Dementia and Delirium Flashcards
(32 cards)
1
Q
What is dementia?
A
- Global impairment of cognition and functioning acquired (later in life) that is progressive and irreversible
- Domains include:
- Memory
- Language (aphasia)
- Praxis (motor planning) - apraxia
- Visuouspatial
- Executive planning
- Social/personality
- The 5 A’s
- Amnesia - memory loss
- Aphasia - language problems
- Apraxia - difficulties performing motor actions
- Agnosia - inability to recognise items, faces, people
- Associated symptoms - non-cognitive like mood/anxiety problems, aggression, hallucinations, delusons, personality changes
2
Q
How are patients with dementia assessed?
A
- Patient’s history
- Informant history
- Daily activities
- Cognitive assessment (AMT>MMSE/MOCA>ACE-R>Neuropsychology input)
- Physical examination (i.e. abnormal movements, ataxia, praxis, eye movements, frontal release signs)
3
Q
What are the elements of a cognitive history?
A
- Memory (impaired abiloty to acquire and remember new information)
- Executive function (impaired reasoning and handling of complex tasks, poor judgement)
- Visuospatial (impaired abilities)
- Language (impaired language functions)
4
Q
What are the causes of rapidly progressive cognitive impairment? (VITAMINS)
A
- V – Vascular
- I – Infectious (syphilis, HIV, Lyme)
- T – Toxic/metabolic (Wernickes, B12 deficiency)
- A – Autoimmune encephalitis
- M – Metastatic/neoplastic
- I – Iatrogenic/inborn error of metabolism (drugs)
- N – Neurodegenerative (CJD, AD)
- S – Systemic/seizure (hypersensitive encephalopathy)
5
Q
What is episodic memory?
A
- Memory related to specific events
- Localised in the medial temporal lobe and hippocampus
6
Q
What is semantic memory?
A
- Factual things
- Widely distributed in the left temporal lobe and multiple cortical areas but with key linking node
7
Q
What is working memory?
A
- Stored memory for 10-15 seconds but not beyond
- Distributed in frontal, temporal and parietal lobes
8
Q
How are attention, concentration and orientation assessed?
A
9
Q
What is semantic dementia?
A
- Gradual loss of semantic knowledge
- Initial loss of low frequency words
- Surface dyslexia
- Will have difficulty naming pictures and sounds
10
Q
What are the 3Ms of sub-cortical dementia?
A
- Motor
- Mood
- Memory
11
Q
What is the clinical progression of dementia?
A
- Early (problems with topographic memory, progressive amnesia)
- Moderate (visuospatial difficulties, personality/behavioural change, executive function)
- Advanced (global cognitive deficits)
- Average survival 6-8 years from diagnosis
- Poorer outcomes in males, <65 onset, prominent BPSD, physical comorbidities and extensive brain damage
12
Q
Features of delirium (bold for key criteria in ICD-10)
A
- Acute or subacute onset
- Impaired cognition or attention
- Reversible
- Secondary to physical abnormality
- Fluctuating course (may appear normal at times)
- Clouding of consciousness (disturbance of consciousness)
- Reduced ability to direct, sustain and shift attention
- Disorientated
- Psychomotor disturbance
- Emotional disturbance
- Florid hallucinations (visual/tactile)
- Illusions (misperceptions)
- Delusions (often poorly formed and paranoid)
- Behavioural disturbance
- Disturbed sleep-wake cycle (worse at night)
13
Q
Importance of delirium
A
- Mortality rates double in over 65s
- Increases length of stay (9 vs 21 days)
- More likely to be readmitted
- More likely to need institutional care at 1 month
- Up to 50% of cases are not recognised
- Impact on other patients and professionals
14
Q
Management of delirium
A
- Search for a cause
- If you don’t find a cause, search for another cause
- Side room that are clutter free with labels
- Adequate lighting to avoid misinterpretation of environment
- Clear brief communication
- Re-orientation
- Familiar objects and people (avoiding transfers)
- Correct sensory impairments
- Medication (a last resort)
- Benzodiazepines
- Antipsychotics (atypical > typical) - avoid in Parkinson’s Disease
- May need detained under the Mental Health Act
15
Q
Common types of dementia
A
- Alzheimer’s Disease (most common)
- Lewy Body Dementia
- Fronto-temporal dementia
- Vascular dementia
- Alcohol related dementia (reversible)
16
Q
Alzhermer’s dementia
A
- Neuropathology
- Atrophy
- Flattened sulci
- Enlarged ventricles
- Histological
- Plaques (extracellular, amyloid β peptide deposit, cleaved from amyloid precursor protein/APP)
- Tangles (intracellular, abnormally phosphorylated tau)
- Vacuoles
- Neuronal loss
- Synaptic loss
- Neurotransmitter loss
- Apoptosis
- Risk increases with age (1% at 60, 40% at 85)
- Genetics
- Trisomy 21 - extra APP
- Presenilin 1 and 2 - young onset
- Clinical features
- Gradual onset
- Slowly progressive
- Primarily memory
- Eventual global impairment
- Limited insight
17
Q
Vascular dememtia
A
- Neuropathology
- Infarcts
- Small vessel disease
