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Cognitive Communication Disorders > Exam 1 (weeks 1-3) > Flashcards

Exam 1 (weeks 1-3) Flashcards

1
Q

Cog-Com skills

A

problem-solving, planning, decision-making, behavior regulation, social communication

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2
Q

Associated cognitive function

A

Attention, memory, reasoning, inferencing, abstract thinking, etc.

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3
Q

Associated communication function

A

Prosody, facial expression, social scripts, turn taking, non-literal language, etc.

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4
Q

Cognitive Communication

A
  • language in use, not structure
  • functional communication
  • cognitive processes supporting functional communication
  • neurological structure and functions supporting cognitive processes
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5
Q

functional communication

A
  • communicating wants and needs
  • communicating emotional state appropriately
  • taking social context into account
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6
Q

Injuries that cause cog-com dis

A
  • cerebrovascular accident (CVA), aka stoke
  • trauma
  • sudden onset, subsequent recovery
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7
Q

CVA (stroke)

A
  • caused by clot or hemorrhage
  • disrupt blood flow and cause cell death
  • localized damage
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8
Q

trauma

A
  • closed or open (through dura) head injury
  • penetrating (always open) or blunt (either)
  • impact and movement cause causes cell death
  • swelling, bleeding, and neurochemical changes exacerbate and can have global impact
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9
Q

Disease that cause cog-com

A
  • multiple possible disease processes
  • micro changes lead to macro differences
  • progressive deterioation
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10
Q

multiple possible diseases process

A
  • multi-infarct
  • protein clumps or other cell abnormalities
  • lead to cell death and atrophy
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11
Q

Micro-changes lead to macro differences

A

global impact possible

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12
Q

causes of cog-com dis

A

CVA, trauma, and disease

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13
Q

cognitive communication profiles

A
  • dementia
  • traumatic brain injury (TBI)
    right hemisphere disorder (RHD)
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14
Q

not a one to one correspondence

A
  • CVA and trauma can lead to RHD or TBI
  • Multiple CVA and repeated trauma can lead to dementia
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15
Q

Hippocampus

A

the main area for memory formation

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16
Q

damage to fornix

A

results in amnesia, important structure for memory formation

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17
Q

occipital lobe

A

vision- in between preoccipital notch and the parieto-occipital sulcus

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18
Q

parietal lobe

A
  • somatosensory (post central )
  • sensory homunculus
  • pain and temperature
  • integrative! (making sense of signals)
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19
Q

temporal lobe

A
  • receptive language (left side only)
  • memory
  • hearing (auditory processing cortex)
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20
Q

frontal lobe

A
  • executive function
  • primary motor (precentral gyrus)
  • expressive language
  • Brocas area
  • memory attention, decision making, impulse control
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21
Q

Limbic system

A
  • emotion regulation
  • memory consolidation (Papez)
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22
Q

basal ganglia

A

motor coordination/ feedback loop

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23
Q

cerebellum

A
  • memory/sensory (proprioception) integration
  • cognitive involvement
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24
Q

Meninges

A
  • skull
  • dura mater (outermost layer)
  • arachnoid (blood vessel)
  • subarachnoid space (present) where the cerebralspinal fluid lives
  • pia mater
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25
Q

Apoptosis

A
  • diminishing of neurons as we age
  • neuronal “pruning” as part of the normal aging process throughout the life span
  • hard to quantify (20-40% of brain cells)
  • appears as widened sulci and ventricles on imaging
  • not equally disrupted: (hippocampus and frontal lobe)
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26
Q

What abilities so we lose in normal aging?

A
  • processing speed
  • word finding abilities
  • short term memory
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27
Q

Aging brain unique to humans?

