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Recognising and managing early dementia

Dementia (mate wareware - see below) is a growing healthcare challenge. There are an estimated 70,000 people with dementia in New Zealand; this number is predicted to increase to over 170,000 by 2050, due to factors such as population growth and increased longevity.* Without a curative treatment or ability to prevent progression of dementia, the main management goal, as for other terminal conditions, is to help people maintain their quality of life for as long as possible. Early diagnosis enables patients and their family/whānau to access support, information and appropriate symptomatic treatments, and allows time to plan for the future.

*Estimates from the Alzheimers New Zealand/Deloitte Dementia Economic Impact report (2016)

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Published: 21 February 2020 | Updated: 6 August 2020

6 August, 2020: MoCA replaced by Mini-ACE, now the preferred cognitive screening test in New Zealand

Mate wareware (pronounced “ma-te wah-ree wah-ree”), meaning to become forgetful and unwell, was identified as a preferred term in te reo Māori for dementia in a large qualitative study including 223 kaumātua (elders).1

Key practice points:

  • Discussions about cognitive decline and dementia (mate wareware*) can be difficult; patients or their family/whānau may be reluctant to disclose symptoms due to fear, embarrassment, shame or denial
  • Symptoms of cognitive decline should be assessed when first reported or noticed. In many cases, reassurance that the symptoms are due to age-related cognitive decline will be appropriate. However, if the symptoms are indicative of a potentially clinically significant change in cognitive function or are affecting the person’s activities of daily living, they should be assessed for dementia.
  • The initial consultation should focus on the clinical history (obtained from the patient and someone who knows them well), investigations to exclude other causes of cognitive impairment (e.g. medicine adverse effects, delirium, depression) and evaluation with a cognitive assessment tool.
  • Most patients with dementia can be diagnosed and managed in primary care. Referral to secondary care is appropriate if there is diagnostic or management uncertainty.
  • Allow additional time when discussing a dementia diagnosis with a patient and their family/whānau to explain what the diagnosis means, how it was made, the management plan and where to access support
  • Strongly encourage early engagement with the local branch of Alzheimers New Zealand or Dementia New Zealand as these organisations are often the main providers of personal support, information, dementia service navigation, “living well” services and programmes such as cognitive stimulation treatment
  • There are currently no treatments available that can cure or prevent the progression of the common subtypes of dementia such as Alzheimer’s disease or vascular dementia. Non-pharmacological and pharmacological interventions may help to delay or slow the development of cognitive and functional symptoms.

* A term for dementia in te reo Māori, meaning to become forgetful and unwell

Part 1: Making a dementia diagnosis

Dementia is not an inevitable part of ageing and not all changes in cognitive function are indicative of dementia, however, it is important that symptoms are investigated when first reported, e.g. by the patient or a family/whānau member, or noticed, e.g. by the primary care team.2 Other scenarios where assessment of cognitive function should be considered in older patients include after a fall or other significant medical event, motor vehicle accident or a safety incident at home, e.g. unattended cooking causing a fire. Patients or their family/whānau may be reluctant to discuss the symptoms, e.g. due to fear, shame or denial, however, timely assessment enables primary care to provide reassurance to people who are experiencing normal age-related cognitive decline, prompt treatment to those with reversible causes of cognitive impairment, and earlier diagnosis in those with dementia.

Investigating the cause of cognitive impairment will usually require at least two consultations: an initial consultation where the patient history and clinical investigations are undertaken and a follow-up where the outcome is discussed.

