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45 Cards in this Set

  • Front
  • Back
Dementia definition
Normal part of aging
rising as cause of dealth
‘A disorder which involves cognitive and
functional decline often accompanied by
behavioural disturbance and psychosis’

 While the risk of dementia increases with age,
dementia is not a natural part of ageing
Dementia in Australia - occurence with age and total number
 Prevalence increases with age
 65 years and over 1 in 15
 80-84 years 1 in 9
 85 years and over 1 in 4
 Dementia sufferers
 2008: 227,000
 2050: 730, 000`
where will there be higher levels of dementia
what percentage of years does it contribute to living with disability
The rate of increase is predicted to be three to four
times higher in developing areas. This is because of
the rapid ageing of developing countries
 According to the Global Burden of Disease estimates
for the 2003 World Health Report, dementia
contributed 11.2% of years lived with disability in
people aged 60 years and older; more than stroke
(9.5%), musculoskeletal disorders
(8.9%),cardiovascular disease (5.0%), and all forms of
cancer (2.4%)
Difference between AD and normall
age-rellatted memory changes
Alzheimer’s disease
Forgets entire experience
Rarely remembers later
Gradually unable to follow
written/spoken directions
Gradually unable to use notes as
reminders
Gradually unable to care for self
Difference between AD and normall
age-rellatted memory changes
Age related memory loss
Forgets part of an experience
Often remembers later
Usually able to follow
written/spoken directions
Usually able to use notes as
reminders
Usually able to care for self
Why early detection?
Dementia Symptoms
 Early stages
 memory disorders
 problems of orientation
 reduced ability to engage in abstract
reasoning
 learning disabilities
 impaired ability to perform in social and
economic spheres
 word finding problems
 limited visual-spatial abilities
 trouble with construction, i.e. drawing
Dementia Symptoms
 Later stages
 intellectual activity ceases
 apathy
 vegetative state
 muscles weakness
 the person becomes incontinent, including
loss of control of bowel and bladder
Identifying people at risk
 Demonstration of trouble with
construction can be obtained by
asking the patient to draw
something.
 Example of a clock drawn by a
patient who was told to put the hours
on it, and set the time at three-thirty.
 Mini-Mental State Examination
(MMSE) used to grade and monitor
dementia
Cognition and Disease Progress
Types of Dementia and occurence
60%
Alzheimer’s Disease
15%
Vascular dementia
10% lewy body
7% fronto temperol
3% parkisons diesease dementia
7% other
Alzheimer’s Disease - cause
 Caused by aggregation of beta-amyloid
protein in certain areas of brain tissue
 Characteristic plaques and tangles
 Progressive destruction of neurons
Alzheimer’s Disease - onset of symptoms, continue of symptoms, life expectency
 Gradual onset of symptoms
 Initial forgetfulness progresses to profound
memory impairment
 Deterioration in ADLs, behavioural changes
 Later stages - loss of motor skills and
speech
 Life expectancy 8 -10 years
Vascular dementia- risk factors, whats lost, whats preserved, what clincial findings present, progression
Onset may be abrupt or staged
 Patients often have risk factors: diabetes, smoking,
hypertension
 Most patients present with signs of stroke or ischaemic
heart disease
 Often imaging evidence of cerebrovascular disease
 Physical problems such as incontinence, gait disturbance
 Emotional lability and impaired judgment
 Relative preservation of verbal memory and personality
Dementia with Lewy Bodies - clinical occurences, overlap with what disease, onset, sypmtoms, what drugs effective
Lewy bodies found in high numbers in brain cortex
 Neurons degenerate
 Overlap with Parkinson’s
(where lewy bodies
are found in mid brain)
 Progression rapid: severe
dementia and parkinsonism
within 1-2 years
 Frequent visual hallucinations/
delusions
 Sensitive to antipsychotics
Fronto-temporal dementia - sypmtoms matched to progression, age, risks,
 Occurs in younger patients – under 65yrs
 Often patients have family history
 Personality change and social
disinhibition early signs
 Language problems
 Memory deficits occur late in disease
Many patients have mixed dementia
 20-40% of dementia patients
 Often one type dominant
Reversible causes of
dementia
D drugs
E emotional illness (depression)
M metabolic / endocrine (hypothyroidism)
E ear / eye / environment
N nutritional / neurological
T tumours / trauma
I infection
A alcoholism / anaemia / atherosclerosis
Cognitive impairment and
medication - why drug history important, what drugs impliacated, what symptoms, what should be done b4 dementia is diagnosed
 Taking a thorough drug history is important when
assessing an older patient, as use of medications may be
the most common and most easily reversible factor
contributing to cognitive impairment.
