Update On Management of BPSD

Update on management of BPSD
Henry Brodaty
Dementia Collaborative Research Centre, UNSW
www.dementiaresearch.org.au
Translating dementia research into practice
Potential conflict of interests

• Advisor, consultant, remunerated speaker and/or
investigator:
– Parke-Davis, Eisai, Pfizer, Sanofi, Servier
– Janssen, Lilly, Hoechst-Marion-Roussel
– Lundbeck, Novartis, AstraZenica, Elan, Wyeth
– Neotherapeutics, Cromedica, Voyager, Searle,
Quintiles

What are BPSD?
• Agitation • Depression
• Aggression • Anxiety
• Calling out/ screaming • Apathy
• Disinhibition (sexual) • Delusions
• Wandering • Hallucinations
• Night time disturbance • Irritability
• Shadowing • Elation/euphoria
• Swearing
Why are BPSD important?

• Ubiquitous, >90% of PWD during course
• Distress to PWD and to caregivers
• Increase rate of institutionalisation
• Higher rate of complications in hospital
• Faster rate of decline
• Associated with increased mortality

Effects of BPSD
• Residents with BPSD are more likely to1:
– be physically restrained
– receive antipsychotic medication
– negatively influence other residents
• BPSD increase the cost of institutional care for
persons with dementia2
• BPSD, especially aggression3 & calling out4,
increase nurse stress
Maslow K 1994; 2O’Brien JA et al, 2000; 3Rodney, 2000; 4Draper et al, 2000
1
Prevalence of BPSD
• In community
– 2/3 PWD have at least one behavioural Sx
– 1/3 PWD have significant level of symptoms
• In developing countries similar rates
• In residential care
– 40- 90% RWD have BPSD
– Rates in similar NHs vary >3-fold
1
Lyketsos et al, Am.J. Psychiatry, 2000; 157:708-714;
2
Prince M et al 2004; 3Brodaty H et al, 2001;
4
Seitz et al, Int Psychogeriatrics, 2010; 22:1025–1039
Aetiology of BPSD
• Biological
• Psychological
• Interpersonal
• Environmental

Biological causes - intrinsic
• Frontal pathology (behavioural disturbance,
disinhibition, depression)
• Basal ganglia lesions (delusions)
• Temporal lobe (delusions, hallucinations)
• Locus coeruleus (psychosis, depression)
• Chemical changes – serotonin, NA, DA
• Genes – serotonin, dopamine receptors
• Family history of psychiatric disorder
Biological causes - extrinsic

• Acute medical illness
• Medication
• Pain syndromes
• Constipation
• Sensory impairments
• Fatigue
• Fears
• Basic needs (hunger, thirst...)
• Psychiatric syndromes
The bio-psycho-social framework
Socio- Interpersonal
environmental
Biological Psychological

Environmental Unmet needs; unable
vulnerability → to comprehend or
↓threshold for make needs known2
stress or stimuli1
Neurological Behavioural: triggers
deterioration → and feedback from
behavioural others control
disinhibition4 behaviours 3
Hall and Buckwalter 1987; 2 Algase et al, 1996; 3 Teri & Logsdon 2000; 4 Cummings JL
1
Before intervening …
1. Is the description accurate?
2.Identification of target behaviour

3.Does behaviour require intervention?
4.Careful diary of behaviours
5.Exclude non-dementia causes
6.Correct sensory impairment - hearing, vision
Socio-
environmental Interpersonal
How to intervene: Environment
• Modify environment rather than person

• Avoid too much or too little stimulation
• Adequate space
• Privacy available
How to intervene: Environment

• Secure grounds • Colour, furnishings,
architecture
• Personalised space
• Lighting
• Non-institutionalised
environment • Resident mix
• Home-like • Size of residential
facility

