Session 9 Flashcards
What is Dementia?
A chronic, progressive syndrome of insidious onset involving decline in higher cortical function.
Can be further divided into: early onset and late onset dementia. Depending on symptoms manifesting before or after the age of 65.
Cognitive symptoms:
- Impaired memory (temporal lobe involvement)
- Impaired orientation (temporal lobe involvement)
- Impaired learning capacity ((temporal lobe involvement)
- Impaired judgement (frontal lobe involvement)
Non-cognitive symptoms:
- Behavioural symptoms
- Agitation
- Aggression (frontal lobe involvement)
- Wandering
- Sexual disinhibition (frontal lobe involvement)
- Depression and anxiety
- Psychotic features:
- Visual and auditory hallucinations (hallucinations=false perceptions)
- Persecutory delusions (delusions=false beliefs)
- Sleep symptoms
- Insomnia
- Daytime drowsiness (decreased cortical activity)
Diagnosis
- By exclusion
- Exclude organic causes of cognitive decline
- Hypothyroidism
- Hypercalcaemia
- B12 deficiency
- Normal pressure hydrocephalus
- Abnormal gait
- Incontinence
- Confusion
- Exclude delirium
- Exclude organic causes of cognitive decline
- Look for features of progressive cognitive decline, impairment of activities of daily living in a patient with a normal conscious level (cf. delirium where conscious level is diminished with acute cognitive decline)
Five types:
- Alzheimer’s Disease
- Vascular Dementia
- Frontotemporal Dementia
- Dementia with Lewy bodies
- AIDS Dementia Complex
Pathological Features, Presentation, Treatment, Risk factors of Alzheimers
Pathological features
- Macroscopic
- Global cortical atrophy. Mostly frontal, parietal and temporal lobes
- Sulcal widening
- Enlarged ventricles (primarily lateral and third affected)
- Microscopic
- Plaques
- Composed of amyloid beta, derived from proteolytic breakdown from β-amyloid precursor protein.
- Tangles
- Hyperphosphorylated tau
- It is believed that plaques and tangles kill neurones. Since neurogenesis is limited in the CNS any neurones that die are unlikely to be replaced
- • Predominant neurones affected
- Cholinergic (treatments target this)
- Noradrenergic
- Serotonergic
- Those expressing somatostatin
- Early-onset :
- β-amyloid precursor protein (β-APP)
- Presenilin 1
- Presenilin 2.
- Late-onset :
- Apolipoprotein E gene
- Plaques
Presentation:
- Deterioration in memory.
- Deterioration in spatial navigation.
- Difficulty in executive functions :
- Language
- Visuospatial functioning
- Calculation
- Affecting activities of daily living
Treatment (Not to cure but supportive):
- Acetylcholinesterase (AChE) inhibitors
- These medicines increase levels of acetylcholine, a substance in the brain that helps nerve cells communicate with each other.
- Donepezil, galantamine and rivastigmine can be prescribed for people with early- to mid-stage Alzheimer’s disease.
- Memantine
- This medicine is not an AChE inhibitor. It works by blocking the effects of an excessive amount of a chemical in the brain called glutamate.
- Memantine is used for moderate or severe Alzheimer’s disease. It’s suitable for those who cannot take or are unable to tolerate AChE inhibitors.
- It’s also suitable for people with severe Alzheimer’s disease who are already taking an AChE inhibitor.
- Antidepressants
- Treat depression and behavioural symptoms
- Cognitive stimulation therapy and rehabilitation
- Group activities and exercises designed to improve memory and problem-solving skills.
- Working with a trained professional, such as an occupational therapist, and a relative or friend to achieve a personal goal, such as learning to use a mobile phone or other everyday tasks. Cognitive rehabilitation works by getting you to use the parts of your brain that are working to help the parts that are not.
- Care support
- Care home or support care at home.
