Dementia Note

The timely diagnosis of dementia
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MODULE NOTES
THE TIMELY DIAGNOSIS OF DEMENTIA

Table of contents:
1. 2. 3. 4. 5. 6. 7. Abbreviations Definitions How common is dementia? Characteristics of dementia Risk factors associated with dementia Protective factors associated with dementia Diagnosing dementia 7.1 Timely diagnosis 7.2 Consequences of not recognising dementia 7.3 How to make the diagnosis 7.3.1 Diagnostic criteria for dementia 7.3.2 Biomedical Imaging 7.3.3 Barriers to diagnosis 7.4 Identifying the type of dementia 7.5 Population Screening vs. Case finding 7.6 What is mild cognitive impairment (MCI)? 7.6.1 Conversion to dementia 7.7 Physical comorbidities of dementia 7.8 Natural history 7.9 Common conditions which may cause or aggravate dementia 8. Treatment of dementia 8.1 The early to middle stages 8.1.1 Links between cardiovascular and dementia risk reduction factors 8.2 Established dementia what can we do 8.2.1 Pharmacy Review 8.3 Functional assessment 8.4 Management plan 8.5 What are Behavioural & Psychological Symptoms of Dementia (BPSD)? 8.5.1 Differential diagnosis of BPSD 8.5.2 Aetiology of BPSD 8.5.3 Managing behavioural and psychological symptoms of dementia (BPSD) and co-morbidities 8.6 Non-pharmacological management of dementia 8.6.1 Psychosocial treatments 8.6.2 Management of behavioural symptoms 8.6.3 Management of psychological symptoms 8.6.4 Pharmacological treatment 8.7 The end stages 8.7.1 The Carer and the patient 8.7.2 Palliation and management of severe distress in dementia 9. Role of GPs and practice nurses 9.1 Breaking the news 9.1.1 Fears expressed by families 9.1.2 Issues to discuss with family 10. Who to call for help 11. Resources 12. References
1. Abbreviations
A AChEI AD ADAS-Cog Amyloid-A Acetyl cholinesterase Inhibitor Alzheimer's Disease Alzheimer's Disease Assessment Scale, cognitive sub-scale
http://thinkgp.com.au/flash/2123_dementia_1/files/dementia_notes.html
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ADL BPSD
Activity of daily living Behavioural and psychological symptoms in dementia Dementia Collaborative Research Centre Dementia with Lewy Bodies Functional Magnetic Resonance Imaging
DCRC DLB FMRI, fMRI FTD, FTLD
Fronto-temporal dementia, Fronto-temporal lobar degeneration Hydrocephalus Hippocampal volume Mild Cognitive Impairment Mini-Mental State Examination Positron Emission Tomography Preferred Priorities for Care Standardised Mini-Mental State Examination Single Photon Emission Computed Tomography White Matter Hyperintensity
HC HV MCI MMSE PET PPC SMMSE SPECT WMH
2. Definitions
1. Dementia is defined in DSMIV as A decline in multiple areas of cognitive function i.e. memory, intellect and personality in an alert (non-delirious) patient, progressive and irreversible, causing significant impairment in social or occupational functioning for diagnosis. (American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision (DSM IV
TR))
2. DSM5, released in May 2013, defines Major Neurocognitive Disorder as: Substantial cognitive decline > 1 domain based on concerns of individual, knowledgeable informant or clinician Decline in neurocognitive performance, typically involving > 2 SDs below appropriate norms (ie < 3rd percentile) on formal testing or equivalent clinical evaluation Cognitive deficits interfere with independence (ie requiring minimal assistance with IADL) Cognitive deficits not exclusively in the context of delirium and not primarily attributable to another mental disorder (eg, major depression, schizophrenia) 3. DSM5 defines Minor Neurocognitive Disorder as: Modest cognitive decline > 1 domain based on concerns of individual, knowledgeable informant or clinician Decline in neurocognitive performance 1-2 SDs <appropriate norms (ie between 3rd and 16th percentiles) on formal testing or equivalent clinical evaluation Cognitive deficits insufficient to interfere with independence (IADLs, like more complex tasks, paying bills, meds, preserved), but > effort, compensatory strategies or accommodation required Cognitive deficits not exclusively in the context of delirium and not primarily attributable to another mental disorder (eg major depression, schizophrenia) 4. Dementia is also described as: ...an umbrella term for a range of conditions (see Types of dementia 7.4). It is characterised by loss of memory, and impairments in thinking and problem-solving capabilities. Features may include impairment in language, memory, perception, and cognitive skills. These may result in loss of intellect, personality, rationality, social skills and normal emotional reactions. Dementia results from degeneration of nerve pathways and the conditions associated with it are typically progressive. (Phillips et al 2010) 5. Delirium is defined (DSMIV) as follows: A delirium is characterized by a disturbance of consciousness and a change in cognition that develop over a short period of time. The manual states: The essential feature of a delirium is a disturbance of consciousness that is accompanied by a change in cognition that cannot be better accounted for by a pre-existing or evolving dementia. The disturbance develops over a short period of time, usually hours to days, and tends to fluctuate during the course of the day. There is evidence from the history, physical examination, or laboratory tests that the delirium is a direct physiological consequence of a general medical condition, Substance Intoxication or Withdrawal, use of a medication, or toxin exposure, or a combination of these factors.
3. How common is dementia?

1. In 2011, there were an estimated 298,000 people with dementia, of whom 62% were women and 70% lived in the community. Among Australians aged 65 and over, almost 1in 10 (9%) had dementia, and among those aged 85 and over, 3 in 10 (30%) had dementia. 2. There were an estimated 23,900 Australians under the age of 65 with dementia in 2011. (AIHW 2012)
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Source: 14 essentials in the practice & art of diagnosis & management of dementia Professor Henry Brodaty 21/05/2011
4. Characteristics of dementia
Early Warning signs may include (BridgesWebb 2003) 1. Memory problems: a. Trouble recalling time or date. b. Impaired ability to recall events or conversations. c. Losing items. d. Repetitive questioning. 2. Cognitive problems include: a. Abandonment of complex problems finances. b. Difficulty recognising familiar objects or people. c. Cannot follow the plot or story. d. Language problems. e. Delirium. f. Reduced competence in making decision & plans. g. Lack of attention to detail. 3. Behavioural problem include: a. Withdrawal and/or inertia. b. Inflexible attitude to stubbornness. c. Irritability. 4. Specific incidents may include: a. Confusion or unhappiness while in unfamiliar environment. b. Neglect of longestablished behaviour for example, not going to regular bowls activity or not baking familiar dishes
or changes in usual routines.
5. Risk factors associated with dementia

1. The following risk factors were listed by Phillips (Phillips et al, 2010): "Well established Old age Genetic factors: Down Syndrome Apolipoprotein E status Genetic mutations (rare) Family history of Alzheimers disease Likely Hypothyroidism Vascular risk factors: Smoking currently High blood pressure (mid-life) Diabetes (generally Type 2) Atrial fibrillation Obesity in mid life Less Likely Depression Elevated homocysteine
Head injury (especially more severe) Low level of education Low birth weight for gestational age
Fatty diet
The risk factors for vascular dementia include many of the above plus male gender, cardiac disease or major cardiac surgery, obesity, stroke, family history of vascular disease and elevated cholesterol. As yet, no amenable risk or protective factors for dementia with Lewy bodies and fronto-temporal dementia have been identified. 2. Communication in 2013 from Prof H Brodaty suggests that the head injury may only have weak link as a risk factor.
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6. Protective factors associated with dementia

Activities which may reduce the risk of developing dementia include management of the following: (Phillips et al 2010) 1. Diet and nutrition: a. A reduced dementia risk is associated with moderate to high intake of polyunsaturated and monounsaturated fats. b. It is recommended that Folate and B12 levels are checked, despite it not being clear the role these play in the development of dementia.
Communication in 2013 from Prof H Brodaty suggests that there is currently no compelling evidence to treat all patients with B12 and folate.
c. There is not at present convincing evidence that antioxidants can prevent dementia, but this does not indicate that they are ineffective. d. Some studies suggest that omega-3 fatty acids (for example, fish oil) may reduce risk of dementia, as could mild to moderate alcohol consumption. A high intake of saturated fat is a risk factor for Alzheimers disease and vascular dementia. e. Alcohol intake associated with a lower risk of dementia appears to range from 1 up to 4 standard drinks per day. f. Anyone who drinks excessive amounts of alcohol over a period of years may get alcohol related dementia. Males who drink more than six standard alcoholic drinks a day, and women who drink more than four, seem to be at increased risk of developing alcohol related dementia. Alcohol Related Dementia (www.fightdementia.org.au) 2. Activity: a. Physical activity: several observational studies have found an association between physical activity in mid to late life and a lower risk of cognitive decline and dementia. Physical activity has numerous health benefits and may reduce cardiovascular risk factors, improve blood flow to the brain and possibly stimulate nerve cell growth and survival. b. Mental activity: these include hobbies as well as excursions and it has also been noted that a higher level of education is associated with a lower risk. It seems that complex mental activity throughout all stages of life may reduce the likelihood of developing dementia. 3. Vascular risk factors: a. Hypertension in mid-life is a risk factor and there is evidence that the treatment, and better management, of high blood pressure may limit cognitive decline. b. Type 2 diabetes and hyperlipidaemia are risk factors. c. Current smoking is a risk factor. 4. Some doctors suggest that further research into the limitations of existing studies is needed before any recommendations on interventions to reduce dementia risk can be made. However, others highlight there is good evidence that preventative strategies including physical, mental and social activity together with good nutrition and control of vascular risk factors may reduce the risk or delay the onset of dementia. Encouraging people of all ages, and particularly those in their forties and fifties, to reduce their risk of dementia will enhance physical health as well as brain health and can do no harm. (Phillips et al 2010)
7. Diagnosing dementia 7.1 Timely diagnosis (Phillips 2010)

1. The benefits of a timely diagnosis include: a. Making the correct diagnosis as other conditions may cause similar symptoms. This allows for the correct management to be instituted early. b. Planning for long term care if the diagnosis is dementia. If the diagnosis is made in a timely fashion, the patient is given the opportunity to participate in decision making and planning. c. Earlier access to medications for Alzheimers disease. d. Management of other comorbid conditions and of risk factors. e. Review of current medications to exclude any which may be contributing to the symptoms of dementia. 2. Diagnosis at specialist staffed memory clinics is higher as well as more accurate than in general practice. There is more difficulty at the primary care level, particularly due to patient caseload. (Turner et al 2004). A range of care providers may be involved in the diagnosis at both primary care and specialist levels. Others available assessment services include Cognitive, Dementia and Memory Services CADMS (www.health.vic.gov.au) in Victoria and Aged Care Assessment Teams ACAT (www.agedcareaustralia.gov.au) or similar in other states. a. Pathology may precede dementia by 2030 years. Symptoms to diagnosis gap is usually 23 years. (personal communication Prof H Brodaty February 2013). b. See Figure 1 below for Early diagnosis and management of dementia in general practice flow chart cited in (Yates & Pond 2012).
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Figure 1. Early diagnosis and management of dementia in general practice. Reproduced with permission Dr Mark Yates.
7.2 Consequences of not recognising dementia

1. 2. 3. 4. 5. 6. 7. Missed reversible causes. Failure to intervene symptomatically. Failure to provide assistance/community support for ADL dysfunction. Missed opportunities re AChEI. Dangerous decision making e.g. still driving? Struggling families, misunderstanding. Missed opportunity for long term planning issues.
7.3 How to make the diagnosis (Phillips et al 2010)

