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

Normal pressure hydrocephalus pathology, S+S, treatment
Pathology: impaired CSF reabsorption, reducing CSF production so ICP isn’t raised. S+S: gait disturbance, ataxia, dementia + urinary incontinence Treat with a shunt

Cruetzfeld Jakob disease
Prion disease causing rapidly progressive dementia and myoclonic jerks
EEG changes
Hummingbird sign

Organic syndromes causing psych symptoms
Cushings - depression (+ weight gain, thin skin, kidney stones, HTN, loss of periods) Hypothyroidism - depression (+weight gain, lethargy, constipation) Hyperparathyroidism - depression (+N+V, polydipsia/uria, fatigue, bone pain) Acute porphyria - anxiety, confusion, hallucinations (+red urine, abdo pain, vomiting)
Treatment of dementias (memory loss, depression, psychosis)
1st line = Cholinesterase inhibitors for Alzheimers + DLB Memantine - NMDA receptor antagonist = 2nd line for Alzheimers + DLB SSRI (citalopram) for depressive symptoms Minimise use of APs Quetiapine for psychosis - don’t use typical APs due to risk of EPSEs
Delirium S+S, treatment
Rapid onset, fluctuating, altered consciousness, distubed sleep-wake cycle Hyper or hypoactive Disorientation to time and place, immediate recall impaired Treatment: supportive, use haloperidol to sedate if needed
Psychological treatment of dementias
Comfortable environment Visual/ hearing aids Support groups/ respite care Counselling
Social treatment of dementias
Patient safety at home Mobility help Restrict driving Legal counsel - power of attorney Monitor meds compliance
What to give to someone with dementia + gastric ulcers?
NMDA receptor antagonist eg memantine
What scores on MMSE + ACE III indicate dementia?
MMSE: 20-26 = mild cognitive impairment;
10-20 = moderate impairment;
<10 = dementia
ACE III <82 indicates likely dementia
What is pseudodementia?
Temporary dementia caused by depression, other mental disorders, psychoactive drugs
Can be reversed with correct management of underlying cause