Enhanced Environment
Good evidence for

• Careful optimisation of level of
stimulation
– Reduce unhelpful stimuli (eg noise or
busy entry doors)
– Optimise helpful stimuli (eg light)
• Good visual access to toilets
Fleming R – www.dementiaresearch.org.au
Wander garden
Outside
space only
beneficial in
combination
with staff
interaction
Moderate evidence
• Small unit size
– hard to differentiate effect of unit size
from staff related factors
• Opportunity to engage in ordinary
ADLs
– again, hard to differentiate from staff
support/engagement
Interesting – but no good evidence
• Signage
• Display of
personal
memorabilia
Snoezelen: multisensory stimulation1

• Significant treatment effect
– Apathetic behaviour ↓
– Loss of decorum ↓
– Rebellious behaviour ↓
– Aggressive behaviour ↓
– Depression ↓
– Well-being during morning care↑
• Numbers small, methodology moderate
Van Weert et al, JAGS 2005;53: 24–33
Verkaik R et al, IJGP 2005;
Translating dementia20: 301–314
research into practice
Partner logo here
Aroma therapy
Lavender Lemon Balm
moderate evidence from Cochrane review

Partner logo here
Lavender oil Holmes et al. (2002)

• Communal area of dementia ward sprayed
with 2% lavender oil or water for 2 hours
daily on alternate days
• All 15 participants had severe dementia and
daily agitation
• Observer wearing nose clip rated behaviors
• Median behavior scores 20% lower while
exposed to lavender vs water (p=0.016)

Partner logo here
Lemon balm (melissa officinalis)
• Antibacterial (eugenol)
• Antiviral (tannins)
• Mild sedative or calming
agent (terpenes)
• Antioxidant activity
Partner logo here
Lemon balm Ballard et al. (2002)

• RCT 71 severely demented NH residents
with clinically significant agitation
• Massaged lightly on the face and arms with
either lemon balm or sunflower oil for 1-2’
twice daily for four weeks
• Blinded ratings of CMAI before and after
• Scores on CMAI fell by 35% in Melissa
group vs 11% for sunflower oil (p<0.0001)
• Positive changes too in social engagement
and constructive activity
Partner logo here
Light therapy
• Five studies met criteria; only 3 able to be included

• No adequate evidence of effectiveness of BLT
Forbes D, Morgan DG, Bangma J et al; Cochrane Review 2004, updated 2006
Pets and robotic pets

Review on animal-assisted
therapy (AAT)1
• 11 papers examining the impact of AAT on BPSD
regarding their ability to
– Reduce agitation
and/or aggression
– Promote social
behaviour
– Improve nutrition
– Role of pet substitutes
Filan & Llewellyn-Jones (2006) Int.
1
Psychogeriatr; 18:4, 597-611

Socio-
BPSD outcome
from family CG
interventions in
community
3279 dyads
17 studies ES = 0.34
(95% CI 0.20 – 0.48, p<0.01)
Brodaty and Arasaratnam

2012 in revision
CG reactions to
BPSD from CG
interventions for
BPSD
12 studies ES = 0.15
(95%CI 0.04 – 0.26, p=0.006)
Brodaty and Arasaratnam

2012 in preparation

CGs administer behavioural treatments
for depression to patients with AD 1
• Behaviour therapies (pleasurable events
schedule or problem solving techniques) 
pt depression Sx & Dx better than controls
• Improvements maintained @ 6 mnths
• Bonus: CGs’ depression better
Teri et al, J. Gerontol. 1997; 52B:159-166
1
CGs as behaviour therapists Teri et al. (2000)
• 148 people with AD + agitation > wkly

• RCT 11 comprehensive behavior training
sessions for family CGs vs placebo vs
haloperidol (mean final dose 1.8mg daily) vs
trazodone, mean final dose 200mg daily)
• Attrition rate high (39%) over 16wks due to
adverse effects with haloperidol and more
agitation with Behaviour Mx and trazadone
• Similar rates of improvement = 31- 41%,

