Behav. Sci. Dementia

Question 1

what are age-associated cognitive changes?

Answer 1

• difficulty retrieving words and names
• slower processing speed
• difficulty sustaining attention when faced with competing environmental stimuli
• learning something new takes a bigger effort
• no functional impairment

Question 2

how does dementia occur?

Answer 2

on a continuum (normal aging, followed by mild cognitive impairment, followed by dementia)

Question 3

mild cognitive impairment definition

Answer 3

• memory complaint corroborated by an informant
• objective memory impairment for age and education
• preserved general cognition
• normal activities of daily living can still be done
• not demented

Question 4

amnestic MCI

Answer 4

• memory loss not meeting the criteria for dementia
• progresses to AD at rate of 10%-15% per year vs. 1%-3% incidence in the general population
• may be the earliest phase of AD
• clinical diagnosis because no “MCI test”

Question 5

DSM-IV diagnostic criteria for dementia

Answer 5

memory decline/impairment and at least one of the following:
aphasia (language decline)
impaired executive function
apraxia (inability to do certain actions)
agnosia (inability to interpret sensations)
-cognitive deficits must impact social/occupational function

Question 6

early-onset AD

Answer 6

occurs btw 30-60

rare; familial in most cases

Question 7

what are the gene mutations present in early-onset AD?

Answer 7

1,14,21
1 - presenilin 2 mutation
14- presenilin 1 mutation
21 - abnormal amyloid precursor protein

Question 8

late-onset AD

Answer 8

MC
develops after 60
combination of factors

Question 9

which gene is implicated in late-onset AD?

Answer 9

chromosome 19 - apolipoprotein E4 gene

Question 10

what is present in the brain of someone with AD?

Answer 10

amyloid plaques (alpha beta) both extracellular and in arteries (amyloid angiopathy)
neurofibrillary tangles (intracellular inclusions of tau)

Question 11

what is disproportionately atrophied in AD?

Answer 11

hippocampus (memory!)

Question 12

what does silver stain show?

Answer 12

neuritic plaques and neurofibrillary tangles in AD brain

Question 13

congo red shows what?!

Answer 13

amyloid in plaques

Question 14

what are the cleave sites on APP?

Answer 14

40 and 42 - 42 is worse

Question 15

mutations in which gene is responsible for the large majority of cases of autosomal dominant alzheimer’s?

Answer 15

presenilin

Question 16

how does a neuritic plaque appear?

Answer 16

dense central core of compact amyloid surrounded by a clear zone and a peripheral corona or halo

Question 17

what is the patient at risk for when they have amyloid angiopathy?

Answer 17

hemorrhage

Question 18

why does the body have difficulty clearing neurofibrillary tangles?

Answer 18

insoluble - body can’t clear

Question 19

how do neurofibrillary tangles appear?

Answer 19

flame shape (form shape of neuron)

Question 20

what are the neurofibrillary tangles?

Answer 20

hyperphosphorylated tau (microtubule-associated protein)

Question 21

frontotemporal lobar degeneration gene

Answer 21

FTLD-tau (can also have TDP or FUS associated)
earlier onset than AD
affects anterior frontal and superior temporal lobes, spares occipital and parietal
knife edge

Question 22

what protein is associated with frontotemporal lobar degeneration?

Answer 22

pick bodies (tau) - rounded

Question 23

AD risk factors

Answer 23

increasing age, females, family history, less education, depression, head injury, low folate and vit B12, presence of apolipoprotein E4 allele, alcohol abuse

Question 24

what are the 3 key features of AD?

