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Dementia
Alzheimer’s Disease
Anna Watkinson-Powell
Sheffield Medical School
What is dementia?
Progressive global decline in cognitive function
without loss of consciousness
Delirium
Vascular
events
Depression
Mass lesions
Learning
disability
Brain damage
Causes of dementia
Degenerative
Alzheimer’s
Lewy body
Frontotemporal
Huntington’s
Parkinson’s
Vascular
Vascular dementia
Binswanger’s
CADAISIL
Vasculitis
Rarer causes
Metabolic
Toxic (including alcohol)
Vitamin deficiencies
Mass lesions
Infective
Endocrine
Normal pressure hydrocephalus Chronic subdural haematoma
Pathology
Aggregation beta-
amyloid
Amyloid plaques &
neurofibrillary tangles
Neuronal loss
Cholinergic
hypofunction
Memory
Brain atrophyEnlarged ventricles
How might Alzheimer’s disease
present?
Getting lost Risk at home
Forgetful
Complex tasks Names
Cognitive deficits
• Memory
• Language
• Perceptual skills
• Attention
• Constructive abilities
• Orientation
• Problem solving
• Functional abilities
Change
from
previous
level
Amnesia Aphasia
Apraxia Agnosia
Other features
Behavioural and psychological
symptoms
Apathy
Motor and sensory
impairment and incontinence
Anosognosia
Loss executive function
Impaired visuospacial skills
BPSD
Agitation
Aggression
Disinhibition
WanderingHallucinations
Delusions
Depression
Approach to patient
History
• Patient
• Collateral
• Time
course
• Functional
impairment
• Risk
Mental state
• Cognition
• Behaviour
• Mood
• Insight
Investigations
• Routine
bloods
• Source
infection
• Brain
imaging
Physical
examination
Risk Assessment
• Non-compliance
• Self-neglect: meals, personal hygiene
• Fire
• Exploitation
• Abuse
• Falls
• Wandering
Principals of management
1. Maximise adaptation
2. Maintain function
3. Manage risk
4. Manage BPSD
5. Plan for future
Acetylcholinesterase inhibitors
Acetyl-
cholinesterase
ACHEI
Donepezil
Galantamine
Rivastigmine
Mild-moderate
Nausea, diarrhoea, fatigue,
dizziness
Memantine
NMDA partial
antagonist
Moderate-
severe
BPSD
Address causes
Pain
Physical health
Depression
Environment
Nursing care
Sensory impairment
Non-pharmacological
Multisensory stimulation
Music/dance therapy
Aromatherapy
Massage
Drugs
Risperidone short-term
Alternative atypical
antipsychotics
Only benzodiazepines for
immediate risk
Increased risk
stroke and overall
mortality with
antipsychotics
Further areas of management
Treat depression
Capacity issues
Support for carers
Palliative care
Summary
• Alzheimer’s disease is the commonest cause of
dementia
• The prominent features are amnesia, aphasia, apraxia
and agnosia
• Delirium and reversible causes must be excluded
• ACHEI and memantine may improve cognitive
symptoms
• BPSD can be distressing and need careful management
• Always assess risk
• Needs a multi-disciplinary patient-centred approach

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Dementia

Editor's Notes

  1. This presentation is on dementia, with a focus on Alzheimer’s disease Dementia is an important illness, affecting an estimated 750,000 people in the UK. Prevalence in the over 65s is 5%, increasing to 17% in those over 80.
  2. Dementia is defined as: This distinguishes it from the important differential diagnoses: Delirium is characterised by clouding of consciousness and is often caused by acute illness Symptoms due to vascular events such as strokes have a sudden onset Intracranial masses are more likely to cause focal neurological signs Learning disability and brain damage tend to leave permanent rather than progressive deficits Depression may cause a pseudodementia but cognitive ability returns when the depression is treated
  3. Alzheimer’s disease is the most common cause of dementia. Other degenerative causes include Lewy body dementia, which is characterised by prominent parkinsonian features, fluctuating cognition and visual hallucinations. In frontotemporal dementia, patients are socially disinhibited with episodic memory initially preserved. Huntington’s disease and Parkinson’s disease can also cause dementia. Vascular dementia accounts for 25% of cases, is often stepwise in progression and may be associated with strokes or TIAs and CVS risk factors. Rarer vascular causes include Binswanger’s disease, CADAISIL and cerebral vasculitis. Metabolic causes, such as uraemia and other electrolyte disturbances are rare but important because they are potentially reversible. Other causes include chronic alcohol abuse, thiamine deficiency, intracranial mass lesions, CNS infections and endocrine disturbances. 2 other important differentials are normal pressure hydrocephalus (which presents with a triad of dementia, ataxia and incontinence and which may be amenable to treatment with a shunt) and chronic subdural haematoma following a head injury.