1. Assess symptoms with a good history. 2. Evaluate memory and thinking abilities. 3. Exclude other causes of dementialike symptoms such as: a. Mental disorders such as depression. b. Delirium. c. Abnormal function of liver, kidney, thyroid, hormonal system. d. Nutritional deficiencies and anaemia. e. Poor eyesight or hearing, severe constipation. f. Side effects of medication, diabetes or chronic UTI. 4. If the above are excluded, and criteria are met for dementia, then the next step is to determine the cause. The most common causes are Alzheimers disease, vascular dementia, dementia with Lewy bodies and fronto-temporal dementia.
MEDICAL HISTORY
Complete medical history. Complete family history. Ask about: forgetfulness, orientation, problem solving, coping with everyday life, mood, alcohol consumption and medication usage. Ask about a time frame: when did the changes first get noticed, was it sudden or gradual, how is it progressing? With the patients consent, get information from family members.
MEDICAL TESTING
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Blood and urine: to exclude infection, nutritional deficiency, and evaluate kidney, liver and thyroid function. Refer for genetic testing and counselling in rare cases of early onset familial dementia. INVESTIGATIONS Brain scans (C/T, MRI) looking for evidence of tumour, stroke, atrophy, vascular changes (deep white matter hyper-intensities, haemorrhage), subdural haematoma and increased intracranial pressure. Changes may be modest in early dementia. Abnormal scan does not diagnose dementia, and normal scan does not rule out (early) dementia. These scans may indicate the cause of dementia e.g. vascular changes or stroke, or focal atrophy as in FTD. Investigations used in specialist and research may include: Positron Emission Tomography (PET). See the podcast by Professor Chris Rowe: Podcasts (www.austin.org.au). Single Photon Emission Computed Tomography (SPECT). Functional Magnetic Resonance Imaging (FMRI). PSYCHOLOGICAL EVALUATION COGNITIVE EVALUATION AND SCREENING TESTS Include an evaluation of mental wellbeing as mood may impact on cognition. Consider anxiety and depression.
These determine the degree of cognitive impairment and track progress over time. Mini-Mental State Examination or (MMSE pdf) and the Brief Cognitive Rating Scale. The MMSE is used to determine eligibility for subsidised prescription medications. The Dementia Outcomes Measurement Suite (DOMS) (www.dementia-assessment.com.au) provides more information. The General Practitioner Assessment of Cognition GPCOG (www.gpcog.com.au) a quick, valid, and efficient test for dementia screening in primary care that can use informant information if necessary. The Rowland Universal Dementia Assessment Scale RUDAS (www.fightdementia.org.au) for people from non-English speaking background. The Kimberley Indigenous Cognitive Assessment (www.wacha.org.au) includes several subsections including a cognitive assessment section (KICA-Cog) and a briefer cognitive screen (KICA-Screen) that can be used in conjunction with carer input (KICA-Carer) for people from rural and remote Aboriginal and Torres Strait Islander communities. The Montreal Cognitive Assessment (MoCA) (www.mocatest.org) a brief cognitive screening test which also has a high sensitivity and specificity for detecting Mild Cognitive Impairment (MCI). The MiniCOG (www.alz.org) - composed of a three item recall and clock drawing. It has been established as an effective routine screening test for use in primary care practice. Brief tests may be followed with more detailed testing: Cambridge Cognitive Examination (CAMCOG) (www.cantab.com) Addenbrooke Cognitive Examination- Revised (ACE-R).
(Table based on Phillips et al 2010)
Also see Tests used in diagnosing dementia, as reviewed by Prof David Ames for Alzheimers Australia (pdf).
Test name
Uses
Strengths
Weaknesses
Time to do test (approximate) 3 minutes
MiniCOG
patient consulting alone, GP/ ED
Quick and easy. Good addition to driving medicals 2 sources of information In most practice software
Misses early dementia. No score, pass or fail Needs informant
GPCOG
Designed for GP
6 minutes
MMSE
Widely used, <24/30 for dementia medication Non English speaking background Aboriginal and Torres Strait Islander
Takes time
15 minutes
RUDAS
Widely used by psychologists
Not widely used by GPs
15 minutes
Kimberley Indigenous Cognitive Assessment (KICA)
Acknowledges culture
Target group have varying cultural knowledge
Can take 30 minutes or more
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7.3.1 Diagnostic criteria for dementia

1. In order to meet the former (DSM IV) diagnostic criteria for dementia (pdf), in addition to significant memory problems, the patient needs to have impairment in at least one of the following 4 domains: a. Aphasia: language problems, which may become evident when taking the history e.g. being able to identify an object but not being able to describe the components. b. Agnosia: failing to recognise, especially people e.g. not knowing who family and friends are, with not only the name forgotten but now being aware of ever having known them. c. Apraxia: being unable to carry out purposeful movements despite there not being a motor or sensory impairment e.g. difficulty getting dressed, where there are many details to consider. d. Executive dysfunction: difficulty with sequential activities and planning, poor initiation and difficulty with problem solving and dealing with a change in routine. 2. DSM5 was released in May 2013, and this is the suggested change (www.dsm5.org).
7.3.2 Biomedical Imaging

1. Pittsburgh compound B (11C-PIB) is a radioactive biomarker used in Positron Emission Tomography (PET) for imaging A deposits. 2. PIB is derived from Thioflavin T, a histopathology dye used to stain A plaques. 3. PIB crosses the blood-brain barrier, binds to insoluble species of Amyloid with high affinity and enters brain in sufficient amount to be imaged using PET. It clears rapidly from normal tissues. 4. Fluorodeoxyglucose (18FDG) PET imaging and Magnetic Resonance Imaging (MRI) are other procedure used. 5. MRI is a powerful scanning tool providing high quality anatomical details of brain tissue. 6. Longitudinal repeat MRI scans are useful to assess the cortical atrophy associated with the progressive neuro-degeneration seen in Alzheimers disease. NOTE: 1 4 are currently in the final research phase with Prof Chris Rowe and others at The Austin Hospital in Melbourne. See Preventing the decline of our ageing population Professor Chris Rowe podcasts (www.austin.org.au).
7.3.2.1 ADVANTAGES AND DISADVANTAGES OF THE COMMONLY USED NEUROIMAGING TECHNIQUES 1. C/T scans & non-contrast C/T used as a routine to primarily exclude brain lesions and identify cerebrovascular disease. 2. MRI better resolution than C/T, but takes longer. Apparatus is more claustrophobic and noisy than C/T. MRI provides better images of intracranial structures, especially cerebral white matter and is more sensitive at picking up vascular lesions than C/T. MRI cannot be carried out when a patient has a cardiac pacemaker or metallic intracranial aneurysm clips. MRI is particularly useful in identifying vascular dementia 3. SPET/SPECT involves administration of compounds that are distributed in the brain according to cerebral blood flow, thus showing a measure of cerebral activity. SPECT investigations commonly measure blood flow but muscarinic and dopamine receptors can be imaged. Useful in identification of FTD 4. PET directly measures cerebral metabolic activity and can assess cerebral metabolism, cerebral blood flow and cerebral receptors. Can provide regional comparisons between lobes, as well as absolute cerebral activity. Can be used to image receptor and transmitter systems that may be of use in detailing the pathophysiology of dementia and monitoring treatment response. Recently developed ligands allow imaging of amyloid.
7.3.2.2 C/T, PET AND MRI WHY DO WE NEED MORE THAN C/T: a. C/T detects the treatable causes of dementia like subdural haematomas, tumours and stroke. b. C/T scan will suffice for typical cases of Alzheimers disease. c. More advanced imaging is required for earlier diagnosis of Alzheimers disease, atypical presentations and non-Alzheimers disease dementia. Source: Professor Christopher Rowe presentation.
7.3.2.3 NEURO-PATHOLOGY OBSERVED IN AN MRI 1. Global a. b. c. d. and regional atrophy: Parietal atrophy in early onset AD. Anterior temporal lobe atrophy in Semantic Dementia form of FTD. Frontal lobe atrophy in the behavioural form of FTD. Hippocampal atrophy. i. Not specific present in AD and FTLD. ii. Present but less severe in Vascular Dementia and Dementia with Lewy Bodies. iii. In MCI it is a strong predictor of progression to dementia within 1 2 years. iv. Rating needs to be age adjusted.
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Images courtesy Prof C Rowe, The Austin Hospital, Melbourne 2009.
7.3.2.4 A IMAGING (AVAILABLE IN MELBOURNE AT THE AUSTIN HOSPITAL) 1. A deposition precedes cognitive decline by up to 10 years. 2. Presents an opportunity for Preclinical Diagnosis and preventative intervention.
Alzheimers disease in 2013
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7.3.3 Barriers to diagnosis
(Phillips 2010)
1. GPs limitation: a. Differentiating between normal ageing and dementia. b. A perceived lack of need to make a specific diagnosis no cure, not enough drugs. c. Lack of confidence and training. d. Risk of misdiagnosis which tests really help. 2. Practical limitations: a. Paucity of specialist or memory clinics available. b. Lack of a recognised, quick-to-administer screening tool. c. Lack of time and other chronic conditions to treat. d. The patients impaired ability, which hinders an accurate history and participation in self-care. 3. Negative attitude to dementia: a. The stigma associated with dementia. b. Doubts about the efficacy of medications. c. A perception of the patient as unable to comprehend or cope with the diagnosis. d. The risk of detriment to the doctor-patient relationship. 4. Carers perception: a. Stigma associated with the diagnosis. b. Delay in treatment through a misunderstanding of symptoms by doctors. c. Families arranged support rather than seeking medical advice. d. Stoicism and the perceived need to cope with a difficult situation.
7.4 Identifying the type of dementia