 Many drugs cause a multitude of psychiatric symptoms,
including psychosis, disinhibition, and emotional lability.
Further, there are a number of medications that may be
linked to cognitive impairment by inducing delirium,
confusion or memory loss.
 e.g Anticholinergics, anticonvulsants, tricyclic antidepressants,
benzodiazepines, beta-blockers, histamine-2 antagonists, levodopa,
methyldopa, metronidazole, and salicylates.
 Before dementia can be diagnosed, all psychoactive drugs
should be eliminated if possible.
what is Delirium
 Altered/ fluctuating level of consciousness
 Disturbances in memory, thought and behaviour
 Reversible
 Acute or subacute onset
 Prevalent in dementia patients
 Caused by a variety of illnesses or medications
 Must identify to treat appropriately
Pharmacottherapy ffor Dementtiia - drugs and borad clsses
Symptomatic treatment of Behavioural and
Psychological symptoms of Dementia (BPSD)
 Antipsychotics
 Antidepressants - SSRIs
 Anticonvulsants - Carbamazepine
Disease modifying treatment
 Cholinesterase Inhibitors
 Memantine
Common BPSD
mental health conditions
anxiety
depressed mood
hallucinations
delusions
sleep disturbance
common BPSD
symptoms/signs
aggression
screaming
agitation
wandering
Hoarding
sundowning (worsening of
behaviour from 5pm)
shadowing (following carer
closely)
culturally inappropriate
behaviour
BPSD - costs, most common BPSD- consists of, delusions %, hallucinations BPSD and
 Agitation is the most common BPSD occurring
in over 50% of people with dementia.
 e.g. disinhibition, verbal abuse, hitting out, damaging
property
 Delusions occur in about 30% of people with
dementia. Typically arise in middle to late
dementia
 Hallucinations occur in about 20%. Usually
limited episodes but may be sustained
 Associated with lower function, increased
burden on caregivers and ACH staff, higher
costs of care and admission to ACH
Assessment of BPSD
 Identify and map one target behaviour
 Examine patient to assess for preventable
cause such as delirium, UTI, pain etc.
 Review medication list
 Investigate possible triggers
 Review patient’s psychiatric and social
history
Non-Pharmacollogiicall ttreattment of
BPSD- advantages
Two main advantages of not using drugs:
- Attempts to address reasons for behaviour
- Side effects, drug interactions and limited
efficacy avoided
Behavioural Problems resolved non pharmacologically in dementia
 Social and Environment Interventions
 Music – especially classical
 Decrease aggressive outbursts, agitation, and
anxiety
 Combined with dance or movement, improves
orientation and self-expression
 Exercise
 Improves cognitive function and general wellbeing
 Environmental modification
 Prevent injury or misadventure from wandering
 increase or decrease light or noise
Evidence for non-pharmacological
techniques - and one disadvantage
 Clinical evidence plus a few small studies support nondrug
techniques in individual patients
 Many of the studies are conducted in patients with mild
symptoms
 Two Australian studies demonstrated the best outcomes for
aged care home residents with severe BPSD using
psychosocial interventions, developed in conjunction with
staff, producing strategies workable in the aged care home
environment.