CADRES:
Caring for Aged Dementia Care Resident
Study
• Prospective RCT comparing
– DCM
– Person-centred care (PCC)
– Usual care (UC)
• 4 months intervention, 4m F/Up
• Primary outcome = CMAI
Professor
Lynn Chenoweth
Chenoweth
Translatinget al. Lancet
dementia Neurol;
research into practice 2009
Kitwood PCC
• Care systems
– support needs for love, attachment,
comfort, identity, occupation &
inclusion
– enhance global sense of self-worth &
feeling valued
– reduce BPSD
Person-Centred Care
• Individualised care planning
– not only clinical history
– social & functional history, needs and
preferences
– care staff sensitised to person’s
unique personality & preferences
– interpret responses & behaviours
– adjust care practices accordingly
Dementia Care Mapping

• Derives from PCC
• Detailed, systematic observations of
residents' experiences of well-being and
ill-being
• Feedback to staff
• Assists staff to identify & address factors
that affect the well-being of PWD
• Care plans - change & improve care
practices & environments

Costs per CMAI point averted…
After At Follow-up
intervention
PCC $ 8.01 $ 6.43
DCM $ 48.95 $ 46.89
Chenoweth et al. Lancet Neurology 2009

Socio-
Psychological Mx approaches to BPSD

• 1632 studies identified  162 met inclusion
criteria  9 studies with Level 1 evidence
• Psycho-education for CGs effective
• Benefits lasted months
• Other CG interventions not effective
• Behaviour Mx techniques centering on individual
pts’ or CG behaviours  similar benefits
• Residential care staff education beneficial
• Cognitive stimulation similar effects
Livingston G et al Am J Psychiatry 2005; 162:1996-2021
Conclusions: Psychological
approaches to BPSD
• Music therapy
Useful during treatment
• Snoezelen but not long term
• ? Sensory stimulation
• Interventions that
changed visual
environment looked
promising, but …
…  research required Livingston G et al
1
Am J Psychiatry 2005;
162:1996-2021
Calming music and/or hand massage
10 min
CMAI
ratings
before during immediately after 1hr after
Remington, Nursing Research, 2002

Apathy: non-pharmacological treatment

• Review: 55 non-pharm intervention studies
• 7 intervention categories:
– Exercise, music, multi-sensory, animals,
special care programming, therapeutic
activities & miscellaneous
• Therapeutic activities were most effective
– Standard of research low for other
interventions
Brodaty H, Burns K Am J Ger Psych 2011

Novel strategies
• Humour therapy
• Volunteers
• Integrating kindergarten/ babies
Humour
SMILE Study
Elder clowns & LaughterBosses reduce agitation
Clinically significant?
• 20% reduction in agitation symptoms in SMILE
• The same effect size as is achieved by antipsychotic

medications used to treat agitation
OR
Conclusions
• Humour therapy sustained +ve effect in
reducing agitation (2.64 pnts over 26 wks)
• Management and Laughterboss (staff)
engagement important components
• After adjustment, +ve effects on
depression and QoL
• No adverse effects
• Cannot determine what elements work
• Humour Therapy is popular
Barriers
• Time
• Money
• Staff
• Attitudes
Key elements • Training
• Engagement
• Understanding
• Time

Socio-
Cholinesterase inhibitors for BPSD

• Systematic review & meta-analysis1
• 29 RCTs with mild-moderate AD
• BPSD: cholinesterase inhibitor group
1.72 points on NPI (6 trials) &
0.03 on ADAS-noncog (10 trials) vs placebo
• Modest benefit on BPSD
• Individual symptoms > response
– Apathy, hallucinations
1
Trinh N-H et al JAMA 2003;289:210-6
ChEIs
• Systematic review – only 3/14 RCTs
significant reduction in BPSD Rodda et al., 2009
• Meta-analysis of 9 RCTs  statistically
significant vs placebo but questionable
clinical significance Campbell et al., 2008
• Individual Sx ??more susceptible: apathy,
hallucinations, aberrant motor behaviour,
delusions, anxiety, depression www.ipa-online.org
Memantine for BPSD

