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1

DEMENTIADEMENTIAAN APPROACH TO AN APPROACH TO

MANAGEMENT AND MANAGEMENT AND PREVENTIONPREVENTION

DR. HASANAH CHE ISMAILPSYCHIATRIST

SCHOOL OF MEDICAL SCIENCESUNIVERSITI SAINS MALAYSIA

2

Definition of the dementiasyndrome

• Multiple cognitive deficits – memory loss – aphasia – apraxia – agnosia – disturbance in executive function

• These lead to functional decline

DEMENTIA

3

Causes of dementia

• Common causes: – Depression– Drug toxicity

• Common causes: – Alzheimer's disease– Vascular dementia

• Other causes– Lewy body disease– Pick's disease (dementia

of the frontal lobe type) – Parkinson's disease with

dementia

Reversible dementias Irreversible dementias

4

Differentiating AD from other dementias

Cognitive impairment

Dementia

Alzheimer's disease

Exclude other causes (e.g. delirium and depression, etc)

Exclude other dementias

Differentiating AD from other dementias

5

DEMENTIA

• AD represents over 50% of all dementia cases

• AD prevalence doubles every 5 years after 60 years of age

• AD affects 15 million people worldwide

Alois Alzheimer

Short history

1907 Alzheimer reports the first case of August D

1960s Re-emergence of interest in dementia

1970s Cholinergic deficits in AD identified

1980s First trials of cholinergic enhancing therapies

1994 First cholinesterase inhibitor licensed

Present First launches of Reminyl, a cholinesterase inhibitor and nicotinic modulator

7

Prevalence of Alzheimer’s disease

Kurz A. Eur J Neurol 1998; 5(Suppl 4): S1-8Wimo A et al. Int J Geriatr Psychiatry 1997; 12: 841-56

0

10

20

30

40

50

60

60-64 65-69 70-74 75-79 80-84 85+ 95+

Age (years)

Pre

vale

nce (

%)

1% 2% 4%8%

16%

30%

50%

8

Clinical features of AD

• Loss of cognition– short-term memory– language– visuospatial functions

• Loss of daily function– instrumental activities of daily living (ADL)– self-maintenance skills

• Abnormal behaviour

9

‘‘Normal’ ageing Normal’ ageing vs.vs. dementia dementia

• Multiple cognitive domains affected• Decline of language and orientation• Deterioration in common activities of daily living

10

IPA AD Conference, 1996

Functionalimpairment * IADL * ADL

Insidious onset Cognitive decline* Memory loss * Aphasia * Apraxia * Agnosia * Executive function difficultiesBehavioral signs

* Mood swings * Agitation* Wandering

Age over 60 years

No gait difficulties

AD

Clinical features of AD

11

Natural history of Alzheimer’s disease

1 2 3 4 5 6 7 8 9

0

5

10

15

20

25

30

Time (years)

Symptoms

Diagnosis

Loss of functional independence

Behavioural problems

Nursing home placement

Death

Min

i-Men

tal S

tate

Exa

min

atio

n (M

MS

E) Early diagnosis Mild-to-moderate Severe

Feldman and Gracon. The Natural History of Alzheimer’s Disease. London: Martin Dunitz, 1996

12

Anatomical features of AD

• Gross atrophy

– shrinkage of brain

– thinning of gyri

– widened sulci

Normal brain

Alzheimer brain

The pathological cascade of ADThe pathological cascade of AD

Clinical symptoms

Neurodegeneration

Neurofibrillary tangles

-amyloid

Environmental risk factors

Genetic risk factors

Apo-E

Pathogenetic mutations

APP

PS1,2

Cholinergic dysfunction

TAU hypophosphorylation

14

Acetyl CoAAcetyl CoA++

CholineCholine

AcetylcholineAcetylcholine

N receptorN receptor

The cholinergic system

Presynaptic nerve terminal

Postsynaptic nerve terminal

ChATChAT

ChAT = choline acetyltransferase

AChE = acetylcholinesterase

N = nicotinic

M = muscarinic

N receptorN receptor

M receptorM receptor

M receptorM receptor

= acetylcholine

Important in:Memory and learningSensory and attentional functions

15

Cholinergic dysfunction in AD

Cholinergic neurons Choline uptake Acetylcholine release Choline acetyltransferase Nicotinic receptors

= progressively impaired memory

and cognition

16

NEUROTRANSMITTERACETYLCHOLINENucleus basalis ofMeynert

17

Need for earlydiagnosis

Consistent onset, clinicalpresentation and disease progression

Practicalassessmentmethods

New symptomatictreatments

Patient and caregiver support

Making a diagnosis of AD

IPA AD Conference, 1996

18

PERUBAHANPERUBAHANKOGNITIFKOGNITIF::