 Recent trial of collaborative care management showed
improvement in overall severity of BPSD
 Requires staff, resources, training and time………
Drug treatment of BPSD - in general practice
 Benzodiazepines often used but not
recommended as they cause confusion,
agitation, apathy, falls and social disinhibition
 Treat underlying depression with SSRIs and
behaviour may improve
 Anticonvulsants have been trialed but are not
recommended due to adverse effects and
limited evidence of effect
Antipsychotics
 Most commonly used drug class to manage
BPSD
 In older people the most prevalent indication
for use is for BPSD
 Some modest benefit upon aggression and
psychosis
 Appear to be more effective in patients with
severe symptoms
 Overall evidence for modest effect countered
by high side effect rate
Side effects of typical
antipsychotics
 Associated with a risk of falls, somnolence,
orthostasis
 Cardiac toxicity (i.e. thioridazine)
 Associated with Extra Pyramidal Symptoms
 Parkinsonism (bradykinesia, rigidity, tremor)
 Akathisia
 Tardive dyskinesia: 28% after 1 year,
50% after 2 years,
63% after 3 years
Adverse effects of atypical
antipsychotics in people with
dementia
Cerebrovascular risk:
- CSM (UK) meta-analysis of RCTs for risperidone and
olanzapine in dementia patients.
- risk of cerebrovascular events increased almost four-fold.
Working group for the faculty of old age psychiatry. Summary guidance for the
management of BPSD. March 2004. www.rcgp.org.uk
Mortality risk:
- FDA (US) analysis based on 17 RCT with atypical
antipsychotics
- increased risk of death (1.6-1.7 fold increase)
Singh S, Wooltorton A. ‘Increased mortality among elderly patients with dementia
using atypical antipsychotics.’ JAMA 2005;353:2335-2341.
Behaviours Responding Poorly
to Drugs
wandering, pacing, entering rooms uninvited, attemoting to leave, making disruption vocalisations, voiding inappriopiately
Antipsychotic withdrawal - % of no relapse, process
 UK study examined the effect of ceasing antipsychotic
treatment in 100 aged care home residents, with stable
behaviour/s, who had been treated for at least 3 months.
 Over two thirds of the residents experienced no
deterioration of CB when assessed at 1 month and 3
months after discontinuation.
Ballard C, Thomas A, Fossey J et al. A 3-month , randomised, placebo-controlled,
neuroleptic discontinuation study in 100 people with dementia: the neuropsychiatric
median cutoff is a predictor of clinical oputcome. J Clin Psychiatry 2004;65:114-119.
 A gradual withdrawal is recommended to avoid relapse
and withdrawal symptoms such as tachycardia,
sweating and insomnia.
Disease Modifying
Treatments - classes and names, comparative info
 Cholinesterase Inhibitors
 Donepezil (Aricept ®)
 Rivastigmine (Exelon ®)
 Galantamine (Reminyl ®)
 Tacrine (not available in Australia)
 NMDA Antagonist
 Memantine (Ebixa ®)
 Comparative Information - almost nonexistent
Cholinesterase Inhibitors- benefit, fraction that benefit, time to assessment,
Cholinesterase inhibitors offer modest benefits to patients with mild
to moderate dementia due to Alzheimer’s disease.
 They are expensive, require supervision, improve alertness and
function and maintain cognitive scores at or above the baseline for
up to 12 months, but do not modify the underlying progression
of pathology.
 Open-label trials have shown continued benefit for up to 4 years.
Six month studies suggest that between 5 and 15 patients need
to be started on treatment in order to see a significant
improvement in 1 patient.
 Two out of three treated patients have their apparent rate of
cognitive decline slowed by cholinesterase inhibitor therapy.
 Patients should be treated for at least 2 months at the maximum
tolerated dose of medication before a final assessment of response
is made.
cholinesterase inhibitors - comparative, swapping?