• Reisberg B et al, 2003:
– memantine v placebo
– no effect on reducing NPI
• Tariot et al, 2004:
– memantine + donepezil vs memantine +
placebo – reduction in NPI
• Van Dyck et al, 2007:
– memantine vs placebo, no effect on NPI
Aggression/ Agitation: effects of memantine 1
 Memantine
 Placebo
Prevalence at
Patients [%]
baseline
Emergence post 44 *
52
baseline
Improvement post 76 *
baseline 67
0 20 40 60 80 100 [%]
* p < 0.05 versus placebo
1
Gauthier et al (2005), IJGP, 20, 459-464
Antidepressants for BPSD

Antidepressants in dementia
• Modest evidence of efficacy of antidepressants in
treatment of depression in dementia1,2
– OR = 2.32, 95%CI: 1.04-5.16
– Best evidence is for sertraline (and citalopram)
– AD may be more responsive than VaD
• Some evidence that citalopram useful for
agitation, psychosis 3,4, 5
• Further trials needed
– eg combining drug & psychosocial treatment
1
Bains et al. (2002). Cochrane Review; Issue 4; 2 Thompson et al. (2007) Can J
Psychiatry; 52: 248-255; 3 Pollock et al. (2007). Am J Geriatr Psych; 15: 1-11;
4
Pollock B et al, 2002; 5 Nieth and Gottfries, 1990.
Sertraline for treatment of depression

in AD: Wk-24 Outcomes (DIADS-2)
• 67 Sertraline, 64 placebo; 12 wk RCT + 12 wk
• No between-groups diff. in depression response
– in CSDD score
– remission rates
– secondary outcomes
• SSRI associated > adverse events of diarrhoea,
dizziness, dry mouth, pulmonary SAE (pneumonia)
Weintraub D et al. Am J Ger Psych, 2010;18:332-340
Study of antidepressants for depression in
dementia (SADD)
• Target N = 507; double dummy design
• Compare 2 classes of antidepressants:
• Mirtazapine 15 mg & sertraline 50 mg; 13/day
• Primary outcomes: depression (CSDD); cost
• Secondary outcomes: adverse events,
compliance, patient QoL, cognition, BPSD, carer
burden, carer stress, carer QoL
Banerjee S, HTA-SADD trial, Lancet, 2011

http://www.hta.ac.uk/project/1508.asp
DEMQOL
HTA-SADD Trial 95
90
85
14
80
CSDD Score 75
12
CSDD Score
0 13 39
10
DEMQOL-Proxy
Score
8
100
95
6
0 13 39 90
Visit
Placebo Sertraline 85
Mirtazapine 95% CI
95% CI 95% CI 80
0 13 39
Citalopram vs Perphenazine
• 17 day RCT, 85 Ss with dementia
• 31 citalopram, 33 perphenazine, 21 placebo
• Outcome: Neurobehavioral Rating Scale
• Citalopram and perphenazine improved agitation/
aggression, psychosis & lability/tension
• Citalopram also improved cognition & retardation
Pollock et al. (2002). Am J Psych; 159: 460-465
Citalopram vs Risperidone
• 12 wk RCT of 103 Ss with dementia:
– 53 citalopram, 50 risperidone
• Significant decrease in agitation score
(Neurobehavioral Rating Scale) for
citalopram, but not risperidone
• Citalopram & risperidone both decreased
psychosis scores (suspiciousness,
hallucinations and delusions)
Pollock et al. (2007). Am J Geriatr Psych; 15: 1-11

Partner logo here
Effects of citalopram on BPSD

• Retrospective analysis of CATIE-AD sub-sample
(n=44) started PBO  citalopram
• 60% ↓ irritability and apathy (but n.s.)
• Sig. ↓ hallucinations (? but clinically significant)
Siddique et al. J Clin Psychiatry 2009; 70(6):915-918

Negative effects of antidepressants

on patients with dementia
• Tricyclics = anticholinergic effect
– Impair cognition1
• SSRI = e.g. nausea, nervousness, insomnia, dry
mouth, blurred vision, anxiety symptoms,
sedation, movement disorders, falls 2
For reviews see
1
Brooks & Hoblyn (2007). J. Geriatr. Psych. Neurol.; 20: 199-214
2
Mulchahey et al (1999). Int. J. Neuropsychopharma.; 2: 121-127
Apathy: pharmacological treatment
• Review: 71 trials
• Consistent support for (most to least effective)
– Cholinesterase inhibitors
– Memantine
– (Antipsychotics)
• Relatively weak support for:
– Ginkgo biloba
– Stimulants
– Dopaminergic agonists
– Nimodipine
Berman K et al Am J Ger Psych, 2011
Antipsychotics for BPSD

