Dementia Screening and ManagementWestern HealthDr. Sook Meng LEE

Department of Geriatric Medicine

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Overview

New terminology from DSM V

What are some of the clues GPs might pick up?

What are the reasons to seek early diagnosis? 

What screening tools to use?

Evidence on treatments available and how to subscribe 

Who and how to refer to CDAMS and other services?

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Causes of cognitive declineNormal ageing

Subjective Cognitive Impairment (SCI)

Mild Cognitive Impairment (MCI)

Dementia

Delirium

Depression

Drugs anticholinergic, analgesics, antinauseants, antibiotics (cipro), CNS acting, cardiac, GI, psychotropics, steroids

The 4 Ds

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New DSM V TerminologyNeurocognitive disorder (NCD) vs DementiaDementia typically refers to neurodegenerative disorders in the elderly

DSM expands category to include disorders in younger people

• eg. HIV, traumatic brain injury

Can be single domain

• eg. Amnestic• exception – Major NCD due to Alzheimer’s disease

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Criteria for Neurocognitive DisordersCOGNITIVE disorders

ACQUIRED and represent a DECLINE (ie not developmental)

Presence of underlying brain pathology

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Major and Mild Neurocognitive DisorderMajor Neurocognitive Disorder

• Significant cognitive decline• Interferes with independence• Not due to delirium• Not due to other mental disorders

Mild Neurocognitive Disorder

• Moderate cognitive decline• Does NOT interfere with independence• Not due to delirium• Not due to other mental disorders

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Cognitive domains specified

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When diagnosing, it is just as important to eliminate non-NCD conditions to determine which disease(s) are presentAmnestic syndromes – post-head injuries, psychogenic states, TLE

Depression and Delirium

• Complex relationship• Important – treatable

Other, some possibly treatable/reversible/modifiable, causes of cognitive disorders including systemic, metabolic, endocrine, infective, nutritional, trauma, toxins (medications, alcohol), neurological (NPH, tumors)

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Clues

Vague complaints

Forgetting appointments, scripts

Repetitive, word finding difficulties

Irritable

Recurrent attendance to ED

Decline in previous well controlled illness

Social withdrawal

Holiday dramas

FAMILY MEMBER and carer worried

What are the common causes of NCD?

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Major types of NCDs

Neurocognitive Disorder due to Alzheimer’s disease

Vascular Neurocognitive Disorder

Neurocognitive Disorder due to frontotemporal lobar degeneration

Neurocognitive Disorder with Lewy Bodies

Neurocognitive Disorder due to Parkinsons disease

Traumatic brain injury

Substance/medication-induced

Prion disease

(several others – up to 70 types)

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Alzheimer’s disease (1)

Causes at least 50% of all neurocognitive disorders

Characterised by insidious onset and slow steady progression

Initially, new learning is affected (pervasive forgetfulness), later praxis, language and executive functions, loss of insight (anosognosia)

“Probable” vs “Possible” Alzheimer’s disease

Related to Evidence of AD gene (family history or formal gene testing)

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Alzheimer’s disease (2)

Medial temporal lobe atrophy on MRI – highly predictive of AD

PET scans – PiB PET, florbetapir amyloid PET

NB variant Ads

Specific medication available (cholinesterase inhibitors & memantine- not curative)

Aβ plaques, neurofibrillary tangles, tau pathology

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Vascular neurocognitive disorder (1)

NINDS-AIREN criteria

• Temporal relationship/stepwise – but not always (infarcts may be silent)

• Focal neurology• Neuroimaging evidence

Clinical neurological signs ( motor, sensory, bulbar, gait, executive function, psychomotor slowing, apathy, urinary dysfunction, gait disorders)

Memory deficits often milder than AD – due to retrieval difficulties rather than primary memory disorder, hence benefit from cues

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Vascular neurocognitive disorder (2)

Slowed information processing, difficulty planning, organising, sequencing, set shifting

Management includes optimisation of CVS risk factors inc antiplatelet Tx

Depression, personality change, emotional lability

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Mixed pathologies

Common – especially in the older patients

Community study in those with clinical diagnosis of dementia

• 50% mixed pathology – most common AD and VaD• AD + PDD, AD + DLB

Brain Banks (Europe)

• 53% mixed pathology• Brain pathology also found in those without clinical diagnosis

during life (brain reserve theory)

