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Detailed treatment updates for common conditions

Alzheimer’s disease
Alzheimer’s disease is the most common form of dementia; however, a disease-modifying treatment remains elusive. The impending retirement of the “baby boomer” generation means this condition will create a growing burden on patients, families and the healthcare system. It
is important that dementia is diagnosed early by GPs as there are important steps that can be taken with the patient and family to, hopefully,
delay further cognitive decline, improve related symptoms and provide time to educate and plan for altered behaviour, more dependent
living and significant family decisions. This article on the diagnosis and management of Alzheimer’s disease was written by Jeff Kirwan,
consultant psychiatrist and clinical director, Older Persons’ Health Specialist Service, The Princess Margaret Hospital, Christchurch.

Alzheimer’s the most
common dementia
As with all other developed countries,
New Zealand’s population is rapidly ageing,
for a number of reasons. These include a decline in fertility, an increase in average life
expectancy and the fact the “baby boomer”
generation is now reaching retirement age.
The first of the “baby boomer” cohort were,
of course, born following the end of World
War II – 65 years ago.
Today, in 2010, only 13 per cent of the
New Zealand population is aged 65 years
and over but, by 2021, this is projected to increase to 19 per cent because the large birth
cohorts of the late 1940s and 1950s will move
into this age group. By 2051, a staggering 25
per cent of New Zealanders will be aged over
65 years.
Medical practitioners will see many agedrelated conditions become more evident in
the coming years. These include osteoporosis,
arthritis, cerebrovascular disease (including
stroke), cardiovascular disease and neurodegenerative diseases, such as Parkinson’s disease and dementia.
Consequently, it will become ever more
important for GPs to have a basic understanding of the types of dementia and how
they present and are diagnosed and managed.
Dementia is a chronic brain disorder which produces an
acquired, persistent, global impairment of intellect, memory skills and personality. It is important to note, it is not
normal ageing.
Alzheimer’s dementia is the most common form, ac-

less common causes of dementia, which include Parkinson’s
disease, multiple sclerosis, Huntington’s disease and alcoholrelated dementia.
These different types have different clinical characteristics and may present with different symptoms and signs
although, towards the end stages of the disease, most dementias appear very similar.
It is important to diagnose the particular type of dementia because this can inform prognosis and management, including pharmacotherapy. Although this article focuses on
the diagnosis and management of Alzheimer’s dementia,
the principles of diagnosis and the many non-pharmacological management strategies are relevant to the other forms
of dementia.
There are significant costs associated with dementia and,
in New Zealand, these were estimated to be approximately
NZ$712.9 million in 2008. The burden of dementia on society is made up of not only the direct costs (eg, residential
care and formal supports) but also the burden on patients’
families, whanau and carers. Carers themselves are at risk of
stress, anxiety and depression.
About 80 per cent of people with dementia live in their
own homes, of whom 50 per cent live by themselves. However,
it is also estimated a significant proportion of those living in
residential care have some form of dementia.

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counting for at least 40 per cent of all dementia cases. The
next most common types (Table 1) are vascular dementia
(as a result of cerebrovascular disease) and mixed dementia
(with both Alzheimer’s and vascular pathologies) followed
by Lewy body and all other forms of dementia, such as frontotemporal dementia (eg, Pick’s disease). There are other

1 Everyone will develop dementia if they live long enough.

2 There is a simple diagnostic test to confirm Alzheimer’s
3 A history of head injury or depression increases the risk
of developing Alzheimer’s disease.
4 Medications for dementia are more important than
non-pharmacological treatments.
5 The newer medications now available for dementia are
6 A trial of a cholinesterase inhibitor is reasonable for a patient
with mild-to-moderate Alzheimer’s disease.
Answers on page 31

New Zealand Doctor F 9 February 2011 F 27

HOW TO TREAT alzheimer’s disease


Alzheimer’s worsens
over about a decade

Diagnostic process for Alzheimer’s disease
(Panel 1)
Needs to include medical and psychiatric functional enquiry, and
collateral history
Physical examination
Needs to exclude reversible causes of cognitive impairment
Cognitive examination
Either ATMS or MMSE ± a freehand clock drawing task

Dementia is common and the incidence and prevalence
rates steadily increase with age. Estimates are that approximately 5 per cent of people over the age of 65 have a dementia and this increases to between 20 and 40 per cent of
those over the age of 85 years. It is unusual for Alzheimer’s
disease to occur before the age of 60. Dementia, however,
is not an inevitability of ageing, is not caused by too much
or too little mental activity nor is it prevented by premorbid
intelligence or occupation.
In addition to age, there are other risk factors for
Alzheimer’s disease, which include gender (slightly more
common in women; relative risk [RR] 1.5), smoking, Down
syndrome, head injury, having the apolipoprotein E4 phenotype, a first-degree relative with Alzheimer’s disease (RR
2–3) and a history of depression.