- Home modifications, such as removing loose carpets and potential trip hazards, ensuring the home is well lit, and adding grab bars and handrails
Risk Factors:
- hearing loss
- untreated depression (although this can also be a symptom of dementia)
- loneliness or social isolation
- a sedentary lifestyle
- Cardiovascular diseases
- Smoking
- Diabetes
- Poor diet
- Previous stroke / MI etc
- Hypertension
- Hypercholesterolaemia
Pathological Features, Presentation, Treatment, Risk factors of Vascular dementia
Cognitive impairment caused by cerebrovascular disease (multiple small strokes)
Risk factors same as for any vascular disease (and indeed same as for Alzheimer’s) :
- Previous stroke / MI etc
- Hypertension
- Hypercholesterolaemia
- Diabetes
- Smoking
- Vascular disease
Presentation:
- Step-wise deterioration of cognitive function with focal neurological symptoms.
Treatment (Not curative):
- occupational therapy to identify problem areas in everyday life, such as getting dressed, and help with working out practical solutions
- speech and language therapy to help improve any communication problems
- physiotherapy to help with movement difficulties
- psychological therapies, such as cognitive stimulation (activities and exercises designed to improve memory, problem-solving skills and language ability)
- relaxation techniques, such as massage and music or dance therapy
- social interaction, leisure activities and other dementia activities, such as memory cafes (drop-in sessions for people with memory problems and their carers to get support and advice)
- home modifications, such as removing loose carpets and potential trip hazards, ensuring the home is well lit, and adding grab bars and handrails
- medication for high blood pressure
- statins to treat high cholesterol
- medicines such as aspirin or clopidogrel to reduce the risk of blood clots and further strokes
- anticoagulant medication, such as warfarin, which can also reduce the risk of blood clots and further strokes
- medication for diabetes
- An antipsychotic medicine, such as haloperidol, may be given to those showing persistent aggression or extreme distress where there’s a risk of harm to themselves or others.
- Alzheimer’s disease medications such as donepezil (Aricept), galantamine (Reminyl), rivastigmine (Exelon) or memantine aren’t used to treat vascular dementia, but may be used in people with a combination of vascular dementia and Alzheimer’s disease.
Pathological Features, Presentation, Treatment, Risk factors of Dementia with Lewy bodies
Essentially the same disease as Parkinson’s. If movement disorder followed by dementia then we call this Parkinson’s disease. If dementia precedes movement disorder we call it dementia with Lewy bodies
Pathology
- Aggregation of alpha synuclein
- Forms spherical intracytoplasmic inclusions
- Main deposits found across the brain:
- Substantia nigra
- Temporal lobe
- Frontal lobe
- Cingulate gyrus (found just above the corpus callosum)
- Can label alpha synuclein in the brain using advanced imaging techniques
Presentation (3 core features):
- Fluctuating cognition and alertness
- Vivid visual hallucinations
- Parkinsonian features
- May cause repeated falls
Treatment: (Supportive)
Medicine cannot stop dementia with Lewy bodies getting worse, but for some people it can help reduce some of the symptoms.
- Acetylcholinesterase inhibitors
- Acetylcholinesterase (AChE) inhibitors, such as donepezil (Aricept), rivastigmine (Exelon) and galantamine (Reminyl), may help improve hallucinations, confusion and sleepiness in some people.
- Memantine
- This medicine is not an AChE inhibitor. It works by blocking the effects of a large amount of a chemical in the brain called glutamate.
- Memantine is used for moderate or severe dementia with Lewy bodies. It’s suitable for those who cannot take AChE inhibitors.
