Transcript Dementia and Primary care - Barnet, Enfield and Haringey

Dementia & Primary Care
Dr. Robert Tobiansky (Barnet Consultant)
Dr Jonathan Hare (Enfield Consultant)
Dr. Michael Payne (Haringey Consultant)
Barnet, Enfield & Haringey Mental Health Trust
Overview of clinical aspects of Dementia
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Definition & prevalence of Dementia
Differential Diagnosis
Management & investigations
the role of medication, including ACHEIs
Management as a GP
Community services
Medico-legal issues Consent & Capacity
National Dementia Strategy
Published 2 Feb 2009
 Five year plan
 17 interlinked objectives
 £150 million extra funding
Four key themes
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Improving awareness
Early better diagnosis
Improved quality of care
Delivering the Strategy
Objectives of the National Dementia Strategy
Dementia care pathway
Primary
care
Social
care
Specialist older
people’s mental health
services
Help
seeking
DIAGNOSIS
specialist care
Social care
community &
care homes
Acute
Trusts
1. Encourage help
seeking and referral
2. Locate responsibility for
early diagnosis and care
Primary
Care
Peer & Vol.
Sector
Support
3. Enable good quality
care tailored to dementia
DEMENTIA:
DEFINITION
Dementia
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A syndrome due to disease of the brain
usually of a chronic or progressive nature
Multiple disturbances of higher cortical
function
Global impairment: intellect, memory,
personality
Changes in emotional control, social
behaviour, motivation
In clear consciousness
Decline in usual functional abilities
EPIDEMIOLOGY
OF DEMENTIA:
 Nature Reviews Neurology
 Reitz et al 2011
Epidemiology of Dementia:
 Global prevalence 24 million predicted to double
every 20 years to 2040
 5% over 65 years
 20% over 80 years
 Over 65 years - prevalence doubles every 5 yrs
 Annual incidence c. 9 / 1000 population
Dementia: key points
 Prevalence increases with older age
 rare in < 65, if suspect in younger
patient refer to neurologist
 diagnosis based on History, Physical &
mental state examination & routine
investigations
DEMENTIA:
COMMONEST TYPES
Dementia
Many causes but commonest are:
 Alzheimer’s Disease
 Vascular Dementia
 Lewy Body Dementia
 Alcohol related dementia
 Frontotemporal dementia
Alzheimer’s Disease:
Neuropathology
 Atrophy, widened sulci, shrunken gyri
 Amyloid plaques: extracellular, swollen
neuronal processes with core of amyloid-b(Ab)
 Neurofibrillary tangles (NFTs): intracellular,
hyperphosphorylated Tau (microtubule
assembly protein) forms insoluble aggregates =
PHF
 Widespread loss of neurones & synapses
 Granulovacuolar degeneration
 Gliosis, loss of dendrites
 Hirano bodies (eosinophilic, cigar shaped)
AD: Neurochemical changes
 Best described: diminished Acetyl-Choline, CAT,
cholinergic neurones (Basal n. Meynert)
 Also reduction in GABA, NA, 5HT etc
Risk Factors for AD:
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Age
Family History (genes on chromosome 21, 14, 1, 19)
Down’s Syndrome
Head injury
Limited education
Risk factors for Vascular Dementia (Diabetes,
hypertension, obesity, AF, lipids etc)
AD Genetics 1: Young-onset
 Familial Alzheimer’s Disease - autosomal dominant,
small minority, young onset, APP mutations
– Ch21: beta amyloid precursor protein gene
– Ch14: presenilin 1 gene
– Ch1: presenilin 2 gene
– All lead to Ab aggregation (increased Ab42)
imbalance between Ab production & clearance
AD Genetics 2: late onset
 Non-Mendelian AD
– great majority of cases
– genetic + environmental factors
– first degree relatives of late-onset AD patients have
2x expected lifetime risk
 Ch19: apolipoproteinE; lipid binding protein in 3
isoforms e2; e3; e4
1x e4 = 2-3 fold increase in AD risk
2 x e4 = 5 fold increase in AD risk
Lowers age of onset by 7 years
AD Genetics 2: late onset
 Various other genes implicated with weaker
effects, all thought to involve increased Ab42 e.g:
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Sortilin-related receptor 1 gene (SORL1)
Clusterin gene (CLU)
Complement receptor type 1 gene (CR1)
Phosphatidylinositol-binding clathrin assembly protein
(PICALM) gene
Biomarkers for AD
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Contribute to increased specificity of diagnosis
In AD CSF levels of Ab42 lower (less soluble)
CSF elevated total TAU & Phosphorylated Tau
Total Tau levels increase with AD progression
Structural MRI: medial temporal lobe atrophy