The initial assessment of a person presenting with suspected cognitive decline should focus on the clinical history to establish the:

If possible, information should also be obtained from someone who knows the person well, e.g. a family/whānau member. A questionnaire, e.g. the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE) or Functional Activities Questionnaire (FAQ), may be used to supplement this discussion (see below for links).3

A list of questions that may be included as part of the patient history is available from:

Patient assessment questionnaires for family/whānau are available from:

Consider other explanations for changes in cognitive function

There are many possible causes of cognitive impairment that must be considered when a person presents with memory loss or other cognitive changes, including:5

  • Medicines use, e.g. medicines with anticholinergic action or adverse effects, opioids, many psychotropic medicines, steroids
  • Psychological causes, e.g. depression, anxiety, stress, psychosis
  • Delirium – many potential causes including dehydration, infection, e.g. urinary tract infection or pneumonia, sensory impairment, adverse medicine reaction, immobility, metabolic disturbances, pain, chronic or severe constipation
  • Alcohol or drug misuse – may also cause delirium
  • Metabolic causes, e.g. vitamin B1 or B12 deficiency, folate deficiency, hyperglycaemic hyperosmolar ketosis, hyperthyroidism, hypothyroidism, hyponatremia, hypercalcaemia, hepatic encephalopathy, uraemia
  • Structural brain disease, e.g. subdural haematoma, mass lesion, normal pressure hydrocephalus
  • Neurological infections, e.g. HIV or syphilis
  • Hearing or vision impairments
  • Sleep apnoea –has been associated with white matter abnormalities and impaired cognition, mood and daytime alertness5,6

Also see: “Differentiating dementia, depression or delirium as the cause of cognitive impairment in older people

Investigations to rule out other potential causes of cognitive decline include:

If a treatable cause is identified, manage this as appropriate and then reassess the patient’s cognitive function. It is possible that a treatable cause may have exacerbated the symptoms of previously unidentified dementia.

Consider arranging a head CT

Brain imaging with computed tomography (CT) is recommended when assessing people for dementia to exclude structural cerebral pathologies or potentially reversible conditions, and to assist with subtyping, management planning and as a clinical baseline if a dementia diagnosis is made.8 If subtyping will not change the management plan or the prognosis, e.g. a person of advanced age with established severe dementia, then a head CT may not be necessary.8

N.B. Referral processes, eligibility criteria and access to head CT varies across DHBs; refer to your local HealthPathways or seek advice from a geriatrician or neurologist.

The history, observation and examination will generally guide the clinician as to whether a formal cognitive assessment is indicated. Cognitive assessments can be used to help confirm and quantify cognitive impairments, and to monitor changes in the patient’s cognitive function over time.

Consider a brief test first, followed by a comprehensive cognitive assessment

If cognitive impairment is suspected but you are unsure, a brief cognitive test can be used initially as a screening tool, e.g. the General Practitioner Assessment of Cognition (GPCOG see: "Cognitive testing with the GPCOG"). The GPCOG takes less than five minutes to administer and is validated for use in primary care. If the results suggest impairment or it is already apparent that some impairment is present, a more comprehensive evaluation should be undertaken. The recommended test for use as part of this assessment is the Mini-Addenbrooke’s Cognitive Examination (Mini-ACE or M-ACE - see “Comprehensive cognitive assessment”). This test also takes about five minutes to administer and is validated for use. Mini-ACE will be the recommended test on the cognitive impairment pathway on local Community HealthPathways platforms once they are updated on 1 September, 2020.

Consider the potential limitations of cognitive testing

There are limitations to cognitive testing, particularly in relation to potential biases that may arise due to the person’s educational level, language or cultural identity. A culturally appropriate cognitive assessment tool for Māori that incorporates knowledge from te ao Māori (Māori worldview) is under development. Another limitation of cognitive testing is that it is possible for a person to score quite well and still have significant cognitive impairment; conversely, a person who functions well can score poorly on a cognitive test, e.g. if they are anxious or have mild dysphasia. Therefore, cognitive assessment tools should not be used in isolation to diagnose dementia.

Dementia is a syndrome with a variety of causes. The symptoms of dementia and the rate of progression vary with subtype (Table 2). Alzheimer’s disease is thought to be the most common subtype of dementia in New Zealand, followed by vascular dementia, but mixed pathology is also common.11 Most patients with dementia can be diagnosed and managed in primary care.

