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Lecture 10

Ageing and Cognitive Disorders - Lecture 10 notes.doc

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Department
Psychology
Course
PSYB32H3
Professor
Konstantine Zakzanis
Semester
Winter

Description
Ageing and Cognitive/Psychological Disorders Dementia • gradual deterioration of intellectual abilities • Step wise (dramatic deterioration) vs. Slowly progressive (slow deterioration of cognitive functioning > the way one deteriorates can differ and the distinction between them can differentiate the various dementia disorders from each other • impairment in social and occupational functioning • each dementia syndrome has a unique neuropsychological signature (neuropsychological testing) o patients will display different patterns of neuropsychological deficit, and the pattern is so distinct that often it allows us to tell quite early on in the disorder whether the person might have Alzheimer's, frontal temporal dementia, etc • a diagnosis of dementia is clinical • only at autopsy can it be definitive The Canadian Study of Health & Aging 1. Prevalence of Alzheimer’s and other forms of dementia is 8% 2. Confirmed risk factors for Alzheimer’s (family history – apo-E gene), head trauma, and lower education 3. ½ of Canadians with dementia are institutionalized 4. There are over 60, 000 new cases of dementia per year Alzheimer’s Disease >Cognitive reserve hypothesis: “use it or lose it” – as we age, if we continue to engage in cognitive exercise, we maintain that level of cognition and less likely to lose it. o The notion that high education or continuing to be mentally active, delays the clinical expression of dementia because the brain develops back up or reserve neural structures as a form of neural plasticity. • Characteristics: o Disease usually begins after age of 65 years of age (before 65 = early onset) o Slowly progressive o Early onset that is more progressive than the late-onset o Death after 8-10 years of its diagnosis, usually as the result of physical decline or independent diseases common in old age, such as heart disease o Most common type (55-80% of all dementias) • Neuropathology • Neuropsychological progression o Memory, naming, visualspatial disorder (executive skills are somewhat normal early) • Neuroimaging Neuropathology • Brain with Alzheimer’s = Atrophy: wasting tissue/structure in certain areas (deeper creases). o Specifically the medial temporal lobes (language, hippocampus - memory formations) and parietal lobe (visual spatial deficit) and pre-frontal cortex (problem solving) • 2 types of abnormalities: o Plaques (deposits of a class of protein called amyloid that acculumate in spaces b/w cells of cerebral cortex, hippocampuc, and other areas critical to memory o Tangles (filaments within nerve cells in brain get twisted and tangled)  Everyone has plaques and tangles in brain but the number of plaques and tangles is what differentiates  Literally count the number, certain number = Alzheimer’s (can only be officially determined after autopsy)  Dual diagnosis • DAT Post Mortem o Volume loss in hippocampus and temporal lobes (cortical level of brain – outer layers)  Sub-cortical levels remain intact (working memory, etc) ** Neuroimaging DAT • DAT cannot be definitively diagnosed until the patient had died and a brain autopsy is performed • Advances in neuroimaging techniques (PET, MRI, CT, SPECT) promise the potential of diagnosing DAT in live patients o SPECT Imaging: Temporal-Parietal  hypo metabolism: less blood flow and oxygen to areas of brain o MRI: Hippocampal Atrophy  Neuroimaging is helpful in the diagnosis of DAT, but not a reliable marker Neuropsychological Tests of DAT • Neuropsychological signature of DAT o Memory, naming, visual spatial impairments – profound deificits  Predictive validity of neuropsychological tests when coupled with clinical history is 90-05% (probable diagnosis, not definitive) • Explicit memory impaired because of inability to consolidate new memories/ learn new information • Working memory relatively intact (normal conversations) – digit span normal results • Procedural memory relatively intact (habitual tasks) • Retrieval impaired • Recognition impaired > remembering list of words (i.e. CVLT) Naming • Inability to spit out the word you want to say • Semantic paraphasias (naming closely related objects in semantic network) are common • phonemic paraphasias (first sound of word is same, but incorrect word) are not common o Frontal lobe abnormality *  Circumlocutions (describing the object instead of naming it) are common as well Visual/Spatial Ability The Dementias (*=rare)  Cortical Dementias o Alzheimer’s disease o Primary Progressive Aphasia *  progressive Broca’s Aphasia (left frontal lobes)  naming difficulties > phonemic paraphasias  intact memory o Semantic Dementia *  progressive Wernicke’s Aphasia (temporal lobes)  remain fluent, memory relatively intact  progressive deterioration of comprehension > hard to test o Frontal-temporal dementias ( & Pick’s disease)  earlier onset than Alzheimer’s  perseveration (childlike tendencies)  hypo-orality: desire to put everything in mouth – esp. sweet  Disinhibited type (Phyneus Gage) • “Dirty late” – appear to be normal
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