Dementia & Delirium Flashcards
What is dementia?
A generalised decline of intellect, memory and personality without impairment of consciousness, leading to functional impairment
= Clinical syndrome caused by multiple pathologies
What is presenile dementia?
Onset <65yr
List the clinical features of dementia (6 areas)
1) Cognition
- Poor memory
- Impaired attention
- Aphasia, agnosia, apraxia
- Disorientation
- ‘Personality change’
2) Behaviour
- Odd and disorganised
- Restless, wandering
- Self-neglect
- Disinhibition
- Social withdrawal
3) Mood
- Anxiety
- Depression
4) Thinking
- Slow, impoverished
- Delusions
5) Perception
- Illusions
- Hallucinations
6) Insight
- Impaired
= minimum duration 6 months
What is usually the presentation of dementia?
Poor memory / forgetfulness
Describe the onset of dementia
Usually insidious but can come to notice after an acute deterioration
May be triggered by a change in social circumstance or intercurrent illness
What is apraxia?
Neurological disorder characterised by loss of ability to carry out skilled movements and gestures (despite having the desire and physical ability to do so)
What is agnosia?
Inability to recognise objects / people / sounds / shapes
What % of people have dementia:
1) 75-80yr
2) 80-85yr
3) >85yr
1) 75-80yr = 4%
2) 80-85yr = 10%
3) >85yr = 40%
Is dementia more common in F or M?
4 x more common in M
List some primary degenerative conditions causing dementia (7)
1) Alzheimer’s disease
2) Lewy body dementia
3) Frontotemperoal dementia = Pick’s disease
4) Huntington’s disease
5) Wilson’s disease
6) Multiple sclerosis
7) Motor neron disease
List other irreversible causes of dementia (6)
1) Traumatic head injury
2) Infections: HIV, encephalitis, CJD
3) Vascular: multi-infarct dementia
4) Toxins: alcohol
5) Anoxia: cardia arrest, CO poisoning
6) Metabolic: hepatic encephalopathy, DM
List some potentially reversible causes of dementia (9)
Neurological:
- Normal pressure hydrocephalus
- Intracranial tumour
- Chronic subdural haematoma
Vit deficiencies:
- Vit B12
- Folic acid
- Thiamine
Endocrine:
- Hypothyroidism
- Cushing’s
What are the 5A’s of dementia?
Amnesia Aphasia Agnosia Apraxia Associated behaviours = BPSD (Behavioural and psychological symptoms of dementia)
Outline mild dementia
Memory loss sufficient to interfere with everyday activities
Able to live independently
Outline moderate dementia
Memory loss is a serious handicap to independent living
Only highly learned / very familiar material retained
Individual unable to function without assistance of another in daily living
Outline severe dementia
Complete inability to retain new information
Virtual absence of intelligible ideation
The mind can no longer tell the body what to do
How should dementia be assessed?
1) Detailed hx
- Inc collateral
2) Physical exam
- Inc neuro
3) Cognitive testing
- MMSE
4) Laboratory investigations
5) Imaging
- CT / MRI
(EEG to rule out CJD)
What laboratory investigations can be done for dementia?
FBC LFTs Thyroid function Vit B12 Thiamine Calcium Glucose Urinalysis
If indicated: HIV / syphilis testing
What is the management of dementia?
General:
- Education / support / respite care
- Written care plan
Psychological:
- Structured group cognitive stimulation programme
- For agitation - aromatherapy, dance/music therapy, animal therapy
- Support for carers
Pharmacological:
- ACh inhibitors
- Memantine
- For agitation - antipsychotics and benzodiazepines
- For depression - antidepressants
What should be included in a written care plan?
Views on residential accommodation, end-of-life care, resuscitation
Input from OT, physio, dietician
Give 3 examples of ACh inhibitors
1) Donepizil
2) Galantamine
3) Rivastigmine
How do ACh inhibitors work?
