Older Persons Mental Health Flashcards
Delirium/acute confusional state: Predisposing factors and precipitating events
Predisposing factors include:
age > 65 years
background of dementia
significant injury e.g. hip fracture
frailty or multimorbidity
polypharmacy
The precipitating events are often multifactorial and may include:
infection: particularly urinary tract infections
metabolic: e.g. hypercalcaemia, hypoglycaemia, hyperglycaemia, dehydration
change of environment
any significant cardiovascular, respiratory, neurological or endocrine condition
severe pain
alcohol withdrawal
constipation
Presentation of delirium?
memory disturbances (loss of short term > long term)
may be very agitated or withdrawn
disorientation
mood change/personality changes
visual hallucinations
disturbed sleep cycle
poor attention
Causes of acute confusional state - DELERIUMS
D - Drugs and Alcohol (Anti-cholinergics, opiates, anti-convulsants, recreational)
E - Eyes, ears and emotional
L - Low Output state (MI, ARDS, PE, CHF, COPD)
I - Infection
R - Retention (of urine or stool)
I - Ictal
U - Under-hydration/Under-nutrition
M - Metabolic (Electrolyte imbalance, thyroid, wernickes
(S) - Subdural, Sleep deprivation
Delirium management
Optimise environment:
Provide a calm, quiet environment.
Keep inside lighting appropriate for the time of day.
Plan for uninterrupted periods of sleep at night.
Help the person keep a regular daytime schedule.
Encourage self-care and activity during the day.
TREATMENT OF UNDERLYING CAUSE
the 2010 NICE delirium guidelines advocate the use of haloperidol or olanzapine
Minimise risk of self harm or harm to others with appropariate supervision (1:1, 2:1)
Delerium management specifically in Parkinsons
management can be challenging in patients with Parkinson’s disease, as antipsychotics can often worsen Parkinsonian symptoms
careful reduction of the Parkinson medication may be helpful
use lorazepam rather than haloperidol
if symptoms require urgent treatment then the atypical antipsychotics quetiapine and clozapine are preferred
DSM 5 criteria for delerium
- Due to another medical condition
- Substance intoxication
- Substance withdrawal
- Delirium due to multiple eiteologies
- Medication related
Further specifiers:
Time: Acute - hours/days Persistent: weeks/months
Level of activity:
Hyperactive (increased psychomotor activity - e.g. myocolonus)
Hypoactive (psychomotor retardation)
Mixed (fluctuations between both
Highest prevelance of delirium
In increasing order:
Post repair of fractured hip
Post CABG
Nursing homes
ICU elderly
Terminally ill patients
Clinical course of delerium
Abrupt of acute onset - within days
Fluctuation in symptom severity:
Waxinag and waning, worse at night, may result in diagnostic uncertainty
Clinical course of delirium
Abrupt of acute onset - within days
Fluctuation in symptom severity:
Waxinag and waning, worse at night, may result in diagnostic uncertainty
Symptoms of hyperactive delrium?
Acting disorientated
Anxiety
Hallucinations
Rambling
Rapid changes in emotion
Restlessness
Cognitive defects
Symptoms of hyperactive delirium?
Acting disorientated
Anxiety
Hallucinations
Rambling
Rapid changes in emotion
Restlessness
Cognitive defects
Symptoms of hypoactive delirium?
Apathy
Decreased responsiveness
Flat affect
Laziness
Withdrawal
Cognitive defects
Delirium vs depression vs dementia
Delerium: abrupt, fluctuating, hours to weeks, alertness increased or decreased, activity increased or decreased, attention impaired, orientation impaired
Dementia: slow and incidious, usually stable daily course, lasts years, clear conciousnes, alertness normal, acitivty variable, attention usually normal and orientation is impaired
Depression: Variable onset, stable daily course, variable length, conciousness is clear, alertness normal, acitvity is variable, attention is usually normal, orientation is normal
How might you investigate an acute confusion?
Capillary Blood Glucose
CT head
FBC
LFT
TSH, B12, Folate
RPR
ABG
Levels of any drugs if appropriate (e.g. digoxin)
Urine dip +/- culture
MRI brain (focal neyroloigcal signs, head trauma, no clear cause found)
ECG
EEG (usually generalised slowing, low voltage fast activity in alcohol or sedative hypotonic withdrawal)
Cardiac enzymes
HIV
CXR
ANA RF CRP
Donepezil adverse effects?
is relatively contraindicated in patients with bradycardia
adverse effects include insomnia
Management of the non-cognitive symptoms of dementia?