INGATANINGATANBAHASABAHASAPERTIMBANGANPERTIMBANGAN

19

PERUBAHANPERUBAHANPADA PADA PERSONALITI,PERSONALITI,KELAKUANKELAKUAN::JUGA GEJALAJUGA GEJALAPSIKIATRIPSIKIATRISEPERTISEPERTIDELUSI &DELUSI &HALUSINASIHALUSINASI

20

PERUBAHANPERUBAHANMOTORMOTOR => =>TERBARINGTERBARINGDI ATAS KATILDI ATAS KATIL=>MENELAN=>MENELANTERGANGGUTERGANGGU=>MAUT=>MAUT

21

Dementia  * Insidious onset with unknown date* Slow, gradual, progressive decline* Generally irreversible* Disorientation late in illness* Slight day-to-day variation* Less prominent physiological changes* Consciousness clouded only in late stage* Normal attention span* Disturbed sleep wake cycle; day night

* Psychomotor changes late in illness

Delirium   * Abrupt, precise onset, known date * Acute illness, lasting days or weeks * Usually reversible * Disorientation early in illness * Variable, hour by hour * Prominent physiological changes * Fluctuating levels of consciousness * Short attention span * Disturbed sleep wake cycle; hour-to-hour variation * Marked early psychomotor changes

OR

Dementia or delirium

Ham, 1997

22

Dementia  * Insidious onset * No psychiatric history * Conceals disability * Near-miss answers * Mood fluctuation day to day * Stable cognitive loss * Tries hard to perform but is unconcerned by losses * Short-term memory loss * Memory loss occurs first * Associated with a decline in social function

Depression  * Abrupt onset * History of depression * Highlights disabilities * ’Don't know' answers * Diurnal variation in mood * Fluctuating cognitive loss * Tries less hard to perform and gets distressed by losses * Short- and long-term memory loss * Depressed mood coincides with memory loss * Associated with anxiety

OR

Dementia or depression

Ham, 1997, modified from Wells CE, 1979

23

Clinical History

Ask the following questions: * How did it start? Was it sudden or gradual? * How long has it been going on? * Is the situation progressing? If so, how rapidly? * Is it step-wise or continuous? * Is it worsening, fluctuating or improving? * What changes have you noticed? * Has there been a change in personality? * Has the patient suffered any delusions or hallucinations? * Does the patient become agitated or wander?

Diagnosing AD in primary careclinical history, questioning

24

Functional Assessment

Functional Activities Questionnaire (FAQ)1. Dealing with financial matters, paying bills, writing checks2. Keeping records of taxes, business affairs3. Shopping for everyday necessities: groceries, clothes, etc4. Hobbies or playing games5. Making tea, turning the kettle on and off6. Cooking a balanced meal7. Perception of current events8. Level of attention and understanding: books, television9. Memory: remembering appointments and medications10. Getting about: driving or taking public transport

Pfeffer et al 1982

ScoreMaximum

3333333333

Total 30

ScoreActual

Diagnosing AD in primary carefunctional assessment

25

Physical examination

* Life-threatening conditions, e.g. mass lesions, vascular lesions and infections * Blood pressure and pulse * Vision and hearing assessments * Cardiac and respiratory function * Mobility and balance * Sensory and motor system examination (tone, reflexes, gait and coordination) and depressive symptoms (sleep and weight)

Diagnosing AD in primary carephysical examination

26

Laboratory tests

All patients* Complete blood count* Thyroid function* Vitamin B12 and folate* Syphilis serology * BUN and creatinine * Calcium * Glucose * Electrolytes * Urinalysis * Liver function tests

Most patients   * ECG* Chest X-ray

Diagnosing AD in primary carelaboratory tests

27

Neuroimaging

Various CT scan reports in AD * Normal examination for the patient's age * Generalized cerebral atrophy * Small vessel changes, areas of leucoencephalopathy* No signs of subdural hematoma (if head trauma suspected) * Absence of specific areas of cerebral infarctions or evidence of stroke

Diagnosing AD in primary careneuroimaging, computed (axial)

tomography (CT)

28

Cognitive Assessment

Cognitive areaMini Mental State Examination: test outline and scoring

Orientation *What is the (date, day, month, year, season)? * Where are you (clinic, town, country)?