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NCD with Lewy Body Disease (1)

Common accounting 10-25% dementia

Core symptoms

• Insidious onset and progression of debilitating cognition over 1-4 years

• Fluctuating cognition/attention/alertness• Visual hallucinations – well formed and detailed• Parkinsonism develops 12/12 AFTER cognitive

impairment

Suggestive features

• Rapid eye movement (REM) sleep disorder• Neuroleptic sensitivity - worsening of movement

disorder & consciousness

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NCD with Lewy Body Disease (2)

Alpha-synuclein immunohistochemistry

Relative preservation of medial temporal lobe structures (cf to AD)

Occipital hypoperfusion on SPECT

Overlap with NCD associated with Parkinson’s Disease

Onset dementia before motor Sx cf Parkinson’s disease (motor Sx 1st)

Cholinesterase inhibitors can be useful for NCD associated with Lewy Body Disease and Parkinson’s Disease

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NCD due to Frontotemporal lobar degeneration (1)3 subtypes

• Behavioural variant – most common• Progressive non-fluent aphasia• Semantic dementia (fluent but loss of meaning of words & anomia)

Typical age at onset is in the 50’s, median survival 7 years

Often diagnosis missed in the early stages

Behavioural symptoms can precede cognitive symptoms for years

Disinhibition, impulsivity, apathy, OCD signs, loss of empathy

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NCD due to Frontotemporal lobar degeneration (2)

Should consider FTD in DDx if significant personality change occurs

MRI and PET are important for early diagnosis

50% tau pathology chrom 17 (50% +ve FHx in1st degree relative)

Cholinesterase inhibitors – no benefit

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Further considerations

Over 70 types of NCDs

Where NCD is a known association

• Motor neuron disease (FTD)• Down syndrome (AD)

Conditions where symptoms overlap with major types of NCDs eg. Creutzfeldt-Jakob disease (CSF pr 14-3-3), encephalities, Huntington’s disease, psychotic disorders

How to evaluate and manage a person with possible dementia

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Issues around diagnosis

Sometimes seen as normal ageing

Therapeutic nihilism – there is no Rx anyway, so why bother?

Stigma & cultural issues

Many conceal Sx from GP, others lack insight

GPs – difficulty making diagnosis and breaking the news

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Benefits of diagnosis Brodaty et al 78% seek help from GP in the first instance

Benefits of early Dx GP Management

Reversible cause Dementia/depression/delirium screen

A relief If not dementia/ but also if dementia

Education CDAMS, Alzheimer’s Australia

Legal planning EPOA, medical POA, Advanced Directives

Prescribing medications Stop potentially harmful ones. Start cholinesterase

Monitoring medications Webster pack, pharmacy, RDNS

Safety OT, ACAS, CDAMS, falls prevention

Carer health Assess independently

Watch out for delirium Recent change in behaviour

Monitor for behaviour Exclude delirium, antipsychotics last resort, DBMAS

Monitor for depression Geriatric Depression Scale

Modify risk factors BP, diabetes, lipids, alcohol

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Diagnostic Assessment (1)

There is no single test

Clinical assessment – obtain history from family, check for functional decline

Exclude potentially reversible or modifiable causes, and exclude misdiagnosis eg. delirium, depression

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Diagnostic Assessment (2)

General medical, cardiovascular and neurological examination

FBE, ESR, U&E, Ca, LFT, TSH, B12, folate, MSU, CT brain/MRI

Depending on history and clinical findings – syphilis serol, EEG, HIV

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Screening tools and further investigationsScreening tools – GPCOG, MMSE, GDS

RUDAS if CALD background or low education

MOCA/FAB if obvious cognitive deficits but high MMSE & frontal features

Neuropsychology assessment

SPECT, PET (18-FDG PET for FTD, PiB PET for AD)

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Brief and quick – 4 activities (recall name & add, date, clock, current affair)

High sensitivity & specificity (80%)

Probable cognitive impairment if

• Patient score 0-4• Patient score 5-8 and informant score 0-3

As good as MMSE, not affected by culture, but not tested for serial testing

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Mini-Mental State Examination (MMSE)Folstein et al : J Psych Res 1975;12:189-98Score Orientation