NICE does not recommend antidepressants for mild to moderate depression in patients with dementia
antipsychotics should only be used for patients at risk of harming themselves or others, or when the agitation, hallucinations or delusions are causing them severe distress
Pharmacological management of Alzheimer’s disease?
First line: acetylcholinesterase inhibitors (donepezil, galantamine and rivastigmine) as options for managing mild to moderate Alzheimer’s disease
Second line: memantine (an NMDA receptor antagonist) - reserved for
- Pts with moderate Alzheimer’s who are intolerant of, or have a contraindication to, acetylcholinesterase inhibitors
- as an add-on drug to acetylcholinesterase inhibitors for patients with moderate or severe Alzheimer’s
- monotherapy in severe Alzheimer’s
Non-pharmacological management of Alzheimer’s disease
NICE recommend offering ‘a range of activities to promote wellbeing that are tailored to the person’s preference’
NICE recommend offering group cognitive stimulation therapy for patients with mild and moderate dementia
other options to consider include group reminiscence therapy and cognitive rehabilitation
What is Alzehimer’s disease?
Alzheimer’s disease is degenerative condition of the brain that leads to memory loss and ultimately global impairment of brain function.
Most common form of dementia
Risk factors for development of Alzheimer’s disease?
increasing age
family history of Alzheimer’s disease
(5% of cases are inherited as an autosomal dominant trait)
mutations in the amyloid precursor protein (chromosome 21), presenilin 1 (chromosome 14) and presenilin 2 (chromosome 1) genes are thought to cause the inherited form
apoprotein E allele E4 - encodes a cholesterol transport protein
Caucasian ethnicity
Down’s syndrome
Macroscopic pathological changes in Alzheimer’s?
widespread cerebral atrophy, particularly involving the cortex and hippocampus
Microscopic pathological changes in Alzheimer’s?
cortical plaques due to deposition of type A-Beta-amyloid protein and intraneuronal neurofibrillary tangles caused by abnormal aggregation of the tau protein
hyperphosphorylation of the tau protein has been linked to AD
Biochemical pathological changes in Alzheimer’s?
there is a deficit of acetylcholine from damage to an ascending forebrain projection
Neurofibrillary tangles in AD
- paired helical filaments are partly made from a protein called tau
- tau is a protein that interacts with tubulin to stabilize microtubules and promote tubulin assembly into microtubules
- in AD are tau proteins are excessively phosphorylated, impairing its function
‘4 A’s of Alzheimer’s disease’
Amnesia (recent memories lost first)
Aphasia (word-finding problems, speech muddled and disjointed)
Agnosia (recognition problems)
Apraxia (inability to carry out skilled tasks despite normal motor function)
Factors favouring 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
Dementia screening tools?
NICE recommend:
10-point cognitive screener (10-CS)
6-Item cognitive impairment test (6CIT)
The following are often used but not recommended by NICE in the non-specialist setting:
the abbreviated mental test score (AMTS), MOCA, ACE3, General practitioner assessment of cognition (GPCOG) and the mini-mental state examination (MMSE)
A MMSE score of 24 or less out of 30 suggests dementia
Investigating ?dementia
PRIMARY CARE - a blood screen is usually sent to exclude reversible causes (e.g. Hypothyroidism). NICE recommend the following tests: FBC, U&E, LFTs, calcium, glucose, ESR/CRP, TFTs, vitamin B12 and folate levels.
Patients are now commonly referred on to old-age psychiatrists (sometimes working in ‘memory clinics’).
SECONDARY CARE - neuroimaging is performed* to exclude other reversible conditions (e.g. Subdural haematoma, normal pressure hydrocephalus) and help provide information on aetiology to guide prognosis and management
Most common causes of dementia?
Alzheimer’s disease
cerebrovascular disease: multi-infarct dementia (c. 10-20%)
Lewy body dementia (c. 10-20%)
Rare causes of dementia?
Huntington’s
CJD
Pick’s disease (atrophy of frontal and temporal lobes)
HIV (50% of AIDS patients)
Important differentials for dementia?
hypothyroidism, Addison’s
B12/folate/thiamine deficiency
syphilis
brain tumour
normal pressure hydrocephalus
subdural haematoma
depression
chronic drug use e.g. Alcohol, barbiturates
What is Frontal Lobal degeneration? What are the three recognised types?
