Old Age Psychiatry Flashcards
Changes in the worlds population from 2000-2050?
Worlds population >60 years will double from 11% to 22%
By how much is the absolute number of people >60 years of age expected to increase?
From 605 million to 2 billion from 2000-2050
How many people in the UK are >65?
One sixth of the population
10 million
How many people are expected to be >65 years of age in the UK in 2050?
19 million
1/4 of the population
How many people in the UK are over 80?
3 million
What does the national Service Framework for older people (2001) state?
Older people with MH problems should have access to specialist services
What does Everybodys Business (2005) state?
Older people’s MH problems require input from both health and social care, physical and MH services and mainstream and specialist services.
What does No Health Without Mental Health (2011) state?
Services should be age appropriate non discriminatory
Needs based criteria for Older Peoples MH Services for commissioners by RcPsych?
People of any age with primary dementia
People with MI and physical illness or frailty, which contribute or complicate management of their MI
People with psychosocial difficulties related to ageing process or EoL issues or who feel their needs may be best met by a service for older people
What % of carers suffer from depression at some stage?
30%
What are the 10 key points from JCPMH guidance for commissioners of older peoples MH services?
Older people will form a larger proportion of the population
Older peoples MH services benefit from an integrated approach with social care
Older peoples MH services need to work closely with primary care and community services
Services must be commissioned on basis of need and not age alone
Older peoples MH services must address needs of people with functional illness as well as dementia
Older people often have a combination of MI and physical illness
Older peoples MH services must be disciplinary
Older people with MH needs should have access to community CRHTTs
Older people with MH needs respond well to psychological input
Older people should have dedicated liaison services in acute hospitals
What domains need to be taken into account when assessing an older adult with MH problems?
Cognitive assessment
Functional abilities
Physical health issues and how these impact on MH
Role of imaging in dementia daignosis
Assessment of carer needs and holistic approach to care
Physical examination
Assessment of capacity issues
Why is medication regimen and timing so important in Parkinsons?
Failure can result in delirium, depression, slowed cognition and anxiety
How many patients with PD have depression?
2/3
How many patients with PD develop dementia?
40%
Common cognitive deficits in Parkinsons?
Higher executive dysfunction Attention Memory Visuomotor processing Visual attention
How many patients with stroke have delirium?
30-40% after one week
Which diseases commonly result in Charles Bonnet?
Macular Degeneration
Cataracts
Diabetic retinopathy
Which diseases are associated with psychotic sx in the elderly?
Auditory impairment
How do metabolic changes during illness accentuate emotional response to it?
Dehydration Electrolyte imbalance Endocrine changes Infection can all produce affective sx
How common is depression in people with chronic physical health problems?
2-3 times more common
How many patients with chronic physical illness will have depression?
20%
First line treatment for depression in chronic physical illness
SSRI - keep in mind interactions
Intracranial reversible causes of dementia
Normal pressure hydrocephalus
Subdural haematoma
Cerebral tumours
Tertiary syphilis
Systemic disorders which can cause reversible dementia
Alcoholism Anoxia Low BM Myxoedema Vitamin deficiencies Drug or chemical poisoning Pseudodementia Renal/hepatic disease
How many diagnosis of dementia are due to young onset of dementia?
12%
How can alcohol use lead to dementia?
Damage to limbic structures and frontal lobes leading to memory and executive impairments
Which impairment in alcohol-induced dementia can improve with abstinence?
Memory impairment
Which type of memory is affected in alcohol-induced dementia?
Autobiographical
What does neuroimaging show in alcohol-induced dementia?
Generalised cerebral atrophy with frontal preponderance
What happens in normal pressure hydrocephalus?
Dilatation of cerebral ventricles - usually 3rd ventricle, with normal CSF pressure at P.
Triad of sx of normal prssure hydrocephalus?
Dementia
Gait ataxia
Urinary incontinence
Population prevalence of NPH in the elderly
0.4%
Which sx precedes all others in NPH?
Mildly broad based, symmetrical short stepped gait
What type of dementia occurs in NPH?
Progressive slowing of cognitive and motor functioning consistent with pattern of subcortical dementia
What is the pattern of subcortical dementia?
