27. clinical diagnosis of Alzheimer’s Disease A)Definite Alzheimer’s Disease B) Probable Alzheimer’s Disease C) Possible Alzheimer’s Disease
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33. MILD COGNITIVE IMPAIRMENT progression: 25 GDS 3 71 NYU 12 Isolated memory loss 74 Seattle 6 CDR 0.5 72 MGH 15 Questionable dementia 66 Columbia 14 Memory Impairment 74 Toronto 12 MCI 81 Mayo Annual conversion rate to AD % Criteria Mean Age Study
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38. “ Distinguishing Features of Cortical & Subcortical Dementia” Psychomotor retardation Forgetfulness Cognitive dilapidation Impaired insight Poor strategy formulation Aphasia- Amnesia Visuospatial disorder Poor abstraction Aculculia Apraxia Agnosia- loss of the power to recognize the import of sensory stimulus. Intellectual Functions Subcortical Cortical
39. “ Distinguishing Features of Cortical & Subcortical Dementia” Depression (rarely, mania) Indifference Personality/Emotions Subcortical Cortical
40. “ Distinguishing Features of Cortical & Subcortical Dementia” Dysarthria Normal (until late) Speech Subcortical Cortical
41. “ Distinguishing Features of Cortical & Subcortical Dementia” Abnormal (parkinsonian, chorea, dystonia, etc.) Normal (until late) Motor Subcortical Cortical
42. “ Distinguishing Features of Cortical & Subcortical Dementia” Thalamus basal ganglia rostral brainstem Neocortical association areas&hippocampus Anatomy Subcortical Cortical
43. Mixed dementias cortical & subcortical structures are involved
70. AD: Treatment No cure for AD Limited therapy to help symptoms or to slow progression Therapies to improve symptoms: Enhancement of cholinergic system Increase dietary choline: little effect on cognition AChE inhibitors: small cognitive enhancing effect
71. Anticholinesterases, such as donepezil, rivastigmine & galantamine, or NMDA (N-methyl-D-aspartate receptor antagonists (memantine) appear to improve cognitive function to some extent in Alzheimer's disease