Dementia Flashcards
What is Lewy body dementia
Depositions of abnormal proteins called Lewy bodies in brain cells
Course of lewy body dementia
Fluctuating course
Symptoms and signs of lewy body dementia
Global brain dysfunction, visual hallucinations, parkinsonian signs
Areas of brain affected in lewy body dementia
Alpha-synuclein cytoplasmic inclusions in substantia nigra, paralimbic and neocortical areas
Treatment of lewy body dementia
Cholinesterase inhibitors, dopamine replacement, avoiding antipsychotics
Symptoms of frontotemporal dementia
Language, personality and behavioural changes and disorders
Cause of frontotemporal dementia
Severe atrophy of frontal and temporal lobes
Diagnosis of frontotemporal dementia
Microscopy shows severe neuronal loss and gliosis, abnormal protein aggregates
Onset of frontotemporal dementia
Earlier age onset of >35 years
Risk of vascular dementia
Stroke, vascular disease, atherosclerosis of arteries
Time course of vascular dementia
Acute cognitive decline in step-wise course from cerebro-vascular events
Causes of multifactorial vascular dementia
Multiple infarcts producing deterioration, infarcts primarily in white matter.
Associations with subcortical vascular dementia
Small vessel disease, lacunes in basal ganglia, can be small cavitating lesions, small infarcts or enlarged perivascular spaces
Treatment of vascular dementia
Prophylaxis against cerebral emboli with aspirin/warfarin. Control of HTN, and can use AchEI or memantidine
What is dementia
Group of chronic progressing signs and symptoms involving multiple higher cortical functions such as memory, orientation, thinking, language and comprehension
Types and prevalence of dementia
Alzheimer’s - 70%
Dementia with Lewy bodies
Vascular dementia
Frontotemporal dementia
Others such as Huntingtons, Wernickes. CJD
Diagnosis of dementia
History, cognitive testing, MMSE, MOCA, biomarkers, brainscans, bloods, DNA and CSF
Clinical features of Alzheimer’s
Amnesia, aphasia, agnosia, apraxia
Brain pathology in Alz
Enlarged and wider asymmetrical ventricles from atrophy, no well defined cortex, gyri widen, sulci have gaps, atrophy of hippocampus, frontal and temporal lobes
Proteins deposits in Alz
Amyloid protein plaques deposited around neurons and tau proteins tangle within brain
Genetic causes of Alz
Autosomal dominant and sporadic
Autosomal dominant causes of Alz
<65, early onset AD, frontotemporal and huntingtons
Sporadic causes of Alz
> 65 years, late onset AD, dementia with lewy bodies
Drug options for Alz
Anticholinesterases - Donepezil, Galantamine, Rivastigmine. NMDA receptor antagonists - Memantine
When are anticholinesterases used
Given in mild-moderate AD to temporarily improve cognitive function in early stages. Increase cholinergic transmission
Side effects of AChEI
Anorexia, nausea, vomiting, diarrhoea, abdo pain, hallucinations, drowsiness, agitation, dizziness, insomnia, headache, bradycardia
Use of NMDA antagonists
With AChEI in moderate AD or severe AD, or if intolerant to AChEI.
Side effects of NMDA antagonists
Constipation, ehadache, dizziness, drowsiness, HTN, dysopnoea
Cause of Huntington’s disease
Inherited autosomal dominant disorder, usually presenting at 50. Repeats of CAG trinucleotide, more repeats coresponds to earlier onset
Symptoms of Huntington’s disease
Personality change, depression, dementia, choreoathertosis, jerky movements
Diagnosis of Huntington’s
Genetic testing, loss of striatal volume, increased size of frontal horns in lateral ventricles on CT/MRI. Intranuclear aggregates of prtoein
Treatment of Huntington’s
Treat psychosis, depression, chorea. No treatment to stop progression of disability
Prognosis of Huntington’s
After diagnosis patients can live from 5 - 30 years