Pronounced slowness of thought
Difficulties in sustaining, switching attention
Difficulties in planning
How many cases of NPH are idiopathic?
50%
What are 50% of NPH non-idiopathic cases due to?
Mechanical obstruction of CSF flow across meninges due to infection, trauma, SAH etc
Which sx is late sx of NPH?
Urinary incontinence
What does CT show in NPH?
Increased size of lateral ventricles and thinning of cortex
Treatment of NPH
Surgical placement of ventriculo-peritoneal shunt
Which sx is most likely to improve with treatment of NPH?
Gait impairment
What is related to good outcome of NPH?
Mild dementia
Why are subdural veins more vulnerable to tears in the elderly?
Cortical shrinking
When should subdural haematoma (SDH) be suspected?
Changing pattern in cognitive function with risk factors
Risk factors for SDH
Post trauma - elderly after fall, HI Cerebral atrophy Alcoholism Epilepsy Clotting disorders Predisposing drugs such as Warfarin, Aspirin
How many SDH cases have bilateral SDH?
30%
How many patients with SDH have a history of HI?
50%
Common features of SDH
Headache
Drowsiness
Altered consciousness
Confusion - fluctuating severity
What does CT show in SDH
Crescent shaped haematoma compressing sulci and midline shift
When might CT not show a SDH?
First 3 weeks as clot is isodense during early phase
Treatment of SDH
Surgical - burr holes
Conservative - steroids
Complications of surgical treatment of SDH
Seizures
Re-bleeding
Mortality of SDH
10%
Which patients with SDH have highest mortality?
Depressed consciousness level
Bilateral SDH
How does Huntingtons dementia present?
Frontal dementa
movement disorder
Prominent deficits in Huntingtons dementia?
Attention Semantic verbal fluency Processing speed Executive function Recall more affected than recognition
Key diagnostic test for dementia in MS
MRI
Problem with MRI scan in elderly with MS
Distinguishing between demyelination and vascular damage can be difficult in the elderly
How is diagnosis of dementia in MS confirmed?
CSF and evoked potentations
Where is Prion protein coded?
PRNP gene on Chromosome 20
When does prion disease occur?
When protein undergoes changes which render it insoluble
Which diseases are caused by prions?
Spongiform encephalopathies - transmissible dementias
What are the four forms of prion dementia?
Kuru
CJD
Fatal familial insomnia
Gerstmann Straussler Syndrome
Worldwide prevalence of sporadic CJD
0.1 per 100,000
Which prion disease is most common?
CJD
What causes CJD?
Pathological form of prion protein PrPsc
What is the normal form of the prion protein?
PrPc
Difference between PrPc and PrPsc
PrPsc is resistant to proteases, thus leading to accumulation and rapid degenerative changes
Onset of CJD
After 5th decade but can occur at any age
Clinical picture of CJD
Rapidly deteriorating dementia Myoclonus Cortical blindness Cerebellar and EPSE Death within one year
When do fulminant sx develop in CJD?
Within weeks
Which sign becomes prominent as CJD progresses?
Myoclonus
How many CJD cases are sporadic?
85%
How many CJD cases are genetic?
10%
How many cases of CJD result from iatrogenic transmission of transplant surgery?
5%
What types of transplant surgery can lead to CJD?
Transplant of dura, corneal grafts and pituitary growth home
What does CT show in CJD?
Atrophy of cortex, worse centrally
Atrophy of cerebellum
What does MRI show in CJD?
Non-specific basal ganglia hyperintensities
What does EEG show in CJD
Periodic bi or triphasic discharges against slight low voltage background
In which type of CJD is EEG change not seen?
Variant CJD
CSF findings in CJD
14-3-3 protein elevated.
What is 4-3-3?
Normal neuronal protein
Definitive diagnosis of CJD
Post-mortem microscopic exam:
spongiform neural degeneration and gliosis throughout cortical and subcortical grey matter, sparing white matter tracts
Treatment of CJD
Symptomatic; valproate and clonazepam to reduce movement disorder
What is vCJD?