When to refer to secondary care for diagnosis or management advice

Referral to secondary care is appropriate if there is diagnostic or management uncertainty, e.g. due to complexity (see below for examples), or to access management supports that are not available in primary care.

Complexities in people with suspected dementia where referral to secondary care is appropriate include:7

  • Severe behavioural or psychological symptoms, including psychotic symptoms
  • Rapidly deteriorating cognitive function
  • Younger age, e.g. aged < 65 years
  • Atypical presentation
  • History of a significant head injury
  • Chronic neurological disorder, e.g. Parkinson’s disease, Huntington’s disease, Motor Neurone disease or multiple sclerosis
  • Intellectual disability
  • Specific deficits, e.g. speech only

Table 2. Common types of dementia and the distinguishing symptoms and signs12,13

Dementia subtype Symptoms and signs Progression/prognosis

Alzheimer’s disease

  • Short-term memory loss and difficulty finding words, followed by behavioural changes and impaired functioning, with reduced insight
  • Typically gradual onset. It can be difficult to determine exactly when symptoms began. May appear to be sudden onset if a triggering event, e.g. illness or stress, uncovers the underlying decline.
  • Progression is typically slow, i.e. changes occur over several years
  • Life expectancy is an average of eight to ten years following symptom onset, although this varies depending on the patient’s age and other risk factors

Vascular dementia

  • Wide range of symptoms and signs depending on the extent, location and severity of cerebrovascular disease
  • Sudden onset of symptoms after a stroke or more insidious onset with small vessel disease
  • Memory loss can be a symptom but typically less noticeable than in Alzheimer’s dementia
  • Deficits may be found in language, decision-making and information and visuospatial processing
  • Mood changes and apathy are common symptoms
  • Can be co-present with Alzheimer’s disease (referred to as ‘mixed dementia’)
  • Progression depends on the type of disease: small vessel disease progresses slowly, like Alzheimer’s disease, while vascular dementia following a stroke (“multi-infarct dementia”) often follows a stepped progression with long periods of remaining the same and short periods where symptoms worsen
  • Life expectancy is approximately five years after symptom onset, however, there is wide variability. Often the cause of death is stroke or myocardial infarction.

Frontotemporal dementia (FTD)

  • Younger age of onset (e.g. age 50–60 years)
  • Symptoms include changes in personality and behaviour, may include disinhibition and impulsiveness. Memory is usually intact early in the disease.
  • Diagnosis can be easily missed; may require more specialised tests of social awareness or behaviour
  • Rate of progression can vary greatly
  • Life expectancy is an average six to eight years after symptom onset

Dementia with Lewy Bodies or Parkinson’s disease with dementia

  • Suspect if dementia with marked fluctuations during the day, parkinsonian features, visual hallucinations, autonomic symptoms, e.g. postural hypotension, incontinence, sexual dysfunction, or falls
  • Tremor may be less evident in people with dementia with Lewy Bodies than with Parkinson’s disease
  • Sleep disturbances, e.g. rapid eye movement sleep behaviour disorder (shouting out or moving while asleep), can occur many years before the onset of dementia
  • Up to 80% of people with Parkinson’s disease will develop dementia. Symptoms are similar to dementia with Lewy bodies, but the motor symptoms occur before the cognitive symptoms by definition.
  • Dementia with Lewy bodies typically develops and progresses slowly, like Alzheimer’s disease
  • In Parkinson’s dementia, motor symptoms typically develop a year or more before the cognitive and psychiatric symptoms.
  • Life expectancy of a person with dementia with Lewy Bodies is an average of 6–12 years from symptom onset

