Dementia Flashcards
What cognitive defects are seen in patients with dementia?
- Aphasia (impairment in language - affects production/comprehension of speech and ability to read and write)
- Amnesia
- Disorientation
- Agnosia (inability to interpret sensations and thus recognise things)
- Executive Function
- Apraxia (difficulty with motor tasks and understanding instruction to do motor activity)
What is the epidemiology of dementia?
1 in 3 people in the UK
What are the three categories of dementia symptoms?
1) Cognitive impairment
2) Psychiatric or Behavioural disturbances
3) Difficulty with ADLs
What are the 4 As of Alzheimer’ disease
Aphasia
Amnesia
Apraxia
Agnosia
What percentage of dementias is AD?
40% - the most common dementia
What is the aetiology of AD?
Genetic link
What are the risk factors for alzeheimer’s dementia?
- Age
- Caucasian
- Family History
- More common in women
- Head injury
- Vascular disease
- Apolipoprotein E4 variant
What seems to be a protective factor for Alzheimer’s dementia?
Drinking wine
What is the pathophysiology of AD?
Involves a progressive degeneration of the cerebral cortex, and there is widespread cerebral atrophy and progressive NEURONAL DAMAGE. Neurons affected develop surrounding AMYLOID PLAQUES and NEUROFIBRILLARY TANGLES and produce LESS ACETYLCHOLINE.
What is the progression of AD?
It I s linear progression, with a gradual decline
How does AD usually present in general?
Usually insidious in onset and develops slowly but steadily over a period of 7-10 years.
What are symptoms of early-stage Alzheimer’s?
- Memory lapses short term memory goes first
- Forgetting names of people or places
- Difficulty finding words for things
- Inability to remember recent events
- Forgetting appointments
What symptoms are seen as AD progresses?
- Apraxia
- Difficulties with language
- Problems with planning and decision making
- Confusion
- Visuospatial problems
What are the late-stage symptoms of AD?
- Wandering, disorientation
- Apathy
- Psychiatric symptoms depression, hallucinations, delusions
- Behavioural problems disinhibition (over trusting, sexual disinhibition), aggression, agitation
- Altered eating habits e.g. forgetting to eat
- Incontinence
- Self-neglect
What are the DDx of AD?
- Normal ageing
- Other forms of dementia
- Parkinson’s Disease
- Normal pressure hydrocephalus
- Hypothyroidism
- Depression, Schizophrenia -> pseudo dementia
- Neurosyphilis
What investigations are undertaken for AD?
- Screening tools e.g. MSE, MMSE, AMT, ACE, MOCA
- Bloods FBC, U&Es, LFT, CRP, TFTs, Haematinics, Calcium Profile, Vit. D
- Urine
- ECG (AF, see baseline before antipsychotics)
- MRI scans to exclude other neurological pathologies
What is the pharmacological management of AD?
• ANTICHOLINESTERASE INHIBITORS
o Donepezil
o Rivastigime
o Galantamine
o These don’t stop progression of Alzheimer’s but helps maintain function for as long as possible, so hopefully slows progression of disease.
• NMDAr ANTAGONIST (glutamatergic receptor)
o Memantine
• Antidepressants for depression (AVOID TRICYCLICS as can have adverse effect on cognition)
• Antipsychotics only if indicated and not for long-term use, but use for psychotic symptoms
• Benzodiazepines or antipsychotics can be used for acute and short-term treatment if required for aggression/agitation
What non-pharmacological Tx is used for managing AD?
- CBT for those with Alzheimer’s who are suffering from depression or anxiety
- Memory enhancing strategies
- Cognitive stimulation programmes
- Aromatherapy
- Therapeutic use of music and dance
- Exercise
- Animal-assisted therapy
- Massage
- Multi-sensory stimulation
- Reminiscence therapy
What is the epidemiology of Vascular dementia?
17% of all dementia’s in the UK
Is the 2nd commonest dementia
What are the subtypes of vascular dementia (VaD)?
Stroke-related VaD
Subcortical VaD
Mixed dementia
What is included in stroke related VaD?
includes multi-infarct dementia, which is usually the result of multiple infarcts, which may not be recognised in themselves and also includes single-infarct dementia, which occurs after a large stroke.
What are the causes of subcortical VaD ?
small vessel disease/Binswager’s disease
What is mixed dementia?
VaD and Alzheimer’s changes are both found together in the brain on imaging. VaD changes are predominantly seen in the white matter and Alzheimer’s changes are predominantly seen in the cortical grey matter. (HAS A GRADUAL + STEPWISE DETERIORATION)
Where do you usually see brain changes in AD?
Cortical grey matter
Where do you usually see brain changes in VaD?
White matter
What are risk factors for VaD?
- History of stroke/TIA
- AF
- HTN
- Diabetes Mellitus
- Hyperlipidaemia
- Smoking
- Obesity
- Coronary Heart disease
- FHx Stroke or CVD
What is the pathophysiology of VaD?