Vascular Dementias
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Includes Multi Infarct Dementia
Single strategic infarct
Subcortical VAD (Binswangers) / SVD
Hypoperfusion Dementia
Specific Arteriopathies (eg CADASIL)
NINDS-AIREN Criteria for VaD
(Roman et al, 1993)
 Dementia (memory and 2 or more domains)
 Cerebrovascular disease (focal neurology and
CVD on brain imaging)
 Link between the 2 (3 months or
abrupt/fluctuating clinical course)
 Possible VaD if brain imaging negative or
relationship (3/12) not clear
NINDS Neuroimaging Criteria for VaD
 Topography
• Large vessel strokes
• Extensive white matter change
• Lacunes (frontal/basal ganglia)
• Bilateral thalamic lesions
 Severity
• Large vessel lesion of dominant hemisphere
• Bilateral strokes
• WML affecting >25% white matter
(Price et al, 2005)
VAD: Neuropathology:
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Micro – infarcts
Cystic necrosis of infarcted areas
Reactive gliosis
Patches of demyelination of white matter
Risk Factors for VAD:
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Old Age
Family history
Male sex
Geography & race
Hypertension
Smoking
Diabetes
Cardiac arrhythmia
Hyperlipidaemia
Increased homocysteine
Hachinski Ischaemic Score:
 Abrupt onset (2)
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Stepwise deterioration (1)
Fluctuating course (1)
Nocturnal confusion (1)
relative preservation of personality (1)
Depression (1)
Somatic complaints (1)
Emotional incontinence (1)
History of hypertension (1)
History of strokes (2)
Evidence of atherosclerosis (1)
Focal neurological symptoms (2)
Focal neurological signs (2)
< 4 suggests AD > 7 suggests VAD
Dementia with Lewy Bodies
 a progressive degenerative brain
disease
 shares symptoms - and sometimes
overlaps - with Alzheimer’s and
Parkinson’s
Dementia with Lewy Bodies
 Lewy Body = smooth round
intraneuronal inclusion bodies
 LBs throughout cortex, midbrain or
brainstem
 “abnormal protein structures” first
described in 1912 by Frederich Heinrich
Lewy
Criteria for Probable DLB
McKeith et al, Neurology, 2005
 Cognitive decline sufficient to interfere with
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social/occupational function
CORE features (at least one core + one suggestive or 2
core features must be present):
- Fluctuation
- Recurrent visual hallucinations
- Spontaneous parkinsonism
 Suggestive features:
- REM sleep behaviour disorder
- Neuroleptic sensitivity
- Dopaminergic abnormalities in basal ganglia
on SPECT/PET
Features supportive of the Dx of
DLB are:
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Repeated falls
Syncope
Transient loss of consciousness
Neuroleptic sensitivity
Systematized delusion
Hallucinations in other modalities auditory,
olfactory or tactile
DEMENTIA:
GENERAL SIGNS & SYMPTOMS
Dementia: general signs &
symptoms
 Early stages:
– memory impairment, loss of planning, judgement,
difficulty with administrative tasks etc
 Intermediate
– impaired basic ADL can’t learn new information,
increasing disorientation time & place
– increased risk of falls and accidents due to confusion
and poor judgment
Dementia: signs & symptoms
 Severe dementia: no ADL skills, totally dependent for
feeding, toileting, & mobilising. Severe global cognitive
impairment
 risk of malnutrition and aspiration
 poor mobility & malnutrition increases risk of pressure
sores
 Seizures, dehydration, malnutrition, aspiration, pressure
sores
 death from infection (resp., skin, UTI etc)
Dementia: signs & symptoms
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Behavioural problems (BPSD):
Persecutory delusions, suspiciousness in c. 25%
wandering, aggression, agitation
Depressive symptoms in c. 60%
Depression in c. 25%
Dementia: Diagnosis & Investigations
A clinical diagnosis
History from an informant
Physical examination
Medication review
Mental state examination & cognitive assessment
(AMT or MMSE)
 Bloods: FBC / ESR / U+E / LFT / TFT / Glucose /
Ca + Po / B12 + Folate / +/-Treponema serology
 CXR, ECG
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Additional investigations:
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If indicated from history & examination:
CT: cortical atrophy, widened ventricles in AD.
Evidence of vascular disease in VAD. Exclude SOL
MRI: v. sensitive for VAD
SPECT valuable in differentiating AD, VAD, FTD (DAT
scan for suspected DLB)
EEG (non-specific diffuse slowing of alpha rhythm.
