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 Christie OPTIMA, University of Oxford Oxford Memory Assessment Clinic. DEMENTIA An Epidemic. Estimated that at least 15 million people are affected worldwide - PowerPoint PPT Presentation


  • Understanding the Person with Dementia Oxford Brookes University

    What is dementia?How do we diagnose it?What can we do?

    Sharon ChristieOPTIMA, University of OxfordOxford Memory Assessment Clinic

  • DEMENTIA An EpidemicEstimated that at least 15 million people are affected worldwideIn the UK there are about 800,000 people with dementia, nearly 2/3 of whom have ADAge is biggest risk factor: 1 in 6 in people over 80yrs old1 in 25 from 70-79yrs old 1 in 100 from 60-69yrs oldBut 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 acquired, global impairment of intellect, memory and personality without impairment of consciousness Impacts on normal social and/or occupational functioning Impairment is sustained over time (progressive) What is Dementia?

  • Early ChangesNot remembering appointmentsMisplacing itemsDifficulty remembering recent information or eventsNot recognising facesWord-finding difficultyLack of concentrationDifficulty making decisionsLosing track of timeMistakes in judgement

  • ChangesWithdrawal / lack of confidenceApathy / lacking motivationIrritability / frustrationLose thread of conversation or rambling sentences Accusatory or paranoidUnable to sequence tasksDifficulty reading or writingReacting less quicklySupervision with Activities of Daily Living (ADL)

  • Why are people not referred for assessment? 41% of people with dementia do not have a diagnosisDementia still has a stigma for some people and in society generallyAnxiety and fear of getting a diagnosisLack of insight and denial of a problemSome people assume nothing can be done so may not seek helpGPs may not refer

  • Specialist Assessment GP may refer to:NeurologyGeratologyOld Age Psychiatry / Community Mental Health Team

    Memory Clinics:History including collaborativeMental state examinationCognitive testingPhysical examination inc. neurological examBlood screenScans/Imaging : CT / MRI / PET / DAT

  • Normal AgeingFrom adulthood, memory shows a slow progressive impairment

    Processing is slower

    ? Reduced ability to learn new things

  • Mild Cognitive ImpairmentMCI 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 TumourBrain HaemorrhageNormal Pressure Hydrocephalus

    Alcohol abuseDrug interactionsInfectionMetabolic disordersEndocrine imbalance(eg low thyroxine)Poor nutrition / dehydration (eg low Vit. B12)Trauma

    DepressionAnxiety / stress

  • DementiaCognitive Impairment


    No other cause found

    Affecting function

  • Dementia: major causes estimated from clinical diagnosesAlzheimers disease(62%)Vascular dementia (17%)Mixed dementia (AD & Vascular)(10%)Lewy body dementia (4%)Other rarer forms (5%)eg Fronto-temporal dementia, Korsakoffs, CJD

  • Alzheimers first patientAlzheimer first saw August D. in November 1901: she displayedmemory loss and delusions.She died in 1906.

    Alzheimer described the uniquehistopathology in 1907: the braincontained both plaques(amyloid) and neurofibrillary tangles (abnormal tau protein).

  • Alzheimer-type pathologySilver stained plaques and tangles

    Thick arrow: senile (neuritic) plaqueSmall arrow: diffuse plaqueStar: tangle

  • ADAD - Pattern of degeneration - Pattern of degeneration

  • Accuracy versus p.m. diagnosis 80%

  • Rapid atrophy of medial temporal lobe in ADAt presentation 7 years later MMSE 23 MMSE 13

  • structural MRI shows the shape of the brainStructural MRI

  • 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 Parkinsons disease, and between DLB and Alzheimers disease, can often make it difficult to make a definitive diagnosis.

  • Dementia with Lewy Bodies (DLB)Central feature is progressive cognitive declineCombined with three additional defining features: fluctuations in alertness and attentionrecurrent visual hallucinationsparkinsonian motor symptoms eg rigidity and the loss of spontaneous movement.

  • Differential DiagnosisAD: 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 & DiagnosisSeek reversible causes Identify exacerbating or contributory factors e.g. vitamin deficiencies or hormonal problemsSome types of heart or blood vessel diseaseOptions for drug treatmentsTo allow patients and families to plan, e.g. financial and legal issues, future care preferencesAdvice about coping strategiesAccess 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 BPControl diabetesTreat heart conditionsStroke prevention eg aspirinCorrect vitamin deficiencies

  • What can we do medically?Treatments for Alzheimers disease:

    Cholinesterase Inhibitors (ChEI):Improve chemical messenger levels in brainDonepezil (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 Alzheimers 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 Alzheimers disease processes in their brain before they develop dementia

  • Jack et al, Lancet Neurology, Jan 2010Hypothetical model of dynamic biomarkers of the Alzheimers pathological cascade

    Slide 2: Alzheimers disease (AD): a public health problem

    AD is a progressive neurodegenerative disease affecting at least 15 million people worldwide (Mayeux R and Sano M, 1999). It is the most common form of dementia in later life. As reported from a US community study, the prevalence of AD increases from 3% in those aged 6574 years of age to 18.7% in those of 7584 years of age and to 42% in those of 85 years of age and older (Evans et al., 1989)

    AD imposes direct costs (e.g. clinicians services, hospital care and medications) and indirect costs (e.g. the unpaid informal care provided by family members). There is also the intangible cost of physical and emotional suffering experienced by patients and their families (Bosanquet et al., 1998; Max et al., 1995).


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