The most common early sign of Alzheimer’s
dementia is subtle memory impairment, which
is insidious in onset and slowly progressive
The most common early sign of Alzheimer’s dementia is
subtle memory impairment, which is insidious in onset and
slowly progressive. With time, other symptoms may develop,
such as language difficulties (aphasia), difficulties with motor tasks (apraxia), difficulties recognising things (agnosia)
and difficulties performing higher level functions, such as
planning, sequencing (executive dysfunction).
The DSM-IV criteria for Alzheimer’s dementia require
both memory impairment and one of either aphasia, apraxia, agnosia or disturbance in executive functioning, causing
significant impairment in social or occupational functioning. These changes are required to represent a significant
decline from a previous level of functioning, be of gradual
onset and of continuing cognitive decline, and not due to
any other disorder (neurological, medical or psychiatric).
These criteria contrast with a common condition known
as mild cognitive impairment (MCI), in which there are also
cognitive changes (that may or may not involve memory)
but where the impairment has not resulted in a significant
functional decline.
MCI is a heterogeneous syndrome, which may or may
not lead to a dementia. Amnestic MCI converts to dementia
at a rate of 10 to 15 per cent per year, but some people with
MCI do in fact fully recover.

The duration of the Alzheimer’s dementia is said to be
eight to 10 years from onset to death, on average, and three
to eight years from diagnosis to death, but there is a wide

ATMS, Abbreviated Mental Test Scale; MMSE, Mini-Mental State

Diagnosis of probable Alzheimer’s disease
The diagnosis of probable Alzheimer’s dementia is based
on a history of gradual onset, progressive decline in function, early significant memory impairment and absence of
other causes of dementia detected by history, examination
or investigation (Panel 1).
Given this, the diagnosis of dementia requires a thorough psychiatric and medical examination, including comprehensive history (including collateral history from family
or significant others), examination (physical and cognitive)
and a range of investigations. Confirmation of the disease
requires the presence of neuritic plaques and neurofibrillary tangles, which is only possible at autopsy.
A number of DHBs have Memory Clinics, set up to assist the diagnostic process by providing a standardised and
comprehensive approach. However, with greater numbers
of older people presenting, these services will struggle to
meet future demand.
Increasingly, GPs will need to perform the initial diagnostic work-up, initiate treatment and provide initial management with support from the NGO sector (eg, Alzheimers
New Zealand) and back up from secondary care services for
complex clinical presentations and challenging management issues.
Important aspects of the history are confirmation of the
type of onset and progression of the cognitive changes and
other symptoms. With Alzheimer’s dementia, symptoms
have often been present for a few years before attending for
assessment, and are frequently noticed by family members
rather than the person.
Short-term memory difficulties are prominent early in
the disease, as is disorientation (particularly to time, day,
date, etc.). Long-term memory is typically intact until the
later stages.
Other changes to enquire about are language functioning; often reported are word-finding difficulties and
reduced vocabulary in spontaneous speech and problems
with executive function (eg, planning, organising, making
The “forgetfulness” begins to impact on the person’s
day-to-day functioning, so important aspects of questioning
include the impact on:

Key features of the main types of dementia (Table 1)

Prevalence (approx.) Key features

Additional notes

Alzheimer’s dementia


Progressive cognitive decline plus deficit in
one other area (see text for DSM-IV criteria)

Considerable overlap with VD; and in
such cases it is called mixed dementia

Vascular dementia


Often, but not always, sudden deterioration;
stepwise course but variable; patchy cognitive decline (affecting some cognitive skills
more than others)

Prognosis less predictable than AD; may
have focal neurological deficits; early
pres­ence of urinary incontinence and gait

Dementia with Lewy bodies


Fluctuating cognitive state, visual
hallucinations and parkinsonism

REM sleep disorders common; drawing
and visuospatial skills affected early;
heightened sensitivity to neuroleptic

