Psych: Old Age Psychiatry and Dementia Flashcards
Which patients see old age psychiatry?
any person over 65 with mental health problems referred to secondary care services
What is Charles Bonnet syndrome? What are the risk factors?
complex visual disturbances/ hallucinations a/w eye disease. Usually hallucinations of faces, children and wild animals.
RF: increasing age, M=F
what are the differences with telling whether the diagnosis is delirium or dementia?
delirium: rapid onset, fluctuating, days to weeks (can be months), altered consciousness, impaired attention, immediate recall memory impaired, hypo or hyperactive, disturbed sleep wake cycle (sundowners), usually reversible
dementia: insidious onset, progressive, months to years, clear consciousness, normal attention (unless severe), immediate recall memory usually normal, no psychomotor changes, usually normal sleep wake cycle, irreversible
Give some examples of organic and functional mental disorders/causes?
organic: normal ageing, mild cognitive impairment, Alzheimer’s, uncontrolled diabetes, vascular dementia, reduced B12/folic acid (also macrocytic anaemia sign), reduced thiamine, meds eg benzodiazepines can cause memory loss
functional: depression (pseudo-dementia)
What are the features of the MMSE?
maximum score is 30 points. a score of 20-24 suggest mild dementia, 13-20 suggests moderate dementia, and less than 12 indicates severe dementia
What tests are done in screening confusion (to rule out delirium/reversible causes of confusion)?
Blood tests
o FBC (infection, anaemia [confusion], malignancy)
o U&Es (hyponatraemia [confusion], hypernatraemia)
o LFTs (liver failure with secondary encephalopathy)
o Coagulation/INR (intracranial bleeding)
o TFTs (hypothyroidism [depression & similar presentation])
o Calcium (hypercalcaemia)
o B12 + folate/haematinics (B12/folate deficiency [cognition problems])
o Glucose (hypoglycaemia /hyperglycaemia)
o Blood cultures (sepsis)
Urinalysis
o UTI is a very common cause of delirium in the elderly
o Positive urine dipstick without clinical signs is not satisfactory
o Look for other evidence (increase WCC, suprapubic tenderness, dysuria, offensive urine, positive urine culture
Imaging
o CT head – concern about intracranial pathology (bleeding, ischaemic stroke, abscess)
o Chest x-ray – may be performed if there is concern about lung pathology e.g. pneumonia, pulmonary oedema)
ECG required for some dementia meds
What is the definition of delirium?
acute, transient and reversible state of confusion, usually the result of other organic processes eg infection, drugs, dehydration
What are the 2 types of delirium?
hyperactive - typical: agitation, delusions, hallucinations, wandering, aggression
hypoactive - atypical and often missed or confused with depression; lethargy, slowness, excessive sleeping, inattention
what are the causes of delirium?
CHIMPSPHONED
C - constipation
H – hypoxia/hydration
I – infection
M – metabolic disturbance inc dehydration
P - pain
S - sleeplessness
P – prescriptions/polypharmacy
H – hypothermia/pyrexia
O - organ dysfunction
N - nutrition
E - environmental changes* - inc. emotions/depression/anxiety
D - drugs (over the counter, illicit, alcohol and smoking)
What is the first line diagnostic tool in delirium?
SQID: single question in delirium (SQID)
more confused than normal? yes or no
positive > collateral history
After history and cognitive assessment of suspected delirium, a thorough clinical exam should be performed including what?
- Vital signs (fever if infection, low SpO2 in pneumonia)
- Level of consciousness (GCA/AVPU) – clouding of consciousness often present in delirium
- Evidence of head trauma
- Sources of infection
- Asterixis (uraemia/encephalopathy)
- Confusion screen (bloods, urinalysis, imaging)
what is the definitive, supportive and medical management of delirium?