Other causes or sub-types of dementia include:13

  • Alcohol-related dementia
  • Posterior cortical atrophy (an Alzheimer’s disease variant)
  • Creutzfeldt-Jakob disease
  • HIV-related cognitive impairment
  • Huntington’s chorea
  • “Parkinson’s Plus” dementias, e.g. corticobasal syndrome, progressive supranuclear palsy
  • Multiple sclerosis
  • Niemann-Pick disease type C
  • Normal pressure hydrocephalus
  • Tertiary syphilis

When delivering a dementia diagnosis to the patient and their family/whānau, the discussion should cover:2, 7

  • That the cognitive problems they have been experiencing are more than just normal ageing. It is important to use the terms dementia or mate wareware, rather than euphemistic descriptions, because this enables the patient and their family access to information, support and services.
  • How the diagnosis was made, i.e. by explaining the information obtained from the history, assessment tool(s) and investigations
  • General discussion about the course and prognosis of dementia
  • Non-pharmacological and pharmacological treatment options for symptomatic management
  • Referral for a Needs Assessment, if indicated
  • How to access information and support from their local dementia organisation; either Alzheimers New Zealand or Dementia New Zealand, depending on location
  • Medico-legal issues to consider, e.g. driving, appointing an Enduring Power of Attorney, developing or updating an advance care plan, preparing a will. N.B. These discussions are likely to be ongoing and may not be considered in detail, if at all, at the first follow up appointment.

Allow additional time for this type of consultation. The pace should be guided by the patient and their support people, it is often not possible or advisable to cover everything in one consultation. Provide written information that the patient and their family can take home with them. Alzheimers New Zealand has “About dementia”, “Living well with dementia” and “Supporting a person with dementia” booklets, available from: Information can also be accessed from Dementia New Zealand:

Acknowledge the impact of a dementia diagnosis

A diagnosis of dementia can have a significant impact on a person’s self-esteem, relationships, employment and future plans. When learning about the diagnosis, the patient and their family/whānau may experience a range of feelings including shock, disbelief, anger, fear, hopelessness, despair and grief.14 Some may also feel relief at having an explanation for the changes that have been occurring. Empathy, understanding and sensitivity toward the person and their family/whānau are imperative when discussing the diagnosis and prognosis for a person with dementia. Although the realities of dementia must be discussed, this needs to be balanced by encouraging the person and their family/whānau to focus on what they can do and to keep actively engaged in life.

Diagnosing dementia early allows people to make decisions about their future care and to access support. It also allows for early engagement with interventions that may help to preserve their quality of life for as long as possible. For carers, early diagnosis allows more time for them to adjust to the patient’s changes in function, mood and personality, and to transition into their caregiving role.14 Ensuring that carers have access to support and maintain their own health and wellbeing is a core component of dementia care.

Carers for a person with dementia can access support through the Supporting Families organisation, see:

Perspectives from patients who are living with dementia and their carers are available from:

Part 2: Managing early-stage dementia

Management should focus on slowing symptom development and maintaining quality of life

There are currently no interventions that can cure or prevent the progression of the more common causes of dementia, such as Alzheimer’s disease or vascular dementia. Therefore, the aim of dementia management is to slow the rate of symptom development and help the person maintain their best quality of life (also see: “Providing dementia care for Māori”). Key areas of focus for primary care should include:2

  • Management of co-morbidities and reducing cardiovascular disease (CVD) risk, e.g. stopping smoking, limiting alcohol intake, managing hypertension, diabetes and obesity, optimising diet (e.g. recommend the Mediterranean diet or Dietary Approaches to Stop Hypertension [DASH] diet (see link below). Reducing CVD risk is particularly important in people with vascular dementia.
  • Ensuring annual vision and hearing checks, and timely management of sensory impairment; enlist the help of a partner or family/whānau member if they cannot arrange an appointment themselves
  • Assessing nutrition and hydration (e.g. using the Mini Nutritional Assessment People with dementia are at risk for undernutrition (either generalised protein-energy malnutrition or specific micronutrient deficiency, especially B12 and folate) due to problems with meal planning, shopping, preparing food and eating regularly.
  • Medicine reconciliation, i.e. reviewing medicines regimens and adjusting or stopping treatment as appropriate
  • Risk assessment, e.g. safety while cooking, using electrical appliances, heavy machinery or firearms, driving, falls
  • Reviewing how the patient is managing at home. Recommend strategies to help the patient manage memory loss (see link below). Refer for a Needs Assessment if there is significant carer stress or the patient needs support to remain living independently.
  • Monitoring mental health, stress and coping – both the patient and their caregiver