5 Year, Season, Month, Date, Day.

5 State, City, Suburb, Building, Floor

Registration

3 Repeat and remember: apple, table, penny

Attention and Calculation

5 Serial 7’s, or spell “WORLD” backwards

Recall

3 Recall 3 objects above

Language

2 Name a pencil and a watch

1 Repeat “No ifs, ands or buts”

3 Follow three stage command

e.g. take this piece of paper in your right hand,

fold it in half, put it on the floor

1 Read and obey the following: “close your eyes”

1 Write a sentence

1 Copy intersecting pentagons

Max score=30

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Depressive symptoms

Depressive symptoms 20-40% of cases, more common if previous Hx of depression

More common in earlier stages, especially with Vascular NCD

Correlates with degree of disruption to brain monoamine systems (and possibly retained insight)

Antidepressants indicated if biological symptoms, diurnal variation, agitation/retardation, psychotic features

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Risk factors: most NCDs

Non modifiable

• Age• Apo E4

Potentially modifiable

• CVS risk factors – HT, diabetes, lipids, smoking, strokes, homocysteine

• Head injury, alcohol

Protective

• Physical activity• Education

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Pharmacological treatment

Donepezil (Aricept), Rivastingmine (Excelon) & Galantamine (Reminyl)

• Mild-moderate Alzheimer’s disease – PBS approval• MMSE >10/30• If cultural, aphasic, blind, intellectual impairment – can do CIBIS• Diagnosis made by or in consultation with specialist• May benefit advanced Alzheimer’s disease with BPSD and Lewy

Body Dis

Memantine (Ebixa)

• Alzheimer’s disease – PBS approval• Same requirements, but MMSE 10-14• Can use with cholinesterase inhibitors

Applying for an authority for cholinesterase inhibitors and memantine:

Initial application:

organise a phone order for 1 month (half dose) + 1 repeat (full dose)

send a written application (triplicate PBS form) to Medicare straight away to for 6 month supply to (one month half dose and 5 months full dose)

 To Reply paid 9857 PBS Authority Section, Medicare Australia, GPO Box 9857 Melbourne

The initial application must include

i. Diagnosis of Alzheimer’s Disease, confirmed by, or in consultation with, a specialist ii. Initial MMSE score with date of scoreiii. Sole PBS-subsidised therapy for this condition

If continuing treatment: send a written application (triplicate script) and send off to above. Include:

i. Patient must demonstrate a clinically meaningful response to initial Rxii. Re-assessments for a clinically meaningful response to be undertaken and documented every 6

months. This may include QOL (level of independence,happiness), cognitive function (memory, recognition, interest in environment) & behaviour (hallucinations, delusions, anxiety, marked agitation, aggressive behaviour)

After approval, Medicare Australia will forward both copies of the prescription to the patient or the prescriber

 

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Cholinesterase inhibitors donepezil (Aricept), rivastigmine (Excelon), galantamine (Reminyl)

Modest improvement in cognition, global changes seen, including function

Non-cognitive benefit eg. apathy, psychosis, BPSD

Delay symptoms by 12-18 months

Many get suboptimal dose and compliance an issue

Contraindicated in poorly controlled asthma

Side effects – GI (including weight loss), bradycardia, sleep disturbance, urinary symptoms

BPSD can be exacerbated if stop at late stage

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Memantine (Ebixa)

NMDA antagonist

For moderate to severe Alzheimer’s disease (MMSE 10-14)

Well tolerated – headache, dizziness, anxiety, tiredness

Maintains mobility and independent feeding

Can assist with aggression and agitation

Can give daily dose

5mg for 1 week, then 10mg, then 15mg, then maintain at 20mg

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Dementia and driving

National uniform law requires a patient to advise the local driver licensing authority – penalties for failure to report

Dx dementia – cannot hold unconditional licence

46-76% with mild dementia pass road test, no test is 100% accurate

Clues that the patient may be unsafe to continue driving

• Caregiver concerned• History of crash or traffic fine• Self-imposed restriction (5-fold increase risk of

crashes)• Impulsive or aggressive personality

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CDAMS process – who to refer

Primary target is dementia related illness

Any age (generally over 50)

Would benefit from a formal diagnosis

No previous diagnosis – unless requesting second opinion

Requires multidisciplinary assessment ie. not just neuropsychology

Requires high level/detailed assessment ie usually MMSE ≥ 17

Client agrees to assessment

Had dementia screen +/- ECG

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When we receive a referral

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Questions?