Frontotemporal dementia


Prominent personality change (eg, disinhibition, impulsivity, apathy, emotional unconcern); marked language difficulties can lead
to early mutism; hyperorality; frontal/executive; cognitive slowing; can spare memory;
poor judgement/insight

Onset relatively early (usually before 60
years); frequently preserved abilities of
spatial orientation, praxis and memory
(patients often score well on standard
cognitive tests until late in the illness)

28 F 9 February 2011 F New Zealand Doctor

Blood screening and neuroimaging

Summary of blood screening for dementia
(Panel 2)

Complete blood count
Renal function
Thyroid function
Serum calcium
Vitamin B12
Serum folate

ability to use the phone
ability to manage finances
ability to use transport (including driving), and
compliance with medications.
Even early in the disease it is important to determine
whether there are any behavioural or psychological symptoms. These include anxiety, depression, apathy, agitation,
irritability, aggression, suspiciousness or psychosis (eg, delusions and hallucinations). Sometimes, there can be subtle
personality changes noted by others. Although these usually
appear in the middle-to-late stages, they can in fact be the
presenting symptoms.
Physical examination is required to identify any reversible causes for the cognitive changes.
Cognitive examination needs to be performed and there
are two simple, commonly used office tests. The first is the
Abbreviated Mental Test Scale (AMTS), which is a 10-point
scale that tests predominantly orientation and short-term
memory, together with some items of general knowledge. It
is quick and easy to administer although it is not that sensitive for detecting very early signs of dementia. A score of
eight or less suggests cognitive impairment.
A more detailed and sensitive screening tool is the MiniMental State Examination (MMSE), which is scored out of
30. It is probably the most frequently used cognitive scale,
internationally. The MMSE measures selected aspects of
cognition, such as recent and remote memory, orientation,
attention, reading, language, writing and the ability to copy
or draw designs. A score of 24 or less indicates probable cognitive impairment.
An additional test, which can be very useful, is the freehand clock drawing task. This tests executive planning and
visuospatial skills. The patient is asked to draw (one step at
a time):
• the face of a clock
• then to put the numbers in the correct positions, and
• then to set the time at five to four (or ten past eleven).
The cognitively intact patient should produce a clock
that has a reasonably regular circle as the face and is big
enough to enable placement of the numbers. The numbers
should be regularly spaced and in order.
Cognitive examination can be affected by a patient’s
level of formal education, culture and language ability. It is
always important to make sure they are wearing glasses and
hearing aids, if needed.
Investigations include blood tests (Panel 2) and neuroimaging. Blood tests are also requested to identify any
reversible medical conditions causing cognitive decline.
It is recommended the minimum test panel would be for
complete blood count, electrolytes, renal function, thyroid
function, calcium and vitamin B12 and folate. Additional
tests may be indicated, such as for thiamine (for patients

HOW TO TREAT alzheimer’s disease


Preclinical Alzheimer’s disease

Mild Alzheimer’s disease

Severe Alzheimer’s disease

who drink high amounts of alcohol), syphilis and HIV (for
high-risk patients).
A CT head scan would be the standard structural neuroimaging procedure recommended. The CT scan may
demonstrate marked cerebral atrophy, especially of the medial temporal lobe/hippocampus, which is suggestive but
not diagnostic of Alzheimer’s dementia.
If present, this would raise the suspicion for Alzheimer’s
dementia in a person with a classical clinical history and if
the other investigations are negative for other reversible
A CT head scan can also identify any significant conditions, such as tumour, haemorrhage, normal pressure hydrocephalus, the presence and degree of cerebrovascular
disease and any regional brain atrophy.
In cases where there are diagnostic uncertainties or if the
patient is under the age of 65 years, an MRI head scan may
be considered. Specialist services may also consider SPECT
scans of the brain for complex diagnostic situations – this allows the functioning of the different parts of the brain to be
measured and then compared to aged-matched population

controls. This technique can be particularly useful if trying
to determine whether the patient has a frontotemporal dementia or Lewy body dementia where this has been unable
to be determined with usual diagnostic work-up.

modation options and other aspects of their personal and
financial affairs.
For family members and whanau, a positive diagnosis
provides an explanation for the changes they have noticed.
It gives an opportunity for education of family members and
can also help them prepare for future caregiving.
With the newer medications available for the treatment
of dementia, typically, the earlier in the course of the disease these are started the better. This is because these medications may stabilise the cognitive decline for a period of
time rather than reverse it.

