GP Presentation:Dementia Update

Belinda McCallConsultant in Elderly Medicine

Trust lead for DementiaLewisham and Greenwich NHS Trust

Scope of the problemWhat is dementiaEarly diagnosisTreatmentBehavioural and psychological symptoms of

dementia and AntipsychoticsThe Lewisham Memory ServiceThe future

Outline

6% of individuals over 651

20% of individuals over 80 850,000 cases in UK currently2

Current cost of dementia £14.3bn – more than stroke, heart disease and cancer combined

Number of people with dementia will increase by 40% in next 15 years

1. Lobo et al 20012. Alzheimer’s research UK 2015

Dementiaepidemiology

2/3 people with dementia are at home Unpaid carers save the tax payer £5.4 billion a

year Annual economic burden of late onset dementia is

£14.3 billion-most falls on families The National Audit Office estimated the xs cost at

more than £6 million / yr in an average general hospital.

NHS care £1.17 billion a year

Costs of dementia

Alzheimer's and other dementias

Is a clinical syndrome Characterised by difficulties in memory, language,

psychological and psychiatric changes, and impairments in activities of daily living.

Is one of the main causes of disability in later life In terms of global burden, it contributes 11.2% of

all years lived with disability Higher than stroke (9.5%); musculoskeletal disorders

(8.9%); heart disease (5%); cancer (2.4%)(Alzheimer’s Society. Dementia UK: the full report.London;AS.2007)

Dementia

Risk factors for AD

Hypthyroidism May lead to a dementia syndrome

Hypercalcaemia May mimic dementia

Hypoglycaemia May be associated with confusion and symptoms similar to dementias

Nutritional deficiencies

May be associated with the dementia syndrome

Kidney and liver disorders

Liver disease and dysfunction, often secondary to alcohol abuse, may lead to the dementia syndrome (90% of alcoholics develop dementia)

Infections

Chronic infections may be associated with a dementia-like condition. Conditions such as borrelioses, neurosyphilis and HIV can lead to dementia and should be considered when the patient's lifestyle or history indicates risk. AIDS-related dementia is probably a direct consequence of HIV infecting the central nervous system (CNS)

Normal pressure hydrocephalus

This is a brain potentially reversible disorder caused by blockage of the flow of the CSF. It leads to enlargement of the ventricles and compression of brain tissue. As a result brain atrophy and dementia can occur. Structural brain imaging techniques such as CT scanning can establish whether this disease has caused the dementia

Some potentially reversible causes of the dementia

syndrome

Cognitive function Progressive loss of short-term memory Difficulty in registration and recall of new information Language problems e.g. repetition Poor or reduced judgement

Behavioural changes Aggression, disinhibition, social withdrawal, wandering,

disorientation Inability to perform usual activities of daily living

Psychiatric problems Associated mood disorder Delusions/hallucinations

Physical debility Self-neglect Incontinence Falls

Clinical Presentation

Common types of dementia:1. Alzheimer’s dementia (60% cases)2. Vascular dementia (20% cases)3. Lewy body dementia (15% cases)4. Frontotemporal dementia (FTD) – 20% cases below

65yrs5. Rarer causes: Hypothyroidism Normal pressure hydrocephalus Dementia in movement disorders e.g. PD, PSP Vitamin B12/folate deficiency Wernicke-Korsakoff dementia Neurosyphilis HIV/AIDS dementia Huntington’s disease Hypercalcemia Creutzfield-Jacob disease (CJD)

Prevalence of Dementia Sub types

Characterised by 3 groups of symptoms Cognitive dysfunction

Memory loss, language difficulties, executive function (loss of higher level planning, intellectual coordination skills), visuospatial skills, attention

Psychiatric symptoms & behavioural disturbances Depression, anxiety, delusions, agitation

Difficulties performing ADLs Complex activities: driving, shopping Basic activities: dressing, eating unaided

A person with AD is 30% more likely to display clinical features of dementia if they have coexisting symptoms of vascular disease(JAMA 1997;277:813-7)

