Dementia Flashcards
Define dementia
Acquired global impairment of intellect, reason and personality without impairment of consciousness that results in impairment of personal ADLs. Must have been going on for longer than 6 months.
Define cognitive impairment
Cognitive Impairment – disturbance of higher cortical functions including memory, thinking, judgement, language, perception, and awareness.
What is mild cognitive impairment?
Mild cognitive impairment is common and psychological – similar to dementia but without effect on ADL.
What cognitive functions are affected be dementia?
Cognitive Functions affected by Dementia
Complex attention
Executive ability – planning, decision making etc.
Learning and memory
Language
Visuoconstructional and perceptual motor ability
Social cognition
What is Alzheimer’s disease?
This develops slowly over many years causing an exaggerated ageing process specifically affecting short term memory, visual/spatial awareness and word finding problems. Changes in mood and behaviour such as loss of motivation/interest. This will present with indifference, delusions, agitation, and behavioural changes. This is due to increased neuronal damage from Neurofibrillary tangles and Senile plaques.
What are neurofibrillary tangles and senileplaques?
Neurofibrillary Tangles (Tau) – Intracellular twisted filaments of Tau protein. Tau normally binds and stabilises microtubules. Tau becomes hyper phosphorylated in AD – Tauopathy.
Senile Plaques (Amyloid)– foci of enlarged axons, synaptic terminals, and dendrites. Amyloid deposition in blood vessels in centre of plaque.
What are the risk factors for alzheimer’s disease?
Risk Factors – 1st degree relative with AD, Down’s syndrome, homozygosity of ApoE,
What is vascular dementia and how does it present?
Signs and symptoms: Abrupt onset with a stepwise deterioration, prominent aphasia, motor dysfunction, mood/behaviour changes and severe depression. Vascular dementia occurs as a result of small blood vessel changes that slowly damage more of the brain or can occur as a result of multiple strokes.
What is parkinson’s disease dementia and how does it present?
Parkinson’s Disease Dementia
Signs and symptoms: Tremors, loss of smell, trouble sleeping, dizziness and fainting, and trouble moving. This simply occurs as Parkinson’s disease progresses into its later stages.
What is fronto-temporal dementia and how does it present?
Signs and symptoms: Most causes personality changes presenting with executive dysfunction, disinhibition, impulsivity, and progressive loss of speech. Later onset memory problems. There is no distinguishing pathophysiology of this type of dementia. Examples include: Pick’s (fronto-temporal dementia), CPA (chronic progressive aphasia) and semantic dementia)
What is huntington’s disease and how does it present?
Signs and symptoms: abnormal involuntary movements, severe decline in thinking and reasoning skills, irritability, depression and mood changes. Generally, this occurs quite young and is hereditary due to a mutated gene on chromosome 4.
What is alcohol related dementia and how does it present?
Signs and symptoms: severe memory problems and problems with thinking and social skills. ARD is an umbrella term that includes Wernicke-Korsakoff Encephalopathy. This is a chronic memory disorder due to thiamine deficiency and is most commonly seen in alcoholics.
What are the general risk factors for dementia?
Female > Males
Education, occupation, and socioeconomic status
APOE e4 allele
Smoking, alcohol, obesity, cholesterol, HTN, DM and cerebrovascular disease
Psychological factors, physical activity, and depression
Describe common symptoms seen in all types of dementia?
Sun downing – worsening of symptoms at night – link to artificial light
Gradual decrease in cognitive function
Confusion
Inappropriate behaviour
Forgetfulness and confabulation
Illusions and hallucinations (often visual)
What is important to ask about in the history of someone with suspected dementia
Full Psychiatric History is good. Asking them to recall simple facts about their life working forward. Activities of daily living when assessing a patient with cognitive decline. If there is no impact on their ADL, then you cannot diagnose dementia.
Collateral history is more important than the history itself, especially important to ask about the timeline of decline.
Describe questionnaires that can be used to test for dementia
- AMTS (abbreviated mental test score)
- 6-CIT (6-item cognitive impairment test) – 0-7 = normal, 8-9 = mild cognitive impairment and 10-28 = significant cognitive impairment
- ACE (Addenbrooke’s cognitive examination) – above 87 is normal, between 83 and 87 is inconclusive and below 83 is abnormal
- GPCOG (general practitioner assessment of cognition) – 9 = no impairment, 5-8 more information required and 0-4 = cognitive impairment. Can also complete a Carer’s version.
- MoCA (Montreal cognitive assessment) – 26 and higher is considered normal
What should you do in the examination of someone with suspected dementia?
Mental state examination
Medication review and physical examination e.g. CVS and neuro (for parkinsonism)
What investigations are important to order in someone with suspected dementia?
Reversible organic causes – U&E, and calcium, LFTs, TFTs, FBC, Folate/B12, Thiamine and Glucose
CT/MRI – to check for reversible causes such as chronic subdural
EEG if suspecting frontotemporal, CJD or seizure disorder
Screen for syphilis and alcohol or drug abuse
How should someone with dementia be managed (excluding drugs)?
