Cognition + Dementias Flashcards
4 areas of cognition to assess
Recent memory Language Visuospatial ability Executive function
Tests for cognition
ACE-III = complex but best AMTS = shorter
Physical tests to order when there is cognitive decline
Bloods: U+E, LFTs, B12 + folate, TFTs, calcium CT head
Frontal lobe deficit symptoms
Behaviour + personality changes
Temporal lobe deficit symptoms
Agnosia, aphasia, hallucinations, visuospatial difficulties, inability to recognise faces (prosopagnosia)
Parietal lobe deficit symptoms
Aphasia, agnosia, visuospatial difficulties, finger agnosia, dyscalculia, apraxia
Occipital lobe deficit symptoms
Visual perception defects: visual agnosia, alexia, prosopagnosia, illusions, hallucinations
Primary dementias
Alzheimers, DLB, frontotemporal (Picks), Huntingtons
Secondary dementias
Vascular, infective, inflammatory, metabolic, endocrine, trauma
Cholinesterase inhibitors: names, action, SE, formulation
Donepezil, galantamine, rivastigmine Increase cholinergic transmission Work for Alzheimers + DLB Side effects: GI, hypersalivation, vivid dreams, HTN, syncope Rivastigmine can come in patches
Alzheimers pathology, risk factors, S+S
Pathology: decreased ACh, extracellular senile plaques made of beta-amyloid, intracellular neurofibrillary tangles, symmetrical atrophy (more pronounced in medial temporal + parietal lobes). Glial proliferation, granulovascular degeneration, Hirano inclusion bodies Risk factors: females, Downs, fam hx, dialysis S+S: insidious onset memory loss + personality changes 5 As: amnesia, apraxia, agnosia, aphasia, associated symptoms (behaviour + personality)
DLB pathology, diagnosis, S+S
Pathology: Lewy bodies = intracellular eosinophilic inclusions, decreased ACh, senile plaques Lewy bodies more present in cortical areas (temporal lobe, cingulate gyrus, insular cortex) vs Parkinsons - more present in basal ganglia S+S: fluctuating cognition, visual hallucinations, Parkinson like symptoms, frequent faints + falls Formally diagnosed with a DaT scan
Vascular dementia pathology, risk factors, S+S
Pathology: multiple infarcts Risk factors: male, CV disease, HTN, high cholesterol, DM, smoking, alcohol S+S: sudden onset, stepwise progression. Commonly mood and behavioural changes Don’t use AChEis
Frontotemporal dementia pathology, S+S, management
Picks disease Pathology: asymmetrical knife blade atrophy, neuronal loss + gliosis Ballooned neurons (Pick cells) + tau-positive neuronal inclusions (Pick bodies) No senile plaques or neurofibrillary tangles S+S: early personality + behavioural changes, pacing + disinhibition, executive impairment Stop anticholinergic drugs
Huntington’s pathology, inheritance, S+S
Onset in 4th/ 5th decade Pathology: abnormal huntington protein leads to neuronal loss in caudate nucleus and putamen (movement) + cerebral cortex (dementia) Autosomal dominant S+S: choreiform movements, progressive dementia, depression