Dementia Flashcards
What is dementia?
An organic syndrome characterized by the loss of cognitive functioning — thinking, remembering, and reasoning — to such an extent that it interferes with a person’s daily life
What age does dementia occur?
- <65yo = early-onset dementia
- 5-10% population over 65yo; 20% population over 80yo
- Alzheimer’s disease (70% dementia) > Vascular Dementia (VD) > Dementia with Lewy Bodies (DLB)
What are the general S/S of dementia?
1st: forgetfulness (stepwise or progressive)
2nd: disorientation (time > place > person) > management problems…
- Wandering
- Sleep-disturbance
- Delusions
- Hallucinations
- Calling out
- Inappropriate behaviour / aggression
What is BPSD?
Behavioural and Psychological Symptoms of Dementia:
(1) Mood changes
(2) Abnormal behaviour
(3) Hallucinations / delusions
What are the investigations for dementia?
Screening tools:
- Risk assess patient
- The abbreviated mental test score (AMTS)
Score <7 suggests cognitive impairment - The mini-mental state examination (MMSE)
Bloods:
- FBC
- TFTs (hypothyroid > cognitive decline)
- LFTs (Korsakoff’s)
- U&Es and dip (infection, diabetes)
- HbA1c / glucose (diabetes)
- Vitamin B12 and folate
CT/MRI:
- AD: Generalised atrophy
- VD: Multiple luciencies
- DLB: Mild atrophy
- FT: Frontal lobe shrinkage
Memory Assessment Clinic referral (after GP):
What is AD?
A progressive degenerative disease of the brain accounting for the majority of dementia seen in the UK (70%)
- Onset usually after 65yrs
- Relentlessly progressive
- Early onset > more rapid progression
What are the RFs for AD?
Biological:
- AGE
- Genetics - APEN, APP, ApoE, etc
- FHx of AD
- Caucasian ethnicity
- Head injury
- Vascular RFs e.g. HTN
- Down Syndrome associated with EOS
Psychosocial:
- Low IQ
- Poor education level
What are the pathological changes that occur in AD?
Macroscopic:
- Widespread cerebral atrophy, particularly involving the cortex and hippocampus
Microscopic:
- Cortical plaques due to deposition of type A-Beta-amyloid protein
- Intraneuronal neurofibrillary tangles caused by abnormal aggregation of the tau protein
- Hyperphosphorylation of the tau protein
Biochemical:
- There is a deficit of acetylcholine from damage to an ascending forebrain projection
What are the S/S of AD?
“The Four A’s”
- Amnesia - recent memories lost first; disorientation occurs early
- Aphasia - in finding correct words (Broca’s), speech muddled/disjointed
- Agnosia - typically “Visual” (i.e. prosopagnosia – cant recognise faces)
- Apraxia - tpically “Dressing” (skilled tasks, despite normal motor functioning)
BPSD
Psychiatric presentations
- Delusions (15%)
- Depression (20%)
- GAD
Behavioural disturbances
- Aggression, explosive temper
- Wandering
- Sexual disinhibition
What is the management of AD?
BIOPSYCHOSOCIAL APPROACH
Pharmacological:
- 1st line (mild to moderate): Cholinesterase inhibitors
e.g. Donepezil, Galantamine, Rivastigmine - 2nd line (moderate or 1st line in severe): NMDA antagonist
e.g. Memantine
Psychological:
- 1st line: Structural group cognitive stimulation sessions (mild to moderate AD)
- Exclude depression or GAD
- NICE recommend offering ‘a range of activities to promote wellbeing that are tailored to the person’s preference’
- Other: group reminiscence therapy, validation (reassure) therapy, multisensory therapy (improve other senses)
Social:
- Explain diagnosis and signpost support
- Optimise health in other areas (i.e. hearing aids, glasses)
- Personal care support, meal support, day centre availability
- Identify future wishes (i.e. advanced directives, lasting power of attorney)
FOLLOW-UP
- Every 6 months with yourself and a single named care manager (with a clearly defined care plan)
Also
- GENERAL: always wear ID, Dossett boxes, change gas to electricity, assistive technology in the house
- CARERS: identify and support any carers involved (signpost information and support; carer’s assessment)
- Legally required to inform DVLA and insurers (if diagnosed with any form of dementia; MCI does not need to inform DVLA)
- Outcome > renew licence each year, revoked licence, maintain licence
What needs to be checked when using cholinesterase inhibitors?
(Raise the ACh available)
Check:
- 1st > ECG
- Side effects – GI (N&V, diarrhoea, anorexia), other (fatigue, dizziness, headache)
What are contraindications to using AChI’s?
- Absolute contraindications – anticholinergics (block ACh from binding), beta-blockers, NSAIDs, muscle relaxants
- Relative contraindications – asthma, COPD, GI disease, bradycardia, sick sinus syndrome, AV block
What is vascular dementia?
