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

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)

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

‘‘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?

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

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)

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

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

Normal Ageing

• From adulthood, memory shows a slow progressive impairment

• Processing is slower

• ? Reduced ability to learn new things

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

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

Dementia

• Cognitive Impairment

• Progressive

• No other cause found

• Affecting function

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

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).

Alzheimer-type pathology

Silver stained plaques and tangles

•Thick arrow: senile (neuritic) plaque•Small arrow: diffuse plaque•Star: tangle

ADAD - Pattern of degeneration - Pattern of degeneration

Accuracy versus p.m. diagnosis 80%Accuracy versus p.m. diagnosis 80%

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

structural MRI shows the “shape” of the brain…

Structural MRIStructural MRIStructural MRIStructural MRI

Healthy elderly64

mild AD67

moderate AD62

Fronto-temporal dementia

Cerebro-Vascular Damage

Small vessel disease

Lewy Body

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.

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. 

Differential Diagnosis

AD: gradual onset / decline Episodic memory, poor orientation,

Vascular: sudden, stepwise deterioration;

area affected; attention, speed, praxis, visual-spatial,

FTD: personality & behaviour

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

What can we do medically?

• Treat vascular risk factors:• Control BP• Control diabetes• Treat heart conditions• Stroke prevention eg aspirin• Correct vitamin deficiencies

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

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

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,

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

Jack et al, Lancet Neurology, Jan 2010Hypothetical model of dynamic biomarkers of the Alzheimer’s pathological cascade