Bovine Spongiform Encephalopathy
What is Bongine Spongiform Encephalopathy?
Prion disease of cows caused by cattle feeds that contained CNS material from infected material.
Incubation period between ingestion of contaminated meat and development of vCJD?
<20 years
Who does vCJD typically affect?
Men in 20s
Characteristics of vCJD?
Anxiety and depressive sx
Personality changes
Progressive dementia
Ataxia and myoclonus
Course of vCJD
1-2 years followed by death
What is diagnostic of vCJD?
Pulvinar sign; symmetric high-signal-intensity changes affecting pulvinar and medial areas of thalamus and tectal plate on FLAR sequence in MRI
How many patients with vCJD had pulvinar sign
> 70%
Does CSF in vCJD show 14-3-3 protein?
Yes
Aside from MRI, how else can vCJD be diagnosed?
Immunostaining from tonsillar biopsy
EEG in vCJD?
No distinctive changes, sometimes diffuse slow waves
Most common Dementia in the developed world?
Alzheimers
Onset of Alzheimers
40-90
Most often >65
Predicted risk of developing Alzheimers in first-degree relatives
15-19%
5% in controls
Relative risk of Alzheimers if you have a first-degree relative with the disease?
3-4 times relative to the risk in controls
Risk of Alzheimers at the age of 60
1%
Risk of Alzheimers at age of 65
5%
Risk of Alzheimers at age 85
40%
How does risk of Alzheimers correlate with age?
Doubles every 5 years
Risk of people >75 for Alzheimers vs Vascular Dementia
Risk is 6x greater for alzheimers than for Vascular DEmentia
In which group of patients is onset of Alzheimers earlier?
FHx of Alzheimers
Proven risk factors of Alzheimers
Age
Downs
Apolipoprotein 4 allele
Likely risk factors of Alzheimers
Female
HI
Postmenopausal oestrogen decline
Possible risk factors of Alzheimers
FHx of Downs
FHx of Parkinsons
Vascular factors
Proven protective factors of Alzheimers
Apolipoprotein 2 allele
Possible protective factors of Alzheimers
Smoking
NSAIDs
Oestrogwn
Premorbid intelligence and education
Which genes are associated with early onset Alzheimers?
Presenilin 2 gene
Presenilin 1 gene
Beta amyloid precursor protein gene
Which chromosome is Presenilin 2 gene on?
1
Which chromosome is Presenilin 1 gene on?
14
Which chromosome is beta amyloid precursor protein gene on?
21
Where on chromosome 21 is beta amyloid precurser protein gene found?
Long arm
What is the major constituent of senile plaques in Alzheimers?
Beta amyloid protein
Describe structure of the beta amyloid protein
42 amino acid peptide that is a breakdown product of amyloid precursor protein
What is the breakdown product of amyloid precursor protein?
Beta amyloid protein
Why are people with Downs at increased risk of Alzheimers?
They have three copies of the amyloid precursor protein gene (found on long arm of chromosome 21)
What can cause excessive deposition of beta amyloid protein?
Downs
Mutation on codon 717 in amyloid precursor protein gene
What imaging can be used to confirm diagnosis of Alzheimers?
Amyloid PET scanning
What increases risk of late onset Alzheimers?
Apolipoprotein allele 4
Where can Apolipoprotein allele 4 be found?
Chromosome 19
Risk of Alzheimers if you have one copy of the Apolipoprotein allele 4 gene?
3x
Risk of Alzheimers if you have two copies of the Apolipoprotein allele 4 gene?
8x
Criteria for diagnosis of probable Alzheimers
Clinical examination and documented by MMSE, Blessed Dementia scale or confirmed by neuropsychological tests.
What features are required for a diagnosis of Alzheimers?
Deficits in 2 or more areas of cognition
Progressive worsening memory and other cognitive functions
No disturbance of consciousness
Absence of system disorders or other brain diseases that could account for progressive deficits
What is CT used for in diagnosis of Alzheimers?
Exclude treatable causes
CT findings in Alzheimers
Cortical atrophy; particularly over parietal and temporal lobes
Dilatation of third ventricles
What CT findings correlate with cognitive impairment?