Antipsychotics for agitation,
aggression and psychosis
DB RCTs
• Haloperidol1,2
• Risperidone2,3,4
• Olanzapine5,6
• Quetiapine 7
• Ariprazole 8
1
De Deyn et al 1999; 2Devanand et al 1998; 3Katz et al.1999; 4 Brodaty et al. 2003; 5Meehan et
al. 2002; 6Street et al. 2000; 7Zhong KX et al, 2007; 8 Mintzer et al, 2007
Agitation/aggression in NH residents
with dementia (CMAI aggression)
baseline week 4 week 8 week 12 end point
0
-1
Reduced agitation/aggression
-2
Placebo
-3 Mean dose
-4 1.06 mls
-5
-6
-7
-8 * pRisperidone
< 0.05
*
-9 Mean dose
0.95mg
-10 *
CMAI, Cohen Mansfield*Agitation Inventory
Translating dementia research into practice 1

Brodaty et al 2003
Olanzapine
• NH study in BPSD 5 and 10 mg/day > placebo for

agitation/aggression and well tolerated Street et al, 2000
– 5 mg dose greater efficacy than 10 mg dose
• 2nd trial - doses of 5 and 7.5 mg no better than
placebo in primary outcome of study De Deyn et al, 2004
Aripiprazole for psychosis in NH

residents with AD 1
• RCT (10mg vs 5mg vs 2mg vs placebo)
• 487 NH residents with AD
• Results:
– 10mg > placebo on NPI-NH psychosis
– 5mg > placebo on BPRS, CMAI
– 2mg no effect
– Cerebrovascular AEs x2 with dosage 
1
Mintzer et al (2007): Am J Geriatr Psychiatry, 15:11, 918-931
Aripiprazole for psychosis in NH
residents with AD 1
• DB RCT, n=131 aripiprazole, n=125 controls
• No difference in primary outcomes between
groups for NPI- psychosis or CGI severity scores
• Benefits on secondary measures (NPI total, CGI,
CMAI, CDS, Brief Psychiatric Rating Scale)
1
Streim et al (2008): Am J Geriatr Psychiatry, 16, 537-550
CATIE-AD
• 42 sites, 421 pts randomised to olanzapine
(5.5mg), quetiapine (56.5mg), risperidone
(1mg) or placebo
• Time to discontinuation
– Overall =
– Because of lack of efficacy: OLZ & RIS <
QTP & PBO
– Because of AEs: OLZ 24%, RIS 18%, QTP
16%, PBO 5%
• CGIC – ns
Schneider L et al NEJM 2006
Meta-analysis of RCTs
• Meta-analysis from 13 studies 1:
– Mean ES in Rx group = 0.45
– Mean ES in placebo gp = 0.32
• In summary
– Effect sizes of atypical
antipsychotics for behavioural
problems are medium and not
statistically better than placebo
Yury C & Fisher J, Psychotherapy and Psychosomatics 2007
Antipsychotics associated
with increased risk of
cerebrovascular AEs & deaths

Meta-analysis of RCTs
• Meta-analysis from 16 RCTs:
– MR 3.5% in Rx group
– MR 2.3% in placebo gp1
• In summary
– Risk of harm too small to
appear in population-based
analyses
1
Schneider LS et al,
– ? similar risks for other
JAMA 2005 medication classes (but
subjected to less scrutiny)
Recommended dosing for BPSD