Definitive: Identify and treat the underlying cause
Supportive
* Consistent care team, ensure access to aids, glasses, hearing and walking sticks, Enable independent activity where possible
* Access to a clock and other orientation reminders, have familiar objects (e.g. photos/clothes), involve friends and family, control surrounding noise, adequate lighting and temperature
Medication
* Avoid unnecessary medications where possible, can worsen delirium
* Wandering is not absolute indication for sedation
* Lorazepam is the first line benzo (0.5mg starting dose – 1mg) due to its rapid onset and short half life
o MAX DOSE is 2mg in 24 hours
* If already on benzos or at risk of respiratory depression then haloperidol is first line option (at a low dose in the elderly – 0.5mg)
o Contraindicated in parkinsons, dementia with LB or prolonged Qtc
What is the prognosis of delirium and what is the prevention?
post discharge: behaviours can continue for up to 6 months after the cause has been treated - make family and carers aware
prevention: avoid drugs known to preciptate delirium (opiates and benzos), identify patients at high risk and observe for early signs, assess pain control and drugs, employ supportive and environmental management approaches for all patients, regardless of delirium risk
Is dementia a normal part of ageing? What is the criteria to be classed as dementia? What is dementia associated with (biologically)?
it is NOT a normal part of ageing
must be of at least 6 months duration and affect activities of daily living
associated with decreased amount of acetlycholine in the brain
What is the rule of 1/3 of cognitive impairment with dementia patients?
1/3 get better
1/3 stay the same
1/3 develop dementia
What are the 5 A’s of dementia?
amnesia - memory impairment
agnosia - recognition
apraxia - motor skills eg dressing
aphasia / agnosia - speech and language
associated behaviours - BPSDs
What s the role of the temporal lobe?
hearing
language comprehension (wernicke’s area)
memory / information retrieval
facial recognition
feelings
What is the role of the frontal lobe?
motor control (premotor cortex)
problem solving (prefrontal area)
speech production (broccas area)
thinking, planning, emotions, behavioural control, decision making
What is the role of the parietal lobe?
body orientation / sensory discrimination / visuospacial
touch perception (somatosensory cortex)
In which dementia are BPSDs most common?
fronto-temporal dementia
can occur in all dementia subtypes but don’t occur in everyone
How do you tell the difference between delirium and BPSDs?
differentiate with timeline (acute vs progressive) and baseline level with a collateral history
what are the behavioural and psychological symptoms of BPSDs?
behavioural:
Wandering
Restlessness
Pacing
Agitation
Disinhibition
Screaming
Physical aggression
Swearing
Apathy
Repetitive
psychological:
Anxiety
Misidentification
Depressed
Insomnia
Delusions (depth perception issues, forget where they place things and think people are “stealing” from them)
Hallucinations
What are the causes of BPSDs?
PINCH ME
Pain
INfection
Constipation
Hydration
Medication
Environmental
How do you assess BPSDs?
Behavioural assessment –ABC
o Antecedents – what happened before?
o Behaviour – what was the behaviour?
o Consequences – what was the consequence?
Physical assessment - e.g. are they in pain?
Mental state assessment to consider alternative causes and treatments – e.g. depression or sleep disturbance
Collateral history
Look at the mnemonic PHONED as a guide for assessing causes of symptoms in people with dementia
Refer if necessary to Medicine for the Elderly or Old Age Psychiatry
What are the differentials of BPSDs?
BIO: pain, delirium, constipation, dehydration, stroke etc.
PSYCHO: depression, anxiety, deterioration of dementia
SOCIAL: links to environmental changes, approach of staff
What is the management of BPSDs?
Treat the cause
If necessary refer to medics
Environmental modification and practical management (e.g. education for family / staff)
Medication as a last resort
Memantine
o Antipsychotics
Only Risperidone is licensed for management of agitation
Side effects are greater in older people
Avoid using it if possible due to the associated risks:
Parkinsonism
Falls
Stroke risk (2-3 times baseline risk)
Cardiovascular risks
Death
If it is used then the lowest possible dose should be prescribed for a time limited period
Often inappropriately prescribed to ‘control’ BPSD
What are the differentials of dementia?
