Dementia Flashcards
dementia
global deterioration of intellectual function in the face of unimpaired consciousness
impaired cognition - memory, abstract thinking, judgement, processing/organizing daily lives
assessment
general medical and neurological history, neurobehavioural and psychiatric history, toxic/drug history, family history
assess mental state → level of consciousness, orientation, memory, attention + concentration, knowledge, language
MMSE/MOCA - quantification measures decline over time
pathology
deficits depend on the initial affected area of brain and the rate of progression
progression of deterioration of intellectual function
acute = weeks - encephalitis
subacute = months - CJD
chronic = years - Alzheimer’s disease
frontal lobe
motor speech area - speech apraxia
pre-motor cortex - behavioural changes
also: Pick’s, Huntington’s
parietal lobe
visuo-spatial orientation
constructional apraxia (inability to draw/copy)
disturbances in cognitive function
dysfunction in frontal lobe
lead to abnormal reflexes → primitive
primitive reflexes
present as babies but fade → return in dementia
- pout reflex - lips pout when tapped
- glabellar reflex - cannot inhibit blinking response to stimulation
- grasp reflex - stroking palm induces grasp
- palmo mental reflex - scratching hand causes contraction of chin muscles
causes
- degenerative
- cerebrovascular
- structural
- infection
- toxic/metabolic
- immune/cancer
- depression
degenerative cause
most common cause (80-85%)
dysfunction + degeneration of neurons and brain cells
age progression
vulnerable regions: parietal, temporal - hippocampus (memory + cognition)
specific targets: Huntington’s = basal ganglia; Parkinson’s = substantia nigra
protein misfolding + abnormal deposition
cerebrovascular cause
2nd most common cause
inflammation of blood vessels - CNS vasculitis
laboratory investigations
clinical history/exam
blood tests/screens for treatable causes, infections
neuroimaging
Alzheimer’s disease
irreversible, progressive - destroys memory + thinking
risk increases with age
disrupts neuron communication, metabolism, + repair
most common cause of dementia
Alzheimer’s clinical features
memory impairment
hallucinations
paranoia
cognitive impairment, personality changes, disorientation
motor and gait disturbances
falls
seizures
autonomic dysfunction
etiology of Alzheimer’s
familial forms
sporadic (unknown cause) - majority of cases
early onset - 40-50 (usually genetic = APP, presenilin 1 and 2 mutations)
late onset - mostly sporadic; apolipoprotein E4, SORL1, CLU, CR1
amyloid precursor protein
membrane protein important for neuronal growth and repair
secreatases cut it into fragments → B-amyloid is sticky fragment - cling together = plaques
neuropathology of Alzheimer’s
cortical atrophy
synaptic + neuronal loss
neurofibrillary tangles - twisted fibres
B-amyloid plaques - deposition in hippocampus and amygdala
tau proteins
neurotransmitter abnormalities in Alzheimer’s
decreased acetylcholine in cortex and hippocampus
neurons in the basal forebrain synthesize Ach - project forward into cortex → neurons die = deficiency in Ach
Alzheimer’s treatment
cholinesterase inhibitors - more Ach
NMDA receptor blockers - glutamate
less effective over time as cells die = no targets
imaging
CT + MRI - show atrophy in hippocampus
PET scan - visualize amyloid in brain
Lewy Body dementia
fluctuating cognition
recurrent visual hallucinations
Parkinsonism
lewy bodies contain alpha-synuclein protein
loss of pigmented dopamine neurons in substantia nigra
Frontotemporal dementia (Pick’s)
bias to females
younger age
frontal and temporal lobe atrophy
Tau pathology
familial forms - gene on chromosome 17
vascular dementia
10-15%
accumulation of strokes causes progressive loss of function
risk factors: hypertension, diabetes, high cholesterol
