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59 Cards in this Set

  • Front
  • Back
Breakdown of etiology of dementia
(statistical % of causes)
85% due to Alzheimer's, Vascular dementia, or a combo
15% due to variety of other conditions
Common neuroimaging findings in "normal" elderly (2)
Enlarged ventricles and atrophy
Ischemic changes in deep white matter and basal ganglia
Characteristic problems of mild cognitive impairment (4)
Finding words "on tip of tongue"
Trouble recalling names
Misplacing things
In amnestic disorder, memory disturbance must be a consequence of what?
A general medical condition
What part of the brain is most sensitive to ischemia?
Amnestic syndrome can reflect disruption anywhere along what?
Medial hemispheric circuit
How does prevalence of dementia progress after age 65
Prevalence doubles every 5 years
Pick's Disease
Frontal lobe degeneration
(This is a primary dementia)
Far and away the most common cause of dementia
Alzheimer's disease
Development of aphasia in cortical vs. subcortical dementia
Cortical -- aphasia early

Subcortical -- dysarthria early, but NO aphasia
Relative quality of recognition vs. recall in C vs. SC dementia
Cortical -- recognition = recall

Subcortical -- recall is worse than recognition
(if you show them something, they'll recognize it)
Speed of thinking of in C vs. SC dementia
Cortical -- NORMAL speed of thinking

Subcortical -- SLOWED thinking
Proportionality of decline in executive functioning in C vs. SC dementia
Cortical -- decline in executive functioning is proportional to other traits

Subcortical -- early decline in exec. functioning GREATER THAN other deficits
Motor exam finding in C vs. SC dementia
Cortical -- NORMAL motor exam early

Subcortical -- movement disorders are common
What is the only way Alzheimer's can be diagnosed definitively?
At autopsy
Examples of CORTICAL dementia (3)
Pick's Disease
Cortical strokes
Examples of SUBCORTICAL dementia (6)
"Diagnosis" of Alzheimer's must show multiple cognitive deficits w/ both:
Memory impairment AND

One (or more) of following:
Apraxia, Aphasia, Agnosia
Impaired exectuitve functioning
Onset of Alzheimer's typically begins when?
After age 55
How do MMSE scores of Alzheimer's pts. change over time?
2-3 pt. decline per year
What is the mean post-diagnosis survival time in Alzheimer's?
10 years
How is memory first affected by Alzheimer's?
Long-term memory is initially in tact
Short-term memory is impaired
How does the EEG of Alzheimer's pts. change between stages of disease?
Stage 1 - Normal
Stage 2 - Background slowing
Stage 3 - Diffuse slowing
CT/MRI evolution through stages of Alzheimer's
Stage 1 - Normal
Stage 2 - Normal or mild atrophy/ventricular enlargement
Stage 3 - Ventricular dilatation; sulcal enlargement
Progression of PET/SPECT scans in Alzheimer's
Starts off w/ bilateral, posterior, parietal-temporal hypometabolism

Becomes, biparietal AND frontal hypometabolism
Pattern of neuronal loss in Alzheimer's
Two primary brain regions affected by Alzheimer's
Temporal-parietal cortex
Brain regions relatively spared by Alzheimer's
Primary motor, sensory, and visual cortices
What/where are amyloid plaques?
EXTRAcellular lesions
Core of beta-amyloid surrounded by dystrophic neurites
What are neurofibrillary tangles?
INTRAcellular lesions
Made of abnormally phosphorylated microtubules
What are Hirano bodies?
Cytoplasmic aggregates of actin and assoc. proteins

These affect the cytoskeletal structure
Early Alzheimer's changes seen on PET scan
Extensive hypometabolism in temporal-parietal cortex

INCREASED activity in hippocampal area
"revving harder to think"
Later Alzheimer's changes seen on PET scan
Hypometabolism spreads to frontal cortex

BUT, primary motor, sensory and visual cortices rel. spared
Temporal-parietal hypoperfusion is NOT specific to Alzheimer's

What other conditions can cause i (3)?
Sleep apnea
Hypoxic brain injury
Vascular Dementia
% of Alzheimer's cases that are familial
Concordance in Alzheimer's twins
40% for monozygotic
SAME for dizygotic

SO, environmental factors must play a role
Early onset cases of Alzheimer's show links to what chromosomes (2)?
Some late onset and sporadic cases of AD show links to what chromosome?
19 (The gene for ApoE4)
Binds avidly to beta-amyloid
Found in plaques and tangles

1 copy causes 3x greater risk
2 copies causes 8x greater risk
Potential etiologies for Alzheimer's (4)
Acetylcholine deficiency
Excess glutamate
Amyloid hypothesis
ApoE hypothesis
Key points about using cholinergic drugs in Alzheimer's
More effective EARLY

Do NOT change rate of progression of illness
Tacrine (Cognex)
Reversible cholinesterase inhibitor

NOT used anymore
Most pts. couldn't tolerate the high doses
(hepatotoxicity, Inc. gastric acid, N&V)
Donepezil (Aricept)
Cholinesterase inhibitor

Can be take ONCE daily
NOT assoc. w/ liver toxicity
Rivastigmine (Exelon)
Cholinesterase inhibitor

Taken TWICE daily
NOT assoc. w/ liver toxicity
Galantamine (Reminyl)
BOTH a cholinesterase inhibitor
AND a nicotine receptor allosteric modulator
ACh loss in Alzheimer's corresponds to loss of neurons where?
Nucleus Basalis of Meynert
Neurotransmitter that is most depleted in Alzheimer's
Glutamate/Excitotoxicity Hypothesis
Too much glutamate
Thus, too great an influx of Calcium

Calcium activates enzymes that make free radicals
Free radicals injure neuron membranes and organelles

Cell is "excited to death"
2 main treatment implications of glutamate/excitotoxicity hypothesis
Glutamate blockade
Antioxidant Therapy
Memantine (Namenda)
NMDA-receptor antagonist

Approved for moderate to severe Alzheimer's
Can be combined with cholinesterase inhibitors
Which works better in Alzheimer's?

Vitamin E or Selegline
Both are equally effective
Both show little effect on COGNITION

BUT, can potentially slow functional decline
Is it better to use Vitamin E and Selegline in combo, or either alone?
The combination actually performs worse than either drug alone
Amyloid hypothesis
Excessive amyloid accumulation leads to destruction of neurons

Analogy to cholesterol in heart disease
What chromosome is the Amyloid precursor gene on?
Which ApoE allele is linked with the lowest risk of AD?
What is ApoE?
Apolipoprotein involved in clearing lipids in the bloodstream

Binds avidly to beta-amyloid

Has been found in plaques, tangles, and amyloid angiopathies
Which ApoE allele is linked with the highest risk of AD?

Analogy is made to "good" and "bad" cholesterol
5 main steps in treatment plan for AD
Establish alliance w/ pt. and family

Follow cognitive status and treat comorbid problems
Monitor for pt. safety

Consider anti-oxidant therapy
Consider cholinergic/glutamate blocking therapy
Commonly prescribed in AD despite being only 20-30% effective

Should be reserved for severe agitation and psychosis