D – drugs, delirium – drugs causing confusion e.g. opitates/steroids
E – emotions/depression – mood causing them to be slow/deteriorate
M - metabolic disorders - U&E, infections etc
E - eye and ear imparitment – affect concentration and ability to retain information
N - nutritional disorders - underweight
T - tumours, toxins, trauma – brain tumors or anything poisoning them
I - infections - delirium (can be superimposed on dementia so treat delirium and see if dementia persists)
A - alcohol, arteriosclerosis
In what circumstance can you not diagnose dementia?
CANNOT diagnose dementia on top of depression > treat the depression first
What is the ICD-10 definition of dementia?
It is a syndrome due to disease of the brain, usually of a chronic or progressive nature. There is a disturbance of multiple higher cortical functions, including a decline in memory and learning new information. No clouding of consciousness.
It is also accompanied by deterioration in judgment and thinking, processing of new information, emotional control, social behaviour or motivation. For more than 6 months
What does ICD-10 class as mild, moderate and severe dementia?
mild: memory loss is sufficient to interfere with everyday activities but they are able to live independently
moderate: memory loss is a seriosu handicap to independent living and only highly learned or very familiar material is retained. They are unable to function without the assistance of another in daily living.
severe: there is a complete inability to retain new information. There is a virtual absence of intelligible ideation. The mind can no longer tell the body what to do.
What is the most common type of dementia?
Alzheimer’s
What is the pathophysiology of Alzheimer’s? What are the 4 pathologies?
Progressive degeneration of the cerebral cortex (widespread cortical atrophy)
Affected neurons contain amyloid plaques, neurofibrillary tangles (tau) & produce less acetylcholine
1. amyloid plaques
2. cerebral atrophy - most pronounced in the medial temporal lobes (hippocampus is here which is responsible for memory)
3. neurofibrillary tangles
4. reduced levels of acetylcholine
What are the RFs of Alzheimer’s?
Age! W>M
Genetics:
ApoE is a gene related to late-onset Alzheimer’s
APP (amyloid precursor protein): found on chromosome 21 (3 of them in Downs Syndrome) – APP produces amyloid plaques which is a feature of AD. Increased plaques = increased risk of AD
Modifiable: social isolation, risk-factors associated with vascular disease (smoking/alcohol, hypercholesterolaemia, HTN, obesity & diabetes), head injury
What is the overall feature of Alzheimer’s?
insidious and gradual onset with progressive cognitive decline
what are the early features of Alzheimer’s?
memory loss, leading to confusion
e.g. forgetting names of people & places, difficulty finding the words for things, getting lost mid-sentence, inability to remember recent events, getting lost, misplacing things, forgetting appointments
what are the intermediate features of Alzheimer’s?
Difficulties with language (struggling to follow a conversation or repeating themselves)
Visuospacial skills – problems judging distance, stairs, parking, 3D
Apraxia (the inability to perform learned movements) – need to be given step by step instructions
Problems with planning & decision making
Orientation – confused or losing track of the day or date
What are the features of Alzheimer’s in the later stages?
Psychiatric: depression, hallucinations, delusions, insomnia
Behavioural: disinhibition, aggression, agitation, irritable
Wandering & disorientation
Less aware of what is happening around them
Apathy
Altered eating habits, difficulty with walking, increasing frailty
Urinary incontinence
Expressive dysphasia
What are the pathological findings of Alzheimer’s?
- Cerebral atrophy on MRI – most pronounced in the medial parietal temporal lobe (predominantly involves in memory)
- Vascular ischaemic changes
- Widened sulci and dilated ventricles on CT/MRI
- Senile/amyloid plaques deposition. Extraneuronal deposits of amyloid beta protein. Plaques cause inflammation cell death
- Neuro-fibrillay tangles. Intraneuronal hyperphosphorylated tau protein, disrupts cell functions
- Acetylcholine levels reduced (loss of cholinergic neurons
What are the investigations of Alzheimer’s?
- Comprehensive history & physical exam:
- Medication review: are there any contributing factors?
- Formal screen for cognitive impairment: e.g. MMSE/ GPCOG – neuropsychodynamic test can be done by psychologist if borderline score on the ACE
- Exclude reversible organic causes: rule out infection (urine dip, inflammatory markers, FBC), metabolic (TFT, U+Es, calcium)
- Consider MRI, cultures, CXR
- Very important to identify depression!!