Forgetfulness noticed by wife (Case study 1)
Presentation and history
David, a 70-year-old retired mechanic, presents with memory complaints. First noticed by his wife about 18 months ago, possibly
longer, they mainly affect his short-term memory. David manages
to minimise his difficulties but his wife reports he has become
repetitive in conversation, needs reminding about appointments
and his ability to manage their finances has diminished. He keeps
good health and his only medications are aspirin and captopril for
hypertension, which is under good control. Functional enquiry is
negative. He has no history of psychiatric illness and there is no
family history of dementia.
A review shows no evidence of acute illness. David’s pulse is
74bpm and regular and his BP 135/85. Cognitive examination reveals short-term memory loss and an MMSE score of 24/30.
The GP assumes a likely diagnosis of early Alzheimer’s dementia.
Full dementia blood screening tests are performed (CBC, electrolytes, renal function, thyroid function, calcium, vitamin B12 and
folate), which are unremarkable. A CT head scan reveals mild temporal lobe and hippocampal atrophy.
The diagnosis of Alzheimer’s dementia is made and discussed with
David and his wife. Referral to Alzheimers New Zealand is made for
psychoeducation and support for both of them. David is strongly
encouraged to set up an EPOA for Welfare and Property. Discussions about driving reveal no concerns and further assessment is
not required at this stage. David is keen to start any medication
that may help his memory and, with fully informed consent, donepezil is started at 5mg daily for one month increasing thereafter
to 10mg daily.
David’s cognition appears to stabilise over the next 18 months but
then declines, reflected by an MMSE score of 21/30. Options of
switching to rivastigmine or augmenting with memantine are suggested by the local Psychiatrist of Old Age. David chooses to switch
and this provides further benefit over the next 12 months.

There are many benefits of early diagnosis


Early diagnosis increases the time available for future
planning and time to identify and manage appropriate
treatment. It allows the person with dementia to be involved
in decisions regarding their future care, including accom-

Here’S HOw


pAtieNtS ANd
tHeir cArerS fiNd






NOt Helpful




Overall rating of Alzheimers Auckland services (2009 survey)

eNSure yOur pAtieNtS Get Help tOO
please tell them about our free dementia-specific services available
in the Auckland region:
• early stage activity groups

• Socialisation service

• carer education & support groups • Ongoing support and advice

www.alzheimers.co.nz | 0800 004 001

New Zealand Doctor F 9 February 2011 F 29

HOW TO TREAT alzheimer’s disease


Non-drug strategies
are most important
For all dementias, including Alzheimer’s dementia, the
non-pharmacological management strategies are the most
important. These include:
• psychoeduation regarding the diagnosis and management for the patient and their family and carers
• support for the patient and family to ensure carer stress/
burnout is less likely, especially in the later stages of dementia
• the role of Alzheimers New Zealand for psychoeducation and support – this is invaluable when available in
the area, and referral (with the patient’s consent) is recommended
• risk assessment and monitoring of safety – this may include a person’s safety with electrical appliances (eg,
stove, tools), heating (eg, fires, electric bar heaters), security (eg, not securing their house adequately), financial and general vulnerability
• review of ability to drive – the person may require a formal driving assessment
• legal considerations – it is prudent to set up Enduring
Powers of Attorney for both Personal Care and Welfare,
as well as for Property (Finances), while the person with
dementia retains the capacity to do this. Once this capacity is lost and legal solutions are required, this may
need to be done through the Family Court (eg, to obtain a Court Appointed Welfare Guardian or Property
Manager), which can be time-consuming, costly and potentially distressing for the person and the family
• Needs Assessment to assess need for formal supports
(eg, Personal Cares, Domestic Assistance, Respite Care
allocation, Day Care and Carer Support, etc.)
• non-pharmacological treatment of behavioural and
psychological symptoms of dementia – see later in this