Dilatation of 3rd ventricles
MRI findings in Alzheimers
Reduced grey matter, hippocampus, amygdala and temporal lobe volumes
SPECT findings in Alzheimers
Reduction in blood flow in temporal and parietal regions
PET findings in Alzheimers
Reduced blood flow and metabolism in temporal and parietal regions
MRS findings in Alzheimers
Abnormal synthesis of membrane phospholipids early in disease
Amyloid PET imaging findings in Alzheimers
Deposition of beta amyloid
What type of memory loss is seen in Alzheimers?
Short-term memory initially, then long term memory deficit later
Amnesia universal, mainly for recent events
What type of disorientation is seen in Alzheimers?
For time
Language findings in Alzheimers?
Expressive and receptive dysphasia Lexical anomia (word finding difficulties)
Other cognitive deficits in Alzheimers
Apraxia; inability to perform coordinated learnt motor tasks
Agnosia
Impaired visuospatial skills
Impaired exectutive function
Psychiatric sx of Alzheimers
Delusions 15%
Hallucinations 10-15%
Depression 20%
Most common psychiatric sx in Alzheimers
Apathy - 59% Depression - 58% Irritability - 44% anxiety - 44% Agitation - 41%
Most common behavioural sx of Alzheimers
Wandering
Aggressive outbursts
Average survival expectation for patients with Alzheimers?
8 years
Sx correlated with progression of Alzheimers?
Increased agitation Frequent emotional outbursts Night pacing Poor sleep Wandering
Sx in terminal phase of Alzheimers?
Profound disorientation
Amnesia
Incontinent of urine and faeces
Areas of cognition tested in AMTS
Memory
Orientation
Cut off for AMTS?
<8/10
Areas of cognition tested with MMSE
Orientation Memory Concentration Language Praxis Gnosis
Cut-off for MMSE?
24/30
Most widely used cognitive test in Old age Psychiatry?
MMSE
What test is best for screening global cognitive dysfunction?
MMSE
What types of variations is MMSE subject to?
Age
Socio-economic status
Educational achievement
What is MMSE heavily weighted towards?
Verbal performance
What does CAPE stand for?
Comprehensive Clifton Assessment for the Elderly
What does CAPE assess?
Level of disability and estimate need for care
What is the DRS?
Clinical Dementia Rating Scale
Areas of cognition assessed by DRS?
Memory Orientation Judgement & Problem solving Community Affairs Homes and Hobbies Personal Care
What scale is commonly used to assess severity and stage of Alzheimers?
DRS
Cognitive areas of assessment of Addenbrookes
Orientation Registration Recognition Recall Perceptual abilities Language Verbal fluency
Cognitive areas of assessment of NPI
Delusions Hallucinations Agitation Depression Anxiety Euphoria Apathy Disinhibition Irritability Aberrant
What does NPI do?
Rates frequency and severity of a range of neuropsychiatric sx.
What does NPI-NH measure?
Rates of occupational disruptiveness, a measure of caregiver distress.
How long does CAMCOG take to complete?
40 minutes
What does CAMCOG give a score out of?
104
Cognitive areas of assessment tested by CAMCOG?
Orientation Comprehension Perception Memory Abstract Thinking
What does Clock drawing test .. test?
Praxis
Higher executive function
What drugs are used to treat mild to moderate cognitive impairment in Alzheimers?
Cholinesterase inhibitors
Give some examples of cholinesterase inhibitors used in the treatment of mild Alzheimers
Donepezil
Rivastigmine
Galantamine
How do cholinesterase inhibitors work in Alzheimers?
Reduce inactivation of Acetylcholine and thus potentiate cholinergic neurotransmitter, which in turn produces a most improvement in memory and goal-directed thought
Plasma half-life of Donepezil
70 hours
Plasma protein binding of Donepezil
Almost 100%
How does Donepezil work?
Highly selective reversible inhibition of acetylcholine.
Side effects of Donepezil
Mainly GI: Nausea/vomiting Diarrhoea Anorexia Headache/dizziness Syncope Muscle cramps
Which Alzheimers drugs cause more neuropsychiatric adverse effects?