Second most common form of dementia after AD.
It is not a single disease but a group of syndromes of cognitive impairment caused by different mechanisms causing ischaemia or haemorrhage secondary to cerebrovascular disease.
What is the aetiology of vascular dementia?
- Infarcts caused by thromboemboli
- Narrowing of arteries due to HTN
What is the epidemiology of vascular dementia?
- Prevalence of dementia following a first stroke varies depending on location and size of the infarct, interval after stroke, age etc
- Overall, stroke doubles the risk of developing dementia
- Incidence increases with age
What are the RFs for vascular dementia?
(CVD RFs):
- Age
- Male
- Obesity / lack of exercise
- Smoking
- AF
- DM
- HTN
- CVA history (stroke, TIA)
- Hyperlipidaemia
What are the main subtypes of VD?
Stroke-related VD – multi-infarct or single-infarct dementia
Subcortical VD – caused by small vessel disease
Mixed dementia – the presence of both VD and Alzheimer’s disease
What are the S/S of VD?
Patients typically present with several months/years hx of sudden or stepwise deterioration of cognitive function (may follow CVA)
- 1st: emotional and minor personality changes (labile emotion – tearful > elation)
- 2nd: cognitive deficit
Focal neurological signs
- Visual / sensory / motor disturbance
- (S/S reflect site of infarct) – i.e. upgoing plantars, some reserved cognition
Also:
- Co-morbid depression
- Difficulty with attention and concentration
- Seizures
- Memory disturbance
- Gait disturbance
- Speech disturbance
What is the management of VD?
Treatment is mainly symptomatic with the aim to address individual problems and provide support to the patient and carers
Biological:
- Daily aspirin (if indicated due to CVA/AF risk)
- Reduce risk factors (exercise, less alcohol, treat HTN, stop smoking, treat AF, control DM)
- Only consider AChE inhibitors or memantine for people with vascular dementia if they have suspected comorbid Alzheimer’s disease, Parkinson’s disease dementia or dementia with Lewy bodies.
Psychosocial:
- Same as per AD
- Tailored to the individual
- Include: cognitive stimulation programmes, multisensory stimulation, music and art therapy, animal-assisted therapy
- Managing challenging behaviours e.g. address pain, avoid overcrowding, clear communication
What is DLB?
The characteristic pathological feature is alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas.
What is the aetiology of DLB?
- Lewy Bodies (LB) = a-synuclein with ubiquitin
- Spectrum of diseases including Lewy Bodies = DLB …all the way to… Parkinson’s disease (PD)
- In PD, LB are found in the brainstem;
- In DLB, LB are found in the brainstem, cingulate gyrus and neocortex
What are the S/S of DLB?
(≥2 of 3) – general gradual decline:
- Fluctuating confusion with marked variations in alertness levels - may resemble delirium > I.E. has some lucid intervals (unlike other dementias)
- Vivid visual hallucinations (Lilliputian hallucinations) – animals or humans
- Parkinsonism (shuffling gait, bradykinesia, rigidity, amimia – n.b. anosmia is an early sign of PD)
- Frequent falls
- (Co-morbid depression)
- “Hallucinations and slow movements”
PD= parkinsonism > dementia
DLB = dementia > parkinsonism
What is the management of DLB?
Biological:
- 1st line: acetylcholinesterase inhibitors (Donepezil or Rivastigmine)
- Do not offer antipsychotics (increased risk of cerebrovascular disease)
Psychosocial:
- Same as per AD
What is the aetiology of front-temporal dementia?
Atrophy of fronto-temporal regions
- Early onset (20% pre-senile cases) – 40 to 60yo
- 60% sporadic; 40% autosomal inheritance
- “Early-onset dementia > child-like behaviour”
What are the S/S of front-temporal dementia?
3 clinical presentations:
- (1) Frontotemporal dementia > frontal lobe syndrome (disinhibition, social/personality changes)
- (2) Semantic dementia > progressive loss of understanding of verbal and visual meaning
- (3) Progressive non-fluent aphasia > 1st: naming difficulties; 2nd: mutism
Memory tends to be affected much later (unlike in AD where it may be the first thing to be affected)
What is the pathology of front-temporal dementia?
Two pathologies with no correlation to clinical presentations:
- (1) Tau positive – “Pick’s” bodies (hyperphosphorylated tau) = Pick’s disease (3R), CBD (4R), PSP (4R)
- (2) Tau negative – no Tau = FTLD-U (Frontotemporal Lobar Dementia with Ubiquinated inclusions)
What is the management of front-temporal dementia?
Biological:
- Antidepressants (treat frontal lobe syndrome)
Psychosocial:
- Same as per AD
- OT, SALT, physiotherapy
What is the prognosis of front-temporal dementia?