What are the NICE general managements?
Offer a ‘range of activities to promote wellbeing that are tailored to the person’s preference’ – e.g. group cognitive stimulation therapy for those with mild & moderate dementia. E.g. + Group reminiscence therapy
Emotional and carer support
Familiatiry – photos in room same carers etc
Calm, well lit environment,
Communicate calmly and clearly
DO - talk slowly, ask short questions, stay calm
DO NOT - take offence, blame, argue etc.
What is the medical management of Alzheimer’s?
mild-moderate: Acetylcholinesterase inh eg donezepil, rivastigmine or galantamine
moderate-severe: memantine (NMDA) > added on top of donezepil when symptoms worsen
What are the side effects of acetycholinesterase inhibitors?
Decreases anxiety, increases motivation, concentration, ADLs
(Cholinergic side effects) Diarrhoae, incontinence, nausea, vomiting, headache, loss of appetite, dizziness, sleep disorders, GI disturbance = so start at a low dose & titrate up opposite of can’t see, pee, climb a tree
Severe side effects: Slows HR (less so for galantamine), decreases appetite, increased weight loss
What are the contraindications of acetylcholinesterase inhibitors?
heart block, bradycardia, active asthma/COPD/bronchitis (more frequent use of inhaler/beta blockers contraindicated), active peptic ulcer unless on PPI (as risk of bleeding), epilepsy (lowers seizure threshold)
When should acetylcholinesterase inhibitors be given?
Taken in the morning – not on an empty stomach (GI disturbance). May make people sleepy, in which case take it at night
What are the side effects of memantine?
Side effects (less common/severe): Dizziness, constipation, SOB, headache, sedation (taken at bed time), increased BP
Renal function needs monitoring, esp eGFR – must be >49 for more than 10mg
Can affect INR (check if on warfarin)
Which meds should be avoided in Alzheimer’s?
Avoid anti-cholinergic medications (worsen cognitive impairment) E.g. antihistamines, anti-psychotics & tolterodine
What is the second most common type of dementia in over 65s?
vascular dementia
What is the onset of vascular dementia?
sudden onset with stepwise deterioration
fluctuating day to day
What makes vascular dementia different to Alzheimer’s with regards to memory?
vascular dementia has motor and sensory defects alongside memory decline
AD is memory only
What are the RFs for vascular dementia?
high BP, smoking, coronary artery disease, hypercholesterolaemia, diabetes, strokes (lots of small events eg lacunar infarcts which accumulate to cause vascular dementia), M>W, age
What are the symptoms of vascular dementia?
problems with planning, organising, concentrating, memory, language, visuospatial skills; difficulties following steps; slower speed of thought
How do you manage the RFs of vascular dementia?
statins, antihypertensives, diabetes
What are the features of dementia with Lewy bodies?
alpha-synuclein forms into clumps inside neurons (aggregation of alpha-synuclein), starting in areas of the brain that control aspects of memory and movement
What is the triad of Lewy Body dementia?
REM sleep disorder, history of falls (secondary to motor problems) and hallucinations (often of small, non-threatening people/animals [Lilliputian hallucinations])
What are the RFs of Lewy body dementia?
few RFs other than age - no clear family history
What are the clinical features of Lewy Body dementia?
- Progressive ALZ and Parkinsons symptoms
- Early – attention/alertness issues which fluctuate throughout the day
- Visual hallucinations (2/3rds) (more than AD/VD) and delusions
- Parkinsonism (up to 70%) to differentiate between two = what came first the parkinsonism or cognitive decline
If the memory issues more than 12 months after movement issues - PDD
If memory issues within 12 months of movement issues (same sort of time) - LBD
Tactile hallucinations common/”happy” one – animals and babies etc - Risk of falls!
- Fluctuating consciousness
- REM sleep disorders
- 70% have systematised delusions, 40-50% have a depressive episode, risk of falls, syncope
- As it progresses, day-day memory, behaviour challenges and walking gets worse
What will the SPECT (DaT)/PET scan show with Lewy Body Dementia?
reduced DA (reduced striatal uptae of ligand for presynaptic dopamine transporter site in LBD but not AD)
What is the management of Lewy Body dementia?
