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DEMENTIA

Cognitive ageing. Cognitive, or thinking ability is the product of fixed intelligence' , the result of previous thinking , which often increases with age i.e wisdomfluid intelligence i.e. real time information processing which declines modestly in old ageIntellectual function is maintained unt

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DEMENTIA

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    1. DEMENTIA Dr. O.Martinovic, SpR to Dr. Heller

    2. Cognitive ageing Cognitive, or thinking ability is the product of ‘fixed intelligence’ , the result of previous thinking , which often increases with age i.e wisdom ‘fluid intelligence ‘ i.e. real time information processing which declines modestly in old age Intellectual function is maintained until at least 80 years of age, but processing is slower. Non critical impairments include: forgetfulness, reduced vocabulary, slower learning

    3. Impairments in cognitive function without dementia Age-associated memory impairment: older people learn new information and recall information more slowly but their performance is unchanged Minimal cognitive impairment: more broad that memory alone and felt to be pathological i.e. due to cerebrovascular disease, full criteria for dementia are not met. Progression to dementia occurs in 5-10% cases

    4. DEMENTIA Acquired decline in memory and other cognitive functions in an alert( i.e. on-delirious person) that is sufficiently severe to affect daily life. Prevalence increases dramatically with age 1% 60-65 year olds, > 30% of over 85 year olds

    5. Major dementia syndromes Dementia of Alzheimer’s type( 60-70%) Vascular Dementia ( 10-20%) Other neurodegenerative dementias(5-10%) Dementia with Lewy Bodies( up to 20%), PDD, Frontotemporal dementia Reversible dementias ( < 5%), drugs, metabolic, SDH,NPH Mixed pathology

    6. History Take from patient and informant Note onset, speed of progression, symptoms Careful Drug History Progressive decline in cognitive function over the years, ending in complete dependency and death. Deterioration may be stepwise( suggesting vascular ethiology), abrupt (single critical CVA) or rapid ( weeks, months-structural, metabolic or drug cause)

    7. Deterioration occurs in Retention of new information, short term memory loss with repetitive questioning Managing complex tasks Language Behaviour Orientation Recognition Ability to self care Reasoning

    8. Physical examination Look for peripheral stigmata of vascular disease, neuropathy, PD, Thyroid disease, liver disease, malignancy Mental state: R/O DELIRIUM: features include agitation, restlessness, poor attention and fluctuating conscious level R/O DEPRESSION: features include low affect, poor motivation, negative perspective. Perform Geriatric Depression Scale Measure cognitive function Neurophysiological assessment

    9. INVESTIGATIONS Screen for reversible causes:FBC,U+E, CRP,ESR,LFT’s, B12, Ca,TSH, glucose Resting ECG, CXR Neuroimaging: Early onset < 60 Sudden onset or brisk decline Focal neurology High risk of structural pathology CT, MRI, SPECT

    10. DEMENTIA-COMMON DISEASES ALZHEIMER’S DISEASE (AD) Most common cause of dementia syndrome Insidious onset, slow progression over the years Early profound short term memory loss, progresses to include broad , global cognitive dysfunction, behavioural change, functional impairment Behavioural problems common Early onset AD ( <65) is uncommon

    11. VASCULAR DEMENTIA Suggested by Risk Factors: (DM, HTN, SMOKING) Cognitive impairment may be patchy Frontal lobe, pseudobulbar, extrapyramidal features, emotional lability common Urinary incontinence and falls Other features may be cortical mimicking AD, or subcortical( apathy depression) Onset often associated with CVA or deterioration may be abrupt, stepwise

    12. Physical examination often shows focal neurology, suggesting CVA or diffuse cerebrovascular disease( hyperreflexia, extensor plantars,abnormal gait) Other evidence of vascular pathology:AF, PVD Neuroimaging shows: multiple large vessel infarcts,single infarct( i.e. thalamus), periventricular white matter change

    13. Differentiating between Alzheimer’s and Vascular Dementia Presentations overlap, pathologies commonly coexist. Pragmatically: In cases where vascular RF's present, treat them aggressively whether or not there is significant cerebrovascular pathology on imaging A trial of cholinesterase inhibitors

    14. Dementia and Parkinsonism DEMENTIA WITH LEWY BODIES PARKINSON’S DISEASE WITH DEMENTIA

    15. Dementia with Lewy bodies Cognitive and behavioural problems precede motor symptoms Gradual progression, insidious onset Fluctuations in cognitive function and alertness Prominent auditory and visual hallucinations, paranoia, dellusions Haloperidol poorly tolerated, Quetiapine better Levodopa or dopa agonists may worsen the confusion

    16. Parkinson’s Disease With Dementia Typical motor features present Presentation may resemble: AD, VD, DLB Features of PD precede dementia for more than a year Other conditions: MSA, PSP, Corticobasal degeneration may present with both PD and dementia

    17. Less common diseases Frontotemporal dementia: Neurodegenerative disease, insidious onset, slow progression, Early onset behavioural change, language difficulties, mild forgetfulness, loss of insight FTD spectrum: frontal lobe degeneration, Pick’s disease, MND with dementia

    18. Normal pressure hydrocephalus Gait Disturbance Incontinence of urine Cognitive impairment Neuroimaging:enlarged ventricles disproportionate to the degree of cerebral atrophy LP: assess baseline gait and cognition, opening pressure normal, remove 20-30 mls and check for improvement in gait and cognition in 1-2 hrs. Treatment: VP shunt- gait more likely to improve than cognition

    19. Other Dementias Drug/toxin induced: alcohol, psychoactive drugs Infections: neurosyphilis, HIV ( in the young) Vasculitis

    20. Dementia- non Drug Treatment Modify reversible RF’s ( constipation, anaemia, infection) Encourage physical+ mental activity Treat Depression Simplify meds ( Dosett boxes) Organise carers Inform patient and family of legal issues : Driving, enduring power of attorney, Wills Discuss end of life issues( artificial feeding, comfort v.s life prolongation

    21. Risk management Falls Wandering Aggression Self neglect Financial Abuse

    22. Role of cholinesterase inhibitors Donepezil Galantamine Rivastigmine Variable response Symptomatic benefit, the underlying cause continues to progress at the same rate Of the dementias, AD,DLB,PDD have the greatest cholinegic deficit and they benefit most Only in mild to moderate, not severe dementia Effect on the cognitive function is modest. However, even a small improvement in cognition can translate to significant improvement in day-to-day function, reducing carer burden

    23. Managing behavioural problems Agitation, anxiety, irritability trazodone->risperidone->olanzapine Benzodiazepines only for brief anxiety relief Depression : citalopram

    24. Prevention Lifestyle-physical and cognitive activity HRT doubles dementia risk NSAIDs may be protective Antioxidants Antihypertensives Statins

    25. Thank you

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