Frontotemporal lobar degeneration (FTLD) is the third most common type of cortical dementia after Alzheimer’s and Lewy body dementia.
There are three recognised types of FTLD:
Frontotemporal dementia (Pick’s disease)
Progressive non fluent aphasia (chronic progressive aphasia, CPA)
Semantic dementia
Common features of frontal lobal dementia
Onset before 65
Insidious onset
Relatively preserved memory and visuospatial skills
Personality change and social conduct problems
Pick’s disease clinical features including macroscopic and microscopic changes
This is the most common type and is characterised by personality change and impaired social conduct. Other common features include hyperorality, disinhibition, increased appetite, and perseveration behaviours.
Focal gyral atrophy with a knife-blade appearance is characteristic of Pick’s disease.
Macroscopic changes seen in Pick’s disease include:-
Atrophy of the frontal and temporal lobes
Microscopic changes include:-
Pick bodies - spherical aggregations of tau protein (silver-staining)
Gliosis
Neurofibrillary tangles
Senile plaques
What is CPA (chronic progressive aphasia)?
A recognized type of Frontotemporal lobar degeneration
Chief factor is non fluent speech.
They make short utterances that are agrammatic.
Comprehension is relatively preserved.
What is Semantic dementia?
A recognized type of Frontotemporal lobar degeneration
Here the patient has a fluent progressive aphasia.
The speech is fluent but empty and conveys little meaning.
Unlike in Alzheimer’s memory is better for recent rather than remote events.
NICE recommendations re:pharmacological management of frontal-lobal dementia?
NICE do not recommend that AChE inhibitors or memantine are used in people with frontotemporal dementia
What is Lewy-Body Dementia and what is the characteristic pathological feature?
Lewy body dementia is an increasingly recognised cause of dementia, accounting for up to 20% of cases.
The characteristic pathological feature is alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas.
What conditions is Lewy Body dementia associated with?
The relationship between Parkinson’s disease and Lewy body dementia is complicated, particularly as dementia is often seen in Parkinson’s disease. Also, up to 40% of patients with Alzheimer’s have Lewy bodies.
Features of Lewy Body dementia?
- progressive cognitive impairment
- in contrast to Alzheimer’s, early impairments in attention and executive function rather than just memory loss
- cognition may be fluctuating, in contrast to other forms of dementia
- usually develops before parkinsonism
- parkinsonism
- visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen)
Diagnosis of Lewy Body dementia?
usually clinical
single-photon emission computed tomography (SPECT) is increasingly used (dopamine uptake scanning)
What drugs can be used to manage lewy body dementia?
both acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine can be used as they are in Alzheimer’s.
What drugs should be avoided in patients with Lewy Body dementia and why?
neuroleptics should be avoided in Lewy body dementia as patients are extremely sensitive and may develop irreversible parkinsonism
Three core features of Lewy Body Dementia?
Fluctuating cognition
Parkinsonism
Visual hallucinations
What is vascular dementia?
Vascular dementia (VD) is the second most common form of dementia after Alzheimer disease. 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. Vascular dementia has been increasingly recognised as the most severe form of the spectrum of deficits encompassed by the term vascular cognitive impairment (VCI)
What are the main subtypes of vascular dementia?
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
Vascular dementia: risk factors
History of stroke or transient ischaemic attack (TIA)
Atrial fibrillation
Hypertension
Diabetes mellitus
Hyperlipidaemia
Smoking
Obesity
Coronary heart disease
A family history of stroke or cardiovascular
Rarely, VD can be inherited as in the case of CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.
How does vascular dementia present?
Several months or several years of a history of a sudden or stepwise deterioration of cognitive function.
Symptoms and the speed of progression vary but may include:
Focal neurological abnormalities e.g. visual disturbance, sensory or motor symptoms
The difficulty with attention and concentration
Seizures
Memory disturbance
Gait disturbance
Speech disturbance
Emotional disturbance
How is vascular dementia diagnosed?
A comprehensive history and physical examination
Formal screen for cognitive impairment
Medical review to exclude medication cause of cognitive decline
MRI scan – may show infarcts and extensive white matter changes, can show evidence of significant small vessel disease
NICE recommends that diagnosis be made using the NINDS-AIREN criteria for probable vascular dementia
NINDS-AIREN criteria for probable vascular dementia
Presence of cognitive decline that interferes with activities of daily living, not due to secondary effects of the cerebrovascular event
- established using clinical examination and neuropsychological testing
Cerebrovascular disease
- defined by neurological signs and/or brain imaging
A relationship between the above two disorders inferred by:
- the onset of dementia within THREE MONTHS following a recognised stroke
- an abrupt deterioration in cognitive functions
fluctuating, stepwise progression of cognitive deficits
Management of vascular dementia?