Memory *Name three objects. Ask the patient to repeat them

Attention*Serial sevens. Alternatively ask the patient to spell world backwards (dlrow)

Folstein et al 1975

ScoreMaximum

55

3

5

ScoreActual

Diagnosing AD in primary carecognitive assessments, MMSE

29

Cognitive Assessment

Cognitive areaMini Mental State Examination: test outline and scoring

Recall *Ask for the three objects mentioned above to be repeated

Language*Name a pencil and watch*Repeat, 'No ifs, ands or buts’*A three stage command*Read and obey CLOSE YOUR EYES*Write a sentence*Copy a double pentagon

ScoreMaximum

3

213111

Total 30

ScoreActual

Folstein et al 1975

Diagnosing AD in primary carecognitive assessments, MMSE (continued)

30

Cognition * Recall/learning* Word finding* Problem solving* Judgement* Calculation

Function* Work* Money/shopping* Cooking* Housekeeping* Reading* Writing* Hobbies

Behavior* Apathy* Withdrawal* Depression* Irritability

IMPAIRMENT

Adapted from Galasko, 1997

Clinical features of ADMild stage of AD (MMSE 21 30)

31

Cognition * Recent memory (remote memory unaffected) * Language (names, paraphasias)* Insight* Orientation* Visuospatial ability

Function* IADL loss* Misplacing objects* Getting lost* Difficulty dressing (sequence and selection)

Behavior * Delusions* Depression* Wandering* Insomnia* Agitation* Social skills unaffected

IMPAIRMENT

Clinical features of ADModerate stage of AD (MMSE 10 20)

Adapted from Galasko, 1997

32

Cognition * Attention* Difficulty performing familiar activities (apraxis)* Language (phrases, mutism)

Function* Basic ADLs Dressing Grooming Bathing Eating Continence Walking Motor slowing

Behavior* Agitation Verbal Physical* Insomnia

Clinical features of ADSevere stage of AD (MMSE <10)

Adapted from Galasko, 1997

IMPAIRMENT

33

The Clock Draw Test

Cognitive Assessment

Time: 5.00 Score: 7 (normal)

Time: 'no real time' Score: 2 (demented)

Thalmann et al 1996.

Time: .10.30 Score: 3 (demented)

Time: 1/4 past 25 Score: 3 (demented)

Diagnosing AD in primary carecognitive assessment

34

AD prognosisOptimal case

Min

i Men

tal S

tate

Exa

min

atio

n s

core

1 2 3 4 5 6 7 8 9

25 ---------------------| Symptoms

20 |----------------------| Diagnosis

15 |-----------------------| Loss of functional independence

10 |--------------------------------| Behavioral problems

5 |-------------------------------------------|

0 Death |------------------------------------------

Nursing home placement

Feidman and Gracon, 1996Years

35

NEUROPSYCHIATRIC SYMPTOMS @ BPSD

APATHY 72% AGITATION 60%IRRITABILITY 42% PACING ETC 38%DEPRESSION 38% ANXIETY 40%DELUSION 22% HALLUCINATION 10%EUPHORIA 8% DISINHIBITION 38%

36

BPSD

DELUSION :

CROSS SECTIONAL STUDIES 20-50%LONGITUDINAL STUDIES 50-70%

• THEFT• INFIDELITY

• CAPGRAS• PHANTOM BOARDERS

• PICTURE SIGN

37Neuropsychiatric disturbances in

AD

0

10

20

30

40

50

60

70

80

Pat

ien

ts (

%)

Mega MS et al. Neurology 1996; 46: 130–5

38

BEHAVIOURAL CORRELATES

•AGGRESSIVE•ACTIVITY DISTURBANCES

COGNITIVE CORRELATES

•DEMENTIA SEVERITY•LANGUAGE, MEMORY &EXECUTIVE FUNCTION

39Successful cholinergic enhancing strategies in AD

Reduced breakdown of acetylcholine

+

Increased release of ACh into synapse

=

Increased availability of ACh at synapse

40

Patient flow

• AD is prevalent among primary care patients• However, patients and general practitioners

(GPs) are often not aware of this• The diagnosis of AD comes too late• 30 memory clinics in Germany• Patients are normally followed up by GPs

41

Reasons for delayed diagnosisReasons for delayed diagnosis

• Cognitive decline seen as age-related• GPs feel unsure about diagnosis of AD• Lack of practical diagnostic tools• Expected benefits of treatment are low

42

Diagnostic problems and pitfallsDiagnostic problems and pitfalls

• Inadequate diagnostic tools• ‘Normal’ ageing vs. dementia • Interpretation of cerebrovascular findings• Problems of mixed pathologies

43

Diagnostic problems and pitfallsDiagnostic problems and pitfalls

• Inadequate diagnostic tools• ‘Normal’ ageing vs. dementia • Interpretation of cerebrovascular findings• Problems of mixed pathologies

44

Problems of mixed pathologiesProblems of mixed pathologies

• Stroke superimposed on AD• Alzheimer’s plus Parkinson’s disease• Dementia with Lewy bodies

45

• RISPERIDONE: 1-2 mg

• OLANZEPINE: 5-10 mg

• QUETIAPINE: 25-250 mg

• HALOPERIDOL: 0.5-3 mg

ANTIPSYCHOTICS

46

AGITATION

• physical aggression• verbal aggression• active resistance to care giversRx: ANTIPSYCHOTIC ANTICONVULSANT