Increase concentration and duration of action of acetylcholine in CNS
When are ACh used?
Alzheimers disease
- MMSE 10-20 points OR
- agitation not controlled by non-drug measures or antipsychotics
Evidence they can improve cognitive function and behaviour for up to a year (but do not halt or delay progression of disease)
Stop after 6 months if no benefit
What is memantine?
A glutamine NMDA antagonist
When is memantine used?
Improves cognition, mood and behaviour in moderate to severe Alzheimer’s
Not licensed in UK as little evidence and ?cost effective
What antipsychotics are used in dementia? When are they used?
Haloperidol
Olanzapine
Only use if severely distressed / agitated, after other methods eg low-stimulation environment, have been unsuccessful
What is the risk of using antipsychotics?
Inc risk of cerebrovascular events
What benzodiazepines are used in dementia? When are they used?
IM lorzepam - used as an alternative to an antipsychotic for extreme agitation
Avoid wherever possible esp in day
Use when antipsychotics fail
What is the most common form of dementia?
Alzheimer’s disease - 55%
After AD, what are the most common two causes of dementia?
Vascular dementia = 20%
Lewy body dementia = 15%
Describe the pathological findings in AD
Smaller aged matched brain:
- Widened sulci
- Enlarged ventricles
- Cell loss
- Shrinkage of dendritic tree
- Proliferation of astrocytes
- Increased gliosis
- Loss of neurons and synapses
Amyloid plaques
Neurofibrillary tangles
What are amyloid plaques?
Areas of dense, insoluble beta-amyloid peptide surrounded by abnormal neuritis filled with highly phosphorylated tau protein
insoluble beta-amyloid peptide deposits as beta-pleated sheets in hippocampus, amygdala, and cerebral cortex
What are neurofibrillary tangles?
Made up of helical filaments of microtubule-associated protein, tau, in a highly phosphorylated state
Found throughout cortical and subcortical grey matter = cortex, hippocampus and substantia nigra
What genetics are implicated alzheimers disease?
Amyloid precursor protein:
- Long arm of Chr 21
Implicated in beta-amyloid peptide:
- Presenilin 1 = Chr 13
- Presenilin 2 = Chr 1
Apo E4 (risk not causative) = Chr 19
What is the ‘cholinergic hypothesis’?
Neurons (by plaques and tangles) lost tend to be primarily cholinergic suggesting that cognitive impairment in AD is due to a deficit of cholinergic neurotransmission
= development of Ach inhibitors
List some risk factors for AD (9)
1) Age
2) FH
3) APP, presenilin or apoE4 gene mutation carrier
4) Previous head injury
5) Down’s syndrome
6) Hypothyroidism
7) Parkinson’s disease
8) CV disease inc HTN
9) Low level of education or lower IQ
(M=F)
Which Chr codes for the amyloid precursor protein?
Chr 21
What mutations can lead to AD?
Mutations in APP
Mutations in presenilin = encode proteins involved in cleavage of APP to beta-amyloid
- Lead to autosomal dominant form of AD
Mutations in ApoE4
- Inherited autosomal dominant forms of disease
Describe the course of AD
Progressive decline (may not be steady)
Incidental physical illness may cause superimposed delirium resulting in a sudden deterioration in cognitive function from which they may not fully recover
How long does someone typically live after the first signs of dementia? What is the most common cause of death?
5-8 years
Bronchopneumonia
Outline the DSM-IV classification of AD
1) Multiple cognitive deficits manifested by both memory impairment and at least one of aphasia, apraxia, agnosia, or a disturbance in executive functioning
2) The cognitive deficits cause significant impairment
in social or occupational functioning and represent a significant decline from a previous level of functioning
3) Course: gradual onset and continuing cognitive decline
4) Cognitive defects not due to any CNS / systemic / substances which could affect memory or cognition
5) Deficits do not occur exclusively during the course of a delirium
6) Disturbance is not better accounted by another Axis I disorder
What are possible protective factors of AD?