A

-Atrophy of brain normal in humans
- not universal to mammals

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28
Q

different models of aging

A
  • disease/disabled aging
  • usual aging
  • successful aging
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29
Q

disease/disabled aging

A

non-age related disease or pathology

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30
Q

usual aging

A

age-related physiological changes
- renal function
- memory/word finding
- thinning of skin

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31
Q

successful aging

A
  • avoidance of age-related pathology or disease
  • minimal interruption of usual function
  • variable profiles ( not all cognitive abilities are affected the same)
  • protective or detrimental effects of (education, physical health like cardio for cardiopulmonary, mental health, and psychological factors)
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32
Q

Seattle Longitudinal study

A

Looking at people’s cognitive functions and several sorts of standardized tests to determine their cognitive functions as they age in 7-year increments
- higher education good
- physical health (particularly cardio-pulmonary) good
- self-efficacy protective good
- depression is detrimental bad
- neurological changes not 100% predictive of cognitive function

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33
Q

key to Successful Aging

A
  • physical activity
  • positive mental attitude
  • self-efficacy
  • social engagement (high educational level and creativity)
  • not 1:1 of structure and function
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34
Q

implications

A
  • neuroplasticity even in old age
  • mental and physical activity can alter the brain
  • inconsistent cognitive profiles related to both anatomy and physiology
  • mental decline is not inevitable
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35
Q

information processing model of memory a three-stage model

A

sensory input > sensory register (forgetting) > short-term memory (forgetting and rehearsal) > long term memory

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36
Q

retrospective memory

A
  • declarative memory and procedural memory
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37
Q

declarative memory

A
  • semantic memory: I know what a car is.
  • episodic memory: I remember buying my car
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38
Q

procedural memory

A

I remember how to drive a car

39
Q

1-2 seconds time frame

A
  • sensory stage
  • sense organs, primary auditory, somatosensory, and visual cortex
40
Q

0-30 seconds time frames

A
  • immediate (short-term, primary, working)
  • sensory and motor association areas and prefrontal regions
41
Q

30 seconds - days time frame

A
  • recent
  • medial temporal lobes (hippocampus and amygdala), diencephalon (hypothalamus and dorsal medial nuclei of thalamus)
42
Q

days - years

A
  • remote
  • left and right association cortex
43
Q

hippocampal damage

A

impaired formation of new declarative memories

44
Q

damage to the diencephalon (thalamus, hypothalamus)

A

impaired learning and retrieval

45
Q

the function of circuit of Papez

A
  • subset of limbic system interconnections
  • multiple passes through the circuit results in memory consolidation
46
Q

Circuit of Papez steps

A
  • hippocampus
  • mammillary bodies
  • anterior thalamic nuclei
  • cingulate cortex
  • entorhinal cortex (hippocampus/neocortex gateway)
  • back to hippocampus
47
Q

frontal lobe damage

A

inattention, poor short term memory (STM)

48
Q

Amnesia

A
  • deficit in consolidation
  • short term memory intact
  • affects episodic (explicit) memory. Implicit (procedural, habitual) not affected
  • if only memory effected
  • if memory, language, cognitive processes, executive function, etc affected: broader cognitive- communication disorder
49
Q

anterograde amnesia

A

inability to form new long term memory

50
Q

retrograde amnesia

A

recall preciously stored memories

51
Q

Cognitive Reserve

A
  • neurological changes associated with aging do not necessarily correlate with cognitive function
  • bank that we have until neurological changes affect our function
52
Q

neurophysiological compensation

A
  • a person does have a deficit
  • in a sentence comprehension task, older adults were able to use working memory or problem-solving areas of the brain to help with comprehension
  • our brain can REROUTE to other areas if needed
53
Q

Why nuns? in religious order study

A
  • similar lifestyles/routines
  • had the same environmental factors, social factors to help make the study equal
54
Q

How does the religious study relate to the Seattle study?

A
  • not always a simple 1:1 relationship between structure and function
  • support the idea of successful aging
  • promote idea prevention (to some degree) is possible
  • in both studies, higher education, good physical health, self-efficacy, and creativity were protective. Depression and feelings of isolation were detrimental
55
Q

What did the religious study find?

A
  • detrimental to cognitive functioning: psychological stress and feeling of isolation
  • protective factors: being conscientious/ having self-control, size of the social network, creativity
  • depression is detrimental
  • neurological changes don’t predict cognitive function psychological factors may be a better predictor
  • psychological stress bad
  • being conscientious (self-control), good
  • feeling isolated bad
  • size of social network (average 7.5) good
    creativity good
    psychological factors relate to cognitive function, not neurological changes
56
Q

Normal aging

A
  • apoptosis
  • minimal interruption to usual function
  • age-related physiological changes in renal function memory, WORDING FINDING ABILITY, and thinning of the skin
  • decrease the ability of processing speed, intelligence, vocab or syntactic skills, word finding, sense of humor, long-term and short-term memory
57
Q