Acetylcholinesterase & memantine are licenced (Rivastigimine) for challenging behaviours (for LBD and Parkinson’s!)
Non-drug management should be tried first – S&L therapy
Avoid antipsychotics!!! > can make parkinsonism much worse. Quetiapine sometimes used with great caution
Treatment is notoriously difficult and is a fine balance between PD and psychotic symptoms
PD and LBD are caused by low levels of DA and are treated by boosting DA - psychosis is caused by high levels of DA and is treated by reducing it
Neurological symptoms may worsen with neuroleptics
psychological interventions are vital in helping manage the condition
What is the second most common cause of dementia in those UNDER 65s (AD is first)?
frontotemporal dementia (Pick’s disease)
What are the key features of frontotemporal dementia?
Usually onset <65 years
Insidious onset
Relatively preserved memory
Personality change & social conduct issues
2-10 years prognosis
Later stages similar to later stages of Alzheimer’s dementia
what are the 3 subtypes of frontotemporal dementia?
- behavioural variant FTD (PICKS, 2/3rds) - frontal lobe involvement prominent
- progressive non-fluent aphasia (CPA) - slow and progressive (2-3 years); memory etc preserved in early stages
- semantic dementia - slow and progressive (2-3 years); memory etc preserved in early stages. peak age of onset = 55-56 years
what are the symptoms of the 3 types of frontotemporal dementia?
- behavioural:
lose their inhibitions – act in socially inappropriate ways
lose interest in people and things – lose motivation but are not sad unlike in depression
lose sympathy or empathy
show competitive, compulsive or ritualised behaviours
crave sweet or fatty foods, increased appetite, lose table etiquette – puts random objects into mouth
perseveration behaviours - progressive non-fluent aphasia (CPA)
Slow, hesitant speech
Errors in grammer
Impaired understanding of complex sentences, but not single word - semantic dementia
Asking the meaning of familiar words (e.g. what is knife?)
Trouble finding the right word
Difficulty recognising familiar people or common objects
What is the histology of frontotemporal dementia?
- Picks (20-30%) – marked transcorticol ASTROGLIOSIS, Pick cells (characteristic ballooned neurons) and Pick bodies (tau positive neuronal inclusions)
- Also atrophy of frontal and temporal lobes and neurofibrillary tangles
- Non-Picks – spongiform microvacuolation, only mild gliosis
- ‘Knife-blade atrophy’, gliosis & neuronal loss of the frontal & temporal lobes (younger indivisual so generally more accurately seen
What is the management of frontotemporal dementia?
Avoid AChE inhibitors & memantine!!
Treat the presenting symptoms, psychosocial interventions
Speech and language therapy
Some evidence in using SSRI to improve disinhibition
Risperidone is the only antipsychotic licensed for persistent aggression/distress. Use at lowest dose for shortest time (up to 6 weeks)
Supportive care + benzos + SSRIS = for agitation
What are the differences between depression and dementia?
Shorter history, rapid onset
Biologcal symptoms e.g. weight loss, sleep disturbance
Patient worried about poor memory (insight)
Mini-mental test score is variable
Global memory loss (dementia characteristically causes recent memory loss)
What is normal pressure hydrocephalus? and what is the treatment?
IE wet, wobbly and weird
A reversible cause of dementia that can be seen in predominantly elderly patients.
Due to impaired absorption of CSF at the arachnoid villi increased ICP ventriculomegaly. This can be triggered by an insult such as a bleed or head injury.
* Triad of: urinary incontinence, dementia and gait abnormality which develops over several months.
* Neuro-imaging can appear similar to Parkinson’s disease, but being unresponsive to L-DOPA can be used as a sign of normal pressure hydrocephalus.
o Enlarged ventricles with absent sulci [as they are compressed by the sulci] (PD = enlarged ventrciels and prominent sulci)
* Treatment in patients fit for surgery is ventriculo-peritoneal shunting, otherwise they may be managed with conservative treatment and repeated CSF taps.