Pharmacological treatments can delay deterioration
There is currently no cure for Alzheimer’s dementia, although there are large numbers of treatment trials being
conducted around the world.
Pharmacological treatments include medications that
aim to address primarily the cognitive decline (Table 2),
and those that target other behavioural and psychological

symptoms of dementia (BPSD), such as depression, anxiety,
psychosis and aggression.
BPSD can be challenging and distressing and often feature at various stages in the course of dementia. Depression
and anxiety often occur in the early to mid stages of dementia (sometimes even predating the cognitive changes) and
psychosis and aggression more typically in the later stages
of dementia.
In New Zealand, the following medications are available
for the treatment of dementia: the cholinesterase inhibitors
(donepezil, rivastigmine, galantamine) and memantine.
These are popularly known as “cognitive enhancing” medications, which may – for some people – slow the progress
of dementia but they are not effective for all people. These
are symptomatic treatments and are not disease modifying.
They are not subsidised, except for donepezil which received a subsidy in late 2010.
Donepezil and rivastigmine enhance brain acetylcholine
levels by blocking the breakdown enzyme acetylcholinest­
erase. Galantamine inhibits the closely related brain enzyme
butyrylcholinesterase. Blocking either acetylcholinesterase
or butyrylcholinesterase leads to an increase in brain acetylcholine levels, which is one of the main neurotransmitters
known to be depleted in Alzheimer’s dementia.
The cholinesterase inhibitors are approved in New
Zealand for mild-to-severe Alzheimer’s dementia and vascular dementia (Panel 3).
As a general rule, the effects of these three medications are modest. Their benefits are greatest in Alzheimer’s
disease, and slightly less in vascular dementia. There is
only a small body of literature on the use of these drugs
in Lewy body dementia; however, many psychiatrists of old
age believe patient groups with Lewy body dementia and
Alzheimer’s disease with Parkinson’s features may respond
best of all.
The cholinesterase inhibitors are not helpful for frontal
lobe dementia, large single infarcts causing vascular dementia, traumatic brain injury or MCI (note: increased mortality
rate in MCI was reported in one study with galantamine).
These medications may be useful also for neuropsychiatric symptom improvement (ie, mood disorders, apathy, psychotic symptoms, aggression and agitation) and may delay
the emergence of BPSD.

‘Cognitive enhancing’ medications: summary (Table 2)


Site of action





(Panel 3)



Tablets: 5mg daily for 1 month,
then 10mg thereafter; take with or
after food

Effects modest, may
improve/delay BPSD


(Panel 3)

Butyrylcholinesterase Mild-to-moderate

Prolonged release caps: 8mg daily for
1 month then 16mg daily for 1 month,
then 24mg daily thereafter; take with
or after food

Effects modest, may
improve/delay BPSD


Caps: 1.5mg twice daily for 1 month
with or after food, then 3mg twice daily
for 1 month, then 4.5mg twice daily,
then 6mg twice daily (only increase
if tolerated)

Effects modest, may
improve/delay BPSD

Rivastigmine Cholinesterase
(Panel 3)


Transdermal patch: 4.6mg patch daily
for 1 month, then 9.5mg patch daily


NMDA receptor

Moderate-tosevere AD

Effects modest, may
delay agitation, possible
adjunct to donepezil

AD, Alzheimer’s dementia; BPSD, behavioural and psychological symptoms of dementia; NMDA, N-methyl-D-aspartate; VD, vascular dementia

30 F 9 February 2011 F New Zealand Doctor

General points for all cholinesterase inhibitors
(Panel 3)
• A trial is reasonable for all patients with mild-to-moderate Alz­
heimer’s dementia (and some other dementias, as discussed)
• Research does not clearly support the use of one over another
• In clinical practice, donepezil and rivastigmine have tended to
be the favoured agents
• Attempt to titrate up to the maximum dose for greater efficacy
• Give with food
• There are a number of potential side effects, although often
they are mild; the common ones include nausea, dizziness,
tiredness, diarrhoea, syncope, urinary frequency/urgency,
incontinence and a change in parkinsonism
• Side effects can differ between agents
• If gastrointestinal or other side effects occur, they usually
occur at initiation or uptitration and often settle within seven
to 14 days if able to be continued; metoclopramide can be
helpful for nausea or domperidone if parkinsonism is present;
rivastigmine transdermal patches have a lower rate of gastrointestinal side effects
• Take patient’s pulse before prescribing as all cholinesterase
inhibitors can worsen pre-existing bradycardia, especially in
relation to first-degree heart block
• If pulse is below 60bpm, an ECG is recommended and treatment of bradycardia suggested (eg, reduce beta-blocker if
• P-R interval should also be noted as heart block may worsen;
the P-R interval on ECG should be less than 200ms
• Other precautions include past history of gastric/duodenal
ulcer disease, sick sinus syndrome, recent myocardial infarction, urinary outflow obstruction and asthma
• Cholinesterase inhibitors should generally not be prescribed
with an existing anticholinergic (eg, oxybutynin) or agents with
a significant anticholinergic side-effect profile; sometimes,
withdrawal of these medications alone can improve cognition,
and this should be done before prescribing a cholinesterase
• All suggestions need to be read in conjunction with each
product’s data sheet.