It is a group of syndromes of cognitive impairment, which are caused by different mechanisms, causing ischaemia or haemorrhage secondary to CVD (multiple infarcts, one large infarcts or small vessel disease).
These cerebrovascular events cause a cognitive decline.
What is the progression of VaD?
There is a stepwise progression, the steps are caused by subsequent cerebrovascular events
What is the presentation of VaD?
Features that may suggest a vascular cause:
• Focal neurological abnormalities
o Visual disturbances
o Sensory or motor symptoms e.g. dysphasia, hemiparesis, visual field defects
o Extrapyramidal signs e.g. dystonia and parkinsonian features
• Poor attention and concentration
• Seizures
• Depression and/or anxiety accompanying the memory disturbance
• Early presence of disturbance in gait unsteadiness and frequent falls
• Bladder symptoms without demonstrable urological condition
• Features of pseudobulbar palsy
• Emotional problems emotional lability, psychomotor retardation or depression
How is a diagnosis of depression made?
Diagnosis of dementia requires:
• Comprehensive history and physical examination (usually need collateral)
• Formal screen for cognitive impairment with specific notes on both short-term and long-term memory as well as individual cognitive domains which include:
o Orientation – time, place, person
o Attention and concentration ability
o Language function (usually evident during questioning)
o Visuospatial functions
o Executive function problem solving
o Motor control
o Praxis – whether they can get dressed, lay a table etc.
• Medication review to make sure there is no evidence that the cognitive decline could be due to the medication
• Other reversible organic causes need to be excluded e.g. normal pressure hydrocephalus
What would be seen on imaging in order to diagnose VaD?
hypoperfusion lesions (due to ischaemic change) and ischaemic lesions infarcts, cortical lacunae and extensive white matter changes.
What investigations are undertaken for VaD?
• Screening tools e.g. MSE, MMSE, AMT, ACE, MOCA
• Bloods FBC, U&Es, LFT, CRP, TFTs, Haematinics, Calcium Profile, Vit. D
• Urine
• ECG (AF, see baseline before antipsychotics)
• MRI scans to exclude other neurological pathologies
(same as AD)
What are the non-pharmacological Mx options for VaD?
Should be tailored to individual’s preferences • Cognitive stimulation programmes • Multisensory stimulation • Music and art therapy • Dancing • Massage • Aromatherapy • Exercise • Animal-assisted therapy
What factors mat exacerbate violet or aggressive behaviour in dementia patients?
o Overcrowding o Lack of privacy o Boredom or lack of activities o Poor communication o Conflict
What do you assess in order to manage challenging behaviour?
o Physical health o Depression and psychosocial problems o Possible undetected pain or discomfort o Adverse effects of medication o Life history spiritual, cultural and religious identity o Physical environment
What pharmacological Tx can be given for VaD?
NO LICENSED DRUGS
What unlicensed drugs may be used in VaD?
Acetylcholinesterase inhibitor - DONEPEZIL (has been shown to improve cognition and function in some patients with VaD)
GLANTAMINE - also been shown to improve cognition in VaD
What medication would be used for challenging and non-cognitive symptoms?
Only to be used in severe distress or immediate risk to harm to patient or to others
• Antipsychotics are recommended by NICE for severe symptoms e.g. psychosis and/or agitated behaviour causing significant distress
o Olanzapine
o Haloperidol
o Lorazepam
These are usually used IM for immediate behavioural control
• Rapid Tranquilisation lorazepam and haloperidol should be used in combination.
• Antidepressants can be considered if the depression is severe and/or causing decrease in function
What would be prescribed to try and reduce the likelihood of more cerebrovascular events occurring?
Anti-hypertensives (ACE inhibitors, Beta-blockers, CCBs, Diuretics)
Statins
Aspirin (but not if haemorrhagic events)
What are complications of VaD?
- Behavioural problems wandering, delusions, hallucinations and poor judgement
- Depression
- Falls and gait abnormality
- Pressure sores
What is the prognosis of AD?
life expectancy of 7-10 years
What is the prognosis of VaD?
life expectancy of 3-5 years
What are the triad of symptoms seen in Lewy body dementia (pick’s disease)
- Cognitive Impairment
- Parkinsonian Syndrome
- Visual Hallucinations - Lilliputian (not usually distressing)
Of the dementia’s - how common is levy body dementia?
3rd most common in Western world
What are the Dementia Sx seen in typical presentation of Lewy body dementia?
o Memory loss
o Decline in problem solving ability
o Spatial awareness difficulties
• Fluctuating levels of awareness and attention
What are the Parkinsonian Sx seen untypical presentation of Lewy Body Dementia?
o Resting tremor o Rigidity o Poverty of facial expression o Festinating gait o Bradykinesia o Includes frequent falls
What do the visual hallucinations usually present as?
o Lilliputian seeing ‘little people’ – usually see children or dogs, these hallucinations are usually not particularly distressing to the individual.