Smoking Oestrogen NSAIDs Vit E Higher premorbid education
What factors are associated with a worse prognosis with AD?
1) Greater severity at presentation
2) Male, <65yr
3) Parietal lobe damage
4) Prominent behavioural problems
5) Severe focal deficits
6) Depression
7) Absence of misidentification syndrome
What is the management of AD?
AChEIs (2nd gen)
- Donepezil: OD, CI in asthma, GI SE, liver metabolism but non-hepatotoxic
- Rivastigimine: BD, GI SE
- Galantamine: BD
AChEIs (1st gen)
- Tacrine: hepatotoxic, GI SE, QD
Memamtine
Others inc statins / antioxidants eg vit E
What is vascular dementia?
aka multi-infarct dementia
Focal disease results from multiple thrombotic / embolic infarcts in the brain
- Infarcts in midbrain or thalamic region especially severe
Describe findings of vascular dementia on neuroimaging
- Multiple infarctions and ischaemic lesions in white matter
- Atrophy of old infarcted areas
- Infarcts tends to be bilateral
- Lesions involve the full thickness of white matter
- Changes in blood flow in unaffected areas
- Entire brain is smaller and ventricles expanded
Describe the onset of vascular dementia
Late 60s / early 70s
More sudden onset than AD
Pt often present after a stroke or due to a sudden unexplained loss of function
How does vascular dementia often present?
1) Early personality changes (often before memory loss)
2) Fluctuating symptoms
3) Episodes of confusion common esp at night
4) Depression
+/- Fits (10%), TIA, other signs of cerebral ischaemia
What may be found on examination of someone with vascular dementia?
Focal neurological deficits
Signs of CV elsewhere
List clinical features of AD vs vascular dementia
AD:
- Insidious decline
- Poor memory
- Progressive disorientation
- Mood change
- Restless activity
- Insomnia
- Decline in social behaviour
- Personality change
- Dysphasia / dyspraxia
Vascular dementia:
- Stepwise progression
- Patchy impairment of cognitive function
- Poor memory
- Episodes of confusion
- Mood change
- Personality change
- Seizures
- Neurological signs
List some risk factors for vascular dementia
1) Male
2) CVD / HTN / high cholesterol
3) Smoking
4) FH of CVD / cerebrovascular disease
5) AF
6) DM
7) Coagulopathies
8) Polycythaemia
9) Sickle-cell anaemia
10) Carotid disease
What is the life expectancy of vascular dementia following diagnosis? What is the usual cause of death?
4-5yrs
Approx half from IHD, others from cerebral infarction or renal complications
What is Binswanger’s disease?
Small vessel vascular dementia = course may be gradual due to multiple microvascular infarcts
What investigations may be useful in vascular dementia?
Bloods - cholesterol, clotting, ESR, CRP (vasculitis) etc
CVD - ECG, CXR, BP, Echo, Dopplers
What is the management of vascular dementia?
Treat contributing disease
Aspirin OD may delay
General health interventions - diet, exercise, smoking etc
What 3 conditions are ‘Lewy bodies’ seen in?
1) Parkinson’s disease
2) Dementia with Lewy bodies
3) Autonomic failure associated with degeneration of sympathetic neurons in the spinal cord
What is the pathophysiology of dementia with lewy bodies?
Lewy bodies are abnormally phosphorylated neurofilament proteins aggregated with ubiquitin and alpha-synuclein (present in Parkinson’s). They are found in the cytoplasm of neurons in the basal ganglia (brainstem nuclei), paralimbic, and neocortical structures
There is associated neuronal loss leading to decreased ACh however there is minimal cortical atrophy
What are the clinical features of Lewy body dementia?
1) Dementia - relative sparing of memory with fluctuating cognitive ability and level of consciousness
2) Parkinsonism (70%)
- Triad of limb rigidity, bradykinesia and gait disorder
3) Visual hallucinations
- Less commonly auditory
4) Recurrent falls / syncope
5) Depression (40%)
6) Sleep disorders - daytime somnolence
Is Lewy body dementia more common in M or F?