Memantine is a glutamate antagonist – it blocks the
pathological activation of N-methyl-D-aspartate (NMDA)
receptors caused by excessive levels of glutamate. Its action
is believed to be in reducing the cell-damaging effect of
Memantine is licensed for use in moderate-to-severe
Alzheimer’s dementia and there is little evidence to support its use in mild dementia. It may have an anti-agitation/anti-aggression action, but the size of this effect is
small. Memantine may be an effective adjunct treatment to
donepezil for some people.

Switching cholinesterase inhibitors
In time, the beneficial effects of cholinesterase inhibitors fade and there is a more rapid deterioration in cognitive function. At this stage, a switch – between donepezil,
galantamine or rivastigmine – can be appropriate.
In clinical practice, the first medication can be discontinued one day and the new one commenced the next. Dose
titration of the new medication can often be quicker than
for the initiation of the first medication (eg, one to three
week intervals rather than four weekly, but slowing this
down if side effects develop).

Discontinuing cholinesterase inhibitors
The long-term use of cholinesterase inhibitors depends
on a patient’s response to treatment, what the goals of
the treatment are and whether they have been reached.
Discontinuation requires consultation with the carers or
family as, often, by this stage, the person with dementia is
unable to make a fully informed decision.
Permanent discontinuation is appropriate:
• if the patient experiences intolerable side effects
• when there is significant ongoing cognitive deterioration despite the use of these medications (and often
when switching manoeuvres have not been successful)
• when particular treatment end points have been met
(eg, transition from home to residential care, or from
general resthome to dementia resthome care)
• if patients have comorbidities that make continued use
either unacceptably risky or futile (eg, terminal illness).

HOW TO TREAT alzheimer’s disease

When one is fairly certain these medications have lost
their efficacy, they can be reduced and stopped over a
month. If there is a significant worsening of cognition on
reduction or cessation, it is recommended the medication
be reinstated to the former dose within two to three weeks,
and the deterioration may be reversible.
In clinical practice, it is suggested patients try discontinuation while they still have a week or two of the medication left so that, if they need to recommence it, they have a
supply to cover a weekend or times when obtaining a new
prescription may be awkward.
The best time to consider stopping the medication is
when as many other factors (eg, place of domicile, physical
health, etc.) are as stable as possible, so any significant decline can be attributed accurately to the withdrawal of medication rather than to other factors.

Behavioural and psychological
symptoms of dementia
Also called the neuropsychiatric symptoms of dementia,
BPSD can be divided into a number of broad groups:
• psychotic (agitation, hallucinations, delusions, irritability)
• mood (anxiety, depression)
• frontal (disinhibition, euphoria), and
• apathy.
Non-pharmacological interventions, including environmental management, psychosocial/psychological counselling and interpersonal/behavioural management, should be
first line and, only if these fail, be followed by medication.
Pharmacological interventions include psychotropic
medications; however, there are increasing concerns regarding their potential side effects, particularly those of the
atypical antipsychotic drugs (eg, risperidone and olanza­
pine, for cerebrovascular events in patients with dementia).
Other potential adverse effects described for pharmacological interventions when used for BPSD are reduced cognition, drowsiness, gait disturbance, falls and urinary tract
Antipsychotics can be effective for psychotic symptoms
associated with dementia (eg, delusions, hallucinations)
and for people who are significantly aggressive or agitated
without psychoses.
Antipsychotics, however, are not effective for all BPSD;
specifically, wandering, social withdrawal, shouting, pacing, touching, cognitive deficits and incontinence do not
In clinical practice, antipsychotic drugs should be used
in the first instance only if an individual is clearly psychotic,
severely distressed or if there is an immediate risk of harm
to others. Antidepressants can be used for depression, anxiety and sexual inappropriateness, and benzodiazepines for
anxiety, agitation, aggression and sometimes insomnia.