Death in 5-10 years
What factors favour delirium over dementia?
- impairment of consciousness
- fluctuation of symptoms: worse at night, periods of normality
- abnormal perception (e.g. illusions and hallucinations)
- agitation, fear
- Delusions
What is the DSM-V definition of delirium?
- A. disturbance in attention and awareness
- B. disturbance develops over a short period of time (hours to days), represents a change from baseline attention and awareness and tends to fluctuate in severity during the course of the day
- C. an additional disturbance in cognition
- D. disturbances in Criteria A and C are not better explained by another condition
- E. evidence from the history, physical examination or laboratory findings that the disturbance is a direct physiological consequence of another medical condition, substance intoxication or withdrawal
I.E. quick onset, fluctuant, disorientated
What is the epidemiology of delirium?
- On admission - 10-30% of acute adult inpatients aged 65+
- After admission - up to 30% new onset on acute wards, 80% ICU
- Care homes - 20%
- 50% never recognised
What is the aetiology of delirium?
- Infection (UTI, RTI)
- Change in environment
- Medication (anti-ACh, steroids, opiates) memantine (think in AD), steroids
- Alcohol withdrawal
- Surgery
- Pain
- Liver/renal impairment
- Hypoxia
- Hyponatraemia
- Stroke
- Encephalitis
- Constipation
- Urine retention
- Dehydration
What are 2 assessment tools for delirium?
Confusion Assessment Method (CAM):
Delirium requires…
- Feature 1 PLUS feature 2 PLUS feature 3 OR 4
4AT
- Rapid clinical test for delirium
- > 4 suggests delirium
What is the management of delirium?
General
- ADMIT (fluctuating)
- Treat the cause
- Manage aggravating factors (e.g. pain, dehydration, constipation)
- Stop unnecessary medications
Behavioural Management
- Frequent reorientation (e.g. clocks, calendars, verbal reminders)
- Good lighting (gloomy conditions increase risk of hallucinations/illusions)
- Address sensory problems (e.g. hearing aids, glasses)
- Avoid over- or under-stimulation (side room if the main ward is disruptive)
- Minimise change (don’t keep moving the patient, one staff member to engage with the patient each shift)
- Establish a routine (regular toileting and sleep hygiene)
- Remove things that can be thrown or tripped over
- Silence unnecessary noises (e.g. bleeping alarms)
- Allow safe or supervised wandering
Medication
- Small night-time dose of BZN could promote sleep
- If short-term sedation is needed, low-dose typical antipsychotics (e.g. haloperidol) or benzodiazepines can be used
What is delirium associated with causing?
- Increased mortality
- Longer admissions
- Higher readmissions rates
- Subsequent nursing home placement
May take days to weeks to resolve
Some patients do not return to pre-morbid levels
How is delirium prevented?
- Good sleep hygiene without medication
- Minimal moves around hospital
- Encouraging mobility
- Proactive management (minimise dehydration, pain, constipation, urinary retention and sensory problems)
What is the management of normal pressure hydrocephalus?
A ventriculo-peritoneal shunt is first line, to allow CSF drainage into the peritoneal
What is the management of psychosis in the elderly?
- Reduction of sensory impairment
- Exclusion of organic cause or LBD
- Low-dose antipsychotics
How is the MMSE interpreted?
> Any score > 24/30 is considered normal
Cognitive Impairment
- Mild: 18-23 - May require some supervision, support or assistance
- Moderate: 10-17 - Clear impairment, may require 24-hour supervision
- Severe: 0-9 - Marked impairment, likely to require 24-hour supervision and assistance with ADLs
> The raw score may need to be corrected based on educational attainment and age
> Note: patients with depression may often answer with ‘I don’t know’ whereas patients with dementia will attempt to answer all questions
What is Wernicke’s encephalopathy?
A neurological condition due to longstanding thiamine (vitamin B1) deficiency, commonly due to chronic alcohol abuse or malnutrition.
How does Wernicke’s encephalopathy present?
It manifests as the triad of:
- Confusion
- Ataxia (e.g. broad-based gait)
- Oculomotor dysfunction (e.g. CN 6 palsies and nystagmus)
What is a complication of Wernicke’s encephalopathy
Korsakoff’s syndrome
- Manifests as anterograde and retrograde amnesia as well as confabulation (patient unconsciously makes up stories to fill a gap in their memory)
How is someone with AD described compared to VD?
- In AD … “mum just isn’t herself anymore”
- In VD … “mum is a little different and is using her left arm much less”
What are people with DLB at risk of?
High risk of falls due to fluctuating autonomic instability e.g. fluctuating BP
Can you give FGAs in DLB?
Not advised as can severely worsen symptoms