Delta & theta activity
psychometric testing if unusual presentation or
uncertain
NICE/SCIE Guidelines for
Dementia 2006
 MRI is preferred modality, CT can be used
 Structural imaging should be used to exclude other
cerebral pathologies & help establish subtype
 HMPAO SPECT can be used to help differentiate
between AD, VaD and FTD if diagnosis is in doubt
 FP-CIT SPECT should be used to help establish
 The diagnosis of DLB if the diagnosis is in doubt
Additional investigations
 Increasing recognition of value of CSF biomarkers CSFtau & CSF-Aß42 as Diagnostic Markers for
Alzheimer Disease
 these biomarkers may have a role in the clinical workup
of patients with cognitive impairment, especially to
differentiate early AD from normal ageing
 low CSF β-amyloid 1-42, high total tau protein, and
elevated phosphorylated tau181P predict AD
Management of Dementia:
 Treat medical disorders & any causes of disability
(mobility, vision, hearing etc )
 Treat BPSD: depression, psychosis, behaviour
disturbance
 Assess ADLs and maximise function, assess risk
(occupational therapist)
 Finances: LPOA, COP, testamentary capacity, benefits
(attendance allowance), council tax exemption (social
worker),
 Early referral to social services (do not wait for
secondary care)
Management of BPSD in Dementia:
(Iliffe)
 P: Physical: pain, infection,
constipation
 A: Activities of others:
misinterpretation
 I: Intrinsic to dementia: walking,
pacing activity
 D: Depression or delusions
Management of dementia:
 Home alone with support from social services:
 Home with care package eg. carer for personal
& domestic care, meal preparation, shopping,
cleaning, etc. supervise medication
 Meals on wheels
 Day centre to increase socialisation &
stimulation
Management of Dementia:
 Support for carers: Alzheimer’s Society / Age
Concern / BCAS advice & support groups
 Respite care
 DHTT if acute severe behavioural problems
 Higher prevalence of depression & anxiety in
carers
 Alternatives to home care (dependency & risk):
extra care sheltered housing, residential &
nursing homes
 NHS continuing care funding
Management of Dementia: Medication
 Medication for cognitive impairment
(cognitive enhancing drugs)
 Medication for BPSD
Management of Dementia: Medication
 Anti-dementia drugs:
- Cholinesterase inhibitors: (Approved by NICE)
Donepezil (Aricept)
Rivastigmine (Exelon)
Galantamine (Reminyl)
- Memantine (Ebixa) (approved by NICE for severe
Dementia March 2011)
Cholinesterase Inhibitors:
 Cholinesterase inhibitors for Alzheimer's
disease Birks Cochrane Database of
Systematic Reviews
The three cholinesterase inhibitors are
efficacious for mild to moderate Alzheimer's
disease. Despite the slight variations in the
mode of action of the three cholinesterase
inhibitors there is no evidence of any
differences between them with respect to
efficacy.
Memantine (Ebixa)
 Memantine for dementia
Cochrane Database of Systematic Reviews
 Authors' conclusions: Memantine has a small
beneficial effect at six months in moderate to severe
AD. In patients with mild to moderate dementia, the
small beneficial effect on cognition was not clinically
detectable in those with vascular dementia and was
detectable in those with AD. Memantine is well
tolerated.
Future developments:
 Disease modifying drugs:
 2 proteases beta and gamma- secretase
 cleave the APP into A-beta fragments which
form amyloid plaques
 APP Beta secretase Gamma secretase Abeta
 Beta secretase (BACE= beta site APP clearing
enzyme)
 Future development of BACE inhibitors?
 Inhibitors of tangle formation?
Management of Dementia: Medication
for BPSD
 Antidepressants
 Antipsychotics
 Anxiolytics
 Hypnotics
Defensible prescribing of
antipsychotics in Dementia
Consider non-pharmacological alternatives
Address vascular risk factors
Consent / capacity / best interests
Discuss risks & benefits with patients or carers
Identify target symptoms (psychosis, hostility,
aggression)
 Choose effective drug & dose
 Choose time-frame during which to assess benefits
(discontinue if no evidence or if harm)
 If good response review need & aim to withdraw in c
3/12 if possible
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Depression vs. Dementia
Clinical
features
Onset
Duration
Mood
Responses
Memory loss
Self image
Associated
symptoms
Previous
history
Depression
Rapid
Weeks
Depressed
“Don’t know”
Poor concentration
Low self esteem
Anxiety, insomnia,
anorexia, life not
worth living
Past or Fam. Hx.
