Dementia Flashcards
Dementia
defined as a syndrome of progressive impairment in two or more areas of cognition suffienct to interfere with work, social function, or relationships. Areas of cognition include:
- memory
- language
- abstract thinking
- praxis
- visuspatial
- executive function - judgement, speech , plannign
- personality
- social behaviour
Epidemiology
- 60 years - 1% if the population
- 40% >85 years
History
- history from patient and relative, carer, or freind
- enquire about:
- memory problems: forgets names of friends and family; where car parked; recent events
- activities of daily living: continue with normal occupation: perform domestic tasks; Personal care
- personality and mental state: change in character; depression; apathy
- History of verebro- and cardiovascular disease
- alochol intake
- HIV risk?
- medications
- family hsitorye.g AD risk Increases X4 if one first degree relative affected
Examination
- Look for head turning sign - patients looks to spuse when asked a sign
- Gait: marche a petitis pas and lower-half parkinsonism ( Cerebrovascular disease); gait apraxia (NPH)l gait ignition failure- difficult in starting to walk
- Focal neurological signs: hemiparesis, visual field defect, primitive reflexes
- Cognitive examintion:
- attention and concentration (count backwards from 20 to 1), months of th year backwards
- language: - name objects, repeating sentence, writing sentence, reading, understanding commands)
- memory: orientation, recall (immediate and after 5 minutes), episodic memory (memory for events personally experienced)
- semantic memory (general knoweldge about the world)
- praxis: mime combing hair, using tooth brush, dressing
- executive function (testing ability to plan, organize, abstract reasoning)
Symptoms
- Memory loss – this is usually the first symptom to appear
- The damage to brain tissue is not universal, and thus some areas of memory, notably autobiographical and political memory is stored in areas that are less often affected.
- Short term memory is more readily affected, and confusion may often result. For example, patients may buy many identical items of food on separate occasions, and then wonder why their cupboards are full of these items.
- Visuo-spatial problems – patients may be easily disorientated by unfamiliar surroundings
- Emotional disturbance
- Loss of normal social behaviour
- Language problems - Problems both understanding what is being said, and naming objects
- Concentration issues
- Short attention span - Also unable to plan, organise, or sequence activities
- Behavioural changes - Delusions (persecutory), agitiation, aggression, wandering
- Variable mood
- Poor sleep
- Restlessness
- Hallucinations
- Apathy
- Depression / euphoria - Severe depression is rare, due to loss of insight
In later stages of the disease, there may also be:
- Self-neglect
- Change in personality – which generally involves loss of inhibition
- Motor and sensory abnormalities
- Seizures
In very late stage disease there may be:
- The patient may become mute
- They may take little interest in anything
- Parkinsonianism
- Wasting
- Seizures
- Incontinence
Causes
There are many causes of dementia, but the two most common are:
- Alzheimer’s disease (~40-50%)
- Diffuse vascular disease (aka multi-infarct dementia) ~25%
In practice it is often difficult to differentiate the type of dementia present
Investigations
- The main symptom is usually confusion. Diagnosis is usually clinical, and made with the help of the MMSE (Mini-Mental State Exam). Sometimes, IQ tests (Wechsler Adult Intelligence Scale, may also be used).
- However, as confusion is often apparent, you may have to perform many other tests to rule out other differentials. The later on in life the presentation, the less likely it is to be investigated.
- Always assume confusion is due to an acute illness until proven otherwise. This might mean, depending on the history, that you are going to have to do a lot of blood tests:
- Vitamin deficiencies - ↓folate, ↓B12, ↓thiamine – these could be primary deficiencies, or may be alcohol related.
- TFT’s – thyroid problems
- FBC – anaemia
- U+E’s – renal failure / dehydration
- LFT’s – carcinoma, cirrhosis, encephalopathy
- Glucose – diabetes
- CRP/ESR – acute infection
- Imaging of the brain – CT/MRI – this may be used to exclude treatable space occupying lesions, such as:
- Hydrocephalus
- Tumour
- Subdural haematoma
- HOWEVER – the most common abnormality seen on brain scan is general atrophy
Alzheimers disease
- The mean survival is 7 years. Most will survive between 2-7.
- Death usually results from bronchopneumonia
- There is a general atrophy of brain tissue, and the weight of the brain is usually reduced. The frontal and temporal lobes are particularly affected.
- There is often compensatory dilatation of the ventricles, resulting in hydrocephalus.
- The cerebellum and spinal cord are normal
- There is a build up of amyloid plaques in the brain. These are the breakdown products of amyloid factors.