There is no convincing evidence that any of the 3 available
cholinesterase inhibitors is more efficacious than the other 2,
however donepezil’s once-daily dosing regime and fewer adverse
effects should make it the first choice medication for most patients.
 In the event of nonresponse, there is a lack of clear evidence to
indicate that switching to another cholinesterase inhibitor will
produce a response, though individual cases who respond to one
Cholinesterase inhibitors - PBS, other than alzeihmers, severe dementia, long term efficacy
 Only available on PBS as authority
prescription for mild to moderately
severe Alzheimer’s disease
 Limited evidence for use in other
dementias though may be of benefit
 Limited evidence for use in severe
dementia
 Long term use efficacy unknown
Side effects of Cholinergic
Agents - when should care be excercised
Cholinergic stimulation
 nausea / vomiting
 diarrhoea
 anorexia (weight loss)
 dizziness
 dyspepsia
 agitation
 vivid dreams

Care is needed
 bradycardia
 caution in sick sinus syndrome
 monitor in patients receiving
other drugs that slow heart rate
 ulcers (increase risk on NSAIDs)
 COPD and asthma
 ureteric obstruction
 Galantamine is contraindicated in severe renal failure.
Practice points of cholinesterase inhibtiors
 Doses should be titrated to minimise side effects
 If treatment is interrupted may require restart at initial
dose and retitrate.
 Rivastigmine comes as an oral liquid and patch
 Abrupt cessation in patients with dementia with Lewy
bodies may cause a rapid decline in benefits
 Donepezil – morning dose to avoid vivid dreams
 No washout is needed when switching agents or
retitration
PBS Cholinesterase Inhibitors
 Eligible patients
 AD and with mild to moderate disease (MMSE score  10)
 Continued benefit
 Subsidised treatment can only be continued in those
patients who demonstrate evidence of cognitive
improvement (MMSE score  2 points better or ADAS-cog
 4 points better) from baseline.
 Where a patients MMSE score falls below 10 treatment
should be discontinued.
 In patients with noticeable decline in cognition,
behaviour or functional status within 2 weeks of
discontinuation of a cholinesterase inhibitor, drug
therapy should be reinitiated starting with a low
dose and titrating upwards.
Memantine - PBS, NTT, MOA
Regulates glutamate transmission
 Thus may protect neurons from over
stimulation and neurotoxicity
 Approved for moderate to severe
Alzheimer’s disease
 Small benefit on cognition, behaviour and
ADL
 17 patients needed to be treated for 6
months to prevent one incident of agitation
 No effect on course of disease
 Recently approved on PBS
Memantine
clinical trials suggest benefit with combining with donepizil
Prevention benefits?
Dementia process starts long before onset
of clinical symptoms
 Therapies to delay or prevent dementia
developing for 5 years – would reduce
cases by 50% in one generation.
 Many therapies proposed ……….
Preventative therapies- types, evidence
Oestrogen?
 Vitamin E?
 Statins?
 NSAIDS (e.g. naproxen, ibuprofen)?
 Folic acid?
 Gingko biloba?
 …Insufficient evidence to endorse use
Preventative treatment in vascular
dementtiia
Main aim in management of vascular
dementia is to prevent new strokes
 Reduce risk factors for vascular disease
- control BP
- control hyperlipidaemia
- control blood glucose
- address lifestyle e.g. smoking
Prevention of Alzheimer’s
disease
Right now, there's no proven way to prevent the onset of
Alzheimer's disease. Human trials of a promising vaccine
against Alzheimer's had to be stopped several years ago
because some of the people who received the vaccine
developed encephalitis.
 However, you may be able to reduce your risk of Alzheimer's
disease by reducing your risk of heart disease. Many of the
same factors that increase your risk of heart disease can also
increase your risk of dementia. The main players appear to
be blood pressure, cholesterol and blood glucose levels.
 Keeping active —physically, mentally and socially — also
seems to reduce the risk of Alzheimer's disease.