Answer 24

impaired cognition, impaired function, and behavioral disturbances

Question 25

how to tell the difference between depression vs dementia

Answer 25

1. depression will demonstrate less motivation during cognitive testing
2. express cognitive complaints that exceed measured deficits
3. maintain language and motor skills

Question 26

frontotemporal dementia (pick’s disease) vs alzheimer’s

Answer 26

Pick’s has insidious onset, gradual progression
early decline in social interpersonal conduct
early impairment in regulation of personal conduct with loss of insight
early emotional blunting
characterized by behavioral abnormalities
memory loss occurs later

Question 27

treatment for frontotemporal dementia

Answer 27

no role for cholinesterase inhibitors
careful use of atypical antipsychotics (quetiapine, risperdol)
divalproex for behavior control
SSRIs for irritability, depression, impulsiveness

Question 28

pharmacotherapy of alzheimer’s

Answer 28

cholinergic (donepazil - ACE inhibitor)

NMDA receptor antagonists

Question 29

what is the most used class of drugs for AD right now?

Answer 29

neurotransmitter replacement

Question 30

why do anticholinesterases work?

Answer 30

AD results in degeneration of basal nucleus causing acetylcholine deficiency which contributes to the memory deficits

Question 31

what are the anticholinesterases used in AD?

Answer 31

donepezil, rivastigmine, galantamine

Question 32

what is memantine?

Answer 32

glutamate NMDA receptor blocker used in AD

Question 33

what are the options for treating neuropsychiatric disturbances in AD patients?

Answer 33

1. counseling! look for the triggers - behavioral approach
2. antipsychotics (risperidone and haloperidol)
3. antidepressants (sertraline and venlafaxine)
4. anxiolytics (buspirone and lorazepam)

Question 34

vascular dementia

Answer 34

multi-infarct dementia
cerebral amyloid angiopathy (can be in association with alzheimer’s)
hypertension-related small vessel disease

Question 35

what is present in the brain of vascular dementia?

Answer 35

lacunar infarcts
subcortical dementia (cognitive slowing, impaired problem solving, visuospatial abnormalities, disturbances of mood/affect)

Question 36

vascular dementia clinical appearance

Answer 36

“step wise progression” abrupt after CVA, seen with cardiovascular risks
“mixed” dementia with AD or Lewy Body not unusual
emotional lability

Question 37

treatment of vascular dementia

Answer 37

focus on controlling cardiovascular risk factors

also: cholinesterase inhibitors (donepezil, galantamine, rivastigmine)

Question 38

Lewy body dementia

Answer 38

characterized by intracellular, fibriller deposits of presynaptic terminal protein alpha-synuclein (lewy bodies)

Question 39

what are the lewy body disorders

Answer 39

1. parkinson’s

2. dementia with lewy bodies

Question 40

parkinson’s disease

Answer 40

MCC parkinsonism (tremor, postural instability, impaired voluntary movement)
dopaminergic deficit (responsive to L-dopa)

Question 41

lewy body dementia vs parkinsons

Answer 41

lewy body: onset of dementia within 12 months of parkinsonism

parkinson’s: onset of dementia more than 12 months AFTER diagnosis of PD

Question 42

what is needed to make diagnosis of parkinsons’

Answer 42

pallor of substantia nigra AND lewy bodies

Question 43

dementia with Lewy bodies

Answer 43

• memory less affected than AD,
• frontal and subcortical features (deficits in attention and alertness),
• pronounced fluctuations and variations in symptoms
• have vivid visual hallucinations and delusions (including dreams - REM sleep disorder)

Question 44

where are lewy bodies more present in dementia with lewy bodies?

Answer 44

cortical - amygdala and cingulate gyrus most common

Question 45

how do lewy bodies appear?

Answer 45

dark core and pale corona - stain positive for alpha-synuclein

Question 46

Mini Mental Status Exam

Answer 46

used for screening
normal 30-27
mild 30-20
moderate 20-10
severe 10 or lower

Question 47

MoCA (montreal cognitive assessment)

Answer 47

normal more than 26
mild 18-26
moderate 10-17
severe less than 10

Question 48

functional assessment: ADLs

Answer 48

activities of daily living: DEATH

dressing, eating, ambulating, toilet, hygiene

Question 49

functional assessment: IADLs

Answer 49

instrumental ADLs: SHAFT

Shopping, Housekeeping, Accounting, Food prep, Transport