Understanding the Person with Dementia Oxford Brookes University
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Understanding the Person with Dementia
Oxford Brookes University What is dementia?
How do we diagnose it?What can we do?
Sharon ChristieOPTIMA, University of Oxford
Oxford Memory Assessment Clinic
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DEMENTIA – An Epidemic• Estimated that at least 15 million people are
affected worldwide
• In the UK there are about 800,000 people with dementia, nearly 2/3 of whom have AD
• Age is biggest risk factor:
1 in 6 in people over 80yrs old
1 in 25 from 70-79yrs old
1 in 100 from 60-69yrs old
• But some people are affected at a much earlier age (1 in 1400 between 40 – 64yrs old)
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What is Dementia?
• Dementia describes a set of symptoms
• Dementia is a syndrome rather than a diagnosis
• Dementia is not part of normal ageing
• It is caused by diseases of the brain The cause gives us a diagnosis usually probable or possible
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‘‘an an acquired, global impairment of impairment of intellect, memory and personality intellect, memory and personality without impairment of consciousness’ without impairment of consciousness’
Impacts on normal social and/or Impacts on normal social and/or occupational functioning occupational functioning
Impairment is sustained over time Impairment is sustained over time ((progressive))
What is Dementia?
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Early Changes
• Not remembering appointments• Misplacing items• Difficulty remembering recent
information or events• Not recognising faces• Word-finding difficulty• Lack of concentration• Difficulty making decisions• Losing track of time• Mistakes in judgement
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Changes
• Withdrawal / lack of confidence• Apathy / lacking motivation• Irritability / frustration• Lose thread of conversation or rambling
sentences • Accusatory or paranoid• Unable to sequence tasks• Difficulty reading or writing• Reacting less quickly• Supervision with Activities of Daily Living
(ADL)
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Why are people not referred for assessment?
• 41% of people with dementia do not have a diagnosis
• Dementia still has a stigma for some people and in society generally
• Anxiety and fear of getting a diagnosis• Lack of insight and denial of a problem• Some people assume nothing can be
done so may not seek help• GPs may not refer
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Specialist Assessment
GP may refer to:• Neurology• Geratology• Old Age Psychiatry / Community Mental Health
Team
Memory Clinics:• History including collaborative• Mental state examination• Cognitive testing• Physical examination inc. neurological exam• Blood screen• Scans/Imaging : CT / MRI / PET / DAT
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Normal Ageing
• From adulthood, memory shows a slow progressive impairment
• Processing is slower
• ? Reduced ability to learn new things
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Mild Cognitive Impairment
MCI – between normal ageing & dementia
Petersen criteria (2001):
Subjective memory complaint – corroborated byinformant
Objective memory impairment for age(1.5 below standard deviation for normal ageing)
Does NOT interfere with Activities of Daily Living
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Need To Rule Out / Consider:
• Brain Tumour• Brain Haemorrhage• Normal Pressure Hydrocephalus
• Alcohol abuse• Drug interactions• Infection• Metabolic disorders• Endocrine imbalance (eg low thyroxine)• Poor nutrition / dehydration (eg low Vit. B12)• Trauma
• Depression• Anxiety / stress
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Dementia
• Cognitive Impairment
• Progressive
• No other cause found
• Affecting function
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Dementia: major causes estimated from clinical diagnoses
Alzheimer’s diseaseAlzheimer’s disease (62%)(62%)
Vascular dementiaVascular dementia (17%(17%)
Mixed dementia (AD & Vascular)Mixed dementia (AD & Vascular) (10%)(10%)
Lewy body dementiaLewy body dementia (4%) (4%)
Other rarer forms (5%)
eg Fronto-temporal dementia, Korsakoffs, CJD
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Alzheimer’s first patientAlzheimer’s first patient
Alzheimer first saw August D. in Alzheimer first saw August D. in November 1901: she displayedNovember 1901: she displayedmemory loss and delusions.memory loss and delusions.She died in 1906.She died in 1906.
Alzheimer described the uniqueAlzheimer described the uniquehistopathology in 1907: the brainhistopathology in 1907: the braincontained both plaquescontained both plaques(amyloid) and neurofibrillary (amyloid) and neurofibrillary tangles (abnormal tau protein).tangles (abnormal tau protein).