Alzheimer’s Disease (AD)

The pathogenesis of AD is poorly understood

Pathways believed to contribute to neuronal dysfunction and death include:–Decreased acetylcholine synthesis and impaired cholinergic function–Glutamatergic excitotoxicity–Direct toxicity of β−amyloid peptide–Mitochondrial dysfunction–Increased oxidative stress–Activation of apoptotic pathways–Release of inflammatory mediators–Impaired calcium signalling and regulation

•These pathways represent targets for existing and novel AD therapies

Pathogenesis of Alzheimer’s Disease

Multiple cognitive deficits, including memory impairment and at least one of: Aphasia - problems with language (receptive and

expressive) Apraxia - inability to carry out purposeful movements

even though there is no motor or sensory impairment Agnosia - failure to recognise things and especially

people Decreased need for sleep

Cognitive deficits severe enough to interfere with occupational and/or social functioning

Cognitive deficits represent a decline from previously higher function

These deficits do not occur exclusively during the course of delirium

DSM IV Criteria for diagnosis of dementia:

Molecular Targets for Current AD Therapies

Plaques and tangles

senile plaque and neurofibrillary degeneration (silver impregnation)

MCI vs. Alzheimer’s Disease

Criteria for diagnosis: Memory complaints, preferably corroborated by an

informant Impaired memory function for age and education Preserved general cognitive function Intact activities of daily living No evidence of dementia

Prospective studies have shown that people with amnestic mild cognitive impairment are up to 15 times more likely to have developed dementia at follow-up

Mild Cognitive Impairment

Vascular dementia is the second most common cause of dementia, after Alzheimer's disease.

It accounts for up to 20 % of all dementias and is caused by brain damage from cerebrovascular or cardiovascular problems - usually strokes.

It also may result from genetic diseases, endocarditis or amyloid angiopathy.

It may coexist with Alzheimer's disease.

Unlike people with Alzheimer's disease, people with vascular dementia often maintain their personality and normal levels of emotional responsiveness until the later stages of the disease.

People with vascular dementia frequently wander at night and often have other problems commonly found in people who have had a stroke, including depression and incontinence.

In Lewy body dementia, cells die in the brain's cortex , and the substantia nigra. Many of the remaining nerve cells in the substantia nigra contain abnormal structures called Lewy bodies that are the hallmark of the disease.

The symptoms of Lewy body dementia overlap with Alzheimer's disease in many ways and may include memory impairment, poor judgment, and confusion.

Lewy body dementia typically also includes visual hallucinations, parkinsonian symptoms such as a shuffling gait (walk) and flexed posture, and day-to-day fluctuations in the severity of symptoms.

Patients with Lewy body dementia live an average of 7 years after symptoms begin.

There is no cure for Lewy body dementia, and treatments are aimed at controlling the parkinsonian and psychiatric symptoms of the disorder.

Rivastigmine can be used to manage symptoms.

Abnormal processing of tau protein

Insidious onset, slow progression

Predominantly affects the frontal and anterior temporal lobes

Rare over age 65 Behavioural features,

impulsivity, personality change, urinary incontinence, disinhibition

Can develop non-fluent aphasia, economy of speech or repetition

Memory and visuospatial ability are relatively preserved in the early stages

Early diagnosis

• History (collateral)• Cognitive function assessments

AMT < 8 (needs further assessment) GPCOG (9 points) MOCA (30 points) MMSE (30 point)

• Score ≥ 25 (normal)• Score 19 – 24 (mild)• Score 10 – 18 (moderate)• Score ≤ 9 (severe)• Does not test executive function, so possible to have a

normal score and still have cognitive deficits Addenbrooke’s Cognitive Examination (ACE-R) – 100

point• Score < 82 suggestive of dementia

• Clinical examination Exclude other pathology Look for clues of self-neglect

Diagnosis

Early DiagnosisHealthy Individual

Memory Occasional lapses

Orientation fully

Judgement & problem solving

Solves everyday problems

Outside home Independent functioning

At home Activities & interests maintained

Personal care Fully capable

Early DementiaMemory Loss of memory for

recent events

Orientation Variable disorientation in time & space

Judgement & problem solving

Some difficulty with complex problems

Outside home Engaged in some activities but not independently. May appear normal

At home More difficult tasks & hobbies abandoned

Personal care Needs some prompting

Timely diagnosis allows people to make future plans, reduces crises, delays institutionalisation and provides support for carers (Prince et al., 2011).

