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Konstantine Zakzanis

Last lecture  Dementia o Gradual deterioration of intellectual abilities  Worsens over time o Step wise  Functioning at a certain level dramatically drops - continue with life, drop again, continue with life, drop again o slowly progressive  Cognitive and intellectual impairments get worse over time ; continuous o Impairment in social and occupational functioning  Elderly will have cognitive problems with age;  Mild cognitive impairment in specific are such as memory - doesn’t cause deficit in social /occupational functioning o Each dementia syndrome has a unique neuropsychological signature  Cannot be diagnosed definitively when alive; except one  Type and patterns of deficits they display are unique to different dementia  Alzheimer’s – loose memory first  Frontal lobe dementia – lose executive functioning or behaviour problems  Clinical diagnosis  Not until autopsy that they can definitively diagnose o Alzheimer’s  50% of all people diagnosed with Dementia  Usually begins after 65 years of age  Early signs  Memory loss – ask the same question again and again?  Women live longer with Alzheimer’s disease, but die more of it than men because  Confusion, disorientation  Late signs  Lose recognition of others  Forget own identity  Unable to communicate or move around  Slowly progressive – not stepwise  Typically diagnosed as possible/ or probable Alzheimer’s disease and after death  confirms disease  Early onset is more progressive (2 times faster deterioration)  Error in text book  gene factor E4 allele – its actually a risk factor for early onset – chances of getting Alzheimer’s if you have 1 of those genes by 40%  Death after 8-10 years – usually consequences of the disease and old age – pneumonia  Dementia with lewy bodies – in the last 10 years  is as prevalent as alzhiemers  Looks a lot like Alzheimer’s  Different : hallucinations  Neuropathology  Anterior and medial temporal and posterior frontal lobe o Atrophy = brain is wasting away o Enlarged sulci o Hippocampus and enthrional cortex – are first to go in Alzheimer o Parietal lobe = disorientation/special navigation  Neurofibrillary tangles and plaques  We all have plaques and tangles but the accumulation of them will determine deficit  Neuroimaging DAT  Risk factors: o 1. Head injury and 2.depression – bi-product of cognitive reserve rd o 3 risk factor = cognitive reserve: as the notion that high education levels delay clinical expression of dementia because the brain develops back up or reserve neural structures as a form of neuroplasticity ; there is more interconnectivity (AKA more gas in your tank, longer you can go)  Use it or lose it – cognitively active = helps preserve cognitive function  Cognitive activity aids with our crystallized intelligence and not with our fluid intelligence  Crystallized – eg. vocabulary, semantic knowledge – gets better with age and use  Fluid intelligence – eg. novel problem solving, doesn’t improve but declines over the years o Physical activity also helps maintain cognitive function = bringing oxygen to the brain  DAT cannot be definitively diagnosed until the patient had died and the brian autopsy is performed  Advances in neuroimaging techniques PET, MRI, CT and SPECT) promise the potential of diagnosing DAT in live patients o Alzheimer’s disease In-Vivo  SPECT imaging  Hypometabolism = less blood flow to the brain  Helps with pathology but not really – by the time clinicians catch it its too late  Should be found as early as possible because disease cannot be reversed but slowed down by drugs  Hippocampal Atrophy o Neuropsychology of DAT  Memory, naming and visualspatial impairment in early disease = signative of DAT  96% accurate in prediction  Explicit memory is impaired – ask them waht they did last night? They cant remember because they were unable to consolidate information  in hippocampus  is impaired  unable to recall information  Working memory is intact – frontal lobe  Interact, answer questions, appear oriented to
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