Impairment of Consciousness, Memory or Cognition Flashcards
Consciousness definition
Being aware of both the environment and of oneself as a subjective being
- global cognitive function
Cognition definition, 5 main domains and their defects/responsible lobes
Mental activities that allow us to perceive, integrate and conceptualise the world
- global functions of consciousness, orientation, attention
- specific domains of memory, executive function, praxis
Language - dysphasia/aphasia –> receptive dysphasia (understanding; temporal lobe) and expressive dysphasia (speaking; frontal lobe)
Praxis - dyspraxia/apraxia –> loss of ability to carry out skilled motor functions despite intact motor function (frontal lobe)
Perception - dysgnosia/agnosia –> loss of ability to interpret sensory information despite intact sensory function (parietal lobe)
Memory - amnesia –> loss of ability to learn or recall new information (temporal lobe; hippocampus)
Executive function - disinhibition, perseveration, apathy, dysexecutive syndrome –> loss of ability to plan and sequence activities or to use abstract information (frontal lobe; limbic for emotions)
Memory - most common type disrupted, types of memory
One of the most common cognitive domains to be impaired
Explicit/Declarative memory = stored memory which individual is “aware” of, can declare - most commonly disrupted
- -> semantic: facts
- -> episodic: autobiographical events
Types of explicit memory
- short term/working: 15-30 seconds, frontal cortex (digit span, 3 items registration)
- long term recent: mins-months, hippocampus and mamillary bodies (anterograde delayed recall, retrograde recent events)
- long term remote: lifetime, frontal and temporal cortex (past important events)
Implicit/Procedural memory = stored without conscious awareness e.g. speaking a language, riding bicycle
Amnesia - definition, types and related areas of damage
Loss of ability to store new memories or retrieve old memories
Anterograde: unable to store new memories from event onwards
- damage to medial temporal lobes esp hippocampal formation
Retrograde: unable to retrieve memories stored before the event
- damage to frontal or temporal cortex
Key points in Hx taking
Onset (r/o delirium if acute)
Initial problem/most prominent (AD vs non-AD)
Severity – functioning, orientation, frequency, coping mech
Risk assessment - suicide, others, self-neglect (food, fire, abuse, meds, self-care)
BPSD - mood, psychosis, motor dysfunction
Caregiver stress
Examinations of patients
MSE
Cognitive tests
Physical
Functional
Standardised cognitive examinations - purpose, adv and disadv
For SCREENING, NOT DIAGNOSIS!
MMSE
- covers most cognitive domains but NOT TESTING EXECUTIVE functions
- not sensitive to mild cases
- influenced by premorbid IQ, language, culture
- > 25/30 = normal, 21-24 mild dementia, 10-20 mod
Abbreviated mental test
- fast
- not sensitive to mild/moderate cases
- <6/10 = delirium
Clock drawing test
- praxis and executive function
- not sensitive to mild
- very influenced by poor motor control/visual impairment
Addenbrooke’s cognitive examination
- test all domains and sensitive to mild
- lengthy, influenced by premorbid culture/IQ/language
HKMoCA
- tests memory and executive function
- age and education corrected data
HKBC
Physical examination
Neurological exam
Look for:
- reversible causes of impairment e.g. hypothyroid, SOL
- risk factors e.g. hypertension, AF
- Ddx e.g. hemiparesis or visual field defect suggestive of CVA
- self-neglect, falls
Investigations for cognitive impairment
Delirium - acute illness
- ECG, septic screen
Chronic impairment
- VitB12, folate
- TFT for hypothyroid
- Ca for hyperCa
- Glucose, U&E for Cushing’s, Addison’s
- CT/MRI for subdural haematoma, tumour
Differential diagnosis for cognitive impairment
Delirium Dementia Mild cognitive impairment Subjective cognitive impairment Stable cognitive impairment Depression (pseudo dementia) Psychotic disorders Mood disorders Intellectual disability
(Specific syndrome a/w organic brain disease e.g. amnesic syndrome, organic mood/delusional state/personality disorder)
Delirium 譫妄 (zim mong) - general definition, diagnostic criteria
Syndrome of acute generalised cerebral dysfunction characterised by
- ALTERED CONSCIOUSNESS, DISORIENTATION, attention, perception, thinking, memory, emotion, sleep-wake cycle, psychomotor behaviour
- Disturbance in attention and awareness
- Disturbance develops OVER SHORT PERIOD OF TIME and tends to FLUCTUATE in severity during the day
- An additional disturbance in cognition e.g. memory deficit, language, perception, disorientation
- Disturbances are not better explained by another neurocognitive disorder and do not occur in the context of severely reduced level of arousal e.g. coma
- There is evidence that disturbance is direct physiological consequence of another medical condition, substance intoxication or withdrawal or multiple aetiologies
Salient features of delirium
ABRUPT onset
SHORT duration
FLUCTUATION of consciousness during the day, worsening at night
- hypoactive type with drowsiness/coma
- hyperactive type with agitation and hypervigilance
COGNITIVE DYSFUNCTION
- short term and recent memory
