Dementia Flashcards
Dementia
Dementia is thought to affect over 700,000 people in the UK and accounts for a large amount of health and social care spending. The most common cause of dementia in the UK is Alzheimer’s disease followed by vascular and Lewy body dementia. These conditions may coexist.
Dementia- assessment
- diagnosis can be difficult and is often delayed
- assessment tools recommended by NICE for the non-specialist setting include: 10-point cognitive screener (10-CS), 6-Item cognitive impairment test (6CIT)
- assessment tools not recommended by NICE for the non-specialist setting include the abbreviated mental test score (AMTS), General practitioner assessment of cognition (GPCOG) and the mini-mental state examination (MMSE) have been widely used. A MMSE score of 24 or less out of 30 suggests dementia
Dementia: management
- in primary care, a blood screen is usually sent to exclude reversible causes (e.g. Hypothyroidism). NICE recommend the following tests: FBC, U&E, LFTs, calcium, glucose, ESR/CRP, TFTs, vitamin B12 and folate levels. Patients are now commonly referred on to old-age psychiatrists (sometimes working in ‘memory clinics’).
- in secondary care, neuroimaging is performed to exclude other reversible conditions (e.g. Subdural haematoma, normal pressure hydrocephalus) and help provide information on aetiology to guide prognosis and management
Causes of dementia
- Common: Alzheimer’s disease, Cerebrovascular disease: multi-infarct dementia, Lewy body dementia
- Rarer causes: Huntingtons, CJD, Pick’s disease (atrophy of frontal and temporal lobe), HIV
- Important differentials: Hypothyrodism, Addisons, B12/ folate/ thiamine deficiency, syphilis, brain tumour, normal pressure hydrocephalus, subdural haematoma, depression, chronic drug use i.e. alcohol, barbiturates
Vascular dementia
Vascular dementia (VD) is the second most common form of dementia after Alzheimer disease. It is not a single disease but a group of syndromes of cognitive impairment caused by different mechanisms causing ischaemia or haemorrhage secondary to cerebrovascular disease. Vascular dementia has been increasingly recognised as the most severe form of the spectrum of deficits encompassed by the term vascular cognitive impairment (VCI)
Epidemiology of VD
- VD is thought to account for around 17% of dementia in the UK
- Prevalence of dementia following a first stroke varies depending on location and size of the infarct, definition of dementia, interval after stroke and age among other variables. Overall, stroke doubles the risk of developing dementia.
- Incidence increases with age
The main subtypes of VD
- Stroke-related VD – multi-infarct or single-infarct dementia
- Subcortical VD – caused by small vessel disease
- Mixed dementia – the presence of both VD and Alzheimer’s disease
Risk factors for VD
- History of stroke or transient ischaemic attack (TIA)
- Atrial fibrillation
- Hypertension
- Diabetes mellitus
- Hyperlipidaemia
- Smoking
- Obesity
- Coronary heart disease
- A family history of stroke or cardiovascular
How does VD present and inheritance
Rarely, VD can be inherited as in the case of CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy).
Patients with VD typically presents with= Several months or several years of a history of a sudden or stepwise deterioration of cognitive function.
VD: symptoms and speed of progression vary but may include
- Focal neurological abnormalities e.g. visual disturbance, sensory or motor symptoms
- Difficulty with attention and concentration
- Seizures
- Memory disturbance
- Gait disturbance
- Speech disturbance
- Emotional disturbance
VD: diagnosis is made based on
- A comprehensive history and physical examination
- Formal screen for cognitive impairment
- Medical review to exclude medication cause of cognitive decline
- MRI scan – may show infarcts and extensive white matter changes
Diagnosis of VD
Using the NINDS-AIREN criteria for probable vascular dementia
* Presence of cognitive decline that interferes with activities of daily living, not due to secondary effects of the cerebrovascular event= established using clinical examination and neuropsychological testing
* Cerebrovascular disease= defined by neurological signs and/or brain imaging
* A relationship between the above two disorders inferred by: the onset of dementia within three months following a recognised stroke, an abrupt deterioration in cognitive functions. Fluctuating, stepwise progression of cognitive deficits
Vascular Dementia: general management
- Treatment is mainly symptomatic with the aim to address individual problems and provide support to the patient and carers
- Important to detect and address cardiovascular risk factors – for slowing down the progression
Non pharmacological management: vascular dementia
- Tailored to the individual
- Include: cognitive stimulation programmes, multisensory stimulation, music and art therapy, animal-assisted therapy
- Managing challenging behaviours e.g. address pain, avoid overcrowding, clear communication
Pharmacological management: vascular dementia
- There is no specific pharmacological treatment approved for cognitive symptoms
- Only consider AChE inhibitors or memantine for people with vascular dementia if they have suspected comorbid Alzheimer’s disease, Parkinson’s disease dementia or dementia with Lewy bodies.
- There is no evidence that aspirin is effective in treating patients with a diagnosis of vascular dementia.
- No randomized trials found evaluating statins for vascular dementia
Lewy body dementia
Lewy body dementia is an increasingly recognised cause of dementia, accounting for up to 20% of cases. The characteristic pathological feature is alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas.
Lewy body dementia and other conditions
The relationship between Parkinson’s disease and Lewy body dementia is complicated, particularly as dementia is often seen in Parkinson’s disease. Also, up to 40% of patients with Alzheimer’s have Lewy bodies.
Features of Lewy body dementia
- progressive cognitive impairment=typically occurs before parkinsonism, but usually both features occur within a year of each other. This is in contrast to Parkinson’s disease, where the motor symptoms typically present at least one year before cognitive symptoms
- cognition may be fluctuating, in contrast to other forms of dementia
- in contrast to Alzheimer’s, early impairments in attention and executive function rather than just memory loss
- parkinsonism
- visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen)
Diagnosis of lewy body dementia
- usually clinical
- single-photon emission computed tomography (SPECT) is increasingly used. It is currently commercially known as a DaTscan. The sensitivity of SPECT in diagnosing Lewy body dementia is around 90% with a specificity of 100%
Management of Lewy body dementia
- both acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine can be used as they are in Alzheimer’s.
- neuroleptics should be avoided in Lewy body dementia as patients are extremely sensitive and may develop irreversible parkinsonism. Questions may give a history of a patient who has deteriorated following the introduction of an antipsychotic agent
