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 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 impairment of intellect, memory and personality without impairment of consciousness’ ‘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 () 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 by informant 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 disease(62%) Vascular dementia (17% Vascular dementia (17%) Mixed dementia (AD & Vascular)(10%) Lewy body dementia (4%) Other rarer forms (5%) eg Fronto-temporal dementia, Korsakoffs, CJD

Alzheimer’s first patient Alzheimer first saw August D. in November 1901: she displayed memory loss and delusions. She died in Alzheimer described the unique histopathology in 1907: the brain contained both plaques (amyloid) and neurofibrillary 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%

Rapid atrophy of medial temporal lobe in AD At presentation 7 years later MMSE 23 MMSE 13 MMSE 23 MMSE 13

structural MRI shows the “shape” of the brain… Structural MRI Healthy elderly 64 mild AD 67 moderate AD 62

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; 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 & symptoms Coping strategies for person with dementia and family Driving Power of Attorney / legal matters / finances, benefits Dementia Information Line Carer support group information Services, 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 2010 Hypothetical model of dynamic biomarkers of the Alzheimer’s pathological cascade