Drug Starting Dose range (mg)/ day
Risperidone 0.25 0.5–2 once
Olanzapine 2.50 5–10 once
Aripiprazole 2.00 5–10 once
Quetiapine 25.00 25–150 divided doses
Haloperidol 0.50 0.5–2 once
Ziprasidone* 20.00 40–80 divided doses, meals
(ECG monitoring of QTc required)
Clozapine* 6.25 12.5–100 once or twice
*Information from open-label trials only
www.ipa-online.org/pdfs/IPA_BPSD_Module_6.pdf
Psychotropic medication for
patients with dementia in NHs1
• 633 NH residents with dementia followed 1 yr
• Overall persistence of BPSD (NPI): 79%
• Individual Sx (depression, delusion, agitation/
aggression) resolved at high rate (47% - 58%)
• Persistent psychotropic drug use very common
• No difference in users vs non-users regarding
course of BPSD
1
Selbæk et al (2008): Am J Geriatr Psychiatry, 16:7, 528-536
Continuing vs stopping
neuroleptics in dementia patients?
• 12 months RCT
• Continuous use of neuroleptics vs placebo
• For most AD pts withdrawal had no overall
detrimental effect
• Continuers – worse verbal fluency (p<.002)
• Subgroup of pts with more severe
symptoms (NPI ≥ 15) might benefit from
continuous Rx Ballard et al 2008 PLOS Medicine, 5:587-599
Anticonvulsants for BPSD treatment1
• Literature review of 7 RCT (2 carbamazepine &
5 valproate
• Results (treatment vs placebo):
– 1 study: sig.  BPSD
– 5 studies: no sig. difference
– 1 study: sig.  BPSD
– AEs more frequent in treatment groups
• Might be beneficial for some pts
• Not recommended for routine use
1
Kanovalov et al (2008). Int Psychogeriatr, 20:2
Anticonvulsants at a glance
• No or limited benifit for divalproex sodium1,2
and sodium valproate3
• Modest evidence for carbamazepine4,5 but
further trials needed
1
Porsteinsson et al (2001). Am J Ger Psychiatry, 9:58-66; 2Tariot et al (2005). J
Geriatr Psychiatry, 13:942–949; 3Herrmann et al (2007). Dement Geriatr Cog
Disord, 23:116-119 4Tariot et al (1998). Am J Psychiatry, 155:54-61; 5Olin et al
(2001). Am J Geriatr Psychiatry, 9:400–4051;
Benzodiazepines
• PBO RCTs: BDZ decrease agitated
behaviours during short-term use
• Short-acting BDZs eg oxazepam or lorazepam
that do not accumulate best
– most effective if used for short periods at
low doses (e.g., lorazepam 0.5–2.0 mg/day)
• AEs = Sedation, falls, confusion, amnesia
(Chesrow et al., 1965; Kirven and Montero, 1973;
Covington, 1975; Coccaro et al., 1990)
Analgesics
• Cluster RCT, 60 NHs, 352 residents, 8 + 4wks
• Mod-severe dementia, CMAI > 39
• Stepped analgesia vs usual care
• CMAI ↓17% (9.6 vs 3.4, p<.001)
• CMAI score ↑ in four weeks after stop analgesia
• NPI, Pain scores significantly ↓
Husebo BS et al, BMJ, 2011;343:d4065 doi: 10.1136bmj.d0465

Analgesics
• No analgesic or low dose paracetamol  3g/day
paracetamol (n = 120, 69%)
• Full dose paracetamol or low dose morphine 
5mg bd morphine (4, 2%)
• Low dose buprenorphine or unable to swallow
 buprenorphine patch 5-10µg/h (39, 22%)
• Neuropathic pain  pregabaline 25-300mg/day
(12, 7%)
Husebo BS et al, BMJ, 2011;343:d4065 doi: 10.1136bmj.d0465

Others
• Buspirone • Hypnotics
• Trazadone • Lithium
• Adrenergic • Canabinoids
blockers • Oestrogens
• Selegiline • Androgen blockers
• Opioids
• Melatonin

