Dementia Flashcards
What are the 4 most common types of dementia?
- Alzheimer’s dementia (50%)
- Lewy Body dementia
- Vascular dementia
- Fronto-temporal dementia
What are the 4 A’s of AD dementia?
- Amnesia
- Aphasia
- Apraxia (impaired ability to carry out motor activities despite intact motor function)
- Agnosia (failure to recognise or identify objects despite intact sensory function)
Define dementia
• Progressive, acquired impairment of cognitive function of at least two domains associated with impairment in activities of daily living (not able to function in society)
Clinical diagnosis only
RF for dementia
• Ageing
• F> M
• Head injury: less reserve, and possible inflammation
• Vascular diseases
Lower education (higher education is more reserve) therefore more cases in developing country
DDx for dementia
VITAMIN D VEST
Vitamin deficiency (B12, folate, thiamine)
Intracranial tumour
Trauma (head injury)
Anoxia
Metabolic (diabetes), Mild Cognitive Impairment
Infection (postencephalitis, HIV)
Normal pressure hydrocephalus, or Normal cognitive changes associated with ageing
Degenerative (Alzheimer’s, Huntington’s, CJD), Delerium, Depression, Disability (intellectual)
Vascular (multi-infarct dementia)
Endocrine (hypothyroid)
Space occupying lesion (chronic subdural hematoma)
Toxic (alcohol)
Features on Hx for dementia
• Patients with dementia may have difficulty with
• Learning and retaining new info (memory domain): therefore rely on lists and calendars, also leaving doors unlocked or stove on
• Handling complex tasks (executive function domain): such as banking, bills and payments
• Reasoning (executive function domain): especially adapting to unexpected situations and unfamiliar environments
• Spatial ability and orientation (perceptual domain): getting lost driving and walking
• Language domain: word finding, repetition, confabulation
• Behaviour (frontal lobe - BPSD): agitation, confusion, paranoia
• “geriatric giants”
• confusion/incontinence/falls/polypharmacy
• ADLs and IADLs
• cardiovascular, endocrine, neoplastic, renal
• alcohol, smoking
• OTCs, herbal remedies, medications (sedative hypnotics, antipsychotics, antidepressants,
anticholinergics), compliance, accessibility
• history of vascular disease or head trauma
• collateral history
Sundowning occurs - Sx gets worse at night
Ix for dementia
• Addenbrookes + MMSE (FTD often normal MMSE as it does not test frontal)
• Bloods: B12, folate, TSH (hypothyroid can mimic dementia), syphilis, HIV, ESR (cerebral vasculitis), ammonia if suspect liver disease
• Imaging:
○ CT brain (first line if old)
○ SPECT/PET scans
○ MRI (first line if young)
• Special
○ EEG: looking for non- convulsive seizures but cause focal deficits, prion disease
○ Go no go test (FLD)
○ CSF: looking for amyloid in CSF
Referral: neuropsychologist testing if unclear on diagnosis
Possible CT findings when Ix dementia
§ Vascular dementia, or mixed dementia with vascular cause
§ Ventricular expansion - normal pressure hydrocephalus, must compare with the sulci
§ Brain atrophy
§ Rule out space occupying lesion
MRI findings in dementia
§ Mass of mesial-temporal lobe (hippocampus) - suggestive of Alzheimer’s of disease if reduced mass
§ More subtle vascular changes: deep white matter indicates old infarct change
Non drug Mx of dementia
ABCDS
- Affective disorders and ADLs: change stove, copies of car keys, scheduled toileting to prevent incontinence, maintain routine
- Behavioural problems
- Caretaker, cognitive medications and stimulation
- Directives, Driving
- Sensory enhancement (glasses/hearing aids)
Drug Mx of dementia
Treatment does not stop progression, may only slow the progression. Only for AD and LBD
• Acetylcholinesterase inhibitors: Donepezil, rivastigmine, galantamine
○ Afx: pro cholinergic therefore can lead to urinary incontinence
• NMDA receptor antagonist: memantine - required later in disease progression, decreases onset of hallucinations and aggression
Antipsychotics: in patients with LBD it is BAD, antipyschotics can cause deterioration in cognitive and motor function and may paradoxically increase agitation and worsen behaviour
Pathophysiology of AD
• Largely unknown but main theory is amyloid deposition leading to neuronal cell loss and cortical cell atrophy in frontal, parietal and temporal lobes (hippocampi)
- Usually due to APP (amyloid precursor protein) mutation associated with APOE genetic RF
• Death of cholinergic neurons
- The spread of disease: temporal -> parietal (language) -> frontal (disinhibition)
Natural course of AD
• 2-3 years progressive decline
• MCI -> 10%/year probability to dementia
• Initially short term memory loss
• Then have other domains affected + psychiatric manifestations: deficits in executive function and language, apathy, major depressive disorder
• If parkinsonism present then consider LB dementia
Death from dementia: usually from dysphagia leading to aspiration pneumonia, loss of appetite and cachexia, immunosuppression
RF of AD
• Modifiable: vascular (theory of leaking amyloid) - DM, mid life HTN, mid life obesity, smoking, brain trauma, low education (theory of low neural plasticity)
- Non modifiable: Down’s syndrome (trisomy 21 - APP is on here therefore more precursor around; 40’s), FHx, age, ethnicity
Specific MRI findings for AD
○ Preferential atrophy of hippocampi and precueneus of the parietal lobe
○ Dilatation of lateral ventricles
- Widening of cortical sulci