Ideally, people with dementia, accompanied by their family/whānau or carer, should be reviewed every three to six months to monitor the management plan and address any concerns.

For further information on lifestyle strategies to slow cognitive decline, see:

For practical tips on how to manage memory loss symptoms, see:

Physical activity

People with dementia should be encouraged to engage in physical exercise both for their general health and wellbeing and as a way of slowing cognitive decline; this should ideally include a mix of aerobic and muscle strengthening exercises. Aerobic exercise, e.g. brisk walking, running, cycling, dancing, aerobics, swimming or aqua jogging, has been shown to be most beneficial in terms of cognitive functioning.15, 16 A meta-analysis of 18 Randomised Control Trials (RCTs) including 802 people with dementia found that exercise interventions that included aerobic exercise (walking, running, cycling or dancing) improved cognition, independently of intervention frequency (i.e. <150 or >150 minutes per week).16 Although the same cognitive benefits were not found with non-aerobic exercise interventions (Tai Chi, strength, balance or flexibility training), these exercises should still be recommended for falls prevention.16

Psychosocial stimulation

Cognitive Stimulation Therapy (CST) is a group or individual talking-based intervention recommended for people with mild to moderate dementia.3 CST uses reminiscence (discussing past activities and events), stimulation and reality orientation (understanding the present using visual prompts) tasks, and focuses on opinions and discussions to stimulate language, thoughts and associations.17 A meta-analysis of 14 RCTs including 657 people with dementia found that CST significantly improved cognitive function, communication and social interaction, self-reported quality of life and wellbeing.18 A 2015 pilot of group CST in people with dementia in Auckland found that CST (14 sessions) reduced symptoms of depression, improved quality of life (reported by families and caregivers but not the patients themselves) and showed a trend towards an improvement in memory.19

Availability of CST around New Zealand is variable; check with the local Alzheimers New Zealand or Dementia New Zealand branch to see if a programme is available in your area.

Remaining mentally and socially active is important. All people with dementia should be encouraged to engage in cognitively and socially stimulating activities that are tailored to suit their interests and abilities, e.g. reading, quizzes, crosswords, sudoku, playing cards or board games, learning something new, playing music, dancing or cultural activities. For Māori, cultural activities and utilising te reo Māori are considered protective factors that optimise a person’s functioning within their whānau and community.1 Encourage Māori patients to continue with their roles within the whānau and on the marae, where possible.1

Information for patients about staying active and engaged following a dementia diagnosis is available from:

Acetylcholinesterase inhibitors

An acetylcholinesterase inhibitor such as donepezil (oral, funded), rivastigmine (transdermal patches funded with Special Authority approval – see: “Rivastigmine patch brand change”, oral not funded) or galantamine (oral, not funded) may be considered in people with Alzheimer’s-type dementia, vascular dementia where subcortical ischaemic changes are prominent and dementia associated with Parkinson’s disease/Dementia with Lewy Bodies (unapproved indication). Acetylcholinesterase inhibitors should not be prescribed to people with mild cognitive impairment.2