- DISORIENTATION TO TIME, and often place
- language abnormalities (rambling, incoherent)
PERCEPTION AND THOUGHT disturbance - often present but not essential
- misinterpretations, illusions, hallucinations (esp visual)
- fleeting persecutory or referential delusions
MOOD disturbance
- labile
- range from depression, irritable, euphoric, anxious, angry, fearful, apathy
Sleep-wake cycle disturbance
- reversal of normal cycle e.g. daytime drowsiness, night time hyperactivity
(diffuse slowing on EEG)
Delirium - epidemiology and risk factors
Common, affecting 15% inpatients and 40-60% in the ICU
All age grps can be affected, more common in children and elderly
Risk factors:
- “at risk brain” e.g. pre-existing dementia (50% cases of delirium) or cognitive impairment, previous serious head injury
- serious physical illness
- polypharmacy
- visual impairment (decreased sensory input)
- isolation, stress
Aetiology of delirium
Primary cause often outside brain and multiple aetiologies
Systemic illness
- sepsis and infections e.g. URTI, UTI
- anoxia e.g. CHF, MI, resp failure (COAD, asthma)
- metabolic and endocrine e.g. electrolyte disturbances, hepatic encephalopathy, hypoBG, hyper or hypo-thyroid/PTH/adrenocortical
- nutritional e.g. VitB12, folate deficiency, thiamine
Intracranial causes
- meningitis, encephalitis
- head injury
- SOL, cerebrovascular e.g. TIA
- epilepsy
Drugs (intoxication and withdrawal)
- anticholinergics (worsen dementia brain which already has Ach deficits), BZD, opiates, anti-parki drugs, steroids
- alcohol (delirium tremens), opiates, cannabis, ICE
- poisons (heavy metals, CO)
Management of delirium
Marker of severity of illness (compromised coping) –> MEDICAL EMERGENCY, high mortality
- *Find and treat underlying disorder
- pre-existing RFs, current picture
- CBC, LRFT, TFT, BG, clotting, Ca, P, CRP, Trop-T, ABG
- CXR
- blood and urine cultures
- Urinalysis, urine toxicology
- CT/MRI, LP, EEG if needed
Maintain adequate hydration and diet, maintain physical condition
Consistent routine to meals, care
Environment – quiet/isolated room with no dangerous objects or triggers, light in day and dark at night, safety, maximise visual acuity and auditory input
Improve orientation by clocks
Encourage visit by relatives (give patient reassurance, reduce anxiety)
Meds:
- avoid any unnecessary medication
- sedation if severe sleep disturbance – not BZD since will worsen confusion UNLESS ALCOHOL WITHDRAWAL; zoplicone, haloperidol
- antipsychotics if high risk, aggression – haloperidol
Monitor improvement using abbreviated mental test score – <6/10 = delirium
Ddx of delirium
- *Dementia
- gradual onset, long duration, normal consciousness, intact attention, impaired orientation at late stages, normal sleep-wake cycle, normal mood, paranoid/fixed delusions/perceptual disturbance in later stages, not reversible, progressive course
Depression
- gradual onset, normal consciousness, inconsistent memory, low mood, mood congruent delusions, diurnal variation
Non-organic psychoses
- variable onset, normal consciousness, intact memory, incongruent mood, complex systematised delusions, sometimes reversible, chronic/relapsing course
Dementia (Major Neurocognitive Disorder) - general definition, diagnostic criteria
Most common organic psychiatric condition
Syndrome of acquired progressive generalised cognitive impairment associated with functional impairment but NO CLOUDING OF CONSCIOUSNESS
For >6 MONTHS
- Significant cognitive decline from a previous level in >1 cognitive domains e.g. attention, learning, memory, language, executive function etc. based on:
- concern of the individual, knowledgable informant or clinician
and
- substantial impairment in cognitive performance by standardised testing - Interfere with INDEPENDENCE in everyday activities e.g. finances, managing meds
- Do not occur exclusively in the context of delirium
- Not better explained by another mental disorder e.g. MDD, schizophrenia
Features of dementia
Insidious onset (but can have triggers for acute deterioration)
- Cognition
- memory impairment: recent memory, new learning affected first
- impaired attention
- aphasia (difficulty finding words), agnosia, apraxia
- impaired executive functioning
- disorientation (in later stages)
- personality change - Behavioural and Psychological Symptoms of Dementia (BPSD)
- Behavioural common: disorganised, restless/pacing/shouting, disinhibition (e.g. sexual), social withdrawal, aimless activity, self-neglect, confabulation
- Mood: anxiety, depressed in up to 50% (c.f pseudo dementia), restricted affect
- Thought: slow, impoverished, impaired judgement, low flexibility, incoherent in later stages
- Psychosis: persecutory/paranoid delusions (40%), hallucinations (visual more common as in delirium; 30%), illusions - Functional impairment
- basic or instrumental ADL
- basic = self-care –> eating, dressing, washing, toileting continence, mobility
- instrumental = independent –> cooking, shopping, housework - Neurological
- 10-20% have seizures
Lack insight
Dementia epidemiology - M:F, prevalence
M>F 4:1
25 million ppl worldwide
5% of aged 65+, doubles every 5 yrs until 80
<65 onset = presenile dementia
Causes of dementia - which are reversible?