Depression
Dementia (eg AD)
Insidious
Months/years
Apathy
Minimises errors
Impaired recent memory
Normal
Less common
May be Fam. Hx.
Dementia
Delirium: DSM 4 criteria
 Disturbance of consciousness with reduced
ability to focus, sustain or shift attention
 Change in cognitive function not due to preexisting or evolving dementia
 Development over short period of time – usually
hours or days & tendency to fluctuate during
course of day
Delirium: causes
 Infection
 Drugs (prescribed & illicit, intoxication or
withdrawal)
 Organ failure (cardiac, resp., hepatic, renal)
 Electrolyte disturbance (dehyd. Na/Ca/K)
 Endocrine & metabolic – thyroid, glucose
 CNS- CVA, subdural, SOL
 Nutritional – thiamine
 Malignancy
 hypothermia
Delirium: risk factors
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Age
Illness severity
Dementia & other cognitive impairment
Dehydration
General frailty
Sensory impairment
Alcohol use
Delirium: clinical presentation
 Hyperactive: agitated, hyper-vigilant, restless,
perceptual disturbance, deluded
 Hypoactive: drowsy, apathetic, decreased
speech & movement
 Mixed / fluctuating
Delirium: management
Clarify history
Assessment of physical & mental state
Identify & treat underlying cause
May need to treat neuropsychiatric symptoms
with modest doses of antipsychotics / sedatives
 Well-lit, quiet room, address sensory impairment
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NICE on Delirium (CG 103)
Main focus is prevention in those at risk
Document delirium in all health records
Familiar health carers when possible
Preventive interventions (eg manage pain, sensory
imp., sleep disturbance, multiple meds etc)
 Identify & treat underlying cause
 Communication, reorientation, reassurance
 If distressed – haloperidol or olanzapine
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Dementia in Primary care
 Av. Practice list c. 2000: 10-15 patients with
dementia (Iliffe, 2010)
 1-2 new cases per year
 Much greater numbers in care homes & special
populations e.g. Barnet
Dementia in Primary care
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Systematic review of disease progression
Shared care protocols for ACHEIs
Carer needs
Managing: BPSD, continence, frailty, end of life
care & hospital admission
NSF protocols on Dementia
April 2004:
“GP practices, using agreed
protocols, will be diagnosing,
treating and caring for older people
with depression or dementia”
NSF Protocols / Pathways
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Care pathways: key points
Where to refer?
When to refer?
Should you refer everyone?
Chronic disease model
Dementia: when to refer?
 Diagnosis or care plan uncertain
 AD (mixed, DLB) MMSE 10 -20/30 for antidementia drug treatment
 Marked behaviour disturbance, risk of harm to
self or others
 Severe mood or psychotic symptoms
Dementia: when to refer?
Do not need to refer if:
 Diagnosis is apparent & clear management plan
 Patient has already been assessed in secondary
care and care needs are unchanged
 Vascular Dementia without behavioural concerns
 NB do refer directly to social services for needs
assessment
Dementia: management
 Always exclude Delirium
 May need referral to MHSOP, social services,
Alzheimer’s society, Geriatrician, Age Concern
etc
 “chronic disease model” - will need long term
monitoring and regular reviews by primary care
team and in some cases “shared care”
Age Changes Over Time
Prevalence of Dementia BEH
Dementia UK Report 2007
Men
Women
YOD
Total
Barnet:
1262
2358
86
3707
Enfield:
851
1625
61
2537
Haringey:
459
743
40
1242
TOTAL BEH
7486
NICE Dementia Guidelines: Barnet
Dementia UK Report 2007
 3707 people in Barnet have dementia
 This is the single largest number of
all London boroughs
 By 2021 this will have increased by 20%
to 4435 people
Numbers of referrals to MHSOP
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1999
2000
2001
2002
2003
2004
2005
2009
941
1081
1203
1268
1482
1562
1610
1750
Doctors contacts, excluding DNA/cancelled appt.,
counting each patient only once
Investing in treatment of
dementia: medication
 Developments in novel drug treatments specifically for
dementia
 Currently only c. 25% receive specialist assessment &
treatment
 Early referrals: uncomplicated, chance for prevention of
crises
 Drug and non-drug costs
 Disease modifying compounds in development
Investing in treatment of
dementia: other aspects
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More holistic dementia care
aromatherapy, light therapy, massage
interpersonal approaches
training for GPs in recognition & management
training & support for carers
providing a spectrum of care: at home, day care
(available, appropriate), respite care, quality dementia
care homes
DOES THIS PATIENT HAVE
CAPACITY?
