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Dementias Flashcards

1
Q

Diagnostic goal

A

whether or not cognitive changes are above and beyond what we expect from normal aging

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2
Q

Dementia

A

a collection of cognitive/personality/behavioral changes associated with disease progression

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3
Q

Atrophy

A

neuronal loss leading to loss of brain volume

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4
Q

cortical dementia

A

affects behavior, personality, and memory.
-alzheimers, FTD

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5
Q

Subcortical dementia

A

affects motor, processing speed, and attention
-Parkinson’s, Huntington’s

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6
Q

Mixed dementia

A

affects cortical and subcortical areas
-lewy body, vascular dementia

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7
Q

Alzheimer’s Disease

A

most common dementia, 50%
-majority dev after 65
-risk increases with age
-onset can happen as early as 40

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8
Q

Alzheimer’s pathology

A

characterized with abnormal protein deposits (amyloid plaques and tau tangles)
-initial degeneration occurs in the medial temporal lobe (memory), the hippocampus, and the entorhinal cortex
-later spreads to the parietal and frontal cortexes (perceptual, visual, and exec. funtioning)

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9
Q

Alzheimer’s MRI finding

A

temporal and parietal lobe atrophy, enlargement of the ventricles

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10
Q

Mild Alzheimer’s

A

memory lapses, word finding problems, trouble with planning and organizing

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11
Q

Moderate Alzheimer’s

A

more pronounced memory and word finding problems, increased executive concerns, personality changes, changes in sleep patterns

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12
Q

Severe Alzheimer’s

A

brain tissue shrink significantly, severe cog impairments, withdrawl

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13
Q

Alzheimer’s early deficits

A

memory impairment (amnesia), rapid forgetting, impaired learning, semantic memory deficits

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14
Q

Alzheimer’s later deficits

A

global cognitive impairment, visual agnosia, aphasia

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15
Q

Vascular dementia

A

2nd most common (10% pure 15%mixed)
-onset b/t 60-75

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16
Q

VD risk factors

A

stroke, high bp, diabetes, high cholesterol, smoking, obesity

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17
Q

VD course

A

depends on when/where ischemic event occurs in the brain
-often a stepwise pattern (periods of stability followed by rapid deterioration due to additional strokes)

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18
Q

VD pathology

A

cause; cerebrovascular disease or impaired cerebral blood flow
-frontal subcortical profile (slow processing, attention, concentration, exec functioning)
-impaired memory as a consequence of impaired attention/concentration
-spec deficits due to lesion location

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19
Q

Frontal temporal dementia

A

4th most common
-onset b/t 50-60 (earlier than most)
-Risk: genetics and presence of ubiquitin

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20
Q

FTD pathology

A

inclusion bodies and pick bodies
-regional cortical atrophy, predom in frontal or temporal lobes
-degeneration of some aspect of frontal or temporal lobes

21
Q

inclusion bodies

A

accumulation of protein inside cells that are markers of disease

22
Q

Pick bodies

A

tau inclusions and ubiquitin inclusions

23
Q

Behavioral variant FTD

A

atrophy, neuronal loss of the frontal cortex
- tauopathy with tau positive inclusions

24
Q

PPA variants

A

nonfluent/agrammatic, semantic, logopenic

25
Nonfluent/agrammatic PPA
frontal and basal ganglia atrophy -Intact: meaning of words -Impaired: grammar and speech production
26
Semantic PPA
temporal atrophy -intact: fluent speech -impaired: meaning of words
27
Logopenic PPA
temporal and parietal atrophy -intact: comprehension -impaired: word finding
28
PPA vs aphasia from stroke
Aphasia from stroke appears suddenly and does not worsen PPA is a neruodegen disorder and develops gradually and worsens over time
29
FTD behavioral presentation
personality changes consistent with frontal systems dysfunction -loss of social awareness, apathy, social withdrawal, decreased personal hygiene, etc.
30
FTD neruopsych presentation
exec dysfunction, memory dysfunction, language deficits, intact visuospatial and orientation
31
AD vs FTD: AD (memory, rapid forgetting, exec dysfunction, personality change)
memory: early rapid forgetting: present Exec dysfunction: later on Personality change: later on
32
AD vs FTD: FTD (memory, rapid forgetting, exec dysfunction, personality change)
Memory: later rapid forgetting: absent Exec dysfunction: early on Personality change: early on
33
Parkinson's disease/dementia
motor symptoms related to dysfunction w/in nigrostriatal dopaminergic pathways non-motor associated with progressive impairment in other dopaminergic pathways -hypokinetic (loss of muscle movement)
34
PD epidemiology
peak onset around 60 -7-8 years after diagnosis become wheelchair bound -neuropsych involvement predictor of progression rate
35
PD causes
dopamine involved in control and coordination of body movement - loss of dopaminergic neurons in substantria nigra (of basal ganglia) -reduction of dopamine leads to dif with controlling movement *neuronal loss is slow, so symptoms become noticeable after 80% of cells in sub. nigra are gone*
36
PD symptoms
Motor: tremors, slow movements (bradykinesia), involuntary muscle contractions, shuffling gait non-motor: depression, anxiety, apathy, pain, fatigue cog: processing speed, working mem, language
37
PD treatments
L-DOPA: precursor to dopamine that can pass BBB, mod doses decrease motor Deep brain stim: implants electrodes w/in spec brain regions
38
Lewy body
12-27% b/t 50-70 -slow, 5-7 years -cognitive deficits present before motor -punctuated by periods of fluctuation of mental status/orientation
39
LB pathology
lewy bodies that are diffusely spread -brainstem, cortical areas, hippo, midbrain, basal ganglia -
40
LB behavior
fluctuating attention/mental status -parkinsonian symptoms -hallucinations -sleep problems
41
Huntington's disease
hyperkinetic movement disorder -inherited caused by mutations in HTT gene -leads to degeneration of neurons in basal ganglia -30-50 progresses 15 days after onset
42
HD pathology
loss of some neurons in the caudate -indirect b. ganglia thalamocortical circuitry affected -at death, brain volume can be decreased by as much as 25%
43
HD symptoms
chorea (involuntary dance), bradykinesia (slow movement), dystonia (involuntary muscle contractions, parkinsonian, exec function, mem loss
44
ALS (amyotrophic lateral sclerosis)
neruodegen disease that causes progressive loss of motor neurons w/in spinal cord and cranial nerves -results in continual difficulties with controlling voluntary movements -initial presentation can be either limb or bulbar onset
45
ALS early symptoms
limb: muscle twitching, cramps, weakness, stiffness Bulbar: muscle twitches in tongue, slurred speech, chewing and swallowing diff
46
ALS epidemiology
58-80 survival for 3-4 years
47
ALS cog& behavorial
exec dysfunction depression, apathy, low motivation
48
ALS treatment
no cure, slow progression

Phys Psych (21 decks)

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