Dementia syndromes may overlap in individual patients: 1. Alzheimers disease accounts for ~40% dementia cases: a. Insidious onset, slow progression, fluctuating symptoms. b. Impairment of memory, attention and language; apathy or irritability; apraxia. c. Neuroimaging may show cortical atrophy. d. Genetic component: i. Rare genetic mutations can cause early-onset autosomal dominant familial AD, whereby mutations in the presenilin genes (presenilin I and II) and the amyloid precursor protein (APP) gene affect the APP and its metabolism. The amyloid cascade hypothesis suggests that accumulation of beta-amyloid, by overproduction or failure to break down APP, leads to amyloid deposition resulting in amyloid plaques, neurofibrillary tangles and cell death. ii. Apolipoprotein E (ApoE) a protein involved in lipid and cholesterol transport has been identified as a genetic determinant of susceptibility to late-onset AD, although it is not causative in disease onset. There are
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2.
3.
4.
5.
6.
three common alleles for the ApoE gene: e2, e3 and e4. The e4 allele confers an increased risk of AD, whereas the e2 allele may be protective [Poirier, 1993]. Vascular dementia accounts for ~20% dementia cases: a. Onset may be sudden following stroke, stepwise deterioration. b. Cognitive impairment variable; emotional lability, gait abnormalities and urinary dysfunction may be early markers; Parkinsonian motor features. c. Vascular lesions on MRI or CT. d. Risk factors include hypertension, diabetes, smoking, hyperlipidaemia, cardiovascular and cerebrovascular disease. Mixed dementia: Dementia syndromes may overlap in individual patients and patients may have pathology associated with more than one type of dementia. (Bridges Webb 2003) (Barker et al 2002) a. Vascular dementia often coexists with Alzheimers disease. Patients with cardiovascular risk factors are also at risk of developing vascular dementia therefore vascular risk factors should be well-controlled in all patients with dementia. Dementia with Lewy bodies accounts for ~20% dementia cases: a. Patients must have at least two of the following: i. Rapidly fluctuating cognition. ii. Visual hallucinations. iii. Spontaneous motor Parkinsonism. b. Neuroleptic sensitivity is common important to avoid neuroleptic drugs. c. For a diagnosis of dementia with Lewy bodies at least two of the cardinal symptoms of visual hallucinations, parkinsonism and fluctuation in mental state (typically over minutes or hours) must be present. (Alzheimers Australia. Dementia with Lewy Bodies). The clinical course of dementia with Lewy bodies differs from Alzheimers disease. Both memory and the ability to carry out complex tasks may fluctuate rapidly, and clinical features include complex visual hallucinations (48%), auditory hallucinations (14%), paranoid delusions (57%), clouding of consciousness (81%), falls or collapses (38%), depression (38%), and extrapyramidal features (9.5%). (Bridges Webb 2003) d. It is important to identify patients with Lewy body dementia because neuroleptic sensitivity is common (seen in about 60% of patients). These patients have a high risk of increased morbidity and mortality if neuroleptic drugs are prescribed. (Bridges Webb 2003) Fronto-temporal dementia accounts for ~5% dementia cases: a. Fronto-temporal dementia (FTD) sometimes called Picks complex is characterised by focal frontal atrophy with personality and behavioural disturbances, or temporal atrophy with either progressive aphasia or semantic dementia. Onset of FTD is observed in a younger age group than other dementias and diagnosis may be difficult in the early stages of disease. b. Routine neuropsychological assessment procedures such as the Mini-Mental State Examination (MMSE) are usually insensitive at detecting frontal abnormalities, therefore more extensive neuropsychological testing is required to establish frontal deficit in patients suspected with FTD. The clock drawing test may be helpful. c. Presenting features of FTD include: i. Insidious onset and slow progression. ii. Preservation of memory to late-stage disease making diagnosis difficult. iii. Early and prominent personality changes (e.g., apathy, irritability, jocularity, euphoria, loss of personal and social awareness). iv. Loss of tact and concern. v. Impaired judgement and insight. vi. Mental rigidity and inflexibility. vii. Hypochondriasis. viii. Unrestrained exploration of objects and the environment (hyper-metamorphosis). ix. Distractibility and impulsivity, depression and anxiety. x. Language difficulties (e.g., problems with word recall, circumlocution, word repetition also known as gramophone syndrome). xi. Inertia. d. Other features (associated with Kluver-Bucy syndrome): i. Emotional blunting. ii. Hyperorality. iii. Hypersexuality. Other types of dementia include: a. Dementia with Parkinsons disease precedes cognitive decline and the absence of other causes of dementia. b. Alcohol dementia: the condition is indicated by a history of excessive alcohol consumption. c. Traumatic brain injury: this may lead to dementia. Symptoms will vary depending on the type of injury and the area of the brain affected. Unlike other dementias, dementia from head injury often remains stable over time or may even improve. d. Complex congenital syndromes such as Down Syndrome.
7.5 Population Screening vs. Case finding

1. Population screening What is it? all patients over 75. 2. GP Guidelines recommend against population screening. 3. Problems include: a. False +ve (NHMRC study over 50% +ve using GPCOG not demented). b. Screening instruments do not perform well in low prevalence (<15%) populations the positive predictive value drops rapidly. (e.g. 10/100 people aged 75, with dementia, using instrument with 90% sensitivity and a 90% specificity) c. Frustration/overwhelms system e.g. GP spends time/effort refer to memory clinic, referral of large numbers of
people without dementia means that clinic waiting times extend, patients suffer undue anxiety while waiting if they dont have dementia and have to wait longer for medications and services if they do have dementia.
4. INSTEAD a. Screening as part of a package of enhanced care. Screen for dementia in those where you have a high index of suspicion.
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b. Guidelines recommend case finding applying screening instrument to someone who reports symptoms, or in whom you observe symptoms, or about whom relatives report symptoms, likely results in lower rate of false +ve's.
7.6 What is mild cognitive impairment (MCI)?

1. 2. 3. 4. 5. 6. Prodrome to dementia in some cases. A cognitive complaint (self-reported or informant-based). Preserved basic ADLs, intact or minimally impaired complex instrumental ADLs (e.g. finances, driving). Cognitive Impairment not normal for age or education. A decline in cognition evidenced by performance in objective testing. Preserved general cognitive functioning.
Petersen criteria revised for MCI Not normal, not dementia. Self and /or informant report. Impairment on objective cognitive tasks and/or. Evidence of decline over time on objective cognitive tasks. Preserved basic ADLs and minimal impairment of complex function. Generally intact global cognition.
Source: 14 essentials in the practice & art of diagnosis & management of dementia Professor Henry Brodaty 2011.
7.6.1 Conversion to dementia

1. Rates vary about 3-12% per annum. 2. Some studies higher depends on definition use and the population that you follow-up e.g. Community screened versus Clinic presentations. 3. NOT Bad News not invariable, some studies show 50% remain stable, or 40% revert to normal.
7.7 Physical comorbidities of dementia

The following conditions occur significantly more frequently in people with dementia (particularly Alzheimers disease) than in people of the same age without dementia: (Kurrle 2010; DCRC) a. Epilepsy. b. Falls. c. Delirium. d. Frailty. e. Malnutrition. f. Dental disease. g. Visual impairment. h. Sleep disorders. i. Urinary and faecal incontinence.
1. Delirium: a. Occurs in up to 60% of hospitalised older patients. b. 3/4 of patients with delirium have dementia: i. Expect delirium in hospitalised older patients with dementia. ii. Use simple screening test (e.g. Confusion Assessment Method: pdf) regularly. iii. Find cause & treat symptomatically (e.g. fluids, medications, and infection). iv. Nurse in appropriate specialised ward, discourage bed/location changes, avoid restraints though not very many GPs will look after hospitalised patients. 2. Weight loss and malnutrition: a. Associated with AD, also seen in other dementias: patients are likely to lose 10% body weight over course of disease. b. Assess nutritional status at time of diagnosis. c. Nutritional interventions may include: reversible medical/socio-environmental causes, increased calorie/protein intake, daily physical activity. 3. Epilepsy: a. Patients with dementia have approximately 6-fold increase in seizures compared to age matched population. b. Consider the possibility of seizure if occurrence of a faint or funny turn. c. Seizures may be atypical. d. Consider treatment with anticonvulsants. 4. Frailty: a. Reduced physiological reserves: combination of weight loss, low grip strength, self-reported exhaustion, slow walking speed, low physical activity. b. Regular exercise has shown to improve physical function and memory. c. Address nutrition if appetite/weight loss. d. Assess cognitive function in frail patients. 5. Sleep disorders: a. Sleep disturbances reported in < 50% of patients with dementia. b. Severity increases with severity of dementia. c. Inquire about sleep disturbances in patients with cognitive impairment. d. Encourage regular sleep/wake routine. e. Address factors that may disturb sleep e.g. pain, infection, heat, cold. f. Consider physical exercise and adequate daylight.
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6. Oral disease: a. More common in patients with dementia compared with age matched. i. Range of factors: e.g. deterioration in ability to self-care, decreased motivation. b. Patients should be referred for dental consultation to maintain/restore good oral health. c. Consider effect of medications. d. Education for carers. e. Care should be appropriate to stage of dementia. 7. Visual dysfunction: a. Visual dysfunction may be presenting symptom of dementia. b. If no structural cause, consider referral to neurologist/geriatrician. c. Visual problems during course of dementia may impact on assessment tasks & ADLs. d. Review by optometrist/ophthalmologist; correct issues e.g. cataracts, improved lighting. 8. BPSD: a. Always check for physical cause e.g. UTI, pain. b. What is the cause? What is being communicated? c. Try psychosocial intervention first. d. Dementia Behaviour Management Advisory Service (DBMAS)/Behavioural ASsessment & Intervention Service (BAsIS) can assist. e. ChEIs may help apathy, hallucinations. f. Memantine may help agitation/aggression/hallucinations/delusions cluster. g. Citalopram may help agitation, delusions, and hallucinations. h. Antipsychotics have a place for aggression, for psychosis, but CVA & Motor retardation. i. Antidepressants disappointing. j. Informed consent from patient or proxy in writing. k. Review regularly, >3rd monthly.
7.8 Natural history
Source: 14 essentials in the practice & art of diagnosis & management of dementia Professor Henry Brodaty 2011
7.9 Common conditions which may cause or aggravate dementia

1. 1. Common conditions which can cause or aggravate dementia need to be thought of and excluded or managed are: a. Depression. b. Drugs. c. Thyroid disorders (hypo/hyperthyroidism). d. Subdural haematoma. e. Neoplasms. f. Alcohol. g. Intracerebral lesions (tumour, normal pressure hydrocephalus). h. Vitamin B12 deficiency, Folate deficiency. i. Metabolic disturbances (hypo/hyperglycaemia, uraemia, hypo/ hypercalcaemia). j. Water and electrolyte disturbances (dehydration and hyponatraemia). k. Infections (urinary tract, respiratory tract). l. Renal failure. m. Hypoxia. n. Malnutrition. 2. Not only may these conditions aggravate dementia, but also the onset of dementia may lead to deterioration in such conditions, particularly by reducing compliance with medications. In order not to avoid overlooking any co-morbidity which should be managed optimally, it may help to use the assessment form checklist developed by the RACGP. (Bridges-Webb, C., & Wolk, J. 2003: pdf)
NOTE: this is currently under review.
8. Treatment of dementia (Phillips et al 2010)

1. There is currently no cure for dementia.
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2. There are four drugs approved in Australia for the treatment of Alzheimers disease. Donepezil, rivastigmine and galantamine are cholinesterase inhibitors that make more of the neurotransmitter acetylcholine available at brain synapses, and help to enhance memory function. Memantine acts on the neurotransmitter glutamate and can relieve symptoms in middle and later stages of Alzheimers disease. (Phillips et al 2010) 3. Comorbidities such as diabetes, hypertension and hyperlipidaemia need to be assessed and managed. 4. Preventive care should include immunisation, hygiene, rest/sleep, hydration and nutrition and dental care 5. Psychosocial treatments and support such as attention to safety, activities of daily living, activity and stimulation and medication supervision are important. 6. Carer support with medication, activities, education and managing behaviours, as well as education, is required. 7. Planning should commence early, with good communication, including the patient/family/carer in decision making. Recommendations to support organisations like Alzheimers Australia will offer resources for patient and family alike.
8.1 The early to middle stages

1. Risk factor management: Primary and secondary prevention. 2. Pharmacy review. 3. What else can we do? a. Needs assessment ADL dysfunction. b. Positive lifestyle changes. c. Diet/Nutrition. d. Medical, dental, sensory co-morbidities. e. Care planning.
8.1.1 Links between cardiovascular and dementia risk reduction factors
Alzheimers Australia. Towards a National Dementia Preventative Health Strategy, August 2010.
8.2 Established dementia what can we do

1. Evidence for risk factor management includes: a. Hypertension b. Control Diabetes c. Regular exercise 2. Managing other medical, dental and sensory co-morbidities
8.2.1 Pharmacy Review