Primary causes (within brain)
- Neurodegenerative: Alzheimer’s disease, Frontotemporal dementia (Pick’s), Lewy body dementia, Hungtington’s disease, Parkinson’s disease
- Cerebrovascular disease: Vascular dementia
- Tumours, cysts, abscesses, haematomas, normal pressure hydrocephalus
Secondary causes
- Trauma: head injury, punch-drunk syndrome
- Infection: CJD, HIV, Syphilis
- Metabolic: hepatic encephalopathy, Wilson’s disease, thyroid (hyper/hypo), Cushing’s
- Nutritional: thiamine, B12, folate
- Drugs/toxins: alcohol, BZD, CO poisoning
- Inflammatory disorders: SLE, MS
Reversible causes:
- tumours, haematomas, normal pressure hydrocephalus
- thyroid, cushing’s
- nutritional deficiencies
Determining severity of dementia
Mild
- Memory loss: short term
- Disorientation: time
- ADL: normal (function well in community but difficulty in new situations)
- 10-15% convert to dementia each year
Moderate
- Memory loss: short term
- Disorientation: time, place
- ADL: instrumental affected
Severe
- Memory loss: short and long term
- Disorientatino: time, place, person
- ADL: basic and instrumental affected
Cortical, Subcortical and Mixed Dementias
Cortical
- Alzheimer’s, Frontotemporal
- aphasia early, normal speech until late, apraxia, agnosia, normal posture, no extra movements
Subcortical
- all others
- normal language, dysarthritic, normal praxis, no agnosia, stooped or extended posture, tremor/chorea/tics
Mixed
- vascular dementia, infection induced (except HIV)
Importance of differentiating types of dementia
Reversible causes Medication treatment for some C/I drugs for some e.g. antipsychotics in Lewy body Prognosis varies Genetic counselling
Alzheimer’s disease - epidemiology, main features, pathology, risk factors, protective factors
50-60% of all cases of dementia
5% aged 65+, 2x prevalence every 5 yrs after 65, 40% over 85
M>F
Features:
- insidious onset with PROGRESSIVE cognitive decline
- EARLY MEMORY LOSS (recent)
- disorientation is early sign
- signs of parietal lobe dysfunction in later stages – dysphasia, dyspraxia, agnosia
Pathology:
- abnormal protein deposition - extracellular amyloid plaques, intracellular hyperphosphorylated Tau (neurofibrillary tangles)
- inflammatory reactions and neuronal death (Ch neurons primarily) – start at hippocampus and spread (occipital, cerebellum not affected)
Risk factors:
- ageing
- **FHx (3x risk of general population for late-onset)
- ApoE4 (late onset), APP/Presenilin genes (early onset AD form)
- Down’s
- Low education
- Head injury
- Metabolic syndrome: HT, DM, HL, Obesity (also for vascular dementia)
- Hypothyroid, Parkinson’s
- Smoking
- Depression
Protective factors:
- higher education
- cognitive stimulation
- leisure, physical activities
- social engagement
- healthy diet (fruit, veg, fish, mediterranean)
Alzheimer’s disease course, prognosis
Progressive deterioration
Later stages: mute, bedridden, incontinent, very thin
Death due to pneumonia, other complications
Prognosis: mean survival 8-10 yrs after onset
Vascular dementia (multi-infarct dementia) - epidemiology, clinical features, pathology, risk factors, course
Very common in HK (approx 1/3 patients); worldwide 15-20% cases; prevalence 1-4% in 65+
M>F
Onset 60-70s
Features:
- ABRUPT onset
- EXECUTIVE FUNCTION usually affected earlier than memory – problem solving, bad temper, disinhibition
- Hx of HT and atherosclerosis
- focal neurological signs (based on site e.g. thalamic artery - memory; left MCA - language; frontal lobe - behaviour; UMN deficits common)
- patchy impairment of cognition
- fluctuating symptoms with episodes of confusion common at night
- emotional lability
- preserved insight
Pathology:
- evidence of cerebrovascular disease/stroke
- multi-infarct dementia, lacunar infarcts (<1cm), micro infarcts (<1mm), white matter ischaemia, strategically placed infarcts
- large and small vessels both affected
Risk factors:
- FHx or PHx of CVS disease
- smoking
- AF, DM
- other blood related diseases e.g. coagulopathies, sickle cell anaemia, polycythaemia
Course:
- STEPWISE progression
- fluctuating course
- 4-5 years survival after diagnosis; 50% die from IHD
Mixed AD and VaD
Very common!
10%
Similar metabolic risk factors
Lewy body dementia - prevalence, features, pathology, risk factors, prognosis, vs Parkinson’s disease with dementia
10-15% dementia cases; prevalence 0.7% in 65+
M>F
Features:
- FLUCTUATING COGNITION (relative sparing of memory)
- prominent VISUAL HALLUCINATIONS
- signs of Parkinsonism e.g. postural instability, shuffling gait for <1 YEAR before dementia occurred
- high sensitivity to antipsychotics (induces Parkinsonism; higher risk of NMS)
- REM sleep behaviour disorder (early predictor)
- repeated falls
- autonomic symptoms (postural hypotension, SNS disturbances)
Pathology:
- ubiquitin and alpha-synuclein intracytoplasmic deposition in subcortical and cortical regions (Lewy bodies) + Alzheimer type plaques/tangles
- basal ganglia primarily
Risk factors:
- FHx
Prognosis:
- higher morbidity (Parkinsonism affecting movement)
- 4-10 yrs after diagnosis
Parkinson’s disease with dementia
- similar features with Lewy body but
- Dx of Parkinson’s >1 YEAR before dementia
Frontotemporal dementia (including Pick’s) - epidemiology, age of onset, features, associated disease
2%
Second commonest EARLY ONSET dementia (40s)
1/3 familial AD inheritance (Chr 17 Tau, Progranulin gene)
Features:
- early decline in social and personal conduct – DISINHIBITION, impulsivity
- early EMOTIONAL BLUNTING, apathy
- attenuated SPEECH output (prominent aphasia), echolalia, perseveration, mutism if severe
- early loss of insight
- relative sparing of other cognitions
Prognosis:
- some a/w MND (C9orf72 gene)
Huntington’s disease
Rare, early onset neurodegeneration at caudate and putamen
AD inheritance
CAG repeat at Chr. 4
Chorea, Cognitive decline, Depression, Apathy, Anxiety
Imaging appearances for main forms of dementia
(CT if not otherwise specified)
Normal ageing
- progressive cortical atrophy and increasing ventricular size
Alzheimer’s
- none in early stage
- general cerebral atrophy
- widened sulci, dilated ventricles, thinning of width of medial temporal lobe and hippocampus
- PET FDG temporal and parietal low; amyloid, tau +ve
Vascular dementia
- single or multiple infarction areas/ haemorrhages; tend to be bilateral
- cerebral atrophy of old infarcted areas (including frontal lobe; possible ddx for frontal lobe syndrome)
- dilated ventricles
Frontotemporal dementia
- greater relative atrophy of frontal and temporal lobes (hypometab on functional MRI)
- knife-blade atrophy (severe localised atrophic gyri)
- PET FDG frontal and temporal low; tau maybe +ve
Lewy body dementia
- dopamine transporter uptake reduced in basal ganglia on functional MRI or PET-DA
Huntington’s
- dilated ventricles
- atrophy of caudate nuclei
CJD
- normal appearance
Management of Dementia - initial lab tests, general aims for mild/mod/severe cases
Exclude and treat reversible causes or other physical illnesses; basic Ix for baseline
- CBC, LFT, RFT, TFT, glucose, CaPO4, lipids, thiamine, B12, folate
- CT/MRI
Preferably outpatient Tx; inpatient only if very high risk or complex comorbidities
Aim to address:
- cognitive deterioration
- BPSD
- environmental safety
- carer stress
MCI: OPTIMISE cognition and function, prevent onset of neuropsychiatric symptoms
Moderate: stabilise functional impairment (maintain abilities), minimise neuropsychiatric symptoms; supervise daily activity schedule
Severe: stabilise ADL and functioning, maintain social interactions
Non-pharmacological Mx of Dementia + BPSD
FIRST LINE!!!
- may refer old age home, ICCMW, DAY CARE centre, psychogeriatric DAY HOSPITAL for rehabilitation
Psychoeducation to all involved
- dx, course, prognosis, treatment available etc
- realistic expectations and treatment goals
Psychotherapy
- stress reduction, socialisation
- reminiscence therapy
- group cognitive therapy/ cognitive stimulating activities
- aromatherapy, music/dance therapy, massage, animal-assisted therapy for BPSD
Lifestyle
- methods to help forgetfulness e.g. making lists, labelling drawers, pill box, establishing routines, clock with day/date, daytime activities to decrease napping
Diet, exercise, sleep, physical health, decrease CVS risk factors, community psychiatric nurse support
Caregiver training and support groups
- address stress, how to adapt
Pharmacological Mx of Dementia - Alzheimer’s disease
Cholinesterase inhibitors for mod cases
- slows rate of deterioration BY 6 MONTHS (no reversal)
- increase Ach effects on brain
- Donepezil (aricept), rivastigmine (exelon)
- S/E: bradycardia, asthma/COAD exacerbation, perforated peptic ulcer (increase acid secretion)
- –> need to monitor S/E in long term
Memantine for severe cases
- glutamate NMDA receptor antagonist
- restore synaptic signal transmission, may be neuroprotective
- S/E: dizziness, headache
Aducanamab is newest monoclonal Ab which potentially could reverse disease by targeting amyloid protein
NOT FOR NON-AD!!
Pharmacological Mx of BPSD
Not first line - should only use if psychotherapy not effective or high risk symptoms
Mood stabilisers (not Li) for aggression, impulsivity, irritability
Antipsychotics INCREASE RISK OF STROKE and MORTALITY
–> slight increase risk of CVS events
–> only if severely distressing symptoms causing risk (haloperidol, olanazapine)
–> SGA in Lewy body if rly indicated since higher risk of NMS
Antidepressants if MDD
AVOID benzodiazepine due to risk of falls and worsening cognition
Dementia vs Delirium
Onset, Duration Course, Context (any physical illness) Consciousness Attention Mood Perceptual disturbance Sleep-wake cycle Orientation Speech Reversibility
Subjective cognitive impairment
Complain of problems but normal score on standardised test
Can reflect anxiety or depression
Stable cognitive impairment
“One off” insults impairing cognition but not progressive
e.g. CVA, hypoxic brain injury, trauma
Pseudodementia - what is it, how to differentiate from dementia
Important Ddx of dementia
Patients presenting with clinical features resembling dementia due to underlying depression
- poor memory because poor concentration with inadequate registration
- slowness, self-neglect
How to differentiate:
- mood symptoms first
- perform better on memory task when have interest
- unwilling to cooperate in tests
If uncertain: Tx depression, recheck cognition after mood improves
Ddx of psychotic symptoms in elderly
Primary psychotic disorders e.g. schizophrenia
- past hx of psychosis
Mood disorders
- mood disturbances
Dementia with psychotic features
- cognitive decline
Delirium
- sudden change in physical state
Transient global amnesia
Middle or late life
M>F
Abrupt episodes of global loss of recent memory
Alert and orientated
Complete recovery except for amnesia of the episode
Unknown cause, no specific treatment
Amnesic syndrome - definition, features, pathology, causes, course, Mx
Profound disruption of recent memory with minimal/no impairment of other cognitive functions
Features
- anterograde and retrograde amnesia – immediate recall normal but delayed few min impaired
- confabulation
- disorientation to time
- no impairment of other functions (alert, reasonable)
Pathology
- damage to hypothalamic-diencephalic system or hippocampal region
Cause:
- Most common: thiamine deficiency resulting in Wernicke’s encephalopathy (ataxia, opthlamoplegia, impaired consciousness) and then Korsakoff’s syndrome
- –> chronic alcohol use, gastric CA, severe malnutrition
- others: third ventricle tumours (diencephalic), CO poisoning (hippocampal), encephalitis (hippocampal), vascular lesions causing diencephalic or hippocampal damage, MS (diencephalic)
Course - chronic
Mx: oral thiamine if due to deficiency
