Dementia Care

Dementia Care

1. GP Presentation:
Dementia Update
Belinda McCall
Consultant in Elderly Medicine
Trust lead for Dementia
Lewisham and Greenwich NHS Trust

2. Scope of the problem
What is dementia
Early diagnosis
Treatment
Behavioural and psychological symptoms of dementia and
Antipsychotics
The Lewisham Memory Service
The future
Outline

3. *6% of individuals over 65
1
*20% of individuals over 80
*850,000 cases in UK currently
2
*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 2001
2. Alzheimer’s research UK 2015
Dementia
epidemiology

4. *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

5. Alzheimer's and other
dementias

6. *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

7. Risk factors for AD

8. 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

9. *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

10. 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 65yrs
5.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)

11. Prevalence of Dementia Sub types

12. *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)

13. 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

15. *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:

16. Molecular Targets for Current AD Therapies

17. Plaques and tangles
senile plaque and neurofibrillary degeneration (silver impregnation)

18. MCI vs. Alzheimer’s Disease

19. *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

20. *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.

21. 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.

22. *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

23. Early diagnosis

25. •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

26. Early Diagnosis
Healthy Individual
Memory Occasional
lapses
Orientation fully
Judgement &
problem solving
Solves everyday
problems
Outside home Independent
functioning
At home Activities &
interests
maintained
Personal careFully capable
Early Dementia
Memory 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

27. *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?

28. *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?

29. *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

30. *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

31. *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 30months
 
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

32. *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

33. 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

34. *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

35. treatments

36. *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

37. *Alzheimer’s disease
*Mild to moderate
*Anticholinesterase inhibitor (ACI) therapy
*Donepezil (1
st
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

38. 1.5
1.2
0.9
0.6
0.3
0.0
–0.3
–0.6
–0.9
–1.2
–1.5
0 6 12 18 Endpoint 30
Study week
C
h
a
n
g
e

i
n

M
M
S
E
Clinical improvement
Clinical decline
Placebo
Aricept:
5 mg/day
10
mg/day
AriceptAricept trialtrial

Rogers et al. Neurology 1998;50:136–145
MMSE ResultsMMSE Results

39. *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….

40. 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

41. Behavioural and Psychological
symptoms of dementias (BPSD)

42. Definition
Signs 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

43. *Depression
*Anxiety
*Delusions
*Hallucinations
*Paranoid ideas
*Misidentification
*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

44. 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.

45. * 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

46. *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

47. *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:

48. *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

49. *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

50. *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

51. *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

52. Lewisham memory service

53. 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 dementia
A high quality service for the assessment, diagnosis and
management of dementia until end of life
Support and advice for carers and patients about dementia and the
range of services available within the borough
Assessments 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

54. 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 Lewisham
Social 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

55. - 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
Acknowledgemen
t of referral
Triage (Duty)
Waiting-List
Waiting-List
Case
Resolved
without
assessment
Inappropriat
e 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

56. *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?

57. Inpatient Services at UHL

58. *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)

62. *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)

63. *Appointment of specialist dementia nurse
*CQUIN
*Full implementation of pathway
*Weekly Carers café with dementia advisors and carers
Lewisham
*Regular cognition steering group meetings
*Reminiscence pod- oak ward
Inpatients (3)

64. The future

65. 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

66. Systematic review:
*global assessment,
*shared care of cholinesterase inhibitors,
*carer needs.
*BPSD
*Continence
*Frailty
*End of Life care & hospital admissions
Disease progression

67. *Continuity of contact
*Population reach
*Pattern recognition
*Experiential learning
*Problem solving not protocol driven
*Systematised care
Core business in general practice

68. 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

69. 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

70. 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?

71. 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

72. *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 are
due to vascular disease, over weeks are due to depression,
and over months are due to dementia
TIPS FOR NON-SPECIALISTS

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

74. Any questions………………….?
Thank you for listening and