1. Value of medication review in dementia patient: a. Assess impact of current chronic disease management e.g. Lasix and ACh side-effects. b. Watch for anti-cholinergic load e.g. antiemetics, antiParkinsons, antispasmodics. 2. Review sedative and hypnotic drugs. 3. Review and simplify current drug regimen.
8.2.1.1 ACETYLCHOLINESTERASE INHIBITORS (ACHEIS) 1. Three Acetylcholinesterase inhibitors (AChEIs) are currently available in Australia: donepezil, rivastigmine and galantamine. (Alzheimers Australia. The dementia epidemic: Economic impact and positive solutions for Australia) AChEIs act by blocking the breakdown of the neurotransmitter acetylcholine, which is associated with memory. 2. They are the established first-line pharmacotherapy in mild to moderate AD. (Birks 2006). 3. A recent Cochrane review concluded that treatment with donepezil, galantamine or rivastigmine for people with mild, moderate or severe Alzheimers disease produced improvements in cognitive function, global clinical state and measures of activities of daily living and behaviors. None of the treatment effects were large. No difference in efficacy between the three main AChEIs (donepezil, rivastigmine and galantamine) has been reported. (Birks 2006). 4. Currently available drugs do not provide a cure or prevent any further disease progression; clinical trials of AChEIs demonstrate that progression of symptoms of dementia are delayed in the majority of people for 912 months and possibly longer. (Alzheimers Australia. The dementia epidemic: Economic impact and positive solutions for Australia) 5. Although most patients benefit from AChEIs to some extent, but only 5060% show a measurable response to treatment, and it is not possible to predict which patient will respond.(Bridges-Webb et al 2003: pdf)
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6. Side effects are generally mild and transient, and can be minimised by slow dose titration. Nausea, vomiting and diarrhoea occur significantly more frequently in AChEI-treated patients than in placebo groups, although many other types of adverse events have been reported. (Bridges-Webb 2003: pdf). 7. In one large trial, adverse events were reported less frequently with donepezil than with oral rivastigmine. (Birks 2006) 8. Only about one quarter (23%) of patients with mild to moderate AD are taking an AChEI. (Alzheimers Australia. The dementia epidemic: Economic impact and positive solutions for Australia) 9. AChEIs are currently licensed only for Alzheimers type dementia. PBS criteria for reimbursement are complex: (Australian Government Department of Health and Aging. Schedule of Pharmaceutical Benefits for approved pharmacists and medical practitioners February 2007). 10. Please see the PBS requirements for prescribing (please note specialist diagnosis is required in order to access the drug) Body System (www.pbs.gov.au). 11. See the report for a plain language summary regarding the use of drugs in Alzheimers disease Report to the PBAC Review of Pharmaceutical Benefits Scheme anti-dementia drugs to treat Alzheimers Disease (pdf) 12. Contraindications to use of these drugs include: a. Active peptic ulcer. b. Bradyarrhythmias e.g. sick sinus syndrome. c. Asthma (?). d. Previous adverse response. eTherapeutic Guidelines states as follows: 1. These drugs require supervision, improve alertness and function and can maintain cognitive scores at or above the baseline for up to 12 months; however, they do not modify the underlying progression of pathology. 2. Patients should be treated for at least two months at the maximum recommended dose, if tolerated, before a final assessment of response is made. 3. Not all patients benefit from cholinesterase inhibitors; some have modest benefit and a few show significant improvement. Adverse effects, particularly gastrointestinal, prevent the use of these drugs in some patients. 4. There is no convincing evidence that any of the available cholinesterase inhibitors is more efficacious than any other; however, a once-daily dosing regimen and limited requirements for dose titration make donepezil, prolonged release galantamine and rivastigmine transdermal patch easier to use than orally administered rivastigmine. In the event of nonresponse, there is a lack of clear evidence to indicate that switching to another cholinesterase inhibitor will produce improvement. However, individual cases of patients who respond to one drug but not to another have been described. In addition, individuals sometimes vary in their susceptibility to the adverse effects of the available cholinesterase inhibitors.
Drug donepezil
Dosage 5 mg orally, at night for 4 weeks, increase up to 10 mg at night if tolerated
OR galantamine (prolonged release) 8 mg orally, daily for 4 weeks, increase up to 16 mg daily if tolerated. If the patient deteriorates after an initial good response, increase further to 24 mg daily, if tolerated
OR rivastigmine Two patch sizes are available: rivastigmine 4.6 mg/24 hours (9 mg) and rivastigmine 9.5 mg/24 hours (18 mg). OR rivastigmine 1.5 mg orally, twice daily for 2 weeks, increase to 3 mg twice daily; subsequent dose increases to 4.5 mg and then 6 mg twice daily should be based on tolerability and may be considered every 4 weeks. 4.6 mg transdermal, daily for 4 weeks, increase up to 9.5 mg daily if tolerated
Memantine, an antagonist of N-methyl-D-aspartate (NMDA) is marketed as a treatment for moderate to severe Alzheimer's disease and there is some trial evidence that it may be efficacious in mild disease. Treatment may be helpful in patients who are deteriorating following an initial response to a cholinesterase inhibitor, or in previously untreated patients whose dementia is moderate to severe. Memantine may be administered to patients receiving a concurrent
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cholinesterase inhibitor. It may be helpful in mild to moderate Alzheimer's disease for patients unable to tolerate a cholinesterase inhibitor. If sleeplessness is a problem, Memantine should be administered earlier in the day. eTherapeutic Guidelines Memantine 5 mg orally, in the morning in the first week, 5 mg twice daily in the second week, 10 mg in the morning and 5 mg at dinner time in the third week, and 10 mg twice daily thereafter.
Table information sourced from eTherapeutic Guidelines 2012.
8.2.1.2 INITIATION OF THERAPY 1. MMSE score >10: Diagnosis of mildmoderate AD confirmed by specialist. Authority application must include the result of the baseline Mini-Mental State Examination (MMSE) or Standardised Mini-Mental State Examination (SMMSE). If this score is 25 30 points, the result of a baseline Alzheimer's Disease Assessment Scale, cognitive sub-scale (ADAS-Cog) may also be specified. (If an ADAS-Cog score is not supplied with the initial application, this scale cannot be used for the purpose of fulfilling the criteria for continued PBS supply.) 2. This application must be made in writing, but initial supply may be sought by telephone. For telephone applications, up to a maximum of 2 months' initial therapy will be authorised. This telephone application must be followed by a written authority application for no more than 1 month's therapy and sufficient repeats to complete a maximum of up to 6 months' initial treatment. For written applications where no prior telephone approval has been issued, up to a maximum of 1 month's therapy plus 5 repeats will be authorised.
8.2.1.3 CONTINUATION OF THERAPY 1. The PBS criteria for the use of the Acetylcholinesterase inhibitors changed in May 2013. PBS 1 May 2013 Acetylcholinesterase inhibitors (AChEIs) AChEIs established as first-line pharmacotherapy in mildmoderate Alzheimers disease (AD). Available in Australia: donepezil, rivastigmine, galantamine. Do not provide a cure. Provides modest benefit in: Cognitive function. Activities of daily living. Behaviour. Global clinical state.
8.3 Functional assessment (Bridges-Webb 2003)

Consider the following: 1. Targeting services to ADL dysfunction. 2. Carer needs. 3. Driving ability.
8.4 Management plan

1. A GP management plan should outline the patients problems/needs/relevant conditions and the goals/changes to be achieved. It should also include required treatments and services (including patient/Carer actions) and arrangements for treatments/services (when, who, contact details). 2. There are several Medicare Item numbers which may be useful in the assessment and management of patients with dementia. Some are listed below. Please refer to the MBS online for further details. 3. Information on Medicare Item numbers for chronic disease management and CDM plans may be found on the Department of Health and Ageing website. 4. Please check currency of item numbers and benefits on the MBS site. MBS Chronic Disease Management Item Numbers
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Item number 701 Health assessment (pdf) brief
Activity Attendance by a medical practitioner (including a general practitioner, but not including a specialist or consultant physician) to perform a brief health assessment, lasting not more than 30 minutes and, including: a) Collection of relevant information, including taking a patient history; b) A basic physical examination; c) Initiating interventions and referrals as indicated; and d) Providing the patient with preventive health care advice and information.
Fee
Fee: $58.20 Benefit: 100% = $58.20
721 Preparation of a GP Management Plan Medicare Benefits Schedule Item 721 (www9.health.gov.au)
Attendance by a medical practitioner (including a general practitioner, but not including a specialist or consultant physician) for the PREPARATION of a GP MANAGEMENT PLAN (GPMP) for a patient (not being a service associated with a service to which items 735 to 758 apply). This CDM service is for a patient who has at least one medical condition that: (a) has been (or is likely to be) present for at least six months; or (b) is terminal. A rebate will not be paid within twelve months of a previous claim for item 721, or within three months of a claim for items 729, 731 or 732 (for a review of a GPMP), except where there are exceptional circumstances that require the preparation of a new GPMP.
Fee: $141.40 Benefit: 75% = $106.05 100% = $141.40
723 Coordination of Team Care Arrangements Medicare Benefits Schedule Item 723 (www9.health.gov.au)
This CDM service is for a patient who: (a) has at least one medical condition that: i. has been (or is likely to be) present for at least six months; or ii. is terminal; and (b) requires ongoing care from at least three collaborating health or care providers, each of whom provides a different kind of treatment or service to the patient, and at least one of whom is a medical practitioner. A rebate will not be paid within twelve months of a previous claim for item 723, or within three months of a claim for item 732 (for a review of TCAs), except where there are exceptional circumstances that require the coordination of new TCAs.
Fee: $112.05 Benefit: 75% = $84.05 100% = $112.05
729 Contribution to a Multidisciplinary Care Plan, or to a Review of a Multidisciplinary Care Plan, for a patient who is not a care recipient in a residential aged care facility (www9.health.gov.au)
This CDM service is for a patient who: (a) has at least one medical condition that: i. has been (or is likely to be) present for at least six months; or ii. is terminal; and (b) requires ongoing care from at least three collaborating health or care providers, each of whom provides a different kind of treatment or service to the patient, and at least one of whom is a medical practitioner; and (c) is not a care recipient in a residential aged care facility. A rebate will not be paid within twelve months of a claim by the same practitioner for item 721 or 723, within three months of a claim for item 729 or within three months of a claim for item 731 or 732, except where there are exceptional circumstances that require a new contribution to the multidisciplinary care plan.
Fee: $69.00 Benefit: 100% = $69.00
731 Contribution to a Multidisciplinary Care Plan, or to a review of a multidisciplinary care plan, for a resident in an aged care facility (www9.health.gov.au)
This CDM service is for a patient who: (a) has at least one medical condition that: i has been (or is likely to be) present for at least six months; or ii is terminal; and (b) requires ongoing care from at least three collaborating health or care providers, each of whom provides a different kind of treatment or service to the patient, and at least one of whom is a medical practitioner; and (c) is a care recipient in a residential aged care facility. A rebate will not be paid within three months of a previous claim for item 731 or within three months of a claim for item 721, 723, 729 or 732 except where there are exceptional circumstances that require a new contribution to the multidisciplinary care plan.
Fee: $69.00 Benefit: 100% = $69.00
732 Review of a GP Management Plan or Coordination of a Review of Team Care Arrangements Medicare benefits
Attendance by a medical practitioner (including a general practitioner, but not including a specialist or consultant physician) to: (a) REVIEW A GP MANAGEMENT PLAN to which item 721 applies. Where these services were provided by that medical practitioner (or an associated medical practitioner), and not being a service associated with a service to which items 735-758 apply.
Fee: $70.65 Benefit: 75% = $53.00 100% = $70.65
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schedule Item 732 (www9.health.gov.au)
This CDM service is for a patient who has at least one medical condition that: i. has been (or is likely to be) present for at least six months; or ii. is terminal. or (b) COORDINATE A REVIEW OF TEAM CARE ARRANGEMENTS to which item 723 applies. This CDM service is for a patient who: i. has at least one medical condition that has been (or is likely to be) present for at least six months; or is terminal, and ii. also requires ongoing care from at least three collaborating health or care providers, each of whom provides a different kind of treatment or service to the patient, and at least one of whom is a medical practitioner. Each service to which item 732 applies may only be claimed once in a three-month period, except where there are exceptional circumstances that necessitate earlier performance of the service to the patient.
"Dementia, delirium, tobacco use disorder and mental retardation are not regarded as mental disorders for the purposes of the GP Mental Health Treatment items. http://www.health.gov.au/internet/main/publishing.nsf/content/pacd-gp-mental-health-care-pdfqa#1_6 (www.health.gov.au). However, the following item numbers may be applicable if there is a comorbid mental health conditions meeting the requirements of the MBS. MBS Mental Health Item Numbers Item number Activity Fee
2700 Preparation of a GP Mental Health Treatment Plan: website. (effective from 1 November 2011)
2700 PREPARATION by a medical practitioner who has not undertaken mental health skills training (including a general practitioner, but not including a specialist or consultant physician) of a GP MENTAL HEALTH TREATMENT PLAN for a patient (not being a service associated with a service to which items 2713 or 735 to 758 apply) lasting at least 20 minutes. A rebate will not be paid within twelve months of a previous claim for the same item or item 2701, 2715 or 2717 or within three months following a claim for item 2712, except where there has been a significant change in the patient's clinical condition or care circumstances that requires the preparation of a new GP Mental Health Treatment Plan.
Fee: $70.30 Benefit: 75% = $52.75 100% = $70.30
NOTE: dementia itself is excluded from Mental Health plans. However coexisting depression would make the person eligible.
PREPARATION by a medical practitioner who has not undertaken mental health skills training (including a general practitioner, but not including a specialist or consultant physician) of a GP MENTAL HEALTH TREATMENT PLAN for a patient (not being a service associated with a service to which items 2713 or 735 to 758 apply) lasting at least 40 minutes. A rebate will not be paid within twelve months of a previous claim for the same item or item 2700, 2715 or 2717 or within three months following a claim for item 2712, except where there has been a significant change in the patient's clinical condition or care circumstances that requires the preparation of a new GP Mental Health Treatment Plan.
Fee: $103.50 Benefit: 75% = $77.65 100% = $103.50
PREPARATION by a medical practitioner who has undertaken mental health skills training (including a general practitioner, but not including a specialist or consultant physician) of a GP MENTAL HEALTH TREATMENT PLAN for a patient (not being a service associated with a service to which items 2713 or 735 to 758 apply) lasting at least 20 minutes. A rebate will not be paid within twelve months of a previous claim for the same item or item 2700, 2701 or 2717 or within three months following a claim for item 2712, except where there has been a significant change in the patient's clinical condition or care circumstances that requires the preparation of a new GP Mental Health Treatment Plan.
Fee: $89.25 Benefit: 75% = $66.95 100% = $89.25
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PREPARATION by a medical practitioner who has undertaken mental health skills training (including a general practitioner, but not including a specialist or consultant physician) of a GP MENTAL HEALTH TREATMENT PLAN for a patient (not being a service associated with a service to which items 2713 or 735 to 758 apply) lasting at least 40 minutes. A rebate will not be paid within twelve months of a previous claim for the same item or item 2700, 2701 or 2715 or within three months following a claim for item 2712, except where there has been a significant change in the patient's clinical condition or care circumstances that requires the preparation of a new GP Mental Health Treatment Plan.
Fee: $131.45 Benefit: 75% = $98.60 100% = $131.45
2712 Review of a GP Mental Health Treatment Plan (www9.health.gov.au)
Attendance by a medical practitioner (including a general practitioner, but not including a specialist or consultant physician) to REVIEW a GP MENTAL HEALTH TREATMENT PLAN prepared by that medical practitioner (or an associated medical practitioner) to which item 2700, 2701, 2715, 2717 or former items 2702 and 2710 applies or to REVIEW a PSYCHIATRIST ASSESSMENT AND MANAGEMENT PLAN to which item 291 applies (not being a service associated with a service to which items 2713 or 735 to 758 apply). A rebate will not be paid within three months of a previous claim for item 2712 or within four weeks following a claim for item 2700, 2701, 2715 or 2717, except where there has been a significant change in the patient's clinical condition or care circumstances that requires the preparation of a new review of a GP Mental Health Treatment Plan.
Fee: $70.30 Benefit: 75% = $52.75 100% = $70.30
2713 GP Mental Health Treatment Consultation (www9.health.gov.au)
Professional ATTENDANCE by a medical practitioner (including a general practitioner, but not including a specialist or consultant physician) involving taking relevant history, identifying presenting problem(s), providing treatment, advice and/or referral for other services or treatments and documenting the outcomes of the consultation, on a patient in relation to a mental disorder and lasting at least 20 minutes (not being a service associated with a service to which items 2700, 2701, 2715, 2717 or 2712 apply). SURGERY CONSULTATION (Professional attendance at consulting rooms)
Fee: $70.30 Benefit: 100% = $70.30
NOTES: ADL = Activities of Daily Living; IADL = Instrumental Activities of Daily living; ACAT = Aged Care Assessment team; OT = Occupational Therapist.
8.5 What are Behavioural & Psychological Symptoms of Dementia (BPSD)?