Some evidence of increase in quality of life and decrease in carer stress.

Reassures worries taken seriously, confirms suspicions Reduced prescribing conflicts Reduced safeguarding events (ADASS) Lower risk of unnecessary hospital admission (Kernow, BANES) Identification of treatable physical and psychiatric causes Treatment of co-morbid conditions Instigation of pharmacological symptomatic treatments Early diagnosis is still a key aim of current dementia policies in the

Western world, including the UK National Dementia strategy (Department of Health, 2009).

Why diagnose?

No disease-modifying treatments or evidence about risks of diagnosis. There is ongoing debate about the benefits of diagnosing dementia (Fox et al., 2013, Carol Brayne ).

BUT autonomy is a high ethical standard. Doctors have given up deciding whether competent patients should know their diagnosis for other illnesses.

Why not diagnose?

Why not diagnose?

Insidious and variable onset of the syndrome Reluctance to diagnose dementia as it is

such a serious and largely unmodifiable disease

Huge stigma still attached Family members who take over social roles

from the patient, to protect them from difficulties in daily life

Barriers to Early Diagnosis

From the health professional GP writing and inviting the patient Asking if you are allowed to share information with For some enlisting the doctor’s medical “authority”

Helpful strategies

GP education increases the number of suspected dementia cases but not accurate or earlier dementia diagnoses. (Two RCTs)

Six home visits from a specialist geriatric nurse over 30 months increased the rate of accurately diagnosed dementia (One RCT).

Preliminary evidence from non-randomised studies that memory clinics increase timely diagnosis, but not that they increase the overall diagnosis rate.

One non-randomised study of leaflets in community places eg library, found diagnosis rate increased less in intervention borough

The evidence

Often difficult process Problems can be because of professionals,

patients and families Still less than 50% ever – those with a timely

diagnosis must be less Even harder for BME Increasing diagnosis in UK in recent years Trying to develop and test evidence based

interventions

Experience of gaining a dementia diagnosis

In primary care Blood tests:

full blood count, erythrocyte sedimentation rate, urea and electrolytes LFTs, thyroid function tests Vitamin B12 and Folate

Syphilis serology is not recommended as a routine test but can be justified if the apparent course of the syndrome or the presentation is atypical.

Investigations

CT (to exclude intracranial lesions; cerebral infarction and haemorrhage; extradural and subdural haematomas; normal pressure hydrocephalus)

MRI (sensitive indicator of cerebrovascular disease, higher resolution to detect focal atrophy—for example, in hippocampal area)

SPECT (to assess regional blood flow and dopamine scan to detect Lewy body disease)

PET CT

Carotid ultrasonography (if large vessel atherosclerosis is suspected)

Electroencephalography is not part of routine investigations but can be useful if epilepsy or an encephalopathy is suspected

In secondary care

treatments

Non-pharmacological Assistance with ADLs Psychological interventions include cognitive, behavioural and

emotion focused approaches Assistive technology Reduction of carer burden through education and support (respite) Driving

Pharmacological Anticholinesterase inhibitors (Donepezil, Galantamine,

Rivastigmine) Enhance cholinergic neurotransmission by delaying breakdown of Ach Licensed for mild to moderate AD Side effects: GI upset, GI ulceration, headache, sleep disturbance, bradycardias

Memantine Excessive activation of the NMDA (N-methyl-D-aspartate) receptor by glutamate

may contribute to destruction of cholinergic neurones NMDA antagonist Licensed for moderate to severe AD Side effects: headaches, fatigue, hallucinations, constipation