  4. There are 2 characteristic pathological features of Alzheimer’s disease. Aggregation of beta-amyloid resulting in senile plaques and neurofibrillary tangles containing tau protein. These are associated with a loss of neurones in the brain and cholinergic hypofunction. The hippocampus is particularly affected, resulting in prominent memory impairment. MRI imaging shows brain atrophy and enlarged ventricles.
  5. The following is an example of a history taken the daughter of a patient suffering from Alzheimer’s disease, demonstrating some of the most common presenting symptoms. “I’m worried about my Mum. She’s 75 and she’s always been a very sharp and active person but over the last year or so she seems to have gone downhill. To start with she just couldn’t remember people’s names but then she started to forget to lock the door and feed the cat. She seems to struggle with her bank accounts and a few weeks ago I got a call from a neighbour who’d found her wandering down the wrong street. Then last week when I called, she’d left the hob on and now I’m really worried she’s going to have an accident.”
  6. Patients with Alzheimer’s disease have a progressive decline in several cognitive domains. These are: It is important to establish a change from the previous level of function, taking into account the patient’s education and intelligence. There are many tools available to assess cognition, including the MMSE and Addenbrooke’s cognitive examination.
  7. The major manifestations of the cognitive deficits can be thought of as 4 As: Amnesia is the loss of ability to learn, retain and process new information, resulting in short term memory loss. Patients may forget appointments, misplace things and repeatedly ask the same questions. Aphasia is a language deficit. Initially this may result in word-finding difficulty (known as anomia), progressing to impaired comprehension and finally a meaningless babble of words. Apraxia is the failure to carry out complex motor tasks, such as getting dressed in the right order, and can significantly impact on activities of daily living. Finally, agnosia is a loss of ability to recognise familiar objects and faces.
  8. In addition to the 4 As, many patients with AD have impaired visuospacial skills, resulting in them getting lost. Executive function declines, with problems organising and planning and impaired social function. Patients may be apathetic and often lack insight into the problems caused by the disease, which is known as anosognosia. In the later stages of the disease there is motor and sensory dysfunction and incontinence. 90% of patients will display what are known as the behavioural and psychological symptoms of dementia. These include:
  9. Behavioural symptoms may include agitation, aggression, disinhibition and wandering. There may be psychotic features such as visual hallucinations, persecutory delusions or delusions of jealousy. Depression is also common, particularly in the milder stages. BPSD can be distressing for the patients and particularly for carers.
  10. So how should you approach the assessment of a patient with possible AD? The history is very important but remember that the patient may lack insight so it is essential to get a collateral history by speaking to a carer or family member. Establish the time course of symptoms and the patient’s premorbid abilities. AD tends to come on gradually with a slow progressive decline. Find out how the symptoms have affected the patient’s function and never forget to assess their risk (this will be discussed in more detail later). The history should be followed by a mental state examination, focusing on cognition. Also consider the patient’s behaviour, mood and insight. Investigations are necessary to rule out delirium and reversible causes of dementia. This should involve a FBC, U&E, LFTs, blood glucose, B12 & folate, calcium, inflammatory markers, TFTs. A screen for infections, toxicology, ECG and CXR should only be carried out if indicated by the history. Brain imaging, preferably MRI should be performed to rule out a vascular event, mass lesions or NPH. You should also carry out a physical examination, particularly looking for neurological signs, which may point to an alternative cause such as a vascular event or mass lesion.
  11. It is essential to perform a thorough risk assessment of patients with AD. Forgetfulness means patients may be at risk of forgetting to take medications, to prepare meals and eat or to wash. Leaving electrical appliances on is a serious fire hazard. Patients are vulnerable to exploitation, for example financially, and they could be at risk of physical or sexual abuse. Apraxia predisposes patients to falls and patients who wander may get lost or have an accident. Early identification of risks reduces the likelihood of patients having to be admitted acutely to hospital.