Developments in Rx for BPSD
• Cholinesterase inhibitors – for apathy
• Memantine - ?benefit for agitation/aggression/
delusions/ hallucinations
• Antidepressants – citalopram, sertraline,
venlafaxine, mirtazapine
• Risperidone 0.5 - 2mg/day; modal = 1mg
• Olanzapine 5mg/day, up to 10mg/day
• Valproate, carbamazepine – titrate dose against
response, SEs and blood level
• Analgesic stepped approach
Recommendation on the use of

antipsychotics
• Reduce use of antipsychotics in PwD
• If needed, …
– Review risk level
– Ensure good practice with initiation,
maintenance and cessation of
antipsychotics
Bannerjee 2009. The use of antipsychotic medication for people with dementia.
Legal consent for psychotropics
• Depending on jurisdiction a Person
Responsible must give consent (?in writing)
• Survey of 3 NHs; 77 residents without capacity
to give informed consent; on psychotropics1
• Only 6.5% written consent
• + 6.5% partial or attempted consent
1
Rendina N et al, 2009
When everything fails?
• You do everything right but BPSD continues

• Risk to other residents/ staff/ family
• Special care units
– Medium term  transfer back to mainstream
• Intensive care unit for very aggressive/ violent

Clinical conclusions about
management of BPSD
Conclusions I
• Prevent BPSD, e.g.
– PCC, environment, titrate stimulation
– CG and staff training
• Determine cause
• Correct reversible factors
• Start with psychological & environmental
intervention(s)
– except if urgent or sometimes concurrent

II: Understand the person -
Don’t just label the behaviour
• Why is this person behaving this way now?
• Aetiological map → management plan
• Different approaches often together
• Be creative
• Document
• Monitor outcome
• Partnership with family/ carers
Conclusions III
• Pharmacotherapy
– modestly effective for BPSD
– Prescribe judiciously
– Need medico-legal consent
– Start low and go slow
– Review regularly, at least 3 monthly

Thank you
• www.dementiaresearch.org.au
• h.brodaty@unsw.edu.au
Katrin Seeher & Megan Heffernan helped with

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Update on management of BPSD

Translating dementia research into practice

Potential conflict of interests

Translating dementia research into practice

Why are BPSD important?

Translating dementia research into practice

Translating dementia research into practice

Biological causes - extrinsic

Translating dementia research into practice

The bio-psycho-social framework

2.Identification of target behaviour

The bio-psycho-social framework

• Modify environment rather than person

Translating dementia research into practice

How to intervene: Environment

Translating dementia research into practice

Translating dementia research into practice

Good evidence for

Translating dementia research into practice

Snoezelen: multisensory stimulation1

moderate evidence from Cochrane review

Partner logo here

Lavender oil Holmes et al. (2002)

Translating dementia research into practice

Lemon balm (melissa officinalis)

Translating dementia research into practice

Partner logo here

Lemon balm Ballard et al. (2002)

• Five studies met criteria; only 3 able to be included

Pets and robotic pets

Translating dementia research into practice

Psychogeriatr; 18:4, 597-611

The bio-psycho-social framework

Brodaty and Arasaratnam

Translating dementia research into practice

Brodaty and Arasaratnam

Translating dementia research into practice

Translating dementia research into practice

CGs as behaviour therapists Teri et al. (2000)

• 148 people with AD + agitation > wkly

Translating dementia research into practice

Dementia Care Mapping

Translating dementia research into practice

Chenoweth et al. Lancet Neurology 2009

Translating dementia research into practice

Psychological Mx approaches to BPSD

before during immediately after 1hr after

Remington, Nursing Research, 2002

Apathy: non-pharmacological treatment

Brodaty H, Burns K Am J Ger Psych 2011

Translating dementia research into practice

• 20% reduction in agitation symptoms in SMILE

• The same effect size as is achieved by antipsychotic

Translating dementia research into practice

Cholinesterase inhibitors for BPSD

Memantine for BPSD

Antidepressants for BPSD

Translating dementia research into practice

Sertraline for treatment of depression

Banerjee S, HTA-SADD trial, Lancet, 2011

Pollock et al. (2002). Am J Psych; 159: 460-465

Pollock et al. (2007). Am J Geriatr Psych; 15: 1-11