Alzheimer’s disease Mild to moderate

Anticholinesterase inhibitor (ACI) therapy Donepezil (1st line) Galantamine Rivastigmine

Moderate to severe Memantine (NMDA receptor antagonist)

There is no role for the combination use of Donepezil & Memantine at present

Options when patients deteriorate i.e. Move from mild to moderate Continue Donepezil Discontinue Donepezil Switch to Memantine

Treatment

1.5

1.2

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–1.2

–1.5

0 6 12 18 Endpoint 30Study week

Ch

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e in

MM

SE

Clinical improvement

Clinical declinePlacebo

Aricept:

5 mg/day

10mg/day

AriceptAricept trialtrial Rogers et al. Neurology 1998;50:136–145

MMSE ResultsMMSE Results

Over the past 12 years, there have been few candidate drugs for AD and other dementias and frequent failures

Most approaches have targeted amyloid but increasingly anti-tau therapies are being developed

More accurate diagnosis of early AD should improve the development of new treatment options

There are many challenges with clinical trials in (early) AD and different study designs and assessment tools may be needed

In the absence of a cure, treatments targeted at specific behaviours and preventative strategies will be important

Combination approaches may be more productive for cognition, behaviour and to target multiple pathologies beyond amyloid and tau

In development….

Same as cardiovascular prevention but emphasise: Regular exercise Stop smoking Lose weight Social interaction Part of HealthCheck

Especially useful to advise: At risk groups (DES) Worried well Those diagnosed with MCI

Prevention

Behavioural and Psychological symptoms of

dementias (BPSD)

DefinitionSigns and symptoms of disturbed perception,  thought content, mood or behaviour that frequently occur in patients with dementia

1996 International Psychogeriatric Association Consensus

Behavioural and Psychological  (Signs and) Symptoms of  Dementia –

BP(S)SD

Depression Anxiety Delusions Hallucinations Paranoid ideas Misidentificatio

n

Agitation Aggression Wandering Sleep

disturbances Changes in, or

inappropriate eating behaviour

Inappropriate sexual behaviour

Behavioural disturbances Psychiatric symptoms

Ask yourself – how many times have you seen these symptoms in someone with dementia? Remember, dementia is not just having a ‘poor

memory’!

Non-cognitive symptoms of dementia

11 recommendations

• Reducing use is a priority backed up by audit and explicit goals

• Curricula needed

• In reach to homes

• Care Quality Commission

• Access to Psychological Therapies Programme

• People with dementia in their own homes.

750,000 people with dementia in the UK 180,000 people with dementia on

antipsychotics Only 36,000 will derive some benefit from

antipsychotics, but: 1800 additional deaths 1620 additional CVAs

The numbers

Perhaps 2/3 of these prescriptions are unnecessary if appropriate support is available

These include older antipsychotic drugs (e.g. halopeirdol) or newer medications (e.g. quetiapine, olanzapine, risperidone, amisulpride, aripiprazole)

Side effects: greater in older people - increased stroke risk, increased cardiovascular risk, Parkinsonian side effects, falls, additional deaths

These are class effects, not limited to one particular drug

Not licensed for the treatment of agitation (except risperidone)

20-30% of people in nursing homes with dementia are on an antipsychotic

NHS survey 2007/8: 5.3% of people over 65 are prescribed an antipsychotic

These drugs are often inappropriately prescribed to ‘control’ BPSD

Antipsychotics used in dementia

Collateral history is extremely helpful Your clinical assessment:

Behavioural assessment – ABC Antecedents Behaviour Consequences

Physical assessment, e.g. are they in pain?

