Department of
Geriatric Medicine
Dementia Screening
and Management
Western Health
Dr. Sook Meng LEE
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?
Footer Text
2
Causes of cognitive decline
Normal 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
Footer Text
3
New DSM V Terminology
Neurocognitive disorder (NCD) vs Dementia
Dementia 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
Footer Text
4
Criteria for Neurocognitive Disorders
COGNITIVE disorders
ACQUIRED and represent a DECLINE (ie not developmental)
Presence of underlying brain pathology
Footer Text
5
Major and Mild Neurocognitive Disorder
Major Neurocognitive Disorder
•
•
•
•
Significant cognitive decline
Interferes with independence
Not due to delirium
Not due to other mental disorders
Mild Neurocognitive Disorder
•
•
•
•
Footer Text
Moderate cognitive decline
Does NOT interfere with independence
Not due to delirium
Not due to other mental disorders
6
Cognitive domains specified
DSM-IV
• Memory impairment
• Aphasia
• Apraxia
• Agnosia
• Executive
dysfunction
Footer Text
DSM-V
• Complex attention
• Executive function
• Learning & memory
• Language
• Perceptual-motor
• Social Cognition
7
When diagnosing, it is just as important to
eliminate non-NCD conditions to determine
which disease(s) are present
Amnestic 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)
Footer Text
8
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
Footer Text
9
What are the
common causes of
NCD?
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)
Footer Text
11
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)
Footer Text
12
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
Footer Text
13
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
Footer Text
14
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
Footer Text
15
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)
Footer Text
16
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
Footer Text
17
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
Footer Text
18
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
Footer Text
19
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
Footer Text
20
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
Footer Text
21
How to evaluate and
manage a person
with possible
dementia
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
Footer Text
23
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
Footer Text
BP, diabetes, lipids, alcohol
24
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
Footer Text
25
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
Footer Text
26
Screening tools and further investigations
Screening 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)
Footer Text
27
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
Footer Text
28
Mini-Mental State Examination (MMSE)
Folstein et al : J Psych Res 1975;12:189-98
Score
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
Footer Text
1
Read and obey the following: “close your eyes”
1
Write a sentence
1
Copy intersecting pentagons
29
Footer Text
30
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
Footer Text
31
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
Footer Text
32
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
Footer Text
33
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.
ii.
iii.
Diagnosis of Alzheimer’s Disease, confirmed by, or in consultation with, a specialist
Initial MMSE score with date of score
Sole PBS-subsidised therapy for this condition
If continuing treatment: send a written application (triplicate script) and send off to above. Include:
i.
ii.
Patient must demonstrate a clinically meaningful response to initial Rx
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
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
Footer Text
35
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
Footer Text
36
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
Footer Text
37
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
Footer Text
38
When we receive a referral
Footer Text
39
Questions?
Footer Text
40