- levodopa – this can help with movement problems, but it can also worsen other symptoms and needs to be carefully monitored by a doctor
- antidepressants – these may be given if you’re depressed
- clonazepam – this can help if you experience a particular type of rapid eye movement (REM) sleep behaviour disorder
- Do not give antipsychotics (dopamine antagonists) as can cause neuroleptic malignant syndrome, a psychiatric emergency
- Fever
- Encephalopathy (confusion)
- Vital signs instability (tachycardia, tachypnoea (v.sensitive sign), fluctuating BP)
- Elevated creatine phosphokinase
- Rigidity (caused by dopamine antagonism)
- occupational therapy to identify problem areas in everyday life, such as getting dressed, and help make life easier
- speech and language therapy to help improve communication or swallowing problems
- physiotherapy to help with movement
- psychological therapies, such as cognitive stimulation (activities and exercises designed to improve memory, problem solving skills and language ability)
- relaxation techniques, such as massage, and music or dance therapy
- social interaction, leisure activities and other dementia activities, such as memory cafes (drop-in sessions for people with memory problems and their carers to get support and advice)
- home modifications, such as removing trip hazards, ensuring the home is well lit, and adding grab bars and handrails
Risk Factors:
- Age. People older than 60 are at greater risk.
- Sex. Lewy body dementia affects more men than women.
- Family history. Those who have a family member with Lewy body dementia or Parkinson’s disease are at greater risk.
Pathological Features, Presentation, Treatment, Risk factors of Frontotemporal dementia
- Second most common cause of early onset dementia
- Peak onset 55-65 y/o
- Frontal and temporal lobe atrophy
- Symptoms mostly related to frontal lobe dysfunction
- Behavioural disinhibition
- Inappropriate social behaviour
- Loss of motivation without depression (caused by damage to anterior cingulate cortex)
- Repetitive/ritualistic behaviours
- Non fluent (Broca type) aphasia
- Others symptoms:
- Primitive Reflexes: Grasp reflex Palmomental reflex
- Short/long-term memory impairment
- Disorder of language –‘receptive’ dysphasia / fluent aphasia
Treatment
Medicines cannot stop frontotemporal dementia getting worse, but it can help reduce some of the symptoms for some people.
The following medicines may help:
- antidepressants – antidepressants called selective serotonin reuptake inhibitors (SSRIs) may help control the loss of inhibitions, overeating and compulsive behaviours seen in some people
- antipsychotics – these are rarely used, but are sometimes needed if SSRIs have not worked, as they can help control severely challenging behaviour that’s putting the person with dementia or others around them at risk of harm
Non-medicinal supportive treatment:
- occupational therapy – to identify problem areas in everyday life, such as getting dressed, and help work out practical solutions
- speech and language therapy – to help improve any communication or swallowing problems
- physiotherapy – to help with movement difficulties
- relaxation techniques – such as massage, and music or dance therapy
- social interaction, leisure activities and other dementia activities – such as memory cafes, which are drop-in sessions for people with memory problems and their carers to get support and advice
- strategies for challenging behaviour – such as distraction techniques, a structured daily routine, and activities like doing puzzles or listening to music
- incontinence products if needed
Risk Factors:
- Family History
- Age
- Little known
Pathological Features, Presentation, Treatment, Risk factors of AIDS dementia complex
As patients with HIV infection live longer thanks to modern treatments, their chance of developing AIDs associated dementia is increasing
- Pathology
- Entry of HIV infected macrophages into the brain is thought to lead to indirect damage to neurones
- Insidious onset but rapid progression once established
Clinical features (related to global damage but also some manifestations of cerebellar involvement)
- Cognitive impairment
- Psychomotor retardation (slow thoughts and movements, also seen in depression)
- Tremor
- Ataxia
- Dysarthria
- Incontinence
Treatment:
- Anti-Virals (Control)
Risk Factors:
- HIV/AIDS
- Asssociated risks for HIV infection e.g. Multiple partners, unproteced sex etc
Management for patients with dementia
Using the bio-psycho-social model
Biological
- Drugs
- Acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine, galantamine)
- Modest efficacy for mild to moderate Alzheimer’s disease
- NMDA antagonists (e.g. memantine)
- Useful for treating agitation
- NMDA antagonist
- Acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine, galantamine)
Psychological
- Few psychological treatments are available for dementia due to its progressive nature
Social
- Mainstay of management
- Key themes
- Explain the diagnosis sensitively
- Talk about problems that will arise and how they will be managed
- Give results of any special investigations (e.g. scans) o Driving – often a difficult topic to deal with as patients frequently desperate to retain their independence
- Finances
- Will
- Power of attorney
- Day care and respite care (mainly to allow carers to rest and provide supportive environment for patients)
- Residential/nursing home placement
What is delerium, its features and types?