  12. There is no cure for Alzheimer’s disease but much can be done to improve the quality of life of patients and their carers. Management should be aimed at maintaining independence and functioning for as long as possible, whilst minimising risk. This is likely to involve a combination of pharmacological therapy, education and support. Behavioural symptoms need to be managed appropriately and planning for the future is essential. A multidisciplinary care plan approach, with input from a variety of professionals, has the best outcome.
  13. The major class of drugs used in AD are acetylcholinesterase inhibitors, which act on synapses in the brain. Under normal conditions, the neurotransmitter acetylcholine is released by presynaptic neurones and transfuses across the synaptic cleft to act on receptors on the postsynaptic membrane. The Ach is then broken down by the enzyme acetylcholinesterase. Acetylcholinesterase inhibitors inhibit this enzyme, reducing the rate at which Ach is broken down. This increases the concentration of Ach in the synapses and thus increasing cholinergic action.
  14. The three ACHEIs used are donepezil, galantamine and rivastigmine. These are recommended for use in mild to moderate AD, as they slow the rate of cognitive decline. They should be discontinued if there is no improvement or when the cognitive deficits become severe (MMSE<12). The commonest side effects are nausea, diarrhoea, fatigue and dizziness and they should be used with caution in patients with cardiac conduction disorders. Memantine is an NMDA-receptor partial antagonist which is liscenced in the UK for moderate to severe AD with an MMSE<14 or if ACHEI are contraindicated. It has been shown to have a beneficial effect on cognitive and global functional and behavioural symptoms.
  15. When managing BPSD, it is essential to look for potential causes of behaviours as they may be a result of unmet need such as pain, hunger or boredom. Patients should be assessed for any underlying physical illness or depression. Symptoms may improve in a quiet, familiar environment with high quality nursing care and correction of any sensory deficits, so check the need for hearing aids or glasses. If there is no improvement after causes have been addressed, patients should be offered non-pharmacological therapies, such as multisensory stimulation, music or dance therapy, aromatherapy or massage, which should be tailored to the needs and preferences of the patient. Pharmacological treatment should only be used if patients are severely distressed or there is an immediate risk of harm to themselves or others. The only liscenced drug in the UK is the atypical antipsychotic risperidone for up to 12 weeks. Other antipsychotics may be prescribed but only after full discussion with carers and consideration of the risks and benefits. The need for the drug should be regularly reviewed and only considered as a short term measure. There is considerable evidence that antipsychotics increase stroke and mortality risk in patients with dementia and the UK government is currently trying to tackle the significant over-prescribing of antipsychotics in elderly dementia patients, particularly in nursing homes.
  16. It is important to recognise and manage depression in dementia patients. Mild cases may respond to CBT or other non-pharmacological therapies including reminiscence therapy, but more severe cases may require antidepressants. Dementia is a progressive disease and patients will at some point lose the capacity to make decisions about their care. It is important to discuss this as early as possible in order to plan for the future. This may involve making a lasting power of attoryney or an advanced decision as well as considering the future need for residential care. Caring for a person with dementia is hugely demanding and can be very distressing. It is essential that carers are supported with psychoeducation, support groups, respite care and psychological therapy such as CBT if they become depressed themselves. As patients reach the end of their lives, it is important to provide high quality palliative care. They should be encouraged to eat and drink for as long as possible, with dietary advice and swallowing assessments as indicated. Patients who have dysphagia or who do not want to eat should not be artificially fed. They should be regularly assessed for signs of pain and analgesics prescribed if appropriate. CPR is unlikely to be successful so a DNAR is usually appropriate after discussion with the patient or carers.
  17. In summary, dementia is an increasingly prevalent disease, with Alzheimer’s disease the most common cause. Remember the 4 As: amnesia, aphasia, apraxia and agnosia as key presenting features. Always consider and exclude derlirium and reversible causes of dementia. ACHEI and memantine are the mainstay of drug treatment for AD, behavioural symptoms should be managed appropriately and risk should always be assessed. Finally, a multidisciplinary patient-centred approach will have the best outcome for patient’s and carers quality of life.