1. Symptoms of disturbed perception (hallucinations), thought content (delusions) and mood (depression), anxiety. 2. Behavioural changes frequently occurring in patients with dementia: a. Wandering. b. Aggression. c. Sexual disinhibition. d. Screaming. e. Hoarding. 3. Aberrant motor behaviour includes pacing, rummaging, wandering, pointless hyperactivity.
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Grossberg. Int. Psychogeriatrics, 14:27-49.
8.5.1 Differential diagnosis of BPSD

1. Delirium: a. Infection, constipation, pain, medication. 2. Medication: a. Anti-Parkinson medication. b. ACh medications. 3. Changes to the environment or routine.
8.5.1.1 DIAGNOSIS OF DELIRIUM Characteristics Onset Course Duration Attention Sensorium Delirium Acute to sub-acute Fluctuation Hours to days Fluctuates Often impaired, can fluctuate rapidly Usually immediate cause Increased, decreased or unpredictable Impaired, poor attention Dementia Insidious Stable and progressive Months to years Steady Clear until later stages
Etiology Psychomotor activity Cognitive function Perception
No immediate cause Usually normal
Poor memory > attention Simple delusions and hallucinations
Hallucinations (visual), delusions fleeting, not systematised Disrupted or reversed
Sleep/wake cycle
Fragmented
Adapted from: Manepalli N., et al., Primary Psychiatry Vol 14, No 8, 2007.
8.5.2 Etiology of BPSD

1. Biological: a. Alterations in neurotransmitter systems. b. Neuronal loss, tangles and plaques. 2. Unmet needs model. 3. ABC model: Antecedents Behaviour Consequences. 4. Stress threshold model: under and over stimulation.
8.5.2.1 FACTORS CONTRIBUTING TO BPSD
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Gauthier et al., 2010.
8.5.2.2 UNDERLYING CAUSE OF DISTURBING BEHAVIOURS 1. Need to find out. 2. May be multifactorial e.g. insomnia : a. Cant find way back after going to toilet. b. Napping during the day. 3. May include issues relating to the carer: a. Limited understanding of dementia. b. Depression.
8.5.2.3 ASSESS THE BEHAVIOUR 1. Characterize the behaviour precisely with special attention to the circumstances under which it occurs, when it started and whether onset was gradual or sudden. 2. If the behaviour appears inappropriate, consider whether there is an underlying goal (e.g. exit-seeking) or misperception (e.g. misperceiving the corner of a room as a urinal, or another person's bed as one's own). 3. Review the patient's psychiatric history, social history and premorbid personality. 4. Review the medication list with special attention to changes around the time the behaviour started and to drugs known to cause agitation, apathy or confusion. 5. Inquire about life events and the quality of premorbid relationships between carer and patient. 6. Examine the patient with attention to changes in mental status from baseline. Look for signs of painful or uncomfortable physical conditions that may be producing agitation or aggressiveness by increasing physical arousal. If possible, ask the patient to explain the symptom and give an account of his general health and living conditions. 7. Develop two sets of hypotheses on which to base treatment. a. Diagnostic: includes considerations of concurrent mental illness, delirium, painful or uncomfortable physical conditions and drug side effect b. Mechanistic: describes mechanisms of behaviour and includes neurological interpersonal or environmental triggers of behaviour, with possible goal or motives for the behaviour.
NSW Department of Health. (2006). Working with People with Challenging Behaviours in Residential Aged Care Facilities.
8.5.3 Managing behavioural and psychological symptoms of dementia (BPSD) and comorbidities
1. Behavioural complications will affect 90% of patients with AD. Psychological/psychiatric complications include depression, anxiety, psychosis or hallucinations, while non-psychological behavioural complications include agitation, wandering, screaming and aggression. (Bridges-Webb 2003)
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2. These problems warrant treatment when they impact on carers burden or coping ability, affect self-care or social interactions, or when they are likely to lead to institutionalisation. Patients with these behaviours can be difficult to manage but they are often over-medicated; as these behaviours change over time, medication for such complications should be reviewed at least every 6 months. (Bridges-Webb 2003) 3. Regular review and optimal management are required. 4. Avoid polypharmacy where possible: a. Supervision of medication-taking will be required. b. Start with low dose, titrate slowly, monitor for beneficial/adverse effects. 5. Adverse effects are common with psychotropic drug therapy in dementia; the benefits, risks and treatment goals should be discussed with the patient (if possible) and carer, and any unrealistic expectations or fears considered. (Bridges-Webb 2003) 6. Depression: Social stimulation, appropriate activities, plus counselling when appropriate are first-line strategies for depressed mood. Antidepressant drugs are often worth trying; antidepressants such as selective serotonin re-uptake inhibitors (SSRIs) usually being preferable to tricyclics. (Bridges-Webb 2003) 7. Agitation/aggression/psychosis: a. First line: social or environmental manipulation, behaviour modification. 8. Anxiolytic/Neuroleptic drug therapy may be appropriate. Neuroleptics should not be used in patients with dementia with Lewy bodies. (Bridges-Webb 2003) 9. Anxiety states: High anxiety levels such as agitation or aggression may respond to social or environmental manipulation. If not, patients may benefit from behaviour modification, counselling, or anti-anxiety, anti-panic or anti-phobic drug treatment. (Bridges-Webb 2003). Tranquillisers such as haloperidol, olanzapine and risperidone may be considered. Shorter acting minor tranquillisers such as chlormethiazole may be useful for behavioural problems caused by anxiety. (Bridges-Webb 2003) 10. An increased long-term risk of mortality has been associated with patients with Alzheimers disease who are prescribed antipsychotic medications. (Ballard et al 2009) 11. Other: Management of CV risk factors should be optimised as for stroke patients, although polypharmacy and compliance may be an issue. Other medical conditions particularly needing optimum treatment are: dehydration, diabetes (particularly, avoidance of hypoglycaemia), hypoxia, anaemia, postural hypotension, epilepsy, infective illness, pain, and urinary or faecal retention. (Bridges-Webb 2003)
8.6 Non-pharmacological management of dementia