Mental state assessment to consider alternative causes and treatments, e.g. for depression or sleep disturbance

Look at the mnemonic opposite as a guide for assessing causes of symptoms in people with dementia

Refer if necessary to community mental health team

Think ‘PINCH ME’ to identify any treatable causes of symptoms• Pain• Infection• Constipation• Hydration• Medication• Environmental

Simple patient-centred care plans can help prevent and soothe behavioural and psychological symptoms in patients with dementia:

Non-pharmacological interventions for non-cognitive symptoms and behaviour that challenges

Approaches that may be considered, depending on availability, include: Aromatherapy Multisensory stimulation (Rempod @ UHL) Therapeutic use of music and/or dancing Animal-assisted therapy Massage

Pharmacological interventions for non-cognitive symptoms and behaviour that challenges only if they are severely distressed or there is an

immediate risk of harm to the person or others. Should not be used in mild to moderate dementia

NICE GUIDELINES for managing BPSD

Pharmacological agents used only in severe dementia with severe non-cognitive symptoms Discussion with the person with dementia and/or carers about

benefits/risks of treatment. Monitor cognition at regular intervals. Target symptoms should be identified, quantified and

documented. Exclude/treat depression The dose should be low initially and then titrated upwards. Treatment should be time limited and regularly reviewed

(every 3 months or according to clinical need). Risperidone is the only antipsychotic drug licensed for

treating dementia-related behavioural disturbances; it is indicated for short term use (up to 6 weeks), for persistent aggression in Alzheimer’s dementia, unresponsive to non-drug approaches.

Both Risperidone and Olanzapine have the best evidence base for effectiveness compared with placebo for physical aggression, agitation and psychosis

NICE GUIDELINES for managing BPSD

Should always be considered before drug  interventions for BPSD

Difficult to evaluate rigorously Often anecdotal, relatively non‐specific and

rely on enthusiasts May improve QoL through increased

stimulation or increased enthusiasm among  staff and caregivers 

Non‐drug Interventions

Antipsychotics have a focused but limited role in the short term management of severe aggression and psychosis.

The best evidence base for pharmacological treatment is for short term treatment with risperidone as a treatment for aggression.

The evidence base supports the value of simple non drug interventions and intensive staff training in care homes

Recent evidence re-inforces the potential value of analgesia

Lewisham memory service

Commissioned from South London and Maudsley NHS Foundation Trust (SLaM) and Lewisham HealthCare NHS Trust.

The main purpose of the services will be to provide: Single point of access referral point for a single seamless service Early identification of people with a possible diagnosis of dementiaA high quality service for the assessment, diagnosis and

management of dementia until end of lifeSupport and advice for carers and patients about dementia and the

range of services available within the boroughAssessments available at GP surgeries, home, hospital outpatients

and Community Mental Health Team base Nearly 400 referrals in the first nine months of the service (average

of ten per week)

Assessment, Diagnosis and Treatment service

Multi-disciplinary from statutory and non statutory providers:Administrator (South London and Maudsley NHS Foundation Trust (SLaM))Team manager (SLaM)2 x band 6 community practitioners (SLaM)Consultant psychiatrist (SLaM)Consultant geriatrician (Lewisham HealthCare Trust)Assistive technology Occupational Therapist (SLaM)5 x Dementia advisors (MindCare)Carer Support Worker (Carers Lewisham)Pharmacist (NHS LewishamSocial Workers (London Borough of Lewisham and SLaM)GP lead (NHS Lewisham)

Rest of the Memory team is under the existing Community Mental Health Teams (CMHTs)

The Assessment Team

- MindCare- District Nurses- LINK

- Hospital- Social Services

- Health-Checks- Family- Carers

- IAPT- Psychiatry

- Other Hospitals- Neurology

- Carers (direct referral)-CMHT

-- Wards refer to UHL- GPs to refer to UHL memory

clinic directly

GP

Referral to SPA

Case Allocation

SLaM

UHL

Acknowledgement of referral

Triage (Duty)

Waiting-List

Waiting-List

Case Resolved without assessment

Inappropriate Referral

Appointment booked

Appointment Booked

Initial Assessment at home or

clinic

Appointment Day

CT-Scan, ECG Assessment Diagnosis MindCare

Findings discussed at

MDT

Referral for further tests

Test results are

discussed at MDT

Diagnosis made in MDT

Patient advised of

Diagnosis at home or in

clinic

Letter with diagnosis

send to GP within a

week

D/C letter sent to GP this includes advice where to refer to in case of deterioration or change of circumstances. Including a checklist with potential referral options.