Evidence lacking for other supplements
and remedies
A number of other preparations claim to provide
support for cognitive function, including vitamin E,
Ginkgo biloba and other herbal and natural remedies
such as fish oils.
Vitamin E (alpha-tocopherol) is an antioxidant
found naturally in food, especially green vegetables
(particularly those lightly cooked or raw) and fish. The
use of vitamin E supplements is controversial and there
is insufficient evidence to support the efficacy of vitamin
E in the treatment of people with Alzheimer’s disease.
Ginkgo biloba is an extract from the maidenhair tree.
It contains an antioxidant and has been widely used in
China and Europe for memory loss, reduced blood circulation and a wide range of other symptoms.
Research has suggested Ginkgo biloba may help improve symptoms of dementia; however, the research
generally has not been robust. Doses of between 120
and 240mg daily have been reported as being useful.
Patients need to be cautious when taking anti­
coagulants, such as aspirin or warfarin, as these may
interact with Gingko biloba and cause bleeding.
Other herbal medicines and natural remedies include fish oils, which manufacturers claim improve
memory. Unfortunately, there is no good evidence to
support these claims, and natural remedies may also
interact with other medications.

Behavioural and psychological symptoms of dementia tend to be time-limited phenomena in the course of dementia

The onset of therapeutic benefit of these medications is
usually delayed, sometimes by several days or a few weeks.
Potential side effects need to be monitored for closely,
particularly extrapyramidal side effects from antipsychotic
As BSPD tend to be time-limited phenomena in the
course of dementia, it is important use of these medications
is reviewed regularly and the dosages reduced or medication stopped if at all possible. In clinical practice, this review
and trial of dose reduction should be made every two to
three months.

Assessing the need for referral
In most cases, GPs can make the diagnosis of Alzheimer’s
disease, though access to neuroimaging may need to be
done through secondary care. Referral would be recommended for patients under 65 years of age, those with atypical presentations and those with challenging BPSD.
Referral to specialist services differs across the regions of
New Zealand. Referral may be to DHB memory clinics, psychiatry of old age services, geriatric medicine services and
sometimes neurology services. Referrals should include as
much of the diagnostic work-up as possible (eg, relevant history and examination findings, results of blood screening
tests and copies of the cognitive tests/clock-drawing task).
GPs can initiate and monitor cholinesterase inhibitors but
advice from secondary care services about this or any other
aspects of care would be encouraged if problems develop.

Further reading
Perkins C. The New Zealand Dementia Guide. Auckland: Random
House, 2004 – an excellent book for GPs, other health professionals and families.
The Use of Antipsychotics in Residential Aged Care. Clinical
recommendations developed by the RANZCP Faculty of
Psychiatry of Old Age (New Zealand), 2008. Available online
at http://tinyurl.com/4u7f2rb

Patient information and support
Alzheimers New Zealand National Helpline
0800 004 001
Provides direction to its nearest local organisation.
Website www.alzheimers.org.nz
Alzheimer’s Society (UK)
Website www.alzheimers.org.uk
The New Zealand Home Health Association
Provides assistance to find out what home health services are
available. Website www.nzhha.org.nz
A nationwide database directory about services for older people
in New Zealand. Website www.eldernet.co.nz

Poor memory and ‘persecution’ (Case study 2)
Presentation and history
Mary, an 80-year-old widow, presents with failing memory and delusions of a persecutory nature. She lives alone and her daughter
has an Enduring Power of Attorney and lives nearby. Her memory
loss began about three years ago and has gradually and progressively worsened. Mary states that people are coming into her home
and are stealing small items. Her daughter frequently finds these
items around the house and believes her mother is just misplacing
them. Mary is unable to be convinced by this explanation. Mary
has a number of medical problems, including treated hypertension, GORD and mild osteoarthritis; she is on an antihypertensive,
omeprazole and regular paracetamol. Her daughter has observed
Mary no longer performing her personal cares well or maintaining
the house to her previous standard.
A physical review shows no indication of acute illness. Mary is
euthymic. There are no other psychotic symptoms (specifically,
hallucinations in any modality) apart for the persecutory thoughts,
which are judged to be of delusional intensity. Cognitively, Mary
scores 18/30 on the MMSE with deficits in short-term memory,
orientation to time and visuospatial tasks.
The GP believes the diagnosis is likely to be Alzheimer’s dementia
with secondary psychotic symptoms, but a number of differential
diagnoses need to be excluded such as intracerebral pathology
(eg, stroke or cerebrovascular disease, space-occupying lesions)
and systemic illness (eg, metabolic abnormality, etc.).
Full dementia blood screening tests are performed (CBC, electrolytes, renal function, thyroid function, calcium, vitamin B12 and folate), which are unremarkable. A CT head scan reveals pronounced
cerebral and hippocampal atrophy.
Mary and her daughter are advised of the likely diagnosis of Alz­
heimer’s dementia and a referral is placed to Alzheimers New Zealand to provide ongoing support and education, particularly for the
daughter. The GP commences Mary on low-dose haloperidol 0.5mg
in the evening. The GP arranges a Needs Assessment.
A month later, the delusional ideas have reduced significantly and
Mary is tolerating the haloperidol well. Mary is receiving Home Help
and Personal Cares and is eligible for Respite Care if needed. Following discussions with Mary and her daughter, the decision is
made to start donepezil 5mg daily for a month then increasing to
10mg daily to attempt to stabilise her cognition, assist with the
psychotic symptoms, and hopefully to allow the gradual withdrawal
of haloperidol in the next two to three months.