1. Non-pharmacologic approaches conceptualize behavioural symptoms as expressions of unmet needs (e.g., repetitive vocalizations for auditory stimulation); inadvertently reinforced behaviour in response to environmental triggers (e.g., patient learns screaming attracts increased attention); and/or consequences of a mismatch between the environment and a patients abilities to process and act upon cues, expectations, and demands. Treatment goals of non-pharmacologic approaches include preventing, managing, reducing, or eliminating behavioural occurrences; reducing caregiver distress; and/or preventing adverse consequences (harm to caregiver or patient). (Gitlin et al 2012) 2. Education about non-pharmacological strategies is important for: a. Nursing and residential home staff. b. Informal carers and family. c. Behavioural strategies. d. Regular routine. e. Reminders and repetition. f. Social activity, sensory stimulation. 3. Environmental strategies: a. Message systems. b. Clocks & date. c. Home modifications (safe, comfortable, familiar, interesting). 4. The consent to use restrictive practices and medication to manage challenging behaviours by a guardian may vary between the States and Territories in Australia. For instance, in NSW permission to use this line of treatment will be made by the Guardianship Tribunal. This will depend on a thorough, documented assessment of the reasons for the person's behaviour and systematic attempts to use positive non-pharmacological interventions, such as a tailored behavioural or activity program have been trialed and found to be inadequate. a. There have been rigorously designed studies which support the efficacy of non-pharmacological strategies to alleviate behavioural disturbances in elderly persons with dementia, specifically there is evidence to support the efficacy of activity programs, music, behaviour therapy, light therapy, carer education and changes to the physical environment. Individualised programs can be developed by monitoring behaviour first to gain an idea of the cues and triggers of behaviour. (NSW Guardianship Tribunal. Position statement on management of challenging behaviours in people with dementia: pdf) 5. Education about such approaches is very important for both informal carers, and nursing and residential home staff. Books and educational materials from organisations such as Alzheimers Australia, and carer support interventions such as support groups (also organised by Alzheimers Australia) may be helpful, together with GP advice. 6. Some general practical strategies which carers can adopt include: (Bridges-Webb 2003) a. Establish a simple, regular routine that suits the person with dementia. b. Establish a physical environment that suits the person with dementia (safe, comfortable, familiar, and interesting). c. Be prepared for change, understand that dementia is due to a disorder/disease of the brain and that the affected person has reduced ability to control/think/act. d. Ignore unwanted behaviour or walk away; positive reinforcement of adaptive behaviour. e. Expect inconsistencies patient can sometimes do things, sometimes not (like faulty wiring). f. Distract try to focus attention away from what is upsetting the person with dementia. g. Use empathy and humour to defuse tension. h. Maintain respect, avoid infantilisation, dont say to the person I just told you that. i. Slow pace, avoid rush. j. Give repeated explanation and reassurance. k. Use clear, direct, short and simple communication; importance of eye contact, gestures and appropriate touch. l. Break tasks down into small steps.
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m. Look at activities in terms of the steps required to perform them. The person may be able to do some but not all of these e.g. get dressed, if clothes are selected and put out by someone else. n. If resistance encountered with task, try again later. o. Tolerate the behaviour (avoid arguing or scolding). p. Ensure consistency and avoid change wherever possible.
8.6.1 Psychosocial treatments

1. Challenging behaviours (OConnor et al 2009): a. Evidence for aromatherapy, person-centred bathing, individualised music, gentle sounds, muscle relaxation training in managing agitation. 2. Psychological symptoms: a. Carer education, music, gentle exercise, recreation and validation therapy useful for psychological symptoms of dementia. Psychosocial interventions for treating the cognitive and noncognitive aspects of dementia are based on the fact that neurological disease will affect each individual differently depending on the following: Individuals biography. Individuals personality. The presence of coexisting physical and mental health problems. The persons social relationships. The physical environment in which the person is living. Community and cultural understandings of and tolerance for confusion and frailty. The extent and location of the disease.
Source : Prof H Brodaty Lectures in dementia online
8.6.2 Management of behavioural symptoms

Symptom Psychosocial Interventions Limit napping, exercise, cut out caffeine Medication*
Insomnia
Give existing psychotropics in evening, melatonin Little evidence for medication Antipsychotics, AChEIs, SSRIs (low dose may assit), carbamazapine, memantine SSRIs, AChEIs, antipsychotics
Wandering
Environmental change, exercise Consider needs, stimulation and ABC models, communication, caregiver support Use needs model, access, privacy, redirection, tactile soothing, caregiver support Reduce crowding, stimulation, exercise, distraction
Aggression
Sexual disinhibition
Agitation
Antipsychotics, carbamazapine, antidepressants
*Please refer to the full PI for approved indications, dosages, adverse events and drug interactions for medicines used in Australia.
8.6.3 Management of psychological symptoms

Psychosocial Depression Psychosis CBT (mild - mod) Clear communication, reassure CBT, exercise, diversion, reassure Medication* SSRIs AChE inhibitors, Antipsychotics SSRI Avoid benzodiazepines
Anxiety
*Please refer to the full PI for approved indications, dosages, adverse events and drug interactions for medicines used in Australia.
8.6.4 Pharmacological treatment
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1. Antipsychotics little evidence for long term (>12 weeks) treatment. 2. Cholinesterase inhibitors. 3. Antidepressants.
8.6.4.1 TREATMENT OF MOOD AND BEHAVIOUR DISTURBANCE (ETHERAPEUTIC GUIDELINES) 1. Psychotropic medication should only be given for specific indications, after assessment of specific symptoms. 2. Pervasive depression should be treated but remember that antidepressant medication which has an anticholinergic adverse effect should be avoided as they have the potential to compound cognitive deficits. 3. Start with low doses of all psychotropics in patients with dementia and be alert to the side effects of orthostatic hypotension, sedation and parkinsonism. 4. Review regularly and reduce and cease the medication where possible. 5. Do not use first generation antipsychotics in patients where Dementia with Lewy bodies is suspected or in those with Parkinsons disease as there is the potential risk of death in these patients. 6. The second generation antipsychotics (risperidone and olanzapine) may have some impact on the aggression and psychosis accompanying dementia but not all patients will improve. There is an increased risk of cerebrovascular incidents and this is highest in those with existing cardiovascular risk factors that are not well controlled e.g. AF, diabetes or hypertension or a history of stroke. To control hallucinations, delusions or seriously disturbed behaviour, use: risperidone 0.5 to 2 mg orally, daily in 1 or 2 doses. OR olanzapine 2.5 to 10 mg orally, daily in 1 or 2 doses. To relieve symptoms of severe anxiety and agitation, use oxazepam 15 mg orally, 1 to 4 times a day. Benzodiazepines should not be used for longer than two weeks. They exacerbate cognitive impairment, and increase the risk of falls and associated injuries in older people
eTherapeutic Guidelines.
8.7 The end stages 8.7.1. The Carer and the patient
8.7.1.1 ASSISTING WITH CARE 1. The Practice Nurse has become an invaluable team member, often identifying patients who have early dementia when doing a house visit or in assisting the GP with a care or management plan: a. Assessing family or carers ability to cope at home. b. Liaising with Community Nursing services. c. Helping with access to community support services to provide support to family/carers. d. Assisting with other medical needs of the patient.
Differential diagnosis and management in general practice Pfizer SPHERE booklet, 2010.
8.7.1.2 EDUCATION AND SUPPORT 1. Carers may require: a. Education with regard to the illness and its impact on families and carers. b. Assessment and management of physical and mental health problems. c. Assistance with organisation of respite care for patients or transition to residential care. d. Assistance with practical strategies to manage behavioural or cognitive problems. 2. Cognitive behavioural therapy: a. Reduces burden of care. b. Delays institutionalisation and improves survival. c. Improves skills in managing patient behavioural problems. 3. Education and support for carers is vital. (Bridges-Webb 2003) Carer surveys have shown carers would like GPs to: (Nankervis et al 2002) a. Include them in care planning and decision-making. b. Provide plain language information about the patients condition, prognosis and treatment. c. Refer to support groups such as carer associations, health care services and respite care providers. d. Discuss and assess the carers own physical and psychosocial health needs. e. Engage other family members in understanding and sharing care responsibilities. f. Recognize grief and loss on cessation of caring. 4. Training programs for carers have been shown both to relieve strain and to delay institutional placement, and are therefore cost-effective. Carers and family members are critical in determining the environment in which the patient operates and therefore in determining their behaviour. If a carer is stressed and feels out of control, the patient may be more likely to behave in a less consistent and more erratic manner in response to the emotional state of the carer, rather than to the demands of a particular situation. Treatment components include motivation and education, relaxation skills cognitive therapy, problem solving skills training, exposure exercises, sleep management skills training. Stress management strategies include self monitoring, relaxation training, cognitive strategies vs. avoidance, self sacrificing, isolating behaviours. (Brodaty 1989) (Brodaty et al 1993) (Mittelman1993) (Marriott 2000)
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8.7.1.3 CARERS AS PATIENTS 1. The stress associated with caring for a person with dementia should never be underestimated. (Bridges-Webb 2003) It places an extraordinary burden on those who undertake the caring role. Carers are often elderly, or burdened by other family responsibilities, and may experience physical, social and financial burdens as well as psychological stress. (BridgesWebb 2003) 2. Higher levels of depression, psychological morbidity and use of psychotropic medications are seen in carers of those with dementia. Up to 30% of carers will develop a depressive disorder (Bridges-Webb 2003) 3. Behavioural problems in the patient, such as sleep disturbance, incontinence and aggression, correlate more closely with carer stress than either severity of cognitive impairment or duration of dementia. (Bridges-Webb 2003) The spouse often more distressed than other family members. 4. Difficulties experienced with caring can be enough to produce sufficient stress to place either the person with dementia or the carer at risk, or jeopardise the success of community care. (Bridges-Webb 2003) 5. GPs should therefore be vigilant about the health of the carer as well as the patient with dementia. Signs of stress need to be looked for, the stress level assessed, and reviewed at least six-monthly; three-monthly would be ideal. (Bridges-Webb 2003) 6. Ask the carer How is this affecting you? What has changed for you? Ask about the carers mood level. Note any changes in the carers health which could be stress related. The Caregiver Burden Scale may be useful. If the carer has a different GP than the patient with dementia, liaison between the two GPs is suggested. (Bridges-Webb 2003) 7. Counseling could include: a. Recognising carer as equal focus of treatment. b. Acknowledging and giving permission. c. Taking into account premorbid relationship what is driving the care? 8. Support may include: a. Community support: i. Practice and Community Nurses. ii. State Health, local community, other respite centres.
8.7.1.4 DECISION MAKING & LEGAL ISSUES 1. Goal is to promote autonomy and protect from abuse & exploitation. 2. Never write Mrs. X has dementia and lacks capacity unless supported by legal or specialist medical opinion. (Personal communication from Associate Professor Carmelle Peisah, President of the Australian Centre for Capacity [ACCEPD] May 2011). 3. Helps planning, routine care. 4. Use the GP MINILEGAL KIT.
8.7.2 Palliation and management of severe distress in dementia

1. A presentation by Dr Adrian Treloar (2009 pdf) of the NHS discussed distress in patients with dementia and highlighted the following points: a. Severe distress is a far more important concept for the patient than behaviours that challenge etc. as the latter are not patient centred. b. Pain is both mental and physical c. Do not see it as a single entity d. Look underneath it for the cause e. Treat the underlying cause according to good practice advice 2. He stated: Palliative care is about prognosis but also about Palliation of distress and Living well with dementia 3. Distress in dementia may be due to physical, mental or existential pain. 4. Treatment has been broken down into: (Treloar) a. Drugs specifically used to treat cognitive impairment in dementia. b. Drugs for psychosis in dementia and drugs for depression in dementia. c. Management of behavioural and psychological symptoms in dementia (BPSD). d. Management of depression. e. Management of physical pain etc. 5. The presentation lists the signs and symptoms of distress in dementia: a. Anger/Frustration. b. Aggression/Agitation. c. Fear/Anxiety. d. Tearfulness/misery. e. Pain when still. f. Discomfort on moving. g. Restlessness. h. Insomnia. i. Calling out/vocalisation. j. Wandering. k. Autonomic arousal, sweating, tachycardia, hypertension. 6. Underlying causes of severe distress include and each should be managed appropriately: a. Depression. b. Psychosis. c. Pain. d. Poor understanding. e. Fear and anxiety. f. Insomnia. g. Hunger and diet. h. Boredom, isolation and spiritual care. i. Poor Environments including poor staff practices etc.
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Behaviour disturbance is a measure of the trouble caused to others by people with dementia rather than a measure of the patients suffering
8.7.2.1 ADVANCE CARE PLANNING 1. Information may vary between the States. Please see A National Framework for Advance Care Directives (pdf). 2. For NSW Information about advance care planning for General Practitioners (pdf) may provide GPs with information useful for the management of palliative care in their patients with dementia.
8.7.2.2 APPROACH TO PALLIATIVE CARE IN DEMENTIA To live as well as possible until you die. So life is cherished and valued still. And natural death accepted. Life is neither prolonged nor shortened Distress reduction is key. Be willing to limit care to that which is not burdensome. Talk to and discuss with relatives. Remember that palliative care of dementia can provide excellent results.
Adrian Treloar Improving lives UK NHS Trust presentation.
9. Role of GPS and practice nurses

