32. Deterioration of intellect Flashcards
what is dementia
An acquired global impairment of intellect memory and personality without impairment of consciousness, that is usually (but not always) progressive and usually irreversible
Presentation: Progressive IMPairment of Intellect, Memory and Personality resulting in impairment in the activities of daily living.
approach to ?cognitive decline
- rule out reversible causes = PINCH ME, mood, agitation, bleed, hearing loss
- examination: CN, neuro Ul, LL, hearing, cardiovascular (vascular dementia)
- bloods: confusion screen
- imaging: CT head ?bleed - Assess cognitive decline severity eg MMSE
- Get imaging during the work up eg CT or MRI
What assessment tools for dementia are recommended for the NON-specialist setting
10-point cognitive screener (10-CS),
6-Item cognitive impairment test (6CIT)
interpretation of MMSE
<24 = could be dementia
<10 severe dementia
presentation alzhimers
insidious onset, Loss of ability to learn, process and retain new info, memory loss especially for names and recent events, language deficits, rapid forgetting, normal gait and neuro exam early
imaging results alzhimers
generalised atrophy (esp medial temporal and parietal later), beta amyloid plaques amyloid plaques and neurofibrillary (tangles tau protein tangles within brain cells)
management alzhimers
non-pharma
- activities to promote wellbeing
pharma
1. acetylcholinesterase inhibitor eg donepezil, galantamine and rivastigmine)
- memantine (an NMDA receptor antagonist)
what investgation should you do before prescribing acetylcholinesterase inhibitors ?
ECG
Unsafe if have QT prolongation, third degree heart block, sinus bradycardia - always check ECG before prescribing.
adverse effects acetylcholinesterase inhibitors
cholinergic side effects such as diarrhoea, nausea and vomiting, bradycardia, increased salivary production and urinary incontinence.
SE acetylcholinesterase inhibitors
diarrhoea
donezapil - insomnia
SE memantine
constipation
presentation vascualr dementia
abrupt or gradual onset, focal neurological signs, signs of vascular disease, stepwise deterioration in someone with previous cardiovascular illness or events.
pathology/imaging findings vascualr dementia
strokes, lunacar infarcts, white matter lesions, vulnerable to CVS events
what imaging is best for vascualr dementia
MRI
what may be used to help make a diagnosis of vascualr dementia
NINDS-AIREN criteria
- presence of cog decline that interferes with ADLs, not due to secondary effects of CVS event
- cerebrovascular disease as shown by neuro signs and/or imaging
- relationship between the above, inferred by
the onset of dementia within three months following a recognised stroke
an abrupt deterioration in cognitive functions
fluctuating, stepwise progression of cognitive deficits
management of vascualr dementia
- manage CVS risk
eg Antiplatelet therapy (aspirin, clopidogrel), Carotid angioplasty/stenting, BP control, glycaemic control, statins
+ supportive and social prescribing
presentation frontotemporal dementia/picks disease
insidious onset, 50-60yo, rapid progression, sibinhibition, socially inappropriate, poor judgement, apathy, poor executive function, impulsivity.
No movement abnormalities
pathology/imaging frontotemporal dementia
MRI shows significant atrophy of the frontal and temporal lobes. Pick cells and pick bodies in cortex
management of picks disease
supportive care, benzos, antipsychotics
NICE do not recommend that AChE inhibitors or memantine are used in people with frontotemporal dementia
what is Semantic dementia
a type of frontotemporal lobar degeneration
fluent progressive aphasia. The speech is fluent but empty and conveys little meaning. Unlike in Alzheimer’s memory is better for recent rather than remote events.
common features of the frontotemporal lobar dementias
Onset before 65
Insidious onset
Relatively preserved memory and visuospatial skills
Personality change and social conduct problems
triad in pellagra? other fetaures>
Dementia, Dermatitis, Diarrhoea
Other features include hair loss, sunlight sensitivity and glossitis.
cause of pellagra? risk factors?
Caused by vitamin B3 (niacin) deficiency.
Alcoholism and crohn’s are risk factors for pellagra due to malnutrition/malabsorption. Pellagra may occur as a consequence of isoniazid therapy (isoniazid inhibits the conversion of tryptophan to niacin).
tetrad of wernike’s
ataxia, ophthalmoplegia, nystagmus and acute confusional state
where are the lesions in wernikes
mamillary bodies and ventricle walls
which b vitamin is thiamine
B1
what is korsakoffs
irreversible damage and haemorrhage to the mammillary bodies of the hypothalamus and the medial thalamus
features korsakoffs
anterograde amnesia: inability to acquire new memories
retrograde amnesia
confabulation