47

DEPRESSION

• major depression uncommon• depressive symptoms frequent (40%)• more common with F/H• MD may precede the onset of AD

48

• SSRI = FLUVOXAMINE (LUVOX)

• SNRI = VENLAFAXIN (EFFEXOR)

• OTHER NEW ANTIDEPRESSANTS

ANTIDEPRESSANTS

49

• APATHY 70%

• IRRITABILITY 42%

• DISINHIBITION 36%

PERSONALITY CHANGES

50

• most common behavioural change

• indifference, loss of affection, decrease motivation

• independent of depression

• frontal hypoperfusion (mediofrontal)

=> correlates with cognitive decline

APATHY IN AD

51

• ATROPHY OF NUCLEAS BASALIS

• DECREASE CAT SYNTHESIS

• ACETYLCHOLINE DEFICIT

• INTACT CHOLINERGIC RECEPERS

CHOLINERGIC DEFICIT IN AD

52

• improve global function

• enhance cognition

• improve behaviour

• delay nursing home placement

CHOLINESTERASE INHIBITOR [ChEI]

53

• TACRINE

• DONEPEZIL

• RIVASTIGMINE

• GALANTAMINE

CHOLINESTERASE INHIBITORSChEIs

54

Potential caregiver benefits

• No sleep disruption

• Maintenance of ADL

• Suppression of behavioural symptoms

= diminished caregiver burden

55

* Define all contributory factors and other illnesses * Discuss the diagnosis, and differentiate other types of dementia * Withdraw non-essential drugs that may interfere with cognition * Treat or manage concomitant illness (e.g. depression, hearing loss)

The role of the primary care physician in mild to moderate AD

Gauthier, Burns and Pettit, 1997

56

* Discuss the use of symptomatic therapies * Monitor functional ability e.g. driving, safety * Referral to specialist if appropriate * Advise on will-making and advance directives * Refer to local AD association for support * Managing caregivers

The role of the primary care physician in mild to moderate AD

(continued)

Gauthier, Burns and Pettit, 1997

57

The role of the primary care physician in severe AD

* Help caregivers discover and optimize the patient's preserved function * Monitor and treat complications * Facilitate caregiver support (respite and day care programs) * Be aware of caregiver burden and stress * Plan institutionalization, if needed * Assist with end-of-life decisions

The role of the primary care physician in severe AD

Gauthier, Burns and Pettit, 1997

58

CASE-FINDINGSymptomssuggestingcognitive

impairment

MANAGEMENT OF AD *Follow-up *Patient and caregiver counseling *Management and symptomatic treatment *Specialist referral if indicated

CLINICAL ASSESSMENT *Clinical history

*Physical examination *Laboratory tests

*Functional assessment *Cognitive assessment

Functional decline and cognitive impairment

DIFFERENTIAL DIAGNOSIS *Exclude delirium depression other causes of dementia *Evaluate evidence for AD (neuroimaging)

YES

AD diagnosis

Diagnosing AD in primary careA systematic approach summary

59

ABCs of Behavioural Management Strategies

60

Iceberg

80%

20%

61

The caregiving burden in AD

Hours dedicated per patient over 1 month(1 month = 720 hours, including 160 working hours)

• Principal (non-professional) caregiver: 280 hours

• Professional caregiver: 36 hours

Rice DP et al. Health Aff (Millwood) 1993; 12: 164–76Boada M et al. Med Clin (Barc) 1999; 113: 690–5

62

Caregiver burden

Physical problems

Psychological or emotional

problems

Social problems

Financialproblems

Family members (including principal caregiver)caring for Alzheimer patient

Multidimensional: objective/subjective burden

George, Gwyther, Hoening, Montgomery, Platt

63Spanish National Plan for Patients

with AD & other Dementias

“Plan Nacional de Atencion a los Enfermos de Alzheimer y otras demencias”

Six main areas

1. Health services

2. Social services

3. Legal and economic protection

4. Family support

5. Education and training for professionals

6. Research

64

A growing problem

0

5

10

15

20

25

30

35

1980 2000 2025

Years

Mill

ions 1980

20002025

Projected prevalence of dementia to 2025

Alzheimer’s Disease International

65Qualitative changes in the Alzheimer

population in the next decade

Early diagnosis

Impact of drugs

Improvement ofcare provided

by non- professionals

Medicalprogress

Changes in the structure of society

Health and social services

66

Risk factors* Age* Family History of AD (ApoE-4) * Head trauma* Low educational level* Environmental factors* Down’s syndrome

Protective factors * Genetic (ApoE-2)* High educational level* Long-term anti- inflammatory drug use, e.g. NSAIDS* Long-term use of estrogens (in women)

AD risk and protective factors

IPA AD Conference, 1996

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