GPs and practice nurses are critical in the care and management of people with dementia. They are involved in many aspects, including: 1. 2. 3. 4. 5. 6. 7. Identifying patients who have suspected dementia. Excluding (and treating) treatable causes, referring patients to specialist services for further diagnosis. Providing information about diagnosis and prognosis of dementia. Assessing carers ability to cope. Providing information about available services and benefits. Helping with access to a range of support services, providing support to family carers. Attending to the medical needs of people with dementia and their carers.
Pfizer SHERE 2010. Dementia: Differential diagnosis and management in general practice Resource Booklet:
8. This is a useful resource: 14 Essentials for Good dementia care in general practice (pdf) 9. Refer to a specialist if: a. Unsure of diagnosis. b. Patient is young or atypical. c. Symptoms and signs are atypical. d. Psychotic or severe behavioural disturbance. e. Multiple, complex comorbidities exist; or f. Considering cholinesterase inhibitor Rx.
(14 essentials in the practice & art of diagnosis & management of dementia, Professor Henry Brodaty 2011)
GP diagnosis of dementia 1. 74% of people consult a GP first after noticing symptoms of cognitive decline, and 2. 79% consider GPs to be easily accessible. 3. GPs are best placed to identify dementia early. 4. But, GPs do not diagnose about 50% (< 91%) of mild cases.
Source: 14 essentials in the practice & art of diagnosis & management of dementia Professor Henry Brodaty, 2011.
9.1 Breaking the news

1. GPs give many reasons for not breaking the news of dementia (Phillips et al, 2010): a. Difficulties in distinguishing normal ageing from dementia. b. Risks associated with misdiagnosis. c. Uncertainty about whether the person with dementia would want to know the diagnosis. d. Risks associated with the persons reaction to diagnosis. e. GPs see the diagnosis as a specialist one. f. GPs feel they are not equipped to discuss all the issues including legal issues. 2. Breaking the news (Tuffrey-Wijne 2013) (Harvey et al 2007): a. Is best seen as a process, not a single event. b. Usually constitute discrete items or pieces of information. c. Information needs to be broken down into smaller pieces of knowledge. d. These can be added over time. e. Certain aspects should be considered: i. Capacity to understand. ii. The response of the person at each stage. iii. People and support services. 3. Recommended strategies (Schofield et al 2003): a. Prepare patient for possible diagnosis. b. Include others that patient would like present. c. Assess patients perceptions; correct misinformation. (Mueller 2002) 4. And this requires real clinical skill: a. Give patient as much information as desired.
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b. Let patient set pace of disclosure. c. Present information clearly. d. Be reassuring and empathetic. e. Encourage involvement in treatment decisions. f. Discuss patients questions on the same day. g. Beware of overload and strong emotion. h. Provide written information/ summary. i. Acknowledge and discuss patients feelings. j. Provide realistic and honest hope. k. Assure patient of doctors availability. (Mueller 2002) 5. Summarise areas discussed. (Mueller 2002) 6. Offer second appointment shortly after.
9.1.1 Fears expressed by families
(Brodaty, 2011 presentation)
1. Disclosing a diagnosis of dementia can lead to: a. Depression; anxiety. b. Stigma. c. Leprosy syndrome. d. Giving up; decompensating. 2. Family conflict: a. Where money is the issue. b. Family conflict and those who refuse to accept diagnosis. c. Sibling rivalry.
9.1.2 Issues to discuss with family

1. 2. 3. 4. 5. Legal issues. Medication for AD if appropriate. Lifestyle regular exercise, mental stimulation, establish routine. General health blood pressure, other health conditions. Enduring Power of Attorney: a. Power of Attorney relates to money and estate, not health, etc. b. Recommend for all persons diagnosed with dementia (and for all persons >50.) c. Tests for capacity? d. Enduring Power of Attorney applications vary by jurisdiction. e. May come into effect immediately or when triggered. Enduring Guardianship a. Proxy decision maker for services, accommodation, health. b. Triggered by loss of decision making capacity. c. Flexible: 1 or more guardians, severally or jointly, different guardians different powers. d. Prudent to arrange early in dementia. e. Prudent for us all to consider this. Advance Directives: a. Treatment. b. Withholding treatment. c. Participation in research. d. Disposal of body, tissue donation at death, funeral arrangements. Informed consent for medical treatment: a. Person must understand: i. The nature of the treatment. ii. The possible effects. iii. The potential side effects. iv. The alternatives. v. Understanding varies with complexity. vi. Person must be able to communicate understanding and wishes. b. Dementia will affect understanding; holding information in head while weighing up pros & cons; and communication. c. Loss of capacity is a point on a sliding slope. d. If unable to give consent, then proxy consent. e. Who can give proxy consent varies by jurisdiction. In NSW = person responsible. f. If no proxy, Guardianship Tribunal may appoint Public Guardian or similar. Capacity to drive: a. Mentally incompetent can be danger to self and others. b. Level of cognitive impairment poor correlation with capacity to drive. c. Best test is on road. d. Co-pilot, familiar routes only, day time only help but not sufficient. e. Better for specialist to bear blame. f. All persons with dementia will lose ability to drive at some time. As of 2012, a diagnosis of dementia precludes an unconditional drivers licence. (See the Austroads Assessing Fitness to Drive guidelines pdf): i. Approach 1: cancel licence immediately ii. Approach 2: graded restrictions and warning about cessation later. iii. Approach 3: send for On-road Assessment. Note: Poor correlation between cognitive testing and driving performance. Capacity to work: a. Capacity vs. Competency. b. Capacity vs. Safety. c. Decision for employer usually.
6.
7.
8.
9.
10.
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d. May become legal matter e.g. if a doctor, lawyer, architect , judge, politician.
9.1.2.1 LEGAL ISSUES TO CONSIDER (Central Coast Division of General Practice Advance care Planning Fact Sheet pdf) 1. Advance care directive or plan of treatment: a. An Advance Care Directive is a written statement regarding your wishes for your own future health care. An Advance Care Directive can be made now by anyone who has the capacity to do so and is only used at some point in the future if you become incapable of making health care decisions for yourself (through illness of accident). b. When a person does not have the capacity to make their own medical decisions, it is possible for the person responsible to make these decisions on their behalf. The person responsible can state their wishes for the persons health care, based on what they believe is in the patients best interest and reflecting what the patient would have wanted. A Plan of Treatment is a written document made by the person responsible that outlines these wishes. c. Advance Care Directives and Plans of Treatment should both be reviewed regularly to ensure that wishes have not changed. 2. What is Capacity? a. It is important to be clear about someones ability to make their own decisions whether these are financial, personal or health related. A person who is able to understand the question at hand, weigh up and understand the consequences of their own choices is said to have capacity. This person has the right to make their own financial, health and lifestyle decisions. All people are assumed to have capacity. Capacity is only questioned if there is a valid reason to do so (such as advancing dementia, delirium, psychosis etc.). In these cases a capacity assessment is carried out by the health or legal professional involved. 3. Who is the Person Responsible? a. There is a clear hierarchy set out by the Guardianship Act stating which people have the right to make decisions on someones behalf if that person can no longer decide. It is no longer necessarily the persons next of kin. In order, the person responsible is: i. The court appointed or enduring guardian if one has been appointed. ii. The most recent spouse or defacto who has an ongoing relationship with the person. The persons primary unpaid carer. iii. A relative or friend who has a close personal relationship with the person. b. In cases of conflict or absence of an appropriate person the Guardianship Tribunal can advise. Freecall: 1800 463 928. 4. Enduring Guardian vs. Power of Attorney (NSW specific): a. An Enduring Guardian is someone you choose to make personal, health or lifestyle decisions on your behalf if and when you lose the capacity to make decisions yourself. b. A Power of Attorney is a legal document authorising someone else to carry out business, financial or property affairs on your behalf. A standard Power of Attorney ceases to have effect once you lose capacity. An Enduring Power of Attorney remains valid if you lose the capacity to carry out these transactions independently. Enduring Guardianship and Power of Attorney may only be made by someone who has capacity. c. Telephone: 1800 463 928 for free forms.
10. Who to call for help