Multidisciplinary team treating multiple aspects of the disease. If caught early, then education about the disease is important and what they should expect as it progresses.
Be aware of depression and treat accordingly
Early Diagnosis/Referral to memory Clinic is important to optimise medical management, relief of knowing, access to care and services and clinical and cost effectiveness as the drugs are more effective earlier in the disease as well as the cost of them coming to hospital.
FOPAL (Frail Older People’s Advice and Liaison Service)
What is a VARM
VARM (Vulnerable adult risk assessment)
Only done on patients who DO have capacity. Classic examples are patients living in squalor or hoarding.
What cholinergic based pharmacological management is there for dementia?
Cholinesterase inhibitors
Donepezil is a centrally acting acetylcholine esterase inhibitor and has been shown to slow the progression of cognitive, memory and behaviour decline of patients with dementia. Care must be taken if the patient suffers from heart conditions, especially bradycardia. Other types of this drug that can be used are rivastigmine (patch) and galantamine.
AChEi SE - Nausea, vomiting, anorexia, arrhythmias, dizziness, falls, GI bleeds, diarrhoea, insomnia, muscle cramps, anorexia, and bradycardia
Cautions in gastric/duodenal ulcers, bladder obstruction, asthma/COPD, heart block, syncope, and seizures.
Monitoring – check pulse at every appointment and an ECG before commencing
Which NMDA antagonist can be used in dementia
Memantine is an NMDA receptor antagonist which can also be used. This drug is predicted to work based on the glutamine overactive hypothesis of dementia. Used for agitated and challenging behaviour.
No monitoring needed
SE include Headache, Constipation, Drowsiness, drowsiness, seizures Insomnia and nausea.
Cautions – Epilepsy/Seizures and max 10mg od if eGFR < 30
What drugs should be avoided in dementia
Anticholinergic drugs
Benzodiazepines due to falls and cognitive decline
Antipsychotic tranquilisers due to stroke, falls, cognitive decline and movements disorders
Can people with dementia drive?
Dementia is a notifiable disease to the DVLA and patients must be informed of this.
What are BPSD – behavioural and psychological symptoms of Dementia
Main symptoms – agitation, aggression, wandering, sexual disinhibition, shouting out, sundowning, sleep disturbance, depression anxiety and psychosis.
How should BPSD symptoms be managed?
Distraction/redirection Activity scheduling Environmental interventions Compensate for sensory impairments Reminiscence therapy
What pharmacological management options are there for BPSD symptoms of dementia
Only considered if the BPSD symptoms cause individual distress, poor quality of life or there is risk of harm to self or others.
Antidepressants – good for low mood/anxiety and good for sexual disinhibition
Benzodiazepines – Lorazepam, consider risk of over sedation and falls
Analgesia – patch if indicated
Mood stabilisers/Anticonvulsants – Depakote, consider if other options have not worked
Antipsychotics for BPSD
Not routine but can be considered if severe agitation, hallucinations, delusions that cause distress of significant risk of harming themselves/others. Be particularly careful with Parkinson symptoms.
Commonly used – Risperidone (only one that is licensed for BPSD), Quetiapine (1st line for LBD and PDD as lowest risk of EPSE) and Aripiprazole
What is lewy body dementia
Definition – aggregation of lewy bodies in neurones causing a dementia presentation. Less favourable prognosis than Alzheimer’s disease (only 6 compared to 12 years)
Causes – Abnormal collections of alpha-synuclein within neurones forming insoluble fibres which can cause loss of dopamine producing neurones in the substantia niagra which results in the Parkinson like affects. The loss of cognition is due to loss of ACh forming neurones.
Descirbe the signs and symptoms seen in lewybody dementia
Loss of cognition
Impaired attention and visuospatial function (poor judge of distance)
REM sleep behaviour disorder (loss of atonia causing acting out of dreams)
Visual hallucinations quite often with good insight – these will not respond to anti-psychotics but will instead cause severe parkinsonism symptoms
Parkinsonism
Problems with memory retrieval which usually occur late on in the disease
How is a diagnosis of lewy body dementia made?
Only accurate way to diagnose is with an autopsy so diagnosis is only ever probable
Diagnosis should be found early due to risk of poor reaction to antipsychotics
Diagnosis is made from core clinical features of which you need 3: fluctuating cognition, recurrent visual hallucinations, REM sleep behaviour disorder and 1 or more cardinal features of Parkinson’s.
DAT scan – direct antiglobulin test
PET scan to show reduced dopamine transporter uptake in basal ganglia
Low uptake of iodine in a myocardial scintigraphy
Polysomnographic confirmation of REM sleep without atonia
How is lewy body dementia managed?
Anticholinergic (rivastigmine) and dopaminergic agents – however these often cause bad side effects. Donepezil can slow cognitive decline and target hallucinations. Melatonin to combat RBD. Dietary changes to target autonomic symptoms