- Perfusion deficits
- Underlying CV risk factors
- Clinical features
- Quicker onset
- Stepwise deterioration
- Focal cogitive impairment
- Mood disturbance
- Insight retained
- CV history
- Neurological signs
- Hachinski index used for liklihood
18
Q
Lewy Body dementia
A
- Neuropathology
- Atrophy (mid-brain, temporal lobes)
- Substantia nigra
- Limbic areas
- Histological
- Lewy bodies (cytoplasmic inclusion, ubiquitin - protein involved in DNA repair, α-synuclein - presynaptic protein)
- Vacuoles
- Neuronal loss
- Synaptic loss
- Dopaminergic loss
- Apoptosis
- Clinical features
- Gradual onset
- Memory difficulties
- Fluctuates
- Parkinsonism symptoms
- REM sleep disturbance
- Visual hallucinations
NB - If established Parkinson’s disease >12 months alongside cognitive symptoms then Parkinson’s dementia
19
Q
Frontotemporal dementia
A
- Neuropathology
- Atrophy (frontal, temporal lobes)
- Knife blade gyri
- Histological
- Pick bodies (tau +/- ubiquitin but preference for frontal lobes)
- Vacuoles
- Neuronal loss
- Synaptic loss
- Neurotransmitter loss
- Apoptosis
- Clinical features
- Younger onset
- Personality change (i.e. inappropriate, impulsive)
- Speech difficulties
- Hyper-orality
- Frontal release signs (i.e. grasp reflex, glabellar tap reflex)
20
Q
Alcohol related brain damage (ARBD)
A
- Very similar to Alzheimer’s
- Alcohol dependence, alcohol end-organ damage
- Associated amnestic syndrome (low thiamine)
- Wernicke’s encephalopathy (cognitive impairment, ataxia, ophthalmoplegia)
- Korsakoff’s psychosis (anterograde memory loss, confabulation, poor diagnostic critera at present)
21
Q
Normal pressure hydrocephalus
A
- Excessive CSF due to flow issue
- Cognitive impairment, ataxia, urinary incontinence
22
Q
Creutzfeldt-Jakob Disease (CJD)
A
- Prion - abnormally folded protein (infectious but not alive)
- Sporadic
- Rapidly deteriorating dementia, early death
23
Q
How is dementia diagnosed?
A
- Clinical history
- Physical (including neurological) examination
- Cognitive testing
- Abbreviated Mental Test (AMT) - rapid screening
- MMSE - general screening
- ACE-III - gold standard
- Routine investigations
- FBC, U&Es, LFTs, CRP, bone profile, TFTs, B12, folate
- Consider HIV, syphilis, vasculitis and ANA
- Consider infection screen (MSSU, CXR, LP)
- Imaging
- CT brain
- MRI brain
- Functional SPECT
NB - Looking to rule out delirium, reversible dementia, MCI and pseudodementia (i.e. depression, chronic psychosis)
24
Q
General management of dementia
A
- Symptomatic control and QoL measures
- Education
- Maximise physical health
- Maximising function (OT)
- Manage challenging behaviours (stress and distress)
- Maximise suport (SW - POC, NH)
- Planning for future (POA, guardianship, DNAR)
- Palliative care
25
Pharmacological management of dementia
* Avoid benzodiazepines (disinhibition, delirium)
* Cognitive enhancers
* Acetylcholinesterase inhibitors (AChls)
* Donepezil, Rivastigmine, Galantamine
* Block AChl, increase neurotransmitter levels
* Side effects include GI upset, incontinence, bradycardia (AV block) and psychosis
* Glutamate (NMDA) antagonist
* Block NMDA excito-toxicity
* Side effects include HTN, seizures, DVT, hepatotoxicity and psychosis
* Antipsychotics if severe agitation (Risperidone, Olanzapine)
26
Aetiology of delirium
27
Risk factors for delirium
* Older or very young age
* Underlying brain injury
* Blind/deaf
* Post-operative
* Previous substance abuse
* Previous psychiatric illness
* Environmental dislocation
* Sleep deprivation
* Sensory extremes
* Sensory overload
* Pain
* Stress
28
Pathogenesis of delirium
* Derangement in normal physiology
* Infection = cytokines, cross BBB, activate reticular activating system
* Cerebral metabolic insufficiency (O2 demand \> supply), ATPase failure
* Impairment of neuronal signalling
* Neurotransmitter changes
* Reduced GABA - neuronal excitability (NMDA unopposed)
* Increased dopamine - psychosis
* Increased serotonin - mood alteration
* Increased noradrenaline - agitation
* Increased cortisol - disruption of circadian rhythm
29
Assessment of delirium
* Clinical history
* Cognitive assessments (CAM)
* CAM = Confusion Assessment Method
* 1) Acute onset
* 2) Fluctuating
* 3) Disorganized thinking
* 4) Consciousness (alert, hyper-alert, drowsy, stupor, coma)
* Need 1 + 2 (+3 or +4)
* Can also use AMT, MMSE, ACE III
* Physical examination (sepsis, neurological, nutrition)
* Bloods (as per dementia - consider drug levels)
* Toxicology screen
* Infection screen
* Head imaging
* LP
* EEG
30
Risks of medical management of delirium
* Benzodiazepines
* Oversedation
* Airway compromise
* Falls
* Antipsychotics
* Cardio-respiratory collapse (NMS)
* Interaction with illicit medication
* Prolonged QTc (especially haloperidol)
* Increased stroke risk in elderly
* Damage to therapeutic relationship
31
Legal framework
32
Dementia vs Delirium