Rivastigmine
Galantamine
How does Galantamine work?
Direct nicotinic stimulatory action
Cholinesterase inhibitor
Which drug improves sx of dementia in Parkinsons?
Rivastigmine
Which sx of Parkinsons does Rivastigmine improve?
Cognition
ADLs
Most common SEs of Rivastigmine?
Nausea/vomiting
Anorexia
What does Rivastigmine work on?
Acetylcholinesterase
Butyrylcholinesterase
How can Rivastigmine be taken?
PO
Transdermal patch OD
What augmentation is beneficial in Alzheimers?
Memantine and Donepezil
What does Memantine do?
Protects neurons from excessive glutamate which may be neurotoxic
What can Memantine be used for?
DAT
Vascular
Mixed dementia
How does Memantine work?
Non-competitive, PCP-site NMDA antagonist
Most common SEs of Memantine?
Dizziness Headache Fatigue Diarrhoea Gstric pain
Which drug is used in treatment of moderate to severe Alzheimers?
Memantine
Which patients with mild Alzheimers is Memantine used in?
When cholinesterase inhibitors are contraindicated i.e. severe cardiac conduction defects, severe asthma
Why is Tacrine not used for Alzheimers?
Potential for hepatotoxicity
Starting dose of Donepezil for Alzheimers?
5mg OD
Treatment dose of Donepezil for Alzheimers?
10mg OD
Starting dose of Rivastigmine for Alzheimers?
1.5mg BD
Treatment dose of Rivastigmine for Alzheimers?
6mg BD
Starting dose of Galantamine for Alzheimers?
4mg BD
Treatment dose of Galantamine for alzheimers?
12mg BD
Starting dose of Memantine for Alzheimers?
5mg OD
Treatment dose of Memantine for Alzheimers?
10mg OD
Recommendations from Committee on Safety of Medicines re use of Olanzapine and Risperidone for Dementia?
Each associated with 2x increase in risk of stroke and therefore should not be used
Poor prognostic factors in Alzheimers
Male Onset <65 Prominent behavioural problems Parietal lobe damage Depression Severe cognitive deficits Absence of misidentification syndrome
Prevalence of psychosis in people with Alzheimers?
30-50%
Which type of psychosis is more common in Alzheimers?
Delusions
Common delusions in Alzheimers
Capgras Phantom boarder Mirror sign TV sign Magazine sign
What is phantom boarder?
False belief that guests are living in a persons home
What is the mirror sign?
Individual identifies his or her own image as someone elses
What is the TV sign?
Misidentification of TV images as real
What is the magazine sign?
Misidentification of magazine images as real and existing in 3D
What is the second most common cause of dementia?
Vascular
How many cases of dementia are vascular?
20%
What is the NINCDS-AIREN criteria for vascular dementia?
Evidence of CVD both on examination and brain imaging
Relationship between onset of dementia and CVD
How can one show a relationship between onset of dementia and CVD?
Either dementia occurring within 3 months of a stroke or
Abrupt deterioration in cognitive function or fluctuating stepwise course
Most prevalent neurological sx in Vascular Dementia
Reflex asymmetry
What sx are associated with measures of small vessel disease?
Dysarthria Dysphagia Parkinsonian gait disorder Rigidity Hypokinesia
What sx were more likely observed in vascular dementia in the presence of a cerebral infarct?
Aphasia Reflex asymmetry Hemianopia Hemimotor dysfunction Hemisensory dysfunction Hemiplegic gait
What are the three subtypes of Vascular dementia>
Cognitive deficits following single stroke
Multi-infarct dementia
Progressive smell vessel disease - Binswanger’s disease
When are cognitive deficits following stroke often seen?
Following midbrain or thalamic strokes
What happens in multi-infarct dementia>
Multiple strokes leads to stepwise deterioration.
Follows a number of minor ischaemic events
What type of dementia is Binswangers disease?
Subcortical
Characteristics of Binswangers disease?
Slow intellectual decline Slowness of thought Decreased STM Disorientation Motor problems; gait, dysarthria
What happens in Binswangers disease?