Medication offered

D/C no diagnosis

Letter with diagnosis

send to GP within 2 weeks Medication

offered

Telephone follow-up after 1 month and face-to-face follow-up after 4 months. D/C back to GP only once stable.

Review after 2-3 months at clinic and again a 6 months clinic appointment. If stable D/C back to GP

People with cognitive impairment on their screening test

Anyone worried about their memory Younger patients with a family history of AD Patients with cognitive impairment and

behavioural symptoms should be referred to CMHT

Who should be referred?

Inpatient Services at UHL

Development of a dementia pathway based on the health care for London Dementia service guide

Opportunistic screening for confusion of all patients over 75 admitted Acute admissions via A&E Elective admissions via pre-assessment

Implementation of dementia passports and patient identifier for patients with cognitive impairment

Involvement of carers in the patient’s treatment plan

Inpatients (1)

Staff training Development of ward dementia champions Review of antipsychotic use in patients

admitted with dementia Participation in National Dementia Audit Guidelines for management of delirium Protocol for the management of patients

with challenging behaviour End of life care for advanced dementia

(PEACE plan)

Inpatients (2)

Appointment of specialist dementia nurse

CQUINFull implementation of pathway

Weekly Carers café with dementia advisors and carers Lewisham

Regular cognition steering group meetings Reminiscence pod- oak ward

Inpatients (3)

The future

Survival with dementia

Median 7.1 years with Alzheimer’s dementia, 3.9 years with vascular dementia. (Fitzpatrick et al J Neurological Sciences 2005)

4.5 years from symptom onset (Xie J et al BMJ 2008; 336: 258-262)

3.5 years from diagnosis (Rait et al, 2010)

Prognosis

Systematic review:global assessment,shared care of cholinesterase inhibitors,carer needs.BPSDContinenceFrailtyEnd of Life care & hospital admissions

Disease progression

Continuity of contact Population reach Pattern recognition Experiential learning Problem solving not protocol driven Systematised care

Core business in general practice

you are very well placed! Dementia is mainly a social disorder GPs are in their communities You know our patients well (biopsychosocial) You are (still) trusted You can powerfully influence local change The Government & NHS are realising you are more important than maybe they thought before

Why GPs

GPs are trusted and therefore in an ideal position to: Discuss the possibility of having dementia Discuss driving Encourage LPA or ACP Review medication (reduce anti-cholinergic burden, de-escalate) Discuss sharing of information Remind patients/carers about local services

Review

Post diagnosis treatment and co-ordination of care for patients with dementia by GPs

BMJ 2012;344:e3086 175 patients with mild – moderate dementia Assessed the quality of life of patients and

caregivers Memory clinics are effective diagnostic facilities Memory clinics were not more effective than

GPs in regard to post diagnosis treatment and care co-ordination for patients with dementia

The Future?

GPs are good at end of life care for cancer…… …so you can apply those skills to dementia: Quality capacity check and documentation Best Interest Decision-making OOH/EPaCCS handover Careful use of DNR forms Involvement of palliative care services Predicting death is more difficult, mistakes normal

End of Life Care

Occasional lapses of memory are common, especially in the presence of physical illness or stress—if in doubt, offer to see someone again in three months

If you ask a patient a simple question and they immediately turn their head to the spouse, suspect dementia

If you suspect dementia, take a history from an informant

Have a low threshold for referring someone to a memory clinic if you suspect he or she may have dementia

Always consider dementia when seeing a patient, especially an older patient who complains of memory problems

Generally, memory problems developing over days aredue to vascular disease, over weeks are due to depression, and over months are due to dementia

TIPS FOR NON-SPECIALISTS

http://www.england.nhs.uk/wp-content/uploads/2014/09/dementia-revealed-toolkit.pdf

resources

Any questions………………….?

Thank you for listening and