What other Sx may typically present for Lewy-bpdy dementia that are not part of the triad of Sx?
- Sleep disorders – rapid eye movement sleep disorder, restless legs syndrome, nocturnal cramps
- Fainting spells
What Investigations are done for LBD?
- MMSE/ACE/AMT etc.
- 6-item Cognitive Impairment Test (6-CIT)
- Imaging
- Bloods – FBC ferratin, vitamin B12, folate, U&Es, LFTs, Glucose, TFTs
- ECG
- MSU
What non-pharmacological Tx is used for LBD?
- Carers
- Cognitive stimulation programmes
- Multisensory stimulation
- Music and art therapy
- Dancing
- Massage
- Aromatherapy
- Exercise
- Animal-assisted therapy
What drug is recommended by NICE that may help treating cognitive decline in LBD?
Rivastigime
Giving anti-parkinsonian drugs in LBD may worsen what?
psychosis
Why should neuroleptic drugs be avoided in LBD?
Commonly induce severe sensitivity reactions in LBD patients - increasingly the motor and mental impairment and can increase mortality
What is the life expectance for patients diagnosed with LBD?
5-8 years
When does frontotemporal dementia usually present?
Is early-onset, usually presents <65 years of age and most common presentation peaks in 6th decade but can occur anytime between 3rd and 9th decade
What is the pathophysiology of Frontotemporal dementia?
• Atrophy of frontal and temporal lobes
• May note loss of neurons or gliosis but no increase in plaque formation
• Spongy vacuolisation of the frontal and temporal cortex
• Frontotemporal lobar degeneration
• Tau protein positive histological findings:
o Corticobasal degeneration
o Classic PiD (pick’s Disease). Pick bodies and Pick cells are seen histologically
o Progressive supranuclear palsy
What are the three main clinical syndromes of Frontotemporal dementia?
1) Behavioural variant frontotemporal dementia
2) Progressive, non-fluent aphasia
3) Semantic dementia
What are the Sx and signs of Behavioural variant frontotemporal dementia?
o Loss of inhibition
o Inappropriate social behaviour
o Loss of motivation but without depression
o Loss of empathy and sympathy
o Change in preferences
o Repetitive or compulsive behaviours, rituals
o Loss of control over eating or drinking
o Difficulties with planning, organisation or decision making
o Memory and visuospatial skills usually preserved in early stages but deteriorates in later stages
o Lack of insight
o Loss of awareness of personal hygiene and incontinence
o Loss of motivation
o Loss of vocabulary
o Ritualised beliefs
o O/E: may have primitive reflexes, may fine echolalia, perseveration or mutism.
What are Sx and signs of progressive, non-fluent aphasia seen in frontotemporal dementia?
o Slow, hesitant, difficult speech
o Grammatical errors in speech
o Impaired understanding of complex sentences, but can recognise individual words
o Loss of literacy skills
o O/E: may have impaired orofacial movements (difficulty swallowing, coughing, yawning on command, but still present as reflex), may have stuttering, impairment of ability to write and read
What are symptoms and signs for semantic detention seen in frontotemporal dementia?
o Loss of vocabulary with fluency of speech maintained
o Asking meaning of familiar words
o Difficulty finding the right words, have to talk around it or describe it
o Loss of recognition of familiar faces or objects
What investigations would be undertaken for frontotemporal dementia?
- Bloods Dementia screen which includes B12, U&Es, TFTs, ANF, TPHA. Also, FBC, LFTs
- MSU
- Imaging, MRI is preferred
What is the non-pharmacological Tx of frontotemporal management?
- Patient and family education
- Organise social and family care
- Forward planning aid financial, occupational, housing, care
- Anticipate motor and gait difficulties practical aids etc.
- Speech and language therapy
What pharmacological management may be useful in frontotemporal dementia?
- Stop drugs with can exacerbate memory problems or confusion e.g. CNS drugs and anticholinergics
- SSRIs may help with behavioural symptoms
- Atypical antipsychotics for severe behavioural problems e.g. agitation, psychosis
What is the life expectancy for patients diagnosed with frontotemporal dementia?
8-10 years
What are the other types of dementia?
• Alcohol induced incl. Wernicke’s and Korsakoff’s Syndrome
• Drug induced
• Normal Pressure Hydrocephalus (WET (incontinent), WOBBLY (ataxic), WACKY (dementia))
• Parkinson’s disease dementia (diagnosed when Parkinson’s Disease precedes dementia)
• Huntington’s disease dementia (usually early onset 50-60y/o)
• Creutzfeld-Jakod disease (Prions)
• Dementia Pugilistica (Mohammed Ali got this due to repeated blows to the head resulting in brain damage)
• Pseudo dementia
o Depression
Does dementia affect your conscious level?
No (but delirium does)