Acute change in consciousness and cognition
Sometimes called ‘acute confusional state’
Often reversible, due to organic cause
Associated with a variety of insults to the brain which may cause neuronal damage and inflammation
Dementia can predispose to episodes of delirium
Features:
- Rapid onset of confusion
- Clouded consciousness (may be drowsy)
- Fluctuating course
- Maybe transient visual hallucinations
- Often exaggerated emotional responses (e.g. aggression)
Types:
- Hypoactive
- Withdrawn
- Quiet
- Sleepy
- Consequently more likely to be missed / confused with something else
- Hyperactive
- Restless
- Agitated
- Aggressive
- Mood may rapidly fluctuate
- Persecutory delusions (narrative of elusion often not coherent)
- Symptoms worse at start and end of day
- Maybe related to changes in endogenous cortisol levels
What are the main causes of delirium?
Drugs toxicity :
- Withdrawal: alcohol, benzodiazepine, cocaine, coffee
- Anti-cholinergics, opiates, anti-histamines, dopamine agonist, monoamine oxidase inhibitors, levodopa, corticosteroids, beta-blockers, lithium, tricyclic anti-depressants, calcineurin inhibitors
Endocrine :
- Hyper/Hypothyroidism
- Addison’s disease
- Cushing’s disease
Liver failure
Intracranial : stroke, haemorrhage, cerebral abscess, epilepsy
Renal failure
Infections : Pneumonia, UTI, Sepsis, Meningitis
Urinary retention / Faecal retention (Constipation)
Metabolic
- Electrolyte imbalance (sodium, calcium, magnesium, phosphate, glucose)
- Hypoxia
What is the management for delirium?
Find and treat the underlying cause
Calm environment.
Rehydration.
Haloperidol (ONLY IF ESSENTIAL).
Prognosis:
- Increases risk of dementia
- Associated with mortality
- These patients often have lengthy hospital stays and have a high risk of re-admission
Common investigations for all suspected dementia cases
These need to be done within six months of recording a new diagnosis of dementia.
FBC
U&E
ESR or CRP
TFTs
LFTs
Random blood sugar
Vitamin B12 and folate.
Routine syphilis testing is not necessary but should be done if a risk is identified in the history.
Effect on self and carers of looking after someone with dementia
Physical Stress
Emotional Stress
Psychological Stress
Socio-economic effects :
Financial burden - aided by Personal Independence Payment (PIP)
Effect of dementia on healthcare system?
Ageing population so prevalence increasing.
Worsening healthcare expenditure on:
Prolonged hospital admissions
Social care services
Community district nurse services
Strain on GP services
Compare Dementia and Delirium
Dementia:
- Slow onset
- Steady decline
- Hallucinations rare
- Speech often slow
- Normal GCS
- Clear consciousness
Delirium:
- Rapid onset
- Fluctuant course
- Hallucinations
- Speech slow/fast
- Reduced GCS
- Impaired consciousness
How to assess a patient who is unconscious?
Check breathing / central pulse.
Lie them on their left side.
Call for help.
Options to assess consciousness:
- Sternal rub
- Trapezius squeeze
- Fingernails pressure test
Ensure that patient is stable.
Assess Glasgow Coma Score (GCS).
Explain Glasgow Coma Scale
Order primary headache disorders from most to least common. How does pain present differently between them?
• Tension-type headache • Migraine • Medication over-use (more secondary) • Cluster headache
What is temporal arteritis?
- Vasculitis involving small and medium sized arteries of head
- F>M
- >50 years (most common in>75)
Consider in any >50 year old with abrupt onset of headache + visual disturbance or jaw claudication
superficial temporal artery commonly involved
Risk of irreversible loss of vision due to ischemia of CN I
Treat with Prednisolone and confirm with artery wall biopsy
