ��76
160. Marzanski M. Would you like to know what is wrong with you? Ontelling the truth to patients with dementia. J Med Ethics 2000; 26:108-113.
161. Pinner G, Bouman WP. Attitudes of patients with mild dementia andtheir carers towards disclosure of the diagnosis. Int Psychogeriatr2003; 15:279-88.
162. Dautzenberg PL, van Marum RJ, van Der Hammen R, Paling HA.Patients and families desire a patient to be told the diagnosis ofdementia: a survey by questionnaire on a Dutch memory clinic. Int JGeriatr Psychiatry. 2003;18:777-9.
�� ��77
Self-assessment (MCQs)
After reading the Clinical Practice Guidelines, you can claim one CMEpoint under Category III (Self-Study) of the SMC Online CME System.Before you login to claim the CME point, we encourage you to evaluatewhether you have mastered the key points in the Guidelines bycompleting this set of MCQs. This is an extension of the learning processand is not intended to “judge” your knowledge and is not compulsory.The answers can be found at the end of the questionnaire.
Instruction: Choose either “True” or “False”.True False
1. Dementia assessment and evaluation should be performedin the following group of patients:A) Subjects with memory and other cognitive
complaints (either self-report or caregiver-report)B) Routine screening for all older subjectsC) Subjects with progressive forgetfulnessD) Subjects who arouse the physician’s suspicion of
cognitive impairment during interview despiteabsence of memory or cognitive complaints
E) Subjects with strong family history of dementia
2. Diagnosis of dementia
A) Dementia can be diagnosed clinically using DSM-IV criteria for dementia.
B) The patient can be diagnosed with dementia if hehas memory impairment and deficits in one othercognitive domain (agnosia, aphasia, apraxia andexecutive functioning) although these cognitivedeclines do not impair social or occupationalfunctioning.
C) Brief bedside screening instruments (such asECAQ, AMT, CMMSE) may be used to aid in thediagnosis of dementia.
D) Neuropsychological testing is useful in detectingsubtle cognitive difficulties not picked up by briefscreening instruments.
E) Potentially reversible causes of dementia should beexcluded in all patients who meet DSM-IV criteriafor dementia.
Self-assessment (MCQs)
�� ��78
3. Complications of dementiaA) Patients with dementia may present with anxiety
and depression in the early stages of their illness.B) Caregivers of dementia patients with significant
behavioural problems may experience copingdifficulties and caregiver stress.
C) Patients with dementia first experience difficultiesin home functioning.
D) Behavioural problems occur uncommonly inpatients with dementia.
E) Depression, agitation, anxiety, paranoia,hallucinations and sleep problems should be askedfor routinely in patients with dementia.
4. The following are common causes of dementiaA) Alzheimer’s diseaseB) Normal pressure hydrocephalusC) Dementia with Lewy BodyD) Creutzfeld-Jakob diseaseE) Vascular dementia
5. Pharmacological management of dementiaA) Pharmacotherapy is the most important aspect in
dementia management.B) A multi-pronged strategy is required for dementia
management, which consists of patient andcaregiver education, non-pharmacologicalmeasures, pharmacotherapy and comprehensivecaregiver psychosocial interventions.
C) Oestrogen therapy should be considered forprevention of cognitive decline in women withdementia.
D) Acetylcholinesterase inhibitors or N-methyl D-aspartate antagonists for symptomatic treatment ofdementia should only be started after carefulconsideration of expected magnitude of benefit,side-effects, co-morbidites and costs of treatment.
E) Patients started on acetylcholinesterase inhibitors orN-methyl D-aspartate antagonists do not requireregular monitoring and follow-up for side effectsand treatment response.
�� ��79
6. Management of behavioural and psychological symptomsof dementiaA) Pharmacological measures should be instituted
initially for management of behavioural andpsychological symptoms of dementia.
B) Non-pharmacological methods to managebehavioural symptoms of dementia entailsunderstand the aetiology of the behaviour andaddressing the problem at its root cause.
C) Antipsychotics (conventional or atypical) should beused as first line in pharmacological treatment ofdementia.
D) Antidepressants may be used to treat comorbiddepression in dementia.
E) Typical antipsychotics is more efficaciouscompared to atypical antipsychotics.
7. Social and caregiver management of dementia
A) Psychosocial interventions in dementia are targetedmainly at patients with dementia.
B) Family caregivers who face much negativeconsequences as a result of long-term caregivingneed to be helped and supported.
C) Respite care can be offered to relieve the burden ofcaregiving on the family caregiver.
D) In meeting the care needs of the person withdementia and his/her carer, referral to communityresources should be considered.
E) Dementia daycare centres are useful in patients indementia in keeping them active, improve theirsleep and aid in reducing caregiver stress.
�0 ��80
Answers
1 (a) T 5 (a) F1 (b) F 5 (b) T1 (c) T 5 (c) F1 (d) T 5 (d) T1 (e) T 5 (e) F
2 (a) T 6 (a) F2 (b) F 6 (b) T2 (c) T 6 (c) F2 (d) T 6 (d) T2 (e) T 6 (e) F
3 (a) T 7 (a) F3 (b) T 7 (b) T3 (c) F 7 (c) T3 (d) F 7 (d) T3 (e) T 7 (e) T
4 (a) T4 (b) F4 (c) T4 (d) F4 (e) T
�0 ��81
Workgroup members
The members of the workgroup, who were appointed in their personalprofessional capacity, are:
Chairman Dr Chong Mei SianConsultantDepartment of Geriatric MedicineTTSH
Members
Dr Christopher Chen Li-HsianSenior ConsultantDept of NeurologyNNI (SGH Campus)SGH
Prof Kua Ee HeokHead, Dept of PsychologicalMedicine,Yong Loo Lin School of Medicine,NUH
Dr Ng Li LingSenior ConsultantDept of Psychological MedicineCGH
Dr Lim Wee ShiongConsultantDept of Geriatric MedicineTTSH
Dr Chin Jing JihConsultantDept of Geriatric MedicineTTSH
Dr Philip Yap Lin KiatConsultantDept of Geriatric MedicineAH
Dr Chiam Peak ChiangChief & Senior ConsultantDept of Geriatric PsychiatryWH/IMH
Dr Francis Ngui Tet ShinMedical Director Adam Road Hospital
Dr Tan Kok LeongDirectorSinghealth Polyclinics-Outram
Workgroup members
�� ��54
Subsidiary editors
Dr Pwee Keng HoAssistant Director (Health Technology Assessment)Health Services Research & Evaluation DivisionMinistry of Health
Dr Rajni GuptaExecutive (Health Technology Assessment)Health Services Research & Evaluation DivisionMinistry of Health
Acknowledgement:
Dr Edwin Chan Shih-YenHead of Evidence-Based MedicineandDirector of the Singapore Branch, Australasian Cochrane CentreClinical Trials & Epidemiology Research Unit
Dr Miny SamuelSenior Evidence-Based Medicine AnalystandCo-Director of the Singapore Branch, Australasian Cochrane CentreClinical Trials & Epidemiology Research Unit
�� ��This page has been intentionally left blank.
��This page has been intentionally left blank.
ISBN 978-981-05-8095-7