- There is also atrophy of cholinergic fibres that run from the hippocampus to the cerebral cortex. Initially there is a reduction on cholinergic transmission, and later a reduction in the synthesis of acetylcholine, particularly in the cerebral cortex itself.
- The damage is variable, and can occur at different rates in different parts of the brain. Most likely to be affected are the Amygdala, temporal cortex, and a few selected brainstem nuclei.
- There is no change in the number of muscarinic receptors, but the number of nicotinic receptors is reduced.
- In very late stage disease there can be variable depletion of other neurotransmitters
- There may be the excess deposition of beta-amyloid in the brain – leading to the formation of beta-amyloid plaques.
Vascular dementia
- This is the result of many small infarcts. Cerebrovascular disease has to be pretty advanced for vascular dementia to become apparent, as large parts of the cortex have to have been affected.
- The disease will have a step-wise progression, so for instance, there will be no apparent change in the condition, perhaps for many months, and then there is a sudden drop in function. Infarcts are particularly likely to affect function if they damage the white matter.
- As well as dementia, eventually there may be:
- Pseudobulbar palsy
- Shuffling gait with small steps – marche a petits pas – sometimes called atherosclerotic Parkinson’s disease.
- There is often also a history if TIA’s
making a willl
If the disease is discovered early enough, then it is possible to make a will, and/or an advanced directive before the patient becomes to ill for one of these to be accepted by law. The patient must be able to:
- Understand and retain the information involved
- Believe the information is true
- Demonstrate they are able to weigh up the pro’s and con’s of an argument and come to a decision based on these
Treatment
there is no cure- management of disease progression
AD
Anticholinesterase drugs – e.g. donepezil, galantamine, rivastigmine
Mechanism – these drugs work by inhibiting cholesterases, and thus increasing cholinergic transmission within the brain.
Unwanted effects – anorexia, nausea, vomiting, diarrhoea, abdo pain, insomnia, confusion, agitation, headache
Note that some of these effects are similar to the clinical symptoms of Alzheimer’s!
Clinical use – will delay the decline of cognitive impairment in 40% of patients – probably only by about 3-6 months.Probably more effective in those without the gene apoE4.
Important to assess efficacy, and to stop treatment in those who do not respond.
Rapid decline is seen when the drug is stopped in previously responsive individuals
Have functional benefits that may improve QOL.
- NMDA receptor antagonists – memantine
- Mechanism – an inhibitor of glutamate NMDA receptors. It binds selectively, depending on the voltage, and thus prevents excitotoxicity, without altering gluatamtes role in normal memory and learning.
- It can be given WITH anticholinesterases
- Unwanted effects:
- Diarrhoea, insomnia, dizziness, headache, hallucinations
Again, note that some of these are similar to symptoms of dementia!
Clinical use
Usually more well tolerated than anticholinesterases, but probably not as effective
May provide some benefit in cognitive function, and may slow cognitive decline
Not widely used
Drug treatment should only be initiated in those with a MMSE of >12! ###
This is mild to moderate dementia
NICE guidelines state:
Treatment to be reviewed every 6 months
Don’t treat if MMSE <12, as side effects of drug likely to outweigh benefits
Treatment only to be administered and monitored by specialist centres
Don’t rely on MMSE as your only tool for aiding prescribing, e.g. get collateral histories, assess function and behaviour
Drug therapy is controversial
Drugs are expensive
Some trials have shown no benefit of the drugs over placebos
In many cases it is thought that they at least allow a few more months in a home care environmen
- See more at: http://almostadoctor.co.uk/content/systems/neurology-psychiatry/psychiatry/dementia#sthash.RX3hef66.dpuf
Vascular dementia treatment
- Prevention
- Reduction of vascular risk factors:
- Aspirin or warfarin therapy – aspirin often quoted anecdotally, but there is actually now evidence that the sort of low dose therapy that many individuals take provides any benefit against vascular dementia. Some at risk patients may be put on warfarin therapy.
- Controlling BP – use normal system (A-C-D (+B)) for initiating bloop pressure maintenance therapy
- Anticholinesterases and memantine – may have some benefit in vascular dementia.
The burden of care
- The course of the disease is often distressing for both families and patient.
- Supportive care is necessary to ensure the patient stays in a familiar home environment as long as possible. Often the burden of care falls to relatives.
Some recent evidence suggests that engaging in cognitively taxing activities late on in life can protect against dementia!
Vitamin E – has shown in some instances to protect against dementia