Multiple microvascular infarcts of perforating vessels lead to progressive lacunae formation
What does MRI show in Binswangers disease?
Small distinct infarcts (lacunae) or more generalised white matter hyperintensities (leukoariasis)
Risk factors of Vascular Dementia
Old age HTN IHD Smoking EtOH High lipid levels AF FHx Valvular disease Atrial myxoma Carotid artery disease APOE4 allele Polycythaemia Sickle cell anaemia Coagulopathies
What is Haschinski Ischemic score index?
Allows quantification of likelihood of patient having vascular rather than degenerative dementia
Which dementia is more common in males?
Vascular
Which dementia is more common in females?
Alzheimers
Which dementia has focal neurological signs?
Vascular
Which dementia has loss of insight?
Alzheimers
Which dementia has mood sx?
Alzheimers
Which dementia has somatic complaints?
Vascular
What is CADASIL?
Form of vascular dementia
What does CADASIL stand for?
Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy
How is CADASIL transmitted?
AD trait with high penetrance
Where is CADASIL gene?
Long arm of chromosome 19
How do patients with CADASIL gene present?
Recurrent stroke at age of 40-50
Hx of migraine
What do patients with CADSIL later develop?
Subcortical dementia
Pseudobulbar palsy
What does MRI show in CADSIL?
Widespread white matter changes
What does CT show in vascular dementia?
Increased number of infarcts
What does MRI show in vascular dementia?
White matter lesions more numerous and severe than Alzheimers
What does SPECT show in vascular dementia?
Irregular perfusion deficits
What does PET show in vascular dementia?
Cerebral blood flow and metabolism reduced and uncoupled
What does MRS show in vascular dementia?
Absence of phospholipid changes
How many cases of dementia are lewy body dementia (LBD)?
15-20%
How does LBD present?
Progressive dementia with parkinsonism and fluctuation in level of attention and severity of cognitive impairment
What are Lewy bodies?
Eosinophilic intracytoplasmic neuronal inclusion bodies
What are lewy bodies made of?
Abnormally phosphorylated neurofilament proteins which are aggregated with ubiquitin and alpha-synuclein
Where can lewy bodies be found?
Brainstem
Subcortical nuclei
Limbic cortex - cingulate, entorhinal, amygdala
Neocortex - frontal, temporal, parietal lobes
Central feature required for diagnosis of LBD?
Progressive cognitive decline of sufficient magnitude to interfere with normal social or occupational function
Core features of LBD
2 for probable, 1 for possible diagnosis:
Fluctuating cognition with profound variatinos in attention and alertness
Recurrent visual hallucinations - well-formed and detailed
Spontaneous motor features of parkinsonism
How many patients with LBD have motor features of Parkinsonism?
70%
Supportive features for LBD
Repeated falls due to autonomic dysfunction Syncope Transient disturbances in consciousness Neuroleptic sensitivity Systematized delusions Hallucinations
Describe visual hallucinations in LBD
Well formed and detailed
Prevalence rate of delusions in LBD
65%
Prevalence rate of auditory hallucinations in LBD
20%
Prevalence rates of visual hallucinations in LBD
60-80%
LBD and antipsychotics
Patients with LBD are very sensitive to antipsychotics; these can lead to worsening of parkinsonian sx
How many patients with LBD experience life threatening adverse effects to antipsychotics?
50%
Decline rate per year of worsening parkinsonism in LBD?
10% decline per year
Which allele is seen in LBD?
Increased frequency of e4 allele (APOE)
Which memory is spared in LBD?
Short term
Which aspects of cognition are affected in LBD?
Attention
Frontal subcortical skills
Visuospatial ability
CT/MRI findings of LBD
Relative sparing of medial temporal lobe
Associated features of LBD pathologically
Lewy-related neuritis Plaques Neurofibrillary tangles Regional neuronal-loss in brainstem Synapse loss Microvacuolation
Where is regional neuronal loss common in LBS?
Brainstem - locus cereleus and substantia nigra
Nucleus basalis of Meynert
Which drugs improve cognition, delusions and hallucinations in LBD?
Cholinesterase inhibitors