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. Aged Care Assessment Services contact your regional Department of Human Services office. Alzheimers Australia help line Tel: 1800 100 500. Alzheimers Australia NSW Living with memory loss program Alzheimers Australia Your brain matters Aged Care Information line Tel: 1800 500 853. Aged Care Assessment Team finder Behavioural Assessment and Intervention Services (BAsIS): 02 9515 9800. Carers WA: 1300 227 377. Carer Support and Respite Coordination Centre Tel: 1800 059 059. Cognitive, Dementia and Memory Service (CDAMS) Commonwealth Carelink Centre: Services in local area and information on ACAT assessment. Tel: 1800 052 222. Commonwealth Carer Resource Centre (www.carersaustralia.com.au) Tel: 1800 242 636. Centrelink: Financial Support Tel: 13 27 17. Behavioural Assessment Intervention Service / Dementia Behavioural Management Assessment Service (BAsIS/DBMAS): Advisory service to assist carers of people with BPSD living in the community or specialist residential facilities Tel: 1800 699 799. (24 hours) 15. Local Old Age Psychiatry Community Team. 16. National Dementia Helpline Tel: 1800 100 500.
11. Resources
1. Australia Government Department of Health and Ageing: a. Information for the elderly and those caring for them is available online from agedcare AUSTRALIA website: http://www.agedcareaustralia.gov.au/internet/agedcare/publishing.nsf/Content/where+to+start. b. Dementia Resource Guide http://www.health.gov.au/dementia. c. Dementia The Caring Experience: A guide for families and carers of people with dementia. http://www.health.gov.au/internet/main/publishing.nsf/Content/ageing-publicat-carerexp.htm 2. Advanced Care Planning http://www.planningwhatiwant.com.au/advance-care-directive/advance-care-directive-planningwhat-i-want_20130305101645.pdf 3. Aged Care Assessment Teams: Arranges respite care for carers and arranges access to government-funded services to aid daily living. Information and local contact details available from: http://www.agedcareaustralia.gov.au/internet/agedcare/publishing.nsf/Content/How%20to%20get%20an%20assessment 4. Aged Care Insite.
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5. Alzheimers Australia http://www.fightdementia.org.au/ a. Alzheimers Australia information http://www.fightdementia.org.au/help-sheets-and-update-sheets.aspx b. Alzheimers Australia Quality dementia Care booklets http://www.fightdementia.org.au/research-publications/qualitydementia-care-papers.aspx c. Living with Memory Loss program http://www.fightdementia.org.au/services/living-with-memory-lossprogram-1.aspx d. Phillips, J., Pond, D., & Shell, A. (2010). Quality Dementia Care No time like the present: the importance of a timely dementia diagnosis (Vol. 7): Alzheimers Australia. 6. Alzheimers International http://www.alz.co.uk/ 7. Dementia Collaborative Research Centres http://www.dementia.unsw.edu.au/ 8. Behaviour Management A Guide to Good Practice Managing Behavioural and Psychological Symptoms of Dementia. http://dementiaresearch.com.au/images/dcrc/output-files/328-2012_dbmas_bpsd_guidelines_guide.pdf 9. Commonwealth Carelink Centre: Services in local area and information on ACAT assessment. Tel: 1800 052 222. 10. Commonwealth Carer Resource Centre Tel: 1800 242 636 www.carersaustralia.com.au 11. Centrelink: Financial Support Tel: 13 27 17. 12. General Practitioner assessment of COGnition http://www.gpcog.com.au/ 13. Good dementia care in general practice (pdf) 14. National Dementia Helpline: 1800 100 500. 15. Podcast by Professor Chris Rowe Preventing the decline of our ageing population. 16. RACGP guidelines Bridges-Webb, C., & Wolk, J. (2003). Care of Patients with Dementia in General Practice. http://www.dementia-assessment.com.au/measures.html 17. 19. Virtual medical centre http://www.virtualmedicalcentre.com/diseases/alzheimers-disease/71
12. References
1. Alzheimers Australia. Dementia with Lewy Bodies. Available from http://www.fightdementia.org.au/understanding-dementia/dementia-withlewy-bodies.aspx (accessed 6 November 2012). 2. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision (DSM IV TR). 3. Australian Institute of Health and Welfare. (2012). Dementia in Australia. 4. Australian Government Department of Health and Aging. Schedule of Pharmaceutical Benefits for approved pharmacists and medical practitioners February 2007. 5. Australian Government Department of Health and Aging Schedule of Pharmaceutical Benefits November 2010. 6. Ballard, C., Hanney, M. L., Theodoulou, M., Douglas, S., McShane, R., Kossakowski, K., et al. (2009). The dementia antipsychotic withdrawal trial (DART-AD): long-term follow-up of a randomised placebo-controlled trial. The Lancet Neurology, 8(2), 151 - 157. 7. Barker, W. W., Luis, C. A., Kashuba, A., Luis, M., Harwood, D. G., Loewenstein, D., et al. (2002). Relative frequencies of Alzheimer disease, Lewy body, vascular and frontotemporal dementia, and hippocampal sclerosis in the State of Florida Brain Bank. Alzheimer Disease and Associated Disorders, 16(4), 203 - 212. 8. Birks, J. (2006). Cholinesterase inhibitors (ChEIs), donepezil, galantamine and rivastigmine are efficacious for mild to moderate Alzheimer's disease. The Cochrane Library. 9. Bridges-Webb, C., & Wolk, J. (2003). Care of patients with dementia in general practice. Guidelines. RACGP and NSW Department of Health 2003. 10. Brodaty, H., & Gresham, M. (1989). Effect of a training programme to reduce stress in carers of patients with dementia. British Medical Journal, 299(6712), 13751379. 11. Brodaty, H., McGilchrist, C., Harris, L., & Peters, K. E. (1993). Time until institutionalization and death in patients with dementia. Role of caregiver training and risk factors. Archives of Neurology, 50(6):643-650. 12. Crouch, A. M. (2009). Treating dementia. Australian Prescriber, 32, 9 -12. 13. Dementia Collaborative Research Centre Behaviour Management A Guide to Good Practice Managing Behavioural and Psychological Symptoms of Dementia. 2012. 14. Drach LM. Drug treatment of dementia with Lewy bodies and Parkinson's disease dementia-common features and differences Med Monatsschr Pharm. 2011 Feb;34 (2):47-52; quiz 53-4. 15. Erkinjuntti, T., Kurz, A., Gauthier, S., Bullock, R., Lilienfeld, S., & Damaraju, C. V. (2002). Efficacy of galantamine in probable vascular dementia and Alzheimer's disease combined with cerebrovascular disease: a randomised trial. Lancet, 359(9314), 1283 -1290. 16. eTherapeutic Guidelines July 2012 Neurology. 17. Garca Daz F. Breaking bad news in medicine: strategies that turn necessity into a virtue Med Intensiva. 2006 Dec;30 (9):452-9. 18. Gitlin, L. N., Kales, H. C., & Lyketsos, C. G. (2012). Nonpharmacologic Management of Behavioral Symptoms in Dementia. Journal of the American Medical Association, 308(19), 2020 - 2029. 19. Grossberg, G. T. (2002). The ABC of Alzheimer's Disease: Behavioral Symptoms and Their Treatment. International Psychogeriatrics, 14 (Suppl 1), 27-49. 20. Harvey JA, et al Breaking bad news: primer for radiologists in breast imaging. J Am Coll Radiol. 2007 Nov;4(11):800-8. 21. Hersch, E. C., & Falzgraf, S. (2007). Management of the behavioral and psychological symptoms of dementia. Clinical Interventions in Aging, 2 (4), 611621. 22. Kalantarian, S., Theodore A. Stern, T.A., Mansour, M., Ruskin, J.N. Cognitive Impairment Associated With Atrial Fibrillation: A Meta-analysis Ann Intern Med. 5 March 2013; 158 (5_Part_1):338-346 23. Knopman, D. S., Boeve, B. F., & Petersen, R. C. (2003). Essentials of the Proper Diagnoses of Mild Cognitive Impairment, Dementia, and Major Subtypes of Dementia. Mayo Clinic Proceedings, 78, 1290 - 1308. 24. Kral, V A. Senescent forgetfulness: benign and malignant. Can Med Assoc J. Feb 10 1962; 86: 257-60. 25. Kurrle, S., Hogarth, R., & Hill, J. (2010). Physical Comorbidities of Dementia Executive Summary Report And Recommendations: Dementia Collaborative Research Centre University of New South Wales 26. Marriott, A., Donaldson, C., Tarrier, N., & Burns, A. (2000). Effectiveness of cognitivebehavioural family intervention in reducing the burden of care in carers of patients with Alzheimer's disease. The British Journal of Psychiatry (176), 557 - 562. 27. Mueller, P. S. (2002). Breaking bad news to patients. The SPIKES approach can make this difficult task easier. Postgraduate Medicine, 112(3), 15-16, 18. 28. Mittelman, M. S., Ferris, S. H., Steinberg, G., Shulman, E., Mackell, J. A., Ambinder, A., et al. (1993). An intervention that delays institutionalization of Alzheimer's disease patients: treatment of spouse-caregivers. Gerontologist, 33(6), 730 - 740. 29. Moo, L. R. Differential Diagnosis of Dementia. 30. Mrak, R. E., & Griffin, W. S. T. (2007). Dementia with Lewy bodies: Denition, diagnosis, and pathogenic relationship to Alzheimer's disease.
Neuropsychiatric Disease and Treatment, 3(5), 619625.

31. Nankervis, J. M., Waxman, P. J., O'Hara, D., & Burbidge, M. (2002). Caring for family carers in general practice. The Medical Journal of Australia, 177(8), 408 - 410.O'Connor, D. W., Ames, D., & Gardner, B. (2009). Psychosocial treatments of psychological symptoms in dementia: a systematic review of reports meeting quality standards. International Clinical Psychopharmacology. 32. NSW Department of Health. (2006). Working with People with Challenging Behaviours in Residential Aged Care Facilities. 33. Petersen RC. Conceptual overview. In: Petersen RC. Mild Cognitive Impairment: Aging to Alzheimer's Disease. 1-14. New York, NY: Oxford University Press, Inc; 2003.)
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34. Phillips, J., Pond, D., & Shell, A. (2010). Quality Dementia Care No time like the present: the importance of a timely dementia diagnosis (Vol. 7): Alzheimers Australia. 35. Poewe W. Treatment of dementia with Lewy bodies and Parkinson's disease dementia.Mov Disord. 2005 Aug;20 Suppl 12:S77-82. 36. Poirier, J., Davignon, J., Bouthillier, D., Kogan, S., Bertrand, P., & Gauthier, S. (1993). Apolipoprotein E polymorphism and Alzheimer's disease.
Lancet, 342(8873), 697 - 699.

37. Reutens, S., Pesiah, C., & Brodaty, H. (2009). Dementia: to screen or not to screen. Medicine Today, 10(5), 14 - 22. 38. Rowe, C Presentation titled Imaging in Alzheimers Disease. 39. Schofield, P. E., Butow, P. N., Thompson, J. F., Tattersall, M. H., Beeney, L. J., & Dunn, S. M. (2003). Psychological responses of patients receiving a diagnosis of cancer. Annals of Oncology, 14(1), 48-56. 40. Simard, M., & van Reekum, R. (2004). The Acetylcholinesterase Inhibitors for Treatment of Cognitive and Behavioral Symptoms in Dementia With Lewy Bodies. The Journal of Neuropsychiatry and Clinical Neurosciences, 16(4), 409 - 425. 41. Speechly, C. M., Bridges-Webb, C., & Passmore, E. (2008). The pathway to dementia diagnosis. The Medical Journal of Australia, 189(9), 487 - 489. 42. SHERE, Dementia: Differential diagnosis and management in general practice Resource Booklet: Lifeblood, Brain & Mind Research Institute The SPHERE booklet formed part of a Category 2 online education program in the RACGP QA&CPD Program for the 2008-2010 triennium, and was also approved by ACRRM for 2 Professional Development Program (PDP) Core Points. 43. Tuffrey-Wijne I.A new model for breaking bad news to people with intellectual disabilities. Palliat Med. 2013 Jan;27(1):5-12 44. Turner, S., Iliffe, S., Downs, M., Wilcock, J., Bryans, M., Levin, E., Keady, J., O'Carroll, R. (2004). General practitioners' knowledge, confidence and attitudes in the diagnosis and management of dementia. Age and Ageing, 33(5), 461 - 467. 45. Yates, M., & Pond, D. (2012). The dementia pathway. Australian Doctor.
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The timely diagnosis of dementia

THE TIMELY DIAGNOSIS OF DEMENTIA

The timely diagnosis of dementia

DCRC DLB FMRI, fMRI FTD, FTLD

HC HV MCI MMSE PET PPC SMMSE SPECT WMH

3. How common is dementia?

The timely diagnosis of dementia

or changes in usual routines.

5. Risk factors associated with dementia

The timely diagnosis of dementia

6. Protective factors associated with dementia

7. Diagnosing dementia 7.1 Timely diagnosis (Phillips 2010)

The timely diagnosis of dementia

7.2 Consequences of not recognising dementia

7.3 How to make the diagnosis (Phillips et al 2010)

The timely diagnosis of dementia

(Table based on Phillips et al 2010)

Time to do test (approximate) 3 minutes

patient consulting alone, GP/ ED

Misses early dementia. No score, pass or fail Needs informant

Widely used by psychologists

Not widely used by GPs

Kimberley Indigenous Cognitive Assessment (KICA)

Target group have varying cultural knowledge

Can take 30 minutes or more

The timely diagnosis of dementia

7.3.1 Diagnostic criteria for dementia

7.3.2 Biomedical Imaging

The timely diagnosis of dementia

Images courtesy Prof C Rowe, The Austin Hospital, Melbourne 2009.

Images courtesy Prof C Rowe, The Austin Hospital, Melbourne 2009.

Images courtesy Prof C Rowe, The Austin Hospital, Melbourne 2009.

Alzheimers disease in 2013

The timely diagnosis of dementia

Images courtesy Prof C Rowe, The Austin Hospital, Melbourne 2009.

Images courtesy Prof C Rowe, The Austin Hospital, Melbourne 2009.

7.3.3 Barriers to diagnosis

7.4 Identifying the type of dementia

The timely diagnosis of dementia

7.5 Population Screening vs. Case finding

The timely diagnosis of dementia

7.6 What is mild cognitive impairment (MCI)?

7.6.1 Conversion to dementia

7.7 Physical comorbidities of dementia

The timely diagnosis of dementia

7.8 Natural history

7.9 Common conditions which may cause or aggravate dementia

8. Treatment of dementia (Phillips et al 2010)

The timely diagnosis of dementia

8.1 The early to middle stages

8.1.1 Links between cardiovascular and dementia risk reduction factors

8.2 Established dementia what can we do

8.2.1 Pharmacy Review

The timely diagnosis of dementia

Dosage 5 mg orally, at night for 4 weeks, increase up to 10 mg at night if tolerated

The timely diagnosis of dementia

Table information sourced from eTherapeutic Guidelines 2012.

8.3 Functional assessment (Bridges-Webb 2003)

8.4 Management plan

The timely diagnosis of dementia

Item number 701 Health assessment (pdf) brief

Fee: $58.20 Benefit: 100% = $58.20

Fee: $141.40 Benefit: 75% = $106.05 100% = $141.40