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Phys Psych > Dementias > Flashcards

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
Q

Nonfluent/agrammatic PPA

A

frontal and basal ganglia atrophy
-Intact: meaning of words
-Impaired: grammar and speech production

26
Q

Semantic PPA

A

temporal atrophy
-intact: fluent speech
-impaired: meaning of words

27
Q

Logopenic PPA

A

temporal and parietal atrophy
-intact: comprehension
-impaired: word finding

28
Q

PPA vs aphasia from stroke

A

Aphasia from stroke appears suddenly and does not worsen
PPA is a neruodegen disorder and develops gradually and worsens over time

29
Q

FTD behavioral presentation

A

personality changes consistent with frontal systems dysfunction
-loss of social awareness, apathy, social withdrawal, decreased personal hygiene, etc.

30
Q

FTD neruopsych presentation

A

exec dysfunction, memory dysfunction, language deficits, intact visuospatial and orientation

31
Q

AD vs FTD: AD
(memory, rapid forgetting, exec dysfunction, personality change)

A

memory: early
rapid forgetting: present
Exec dysfunction: later on
Personality change: later on

32
Q

AD vs FTD: FTD
(memory, rapid forgetting, exec dysfunction, personality change)

A

Memory: later
rapid forgetting: absent
Exec dysfunction: early on
Personality change: early on

33
Q

Parkinson’s disease/dementia

A

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
Q

PD epidemiology

A

peak onset around 60
-7-8 years after diagnosis become wheelchair bound
-neuropsych involvement predictor of progression rate

35
Q

PD causes

A

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
Q

PD symptoms

A

Motor: tremors, slow movements (bradykinesia), involuntary muscle contractions, shuffling gait
non-motor: depression, anxiety, apathy, pain, fatigue
cog: processing speed, working mem, language

37
Q

PD treatments

A

L-DOPA: precursor to dopamine that can pass BBB, mod doses decrease motor

Deep brain stim: implants electrodes w/in spec brain regions

38
Q

Lewy body

A

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
Q

LB pathology

A

lewy bodies that are diffusely spread
-brainstem, cortical areas, hippo, midbrain, basal ganglia
-

40
Q

LB behavior

A

fluctuating attention/mental status
-parkinsonian symptoms
-hallucinations
-sleep problems

41
Q

Huntington’s disease

A

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
Q

HD pathology

A

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
Q

HD symptoms

A

chorea (involuntary dance), bradykinesia (slow movement), dystonia (involuntary muscle contractions, parkinsonian, exec function, mem loss

44
Q

ALS (amyotrophic lateral sclerosis)

A

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
Q

ALS early symptoms

A

limb: muscle twitching, cramps, weakness, stiffness
Bulbar: muscle twitches in tongue, slurred speech, chewing and swallowing diff

46
Q

ALS epidemiology

A

58-80
survival for 3-4 years

47
Q

ALS cog& behavorial

A

exec dysfunction
depression, apathy, low motivation

48
Q

ALS treatment

A

no cure, slow progression

Phys Psych (21 decks)

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