F
What is the management of Lewy body dementia?
Parkinsonisn treated with L-dopa
Anticholinergics should be avoided as they can increase confusion and visual hallucinations
Atypical antipsychotics should be used over typical:
- Lewy body dementia carries higher risk of neuroleptic malignant syndrome
Psychosocal
What is neuroleptic malignant syndrome? How does it present? What is the management?
Life-threatening reaction to neuroleptic or antipsychotic medication
Symptoms include high fever, confusion, rigid muscles (high CK), variable BP
Raised CK can lead to renal failure
Stop antipsychotic
IV fluids
Dantrolene can be given to stop spasms
Bromocriptine can be given
What is delirium?
aka acute confusional state
Acute impairment of consciousness producing a generalised cognitive impairment
How common is delirium?
Common
15% pt in general medical / surgical wards
List the clinical features of delirium (6 areas)
1) Impaired consciousness
- Disorientation
- Poor attention and concentration
- Loss of memory
2) Behaviour
- Overactive / underactive
3) Thinking
- Muddled
- Ideas of reference
- Delusions
4) Mood
- Anxious / irritable
- Depressed
- Perplexed
5) Perception
- Misinterpretations
- Hallucinations (mainly visual)
Describe the course / onset of delirium?
Acute onset
Fluctuating course
Worse in evening
List some causes of delirium?
1) Systemic infection - UTI, chest, cellulitis, IV lines
2) Neurological infection - meningitis or encephalitis
3) Stroke or MI
4) Trauma or head injury
5) Metabolic failure - cardiac, respiratory, renal or hepatic
6) Hypoglycaemia
7) Electrolyte abnormalities
8) Nutritional deficiencies - vit B12, thiamine, nicotinic acid
9) Drug intoxication or withdrawal
10) Alcohol withdrawal
11) Raised ICP or SOL
12) Postictal states / status epilepticus
What investigations can be for delirium?
Bloods - FBC, U&Es, LFTS, TFTs, calcium, phosphate, magnesium, glucose, lactate, troponin, albumin, paracetamol and salicylate, haematinics
Blood and urine cultures
ABG ECG Urinalysis CXR Further tests eg CT head, LP, EEG
What tests can be performed to quantify cognitive impairment?
Abbreviated mental test score (AMTS)
Mini mental state examination (MMSE)
What is the AMTS?
1) What is your age? (1 point)
2) What is the time to the nearest hour? (1 point)
3) Give the patient an address, and ask him or her to repeat it at the end of the test. (1 point) e.g. 42 West Street
4) What is the year? (1 point)
5) What is the name of the hospital or number of the residence where the patient is situated? (1 point)
6) Can the patient recognise two persons (the doctor, nurse, carer, etc.)? (1 point)
7) What is your date of birth? (day and month sufficient) (1 point)
8) In what year did World War 2 begin? (1 point) (other dates can be used, with a preference for dates some time in the past)
9) Name the present monarch/dictator/prime minister/ president. (1 point)
10) Count backwards from 20 down to 1. (1 point)
Score <6 = delirium
What scores of MMSE indicate delirium?
/ 30
25 or more = normal
21-25 = mild dementia
10-20 = moderate dementia
Less than 10 = severe
What is the management of delirium?
Treat underlying cause
- Oxygen
- Fluids
- Abx
- Pain relief etc
Reassurance and reorientation
- Clock visible at all times
- Pt reminded of time, place regularly
- Routines
Sleep
- Hypnotics eg zopiclone 3.75mg or benzodiazepine eg temazepam 10mg may be needed at night
May need sedatives
- Haloperidol 0.25-2mg every 4hrs or lorazepam
What is the prognosis of delirium?