Test for Capacity – S. 3(1)(c) MCA 2005
A person is incompetent if he is unable:
 To understand the information relevant to the
decision;
 To retain that information; - (s.3(3))
 To use or weigh that information as part of the
process of making the decision; or
 To communicate his decision (whether by
talking, using sign language or any other means)
Definition of Incapacity – (S. 2(1)
MCA 2005)
 “A person lacks capacity in relation to a matter if
at the material time he is unable to make a
decision for himself in relation to the matter
because of an impairment of, or a disturbance in
the functioning of, the mind or brain”  Capacity can fluctuate and a person can
therefore lack capacity in relation to one matter
but not in relation to another – S.2(2)
Principles Regarding Persons who
Lack Capacity
 A person is presumed to have capacity; S.1(2)
 A person is not to be treated as unable to make
a decision unless all practicable steps to help
him to do so have been taken without success;
S.1(3)
 A person is not to be treated as unable to make
a decision merely because he makes an unwise
decision; S.1(4)
Capacity – MCA 2005
 Consideration should be given to the person’s
past and present wishes and feelings and the
beliefs, values and any other factors that would
be likely to be taken into account if the person
had capacity. S.4(6)
 Take into account written statements made while
P had capacity. S.4(6) (see explanatory notes
Capacity – MCA 2005
 Take into account if practicable and appropriate views
of:– Anyone named by the person as someone to be
consulted.
– Anyone engaged in caring for the person or
interested in his welfare.
– Any donee of a LPA
 Will have complied with the law if you reasonably
believe that what you are doing is in the P’s best
interests S.4(9)
Can Dementia be prevented?
 Kurth & Logroscino BMJ 2010:341:310-1
 Modifiable risk factors exist but too early to call
for prevention programmes
Can Dementia be prevented?
 Ritchie et al BMJ 2010:341:
 Cohort study, 1433 people Montpellier followed
from 1999 for7 years
 Predictors of dementia: crystallised intelligence
(vocab & gen. knowledge), Depression, Fruit &
veg consumption, diabetes & apolipoprotein E4
allele
 Theoretical elimination of depression & diabetes
& increase in fruit & veg consumption estimated
would reduce burden of dementia by 21%
Can Dementia be prevented?
 Age & genetic factors strongest risks
 Life-style risk factors modulate the risk for
dementia and Alzheimer‘s disease
 Cardiovascular risk factors
 Nutritional factors
 Behavioural factors (physical & psychosocial
activity)
 Risk appears to be modulated by APO E4 status
 Intervention in middle age may reduce risk
Possible Protective factors:
Weak evidence of protective effect for:
 Mediterranean diet
 Physical activity
 Intellectual activity
Survival after diagnosis of
dementia in primary care
 Rait et al BMJ 2010;341:337
 Health improvement network primary care
database incidence of dementia in primary
care 1990-2007, compare survival from
diagnosis to those without dx
 Cohort of 22529 recorded dx dementia
 Incidence 3-4/1000 person years
 Median survival those 60-69 years was
6.7years (range 3-11)
 Survival for >90 years was 1.9 years(0.7-3.6)
Survival after diagnosis of
dementia in primary care
 Mortality rates 3x higher in first year after
diagnosis of dementia than people
without(RR 3.68)
 2.5x greater risk subsequently
 Median survival signif. lower than screened
populations
CASES
FOR DISCUSSION
Cases for discussion: Case 1
• 88 year old woman with no past psychiatric
history. She lives alone at home , supported by
her daughter who visits 3x weekly.
• The daughter rings you reporting that her
mother has been confused over the past 2 days,
is disorientated in time, claims that strangers
are entering her house and accuses the cleaner
of stealing her purse.
1. What is the most likely explanation for the presentation?
2. How would you assess & manage this situation?
Cases for discussion: Case 2
78 year old man lives at home with his wife. She reports
that he has a 1 year history of increasing forgetfulness. He
is upset as he claims that strange people, including
children, keep entering his bedroom at various times. He
has poor mobility and frequent falls. He has episodes of
marked confusion but at other times can be more lucid.
1. What is the most likely diagnosis and DDx?
2. What neuroimaging might be useful here?
3. What drugs would you consider for the hallucinations?
Cases for discussion: Case 3
 You receive a letter from a solicitor, “your
patient wishes to make a new will… does
he have Testamentary Capacity?”
 “Could you also please tell me if he has
capacity to donate Lasting power of
Attorney?”
How do you proceed?