The treatment effects of acetylcholinesterase inhibitors are generally modest; not all patients will respond to treatment and it is not possible to predict response. There is no evidence that acetylcholinesterase inhibitors prevent the progression of dementia, however, some people may have a temporary improvement in cognition and functionality. A meta-analysis of 43 RCTs including over 16,000 people with Alzheimer’s disease reported that acetylcholinesterase inhibitor treatment resulted in small to moderate improvements in cognitive function, global symptoms and functional capacity.20 Data on neuropsychiatric symptoms are mixed, but suggests that there may be benefits for some symptoms (such as apathy and psychosis) but not others (such as anxiety and aggression).20

Cautions to acetylcholinesterase inhibitor use include sick sinus syndrome or other supraventricular conduction abnormalities, e.g. atrioventricular or sinoatrial block, due to an increased risk of bradycardia. Perform an ECG in all patients prior to initiating treatment to check for pre-existing conduction abnormalities.21, 22

Acetylcholinesterase inhibitors can cause dose-related cholinergic effects, e.g. nausea, bradycardia, vomiting, diarrhoea, dyspepsia, urinary incontinence, dizziness.21 Treatment should be initiated at a low dose and titrated upwards, if tolerated. Patients who have intolerable nausea or vomiting with donepezil tablets can be prescribed transdermal rivastigmine patches.

N.B. The acetylcholinesterase inhibitors available have similar effectiveness; most people will be initiated on donepezil as it is fully funded. If donepezil is not effective, rivastigmine or galantamine may be trialled, taking into consideration the affordability of non-funded treatments. Only one acetylcholinesterase inhibitor should be used at a time.

Treatment effectiveness, adverse effects, adherence and symptom progression should be assessed one month after initiating a acetylcholinesterase inhibitor, and again at three months and six months, if treatment has been tolerated.23 Family and caregivers are well-placed to observe treatment response and adverse effects, however, it is recommended that an objective measure, e.g. Mini-ACE, is also used to monitor treatment effectiveness.23 There is limited guidance on the recommended duration of acetylcholinesterase inhibitor treatment. If the patient experiences significant adverse effects, has poor adherence to treatment or monitoring requirements, is no longer showing benefit from treatment or has not benefitted from treatment, the medicine should be discontinued.23 It is recommended that the dose is stepped down over two to three weeks rather than stopping abruptly, and if there is significant decline, re-start the medicine promptly.23

Refer to the NZF for further information on cautions, dosage, switching from oral to transdermal formulations and monitoring of acetylcholinesterase inhibitor treatment:


Memantine (not funded) may be considered for people with moderate Alzheimer’s disease who are intolerant of or have a contraindication to an acetylcholinesterase inhibitor, or who have severe Alzheimer’s disease.2, 3 Memantine may also be used in combination with an acetylcholinesterase inhibitor by people with moderate to severe Alzheimer’s disease.2, 3 As with acetylcholinesterase inhibitors, the effects of memantine are variable; some may experience benefit, e.g. improved function or slowed rate of decline, while others will not. Memantine is contraindicated in people with a history of seizures and should be avoided in people with severe hepatic or renal impairment.21 Common adverse effects include constipation, hypertension, dyspnoea, headache, dizziness and drowsiness.21

Refer to the NZF for further information on cautions and dosage:

Future articles will cover the management of behavioural and psychological symptoms as dementia progresses and the role of primary care in supporting patients and their families during the palliative phase of dementia care.

Dementia resources for primary care health professionals are available here:

National report

There is a national report associated with this article.

The purpose of this report is to provoke thought and discussion about how and why antipsychotic medicines are prescribed to older patients. The report includes national data, and practice points for reflection. View national report

CME activites

There are CME activites associated with this article.


Thank you to Dr Matthew Croucher, Psychiatrist of Old Age, Canterbury DHB and Senior Clinical lecturer, University of Otago, Christchurch for expert review of this article.

Article supported by PHARMAC

N.B. Expert reviewers do not write the articles and are not responsible for the final content. bpacnz retains editorial oversight of all content.

Ben Gray 21 Feb 2020 13:19
Sharyn Willis, Medical Advisor, bpacnz 21 Feb 2020 16:59

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