Usually gradual reduction of symptoms with effective treatment of cause
Often patchy amnesia following recovery
Approx 20% mortality around that admission, 50% at 1 year
May be a marker for subsequent development of dementia
What cerebral lesions may have psychiatric symptoms?
1) Stroke
2) Cerebral tumours
3) Epilepsy
4) Head injury
What psychiatric symptoms may someone who has had a stroke experience?
Depression Emotional liability Personality changes Behavioural problems Dementia
- High incidence of depression in first year
What psychiatric symptoms may someone who with epilepsy experience?
Auras Hallucinations and other disorders of perception Deja vu Psychosis Neurotic disorders
Can have complex partial seizures of temporal lobe epilepsy, schizophrenia-like psychosis and increased risk of suicide
What may be the organic cause of:
- Depression
- Fatigue and low energy
- Irritability
- Cognitive slowing?
Hypercalcaemia
What may be the organic cause of:
- Emotional disturbance and lability
- Delirium
- Depression
- Panic / anxiety episodes
- Psychotic episodes?
Porphyria (acute intermittent type)
What may be the organic cause of:
- Weight gain
- Depression
- Insomnia
- Loss of libido
Cushing’s disease
What may be the organic cause of:
- Anxiety
- Panic
Associated with HTN
Phaeochromocytoma
What may be the organic cause of:
- Depression
- Sleep disturbances
Hypokalaemia
What may be the organic cause of:
- Weight loss
- Inc appetite
- Anxiety
- Psychosis
- Irritability
- Loss of libido
- Restlessness
- Weakness
Hyperthyroidism
What may be the organic cause of:
- Depression
- Memory problems
- Delirium (33%)
- Psychosis
May present with hepatic or movement disorders, or psychiatric symptoms including dementia
Wilson’s disease
What may be the organic cause of:
- Altered consciousness
- Confusion
- Seizures
- Dysphasia
- Movement disorders
- Sensory changes
- Abnormal behaviour
- Hallucinations
- Nightmares
Viral encephalitis
Many causative organisms eg tick-borne viruses, measles, mumps, rubella, rabies, HS
What may be the organic cause of:
- Depression
- Apathy
- Tiredness
- Weight loss
- Anorexia
- Mild cognitive impairment
Addison’s disease
= Primary adrenal insufficiency
What may be the organic cause of:
- Depression
- Maina
- Schizophrenic-like psychosis
- Cognitive slowing
- Dementia
- Ataxia
- Weight gain
- Depressed mood or psychotic symptoms
- Loss of libido
- Poor memory
Hypothyroidism
“myxoedema madness”
What is the DEMENTIA pneumonic?
Drugs / delirium Emotions / depression Metabolic disorders Eye and ear problems Trauma / toxins / tumours Infections Alcohol / atherosclerosis
What age is frontp-temporal dementia usually diagnosed?
45-65yr
List 3 subtypes of fronto-temporal dementia (FTD)
1) Behavioural variant FTD
- Change in personality, behaviour and interpersonal skills
2) Progressive, non-fluent aphasia
- Loss of language skills
3) Semantic dementia
- Loss of semantic memory
What investigations are performed for FTD?
To determine if there is FTD and what type
- Fluency assessment
- Abstract thinking and metaphor interpretation
- Sorting tasks = Wisconsin sort task
- Stroop tests (eg word ‘orange’ written in blue and you have to say what colour the word is not what the word says)
- Hand-positoning test
- Copying tasks
- Rhythm tapping taska
- Trail making tests
- Cognitive assessments
What does an MRI show in FTD?
Bilateral atrophy of frontal and temporal lobes
What are the histologically different types of FTD?
1) Microvascular (60%)
2) Pick’s type (25%)
3) Combined (15%)
What is Pick’s type FTD?
Presence of Pick’s bodies = intraneuronal masses of cytoskeletal elements
What is the management of FTD?
Unknown aetiology of FTD makes it difficult to manage
- Do not use ACHeis
- Treat symptoms
- ?SSRI beneficial