Treatment is mainly symptomatic with the aim to address individual problems and provide support to the patient and carers
Important to detect and address cardiovascular risk factors – for slowing down the progression
Include: cognitive stimulation programmes, multisensory stimulation, music and art therapy, animal-assisted therapy
Managing challenging behaviours e.g. address pain, avoid overcrowding, clear communication
Consider pharmacological management if mixed subtype
Pharmacological management of vascular dementia
There is no specific pharmacological treatment approved for cognitive symptoms
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.
There is no evidence that aspirin is effective in treating patients with a diagnosis of vascular dementia.
The Deprivation of Liberty Safeguards is the procedure in law used where it is necessary to deprive a patient or resident of their liberty as they lack capacity to consent to treatment or care to keep them safe from harm.
These procedures must be authorised by a supervisory authority e.g. local authority.
What conditions must be met to allow for a DoLS to be put in place?
The following conditions must be met to allow a person to be deprived of their liberty under the safeguards:
The person must be 18 or over.
The person must be suffering from a mental disorder.
The person must be a patient in hospital or a resident in a care home.
The person lacks capacity to decide for themselves about the restrictions which are proposed so they can receive the necessary care and treatment.
The proposed restrictions would deprive the person of their liberty.
The proposed restrictions would be in the person’s best interests.
Whether the person should instead be considered for detention under the Mental Health Act.
There is no valid advance decision to refuse treatment or support that would be overridden by any DoLS process.
Capacity
All patients are initially assumed to have capacity
Capacity is decision-specific e.g. a patient may be able to decide which clothes to wear, but not where is safest to live
Capacity can be impaired permanently, temporarily, or can fluctuate
Patients deemed to have capacity are freely able to make decisions that the healthcare provider thinks unwise or dangerous
What are the 5 principles of the mental capacity act?
- Every adult is assumed to have capacity unless proved otherwise
- A person must be given all practicable help to make their own decisions before they are deemed to lack capacity
- Unwise, unsafe or dangerous decisions does not mean that person does not have capacity.
- All treatment given to a person who lacks capacity must be in the patients best interests
- Anything done for a person who lacks capacity must be done in the least restrictive way possible
An important differential of dementia is pseudodementia, which is primarily associated with cognitive deficits in older patients with depression.
What are the suggestive features?
Short duration of dementia
Equal effect on long and short term memory
Amnesia concerning specific events (often events are emotionally charged)
Often patient will very detailed complaint about memory disturbance
Patient may highlight failures in answers to questions relating to memory
Loss of social skills early in the illness
Patient will often answer “don’t know” to questions, as opposed to guessing close answers
Patient may make little effort in performing tasks
How can capacity be maximised?
Discuss the options in a time and place that helps them to understand and remember what you say.
Ask whether having a friend or relative with them might help them to remember information, or otherwise help them make the decision.
What is delerium?
Acute confusional state, with a sudden onset and fluctuating course.
May be hypoactive or hyperactive - recognised change in conciousness
Onset of 1-2 days.
CHANGE FROM BASELINE
What is Dementia?
Progressive decline in cognitive function usually occuring over several months. It affects many different areas of function, including:
Retention of new information, managing complex tasks, language and word finding difficulty, behaviour, orientation, recognitiion, ability to self care, and reasoning
Alzheimer’s dementia: course and onset, early presenting symptoms, neurological symptoms, mood and behavioral changes, structural brain imaging
Course and onset: Gradual, insidious, slow progression
Early presenting symptoms: Memory impairment
Neurological features: Absent
Mood and behavioral changes: May be minimal initially but pre-existing anixety etc may worsen
Structural behavioral imaging: Volume loss in MEDIUM TEMPORAL LOBE, POSTERIOR CINGULATE
enlargement of cerebral sulci, loss of gyral volume and mild dilation of the ventricular system
Aspects of AMT
What is reversible dementia, and what are some examples of causes?
“Reversible dementias” are conditions that may well be associated with cognitive or behavioral symptoms that can be resolved once the primary etiology is treated
Subdural haematoma
Alcoholic
Normal pressure hydrocephalus