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Alzheimer-type pathology
Silver stained plaques and tangles
•Thick arrow: senile (neuritic) plaque•Small arrow: diffuse plaque•Star: tangle
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ADAD - Pattern of degeneration - Pattern of degeneration
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Accuracy versus p.m. diagnosis 80%Accuracy versus p.m. diagnosis 80%
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Rapid atrophy of medial temporal lobe in ADRapid atrophy of medial temporal lobe in AD
At presentation 7 years laterAt presentation 7 years later MMSE 23 MMSE 13MMSE 23 MMSE 13
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structural MRI shows the “shape” of the brain…
Structural MRIStructural MRIStructural MRIStructural MRI
Healthy elderly64
mild AD67
moderate AD62
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Fronto-temporal dementia
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Cerebro-Vascular Damage
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Small vessel disease
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Lewy Body
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Dementia with Lewy Bodies (DLB)• Build-up of Lewy bodies – accumulated
bits of alpha-synuclein protein - inside the nuclei of neurons in areas of the brain that control particular aspects of memory and motor control.
• Alpha-synuclein accumulation is also linked to Parkinson's disease
• Similarity of symptoms between DLB and Parkinson’s disease, and between DLB and Alzheimer’s disease, can often make it difficult to make a definitive diagnosis.
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Dementia with Lewy Bodies (DLB)
• Central feature is progressive cognitive decline
• Combined with three additional defining features:
• fluctuations in alertness and attention• recurrent visual hallucinations• parkinsonian motor symptoms eg
rigidity and the loss of spontaneous movement.
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Differential Diagnosis
AD: gradual onset / decline Episodic memory, poor orientation,
Vascular: sudden, stepwise deterioration;
area affected; attention, speed, praxis, visual-spatial,
FTD: personality & behaviour
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Importance of early assessment & Diagnosis
• Seek reversible causes • Identify exacerbating or contributory factors e.g.
– vitamin deficiencies or hormonal problems– Some types of heart or blood vessel disease
• Options for drug treatments• To allow patients and families to plan, e.g.
financial and legal issues, future care preferences
• Advice about coping strategies• Access to support from NHS, Social & Healthcare
Services, Voluntary bodies (e.g. AS, Age UK, Young Dementia UK), & others
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What can we do medically?
• Treat vascular risk factors:• Control BP• Control diabetes• Treat heart conditions• Stroke prevention eg aspirin• Correct vitamin deficiencies
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What can we do medically?
Treatments for Alzheimer’s disease:
Cholinesterase Inhibitors (ChEI):– Improve chemical messenger levels in brain– Donepezil (Aricept)– Galantamine (Reminyl)– Rivastigmine (Exelon)– for mild to moderate AD – 50% +/- response rate; 18-24 months
ChEI treat symptoms, not the disease
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What can we do medically?
Treatments for Alzheimer’s disease:
Memantine (Ebixa) - NMDA receptor antagonist • It blocks the chemical glutamate, which is released in
excessive amounts when brain cells are damaged in AD, and causes further damage to the cells.
• For moderate to severe AD
Can also be added to ChEI but not currently available on NHS unless for behavioural symptoms
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What else can we do?
Provide information, support and advice
Clinical staff at clinic (Doctors, memory clinic nurse)
Dementia Advisor at clinic (O.C.C/ Alz Soc/ Age UK)
Information about the disease & symptomsCoping strategies for person with dementia and family
DrivingPower of Attorney / legal matters / finances, benefits
Dementia Information LineCarer support group informationServices, activities,
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What can we do?
• Research into new drugs to protect brain cells, rather than just improve symptoms by helping cells to cope with damaged chemical messenger systems
• Can we interfere / stop the development of amyloid plaques and neurofibrillary tangles (abnormal tau protein)?
• Try to identify people with Alzheimer’s disease processes in their brain before they develop dementia
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Jack et al, Lancet Neurology, Jan 2010Hypothetical model of dynamic biomarkers of the Alzheimer’s pathological cascade