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Dementia and Delirium Flashcards

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
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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)
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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)
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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)
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5
Q

What is episodic memory?

A
  • Memory related to specific events
  • Localised in the medial temporal lobe and hippocampus
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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
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7
Q

What is working memory?

A
  • Stored memory for 10-15 seconds but not beyond
  • Distributed in frontal, temporal and parietal lobes
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8
Q

How are attention, concentration and orientation assessed?

A
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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
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10
Q

What are the 3Ms of sub-cortical dementia?

A
  • Motor
  • Mood
  • Memory
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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
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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)
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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
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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
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15
Q

Common types of dementia

A
  • Alzheimer’s Disease (most common)
  • Lewy Body Dementia
  • Fronto-temporal dementia
  • Vascular dementia
  • Alcohol related dementia (reversible)
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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
Q

Pharmacological management of dementia

A
  • 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
Q

Aetiology of delirium

27
Q

Risk factors for delirium

A
  • 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
Q

Pathogenesis of delirium

A
  • 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
Q

Assessment of delirium

A
  • 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
Q

Risks of medical management of delirium

A
  • 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
Q

Legal framework

32
Q

Dementia vs Delirium

Neurology (26 decks)

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