Delirium

A
  • sudden onset
  • can come and go
  • rapid deterioration
  • confused mental state
  • hypo-aroused
  • transient rapid onset
  • symptoms over lapped with dementia
58
Q

Minor cognitive Impairment

A
  • does not affect ADL’s/ independence
  • gradual onset
  • a significant decline from previous performance in one or more cognitive domains can be attributed to a mental disorder
  • can be prodrome to dementia
  • a future decline not required
  • beginnings of anomia, TOT, memory
59
Q

Normal Pressure Hydrocephalus

A
  • magnetic gait
  • enlarged ventricles
  • affects bladder function
  • treatment via shunt
  • glued feet, no tremors, and bladder dysfunction
  • Gradual CF pressure buildup affects gaits and functions like memory, EF, and language
  • mostly 60 years +
  • enlarged ventricles
  • classic NPH gait pre-shunt
  • similarities to Parkinson’s and Alzheimer’s
60
Q

Frontotemporal dementia nuero bases

A
  • Most likely to have a genetic origin, but has multiple causes
  • Tau and TDP43 protein clumps (Pick bodies)
  • Protein clumps primarily affect frontal and temporal lobes causing reduction in gyri
61
Q

Frontotemporal dementia clinical presentation

A
  • Comprise 2 to 5% of dementia cases
  • Primary initial symptoms are language and behavior related, not memory
  • Two subtypes with slightly different presentation:
    (Pick’s disease & Primary Progressive Aphasia)
62
Q

Frontotemporal dementia disease progression

A
  • Pick’s disease
    Characterized by personality changes first (changes in behavior, judgment, and empathy)
    Speech, language, and memory changes follow
    Onset before 65
  • Primary Progressive Aphasia
    Expressive and receptive language deficits appear first
    Attention, memory, executive functions follow
    Onset before 65
63
Q

Vascular Dementia neuro bases

A
  • Caused by series of lacunar infarcts (small strokes)
  • 2 types of infarcts:
    Large vessel/cortical infarcts (like stroke)
    Small vessel/subcortical infarct (gradual & vague deficits)
  • Often goes along w/ AD
  • Risk factors & medical treatment similar as for CVA
64
Q

Vascular Dementia clinical presentation

A
  • The presenting symptoms depend on where the lacunar infarct took place
  • Unlike AD they often have a more intact awareness of their condition
  • Defined or Gradual onset of deficits dependent upon size and location of affected vessels
  • (Large Vessels) Defined onset; Identifiable areas of damage
  • (Small Vessels) Gradual onset; Vague deficits; often integrative/executive functions
    Step-wise deterioration and intermittent functional plateaus/improvement

**patients that will tell us they’ve had a “mini” stroke

65
Q

Vascular dementia disease progression

A
  • Small vessel/subcortical infarcts:Gradual onset of deficits (often executive functions)
  • Large Vessel/cortical infarcts: defined onset, identifiable areas of damage
  • Can be differentiated by deterioration and intermittent plateaus/improvement
66
Q

Dementia with Lewy body nuero bases

A
  • Caused by build-up of alpha-synuclein protein inside neurons:
    Cortical Lewy bodies
    Brain stem Lewy bodies (in substantia nigra)
67
Q

Dementia with Lewy bodies clinical presentation

A
  • Similar to Parkinson’s Disease in physical symptoms
    Ex: tremors, stiffness, slowness of movement, festinating gait
  • Similar to Alzheimer’s Disease in cognitive symptoms
68
Q

Dementia with Lewy bodies disease progression

A
  • Relative progression of:
    Physical and cognitive features
    Fluctuating cognition
    Hallucinations
    Visuospatial deficits
  • Braak Stages of Progression
    1-2: autonomic & olfactory disturbances
    3-4: sleep & motor disturbances
    5-6: emotional & cognitive disturbances
69
Q

Alzheimer’s Disease Neuro Bases

A

Early onset:
Beta-amyloid overproduction (plaques)
Chromosome 21,14,1
Late onset:
Susceptibility gene and ApoE
Caused by a genetics and the environment

70
Q

Alzheimer’s Disease clinical presentation

A
  • Two or more cognitive areas are affected
  • Memory is affected (new before remote)
  • Decline in language context first before form
  • Apraxia worsens and the perception
  • Impaired ADLs
  • Sundowning
  • Alertness and the circadian rhythm are affected
  • definitive diagnosis at autopsy (plaques and tangles)
71
Q

Alzheimer’s Disease disease progression

A
  • Decreased interest in activities
  • Articulate speech becomes difficult often become mute (severe)
  • Social withdrawals (don’t have memory and language to participate in
72
Q

major neurocognitive disorder

A
  • a significant decline from the previous performance level in one or more cognitive domains
  • deficits not attributable to other mental disorders
  • deficits sufficient to interfere with independence in activities of daily living
    -primary disease to Huntington’s, Parkison’s, and Multiple Sclerosis
73
Q

DSM-5 Minor (MCI, prodromal dementia) and major neurocognitive disorder (dementia)

A
  • Complex attention (all levels and processing speeds)
  • Executive function
  • Learning and memory
  • Language
  • Perceptual-motor function
  • Social cognition
  • Impaired short-term memory
  • Impaired long-term memory
    Memory impairment not required anymore
  • Deficits can be in language, attention, etc.,
    depending on brain areas initially affected
  • Insidious onset
  • Not caused by delirium, schizophrenia, or
    depression
  • Acquired
  • Persistent
74
Q

Warning signs of dementia normal aging

A
  • forgetting names of people you rarely see
  • briefly forgetting part of an experience
  • not putting things away properly
  • mood changes because of an appropriate cause
  • changes in your interest
75
Q

warning signs of dementia- early signs of alzheimer’s

A
  • forgetting the names of people close to you
  • forgetting a recent experience
  • putting things away in strange places
  • having unpredictable mood changes
  • decreased interest in activities
76
Q

How to distinguish a minor neurocognitive disorder from normal aging?

A
  • rate of progression
  • amount of “annoyance” without overt deficit
77
Q

Delirium vs. Dementia

A

Delirium
- confused mental state
- changes in circadian rhythm
- sundowning
-misperceptions
- illusions
- hallucinations
- transient
- rapid onset and offset

dementia
- confused mental state
- changes in circadian rhythm
- sundowning
- misperceptions
- illusions
- hallucinations
- progressive/persistent
- insidious onset, no offset

78
Q

Frontotemporal Dementia

A

About 2-5% of diagnosed Dementia cases
* Multiple causes, similar/distinct profiles
* Protein clumps (Tau and TDP43)
* Primarily affect frontal and temporal lobes
* More likely genetic
* Primary initial symptoms are language and
behavior changes (not memory)

79
Q

Pick’s disease (previously synonymous)

A

Personality (Behavior, judgment, empathy, impulsivity)
changes first
* Speech (motor-speech, fluency), language (syntax,
word finding), and memory follow
* Onset before 65

80
Q

Primary progressive aphasia

A

Onset mostly before 65
* Expressive and receptive language deficits first
* Deficits at sentence or word level
* Attention, memory, executive function deficits follow

81
Q

dementia with lewy bodies

A

About 15% of diagnosed Dementia cases
* Caused by build-up of alpha-synuclein protein
inside neurons
* Cortical Lewy bodies
* Brain stem Lewy bodies (in substantia nigra)
* Similar to PD in physical symptoms
* Similar to AD in cognitive symptoms
* Distinguished by relative progression of physical
and cognitive features, fluctuating cognition,
hallucinations, visuospatial deficits
* Final diagnosis at autopsy (Lewy bodies)

82
Q

Vascular dementia

A
  • about 20% of diagnosed dementia cases
  • not a single disease but a disease process
  • caused by a series of lacunar infarct
  • deficits dependent on areas of infarction
83
Q

Vascular dementia risk factors same for CVA

A
  • hypertension
  • cardiovascular disease
  • diabetes
  • history of stroke
84
Q

Alzheimer’s Disease

A
  • about 65% of diagnosed Dementia cases
  • approx five million in 2014
  • anticipated approximately
  • risked doubles every years post 65
85
Q

Early onset of Alzheimer’s disease

A
  • age 40- 60
  • rare genetic mutation ( dominant gene, 1991)
  • genetic fault in beta-amyloid overproduction
  • 5% of all AD cases
  • chromