Psych - Dementia Flashcards
What is the most comprehensive test of cognitive function?
Addenbrooke’s Cognitive Examination
(ACE-iii or ACE-R for revised)
- Tests 5 basic executive functions
- Score out of 100
- < 82 = considered abnormal (NOT a diagnostic test)
What 5 aspects of cognition does an ACE-iii examine?
- Memory
- Attention
- Fluency
- Visuospatial skills
- Language
N.B. informally it also tests your higher executive function i.e. task planning / management - which requires the above basic executive functions.
Name 2 short/simple cognitive assessments?
-
MOCA (Montreal Cognitive Assessment)
- Score out of 30
- < 26 = suggests MCI (mild cognitive impairment)
- < 17 = suggests dementia)
- MMSE (mini mental state examination) - less used due to copyright issues
What assessment tool can be used to discriminate between dementias with impact on frontal executive function and Alzheimer’s dementia?
Frontal Assessment Battery (FAB)
- Can be used in mildly demented pts or better (MMSE > 24)
- Total score is out of 18 (higher score = better performance)
Dementia syndromes can be divided into cortical and subcortical.
To what do these regions refer to?
How are cortical and subcortical dementia characterised?
Cortical = outer layer i.e. cerebral cortex
Subcortical = areas beneath cortex e.g. basal ganglia, limbic system (amygdala, hippocampus), diencephalon (thalamus, hypothalamus)
- Cortical dementia = early symptoms include higher function difficulty e.g. memory, language, dyspraxia (visuospatial), lack extra-pyramidal features
- Subcortical dementia = early symptoms don’t tend to involve higher function, but do include; behaviour, mood/affect, motor slowing, extra-pyramidal features
Dementia syndromes can be divided into cortical and subcortical.
Give examples of each cortical and subcortical dementia.
Cortical:
- Alzheimer’s dementia
- Lewy-body dementia (memory before motor)
- Fronto-temporal dementia (Pick’s disease)
Subcortical:
- Vascular dementia
- Parkinson’s dementia (motor before memory)
- Wilson’s dementia
- Huntington’s
- HIV/AIDS dementia
- MND / MS dementia
- Alcohol related dementias
Which parts of the brain does Alzheimer’s disease characteristically affect?
- Medial temporal lobe i.e. hippocampus - impacts episodic memory (anterograde amnesia)
- Lateral temporal lobe i.e. Wernicke’s area - can cause receptive dysphasia (difficulty understnading written or spoken language but have fluent speech without meaning i.e. word salad)
- Anterior + inferior temporal lobe - impacts semantic memory (general knowledge e.g. facts, ideas, concepts)
What are the four most common types of dementia?
- Alzheimer’s disease (2/3rds of dementia)
- Vascular dementia
- Lewy Body dementia (~15% of dementia)
- Fronto temporal dementia
What investigations are reccomended for someone with suspected dementia?
-
Bloods:
- Done to exclude reversible causes
- FBC, U&E, LFTs, calcium, glucose, TFTs, vitamin B12 and folate levels
-
MRI / CT:
- Done to exclude reversible causes e.g. subdural haematoma, normal pressure hydrocephalus
What are the recommended pharmacological management steps for Alzheimer’s disease?
-
One of the 3 acetylcholinesterase (AChE) inhibitors - mild-moderate AD
-
Donepezil
- once daily, long-half life, start 5mg and ↑ to 10mg after 1 month
-
Galantamine
- Oral solution, tab and modified release cap
-
Rivastigmine (also a butyrylcholinesterase inhibitor)
- short half life (1hr), BD, daily patch more common
-
Donepezil
-
Memantine (NMDA receptor antagonist) recommended:
- Monotherapy in severe AD OR
- Moderate AD + intolerant / contraindication to AChE inhibitors OR
- In addition to AChE inhibtors for moderate-severe AD
What are the recommended pharmacological management steps for NON- Alzheimer’s disease?
Lewy-Body:
- Offer donepezil or rivastigmine
- Consider galantamine (only if donepezil or rivastigmine not tolerated)
- Consider memantine (if AChE inhibitors not tolerated/contraindicated)
- Some parkinson’s medication (e.g. levodopa) can help with movement impairment
Vascular:
- Only consider AChE inhibitors or memantine for vascular IF they have suspected comorbid AD, PD dementia or Lewy-body
Fronto-temporal dementia or MS cognitive impairment:
- DO NOT offer AChE inhibitor OR memantine
What investigations need to be done prior to starting a AChE inhibitor or NMDA receptor antagonist (memantine)?
-
ECG - to assess HR, arrhythmias and QTc interval
- AChE inhibitors are contraindicated for pts with; bradykinesia, Left Bundle Branch Block or a ↑ QTc interval
- AChE inhibitors also contraindicated if Hx of; gastric ulcers or seizures
-
U+Es:
- Memantine can cause acute renal failure
What are some common side effects of AChE inhibitors?
- Nausea / vomiting
- Diarrhoea
- Urinary incontinence
- Headache / dizziness
- Insomnia
- Muscle cramps
- ↓ Appetite –> weight loss
In addition to cognitive symptoms of dementia, what other categories of symptoms are there?
Non-cognitive i.e.
Behavioural and Psychological symptoms of dementia (BPSDs) e.g.
- Hallucinations
- Delusions
- Anxiety
- Behaviour: marked agitation, aggression, wandering, hoarding, sexual disinhibition, apathy and disruptive vocal activity such as shouting
What psychological treatments are available for the management of cognitive + BPSDs in dementia?
- Cognitive stimulation therapy (CST)
- CBT
- Reminiscence therapy
- Aromatherapy
- Sensory stimulation
- Music therapy
What pathological changes occur to a brain with Alzheimer’s?
Macroscopic:
- Widespread cerebral cortical atrophy
- Medial temporal lobe atrophy (particularly hippocampus)
- Enlarged ventricles (due to cerebral atrophy)
Microscopic:
- Beta-amyloid plaques (cortex)
- Neurofibrillary tangles (intraneuronal aggregation of tau protein)
Biochemical:
- Acetylcholine deficit (due to factors above) - loss of cholinergic neurons and ↓ ACh
Describe dementia in layman’s terms.
A chronic, often progressive, mental disorder caused by brain disease or injury and marked by:
1) memory changes
2) personality changes
3) impaired reasoning / ↓ executive function
4) Impact on ADLs
What are some risk factors for dementia?
- Age
-
Gender:
- Female (AD)
- Male (VD and DLB)
-
Ethnicity:
- South asians and Afro-Caribbean (VD)
- African (AD)
- Depression - if in mid-life or later life
- Head injuries (Parkinson’s dementia)
- Lifestyle factors: smoking, alcohol, exercise, education
How does Alzheimer’s present clinically?
- Four A’s:
- Amnesia (most common)
- Aphasia (language impairment - production or comprehension of speech)
- Agnosia (inability to process sensory info e.g. can’t recognise objects, sounds, smells, get lost etc.)
- Apraxia (motor planning impairment due to brain damage)
- Others:
- Apathy - ↓ motivation + anhedonia
- Misplace / lose items (memory or visuospatial decline)
- ↓ ADLs
- Slow progressive
- Late / early onset
What pattern of inheritance does early onset Alzheimer’s follow?
What genes are involved?
Follows autosomal dominant pattern (50% chance inheritance)
Genes:
- Chromosome 14 PSEN-1 (presenilin 1) gene
- 80% of familial AD
- Symptoms as young as 30yrs
- Chromosome 1 PSEN-2 (presenilin 2) gene
- Symptoms later than PSEN-1
- Chromosome 21 APP (amyloid precursor protein) gene
What genetic disorder conveys a high risk of also developing Alzheimer’s?
Down Syndrome (Trisomy 21)
- 3 copies of APP (amyloid precursor protein)
- 50% of Down’s syndrome people who live to 60 get AD
What are the features of dementia with Lewy-bodies?
-
Progressive cognitive impairment:
- Visuo-spatial decline, language, dyspraxia
-
Parkinsonism triad:
- Bradykinesia, rigidity, tremor
- Visual hallucinations e.g. children/little people or animals
- Autonomic dysregulation: urinary incontinence, constipation
- Sleep disturbances: nightmares, aggressive movements, disturbed sleep
- Antipsychotic sensitivity - can develop irreversible parkinsonism
Which of the following are mandatory parts of a standard dementia screening of an individual with memory loss which are essential for dementia diagnosis? (Select TWO)
- Neuropsychological assessment
- Cognitive testing
- History-taking
- SPECT scan
- Brain imaging - MRI/CT
Although all 5 are useful - these 2 are REQUIRED for dementia diagnosis:
- History taking (most important)
- Cognitive testing
- SPECT scan - type of functional neuroimaging that can help to differentiate between Alzheimer’s and Frontotemporal dementia
- MRI/CT - never diagnostic but could help to settle the diagnosis and show cerebrovascular issues
How would you summarise the treatment available for Alzheimer’s?
(think conservative and pharmacological/medical)
Conservative:
- CBT, Cognitive stimulation therapy
- Aromatherapy, music therapy, reminiscence therapy
Medical:
- AChE Inhibitors (Donepezil, Galantamine, Rivastigmine)
- NDMA receptor antagonist (Memantine)
Vascular Dementia:
- What are the risk factors?
- What is the pathophysiology?
- How would you summarise the treatment?
Risk Factors:
- AF, HTN, hyperlipidemia, smoking, diabetes (all risk factors for stroke/TIA)
Pathophysiology:
- Microvascular disease (e.g. atherosclerosis) –> thrombi / emboli –> infarcts –> neuronal death
- STEP-WISE decline
Treatment:
- Stop smoking
- Manage the same as stroke/TIA:
- Acute: aspirin (2 weeks)
- Prevention: Statin, anticoagulation, antihypertensives
What investigations would you do as part of a confusion screen?
(think: bedise, bloods, imaging)
Beside:
- Clinical history (+ collateral)
- Observations - can identify sepsis
- Physical examination e.g. abdo (suprapubic tenderness - UTI?), head trauma, alcohol withdrawel (tremor, fever, sweating)
- MSE
- Cognitive assessment
Bloods:
- FBC - ↑ WCC (infection)
- CRP - ↑ in context of infection
- U+Es - uraemia, hyponatraemia, hyper/hypocalcemia
- B12 & Folate - deficiency can cause confusion
- TFTs - confusion mor eommon in hypothyroidism
- Glucose - hypoglycaemia
- LFTs - liver failure (hepatic encephalopathy)
- Coagulation / INR - important in context of cranial bleed
Imaging:
- CT head –> MRI head
Anticholinergic drugs DECREASE the effect of AChE inhibitors.
Name some anti-cholingeric drugs.
Image shows anticholinergic burden table - mild, moderate, severe impact on ACh levels and thus their impact on ↓ AChE inhibitor efficacy.
- All antipsychotics have anticholinergic properties
- Beta-blockers + AChE-Is –> ↑ each others effects –> worsening bradycardia + syncope
- Memantine + glutamate-R antagonists (e.g. ketamine, amantadine) –> ↑ each others effects –> pharmacotoxic psychosis
Seperate the following statements by whether they are true of Alzheimers or DLB.
- More common in men
- Gradual decline in cognitive impairment
- Fluctuating cognitive impairment
- More common in women
- Physical deterioration usually at a late stage
- Decrease in facial expression develops later in disease
- Visual hallucinations occur early
- Hallucinations may occur, but in late stages
- Early problems with balance
- Face shows very little emotion from early in the disease
Alzheimers:
- More common in women
- Gradual decline in cognitive impairment
- Hallucinations may occur, but in late stages
- Physical deterioration usually at a late stage
- Decrease in facial expression develops later in disease
DLB:
- More common in men
- Fluctuating cognitive impairment
- Visual hallucinations occur early
- Early problems with balance
- Face shows very little emotion from early in the disease
What do the BMJ list as core clinical features of dementia with Lewy-bodies?
(supportative clinical features or biomarkers are less important but can add to picture)
Core clinical features: (first 3 often occur early)
- Fluctuating cognition + pronounced variability in attention/ alertness
- Visual hallucinations (typically well formed and detailed)
- REM sleep behaviour disorder (RBD - acting out dreams)
- 1 or more parkinsonism features: bradykinesia, rest tremor, rigidity
For PROBABLE DLB diagnosis, 2 or more core clinical features are needed or 1 + indicative biomarkers (see BMJ criteria - don’t need to know)
Supportive clinical features:
- Severe sensitivity to antipsychotics
- Autonomic dysfunction: constipation, orthostatic hypotension, urinary incontinence)
- Postural instability (poor balance)
- Repeated falls
- Delusions
- Depression
What is the pathology underpinning DLB?
alpha-synuclein deposits within neurons in brain
location of lewy-bodies influences symptom profile
What medication can be given to manage REM sleep behaviour disorder (RBD - can be a feature of dementia with lewy-bodies)?
Clonazepam
Benzodiazepine tranquilizer - enhances activity of GABA by binding to benzodiazepine receptor on GABAA
In patients with DLB and who have psychotic symptoms which are making the patient challenging (e.g. shouting, hitting etc) - if you choose to give an anti-psychotic, what are the best choices?
Pts with DLB or Parkinson’s dementia are at risk of antipsychotic sensitivity!!
- Quetiapine (low dose)
- Clozapine (involves a lot of monitoring - thus quetiapine is preferred)
How can you differentiate between DLB and Parkinson’s disease with dementia?
DLB:
- Dementia starts BEFORE and WITHIN 1 YEAR of the onset of PD symptoms
Parkinson’s dementia:
- Dementia starts > 1 YEAR after onset of PD symptoms
Lewy Body Disease:
- If time frame of dementia / PD symptoms is unknown then the name Lewy-Body disease might be used
What are common features of Fronto-temporal dementia
also called Pick’s disease?
- Insidious onset < 65 yrs
- Relatively preserved memory + visuospatial
-
Language issues:
- non-fluent aphasia - slow, hesitant speech, grammer errors, can’t understand complex scentences
- semantic dementia - anomia, describe items, can’t recognise familiar people
-
Personality changes:
- loss of sympathy / empathy
- change in eating habits (e.g. crave sweet or fatty food, no table manners, don’t stop eating / drinking)
-
Social / behaviour problems:
- socially disinhibited + impulsive
- apathy
- repetitive, compulsive ritualised behaviours (hoarding, repeating phrases/gestures)
What are the features (symptoms and radiological) of normal pressure hydrocephalus?
Symptoms:
- Fluctuating dementia and bradyphrenia (slowness of thought)
- Urinary incontinence
- Gait abnormality (often similar to Parkinson’s disease i.e. shuffling)
Radiological:
- Ventriculomegaly - widening of temporal horns of lateral ventricles, enlarged 4th ventricle
- Callosal angle < 90 degrees (angle between superior parts of lateral ventricles)
- Absence of substantial sulcal atrophy
- Tight high convexity - CSF spaces over convexity (superior brain) are narrowed