Quiz answers
1. False. 2. False. 3. True. 4. False. 5. False. 6. True.

New Zealand Doctor F 9 February 2011 F 31



The difference
beTween conTrol
& being conTrolled.
Positive treatment with Methylphenidate for children with
ADHD is well proven,1-4 however, a pill should only ever be
considered part of ADHD treatment.5
While children will benefit from the ability to focus and
learn in the classroom, they also need the space to learn
to cope with their condition.6
Ritalin Long Acting (LA) gives kids 8 hours of cover,
which means good control right through the school day.7
Parents then have the flexibility and control over whether
they think they need to top-up after school or to help them
learn to manage their ADHD.
Plus, Ritalin Long Acting is designed to work with your
patient’s day, not just during it. The unique ‘double peak’
delivery ensures a fast acting onset in the morning to give
them the best start and another in the mid afternoon when
concentration naturally drops.1-4

Give flexibility and control back to your
ADHD patients with Ritalin Long Acting.

Once Daily ■ Long Acting

methylphenidate HCI

References: 1. Biederman J, Quinn D, Weiss M et al. Pediatr Drugs 2003;5(12): 833-841. 2. Silva R, et al. J Child Adolesc Psychopharmacology 2005; 15: 637-654. 3. Lopez F, et al. Pediatr Drugs 2003; 5(8):545-555.
4. Lyseng-Williamson KA Drugs et al. Drugs 2002;62(15): 2251-2259. 5. New Zealand Guidelines for the Assessment and Treatment of Attention-Deficit/Hyperactivity Disorder, Ministry of Health July 2001 6. NICE Guidelines
on Diagnosis and Management of ADHD in Children, Young People and Adults, NCP Guideline, Number 72, 2009. 7. Ritalin Datasheet, Novartis New Zealand Limited.
RITALIN® LA CONTROLLED DRUG B2, Fully funded on the pharmaceutical schedule, Special Authority Criteria Apply. Before prescribing please read the full Data Sheet Presentation: Modified-release caps 10 mg, 20 mg, 30 mg, or 40 mg - bottles of 30.
Indication: Attention-deficit/hyperactivity disorder (ADHD) Dosage: Max daily dose 60 mg. starting dose 20 mg. May begin treatment with 10 mg. Ritalin LA is for once daily administration. Contraindications: Hypersensitivity to methylphenidate or excipients, anxiety,
tension, agitation, hyperthyroidism, pre-existing cardiovascular disorders, MAOI (and within 2 wks), phaeochromocytoma, diagnosis or family history of Tourette’s syndrome. Precautions: Structural cardiac abnormalities or serious cardiac disorders; family history of
sudden death and ventricular arrhythmia; hypertension, monitor BP; pre-existing cerebrovascular abnormalities; psychiatric disorders (or family history); psychosis, mania or acute suicidality; monitor growth; epilepsy; monitor blood counts; children < 6y; pregnancy;
lactation. Interactions: MAOI’s; drugs that elevate BP; anticoagulants; anticonvulsants; alpha-2 agonists; dopaminergic drugs (TCA, antipsychotics); phenylbutazone; alcohol. Adverse reactions: Common: nervousness, insomnia, decreased appetite, drowsiness,
dizziness, dyskinesia, arrhythmias, increase in BP and heart rate, abdominal pain, nausea, vomiting, rash, arthralgia. Rare: angina, blood dyscrasias, psychosis, depressed mood, convulsion, tics, cerebrovascular disorders, abnormal LFT’s, severe skin reactions. Novartis
New Zealand Limited, Auckland. Phone: 09 361 8100 Date of Preparation: 23 Sept 2010. 3618110, RitLA 1210-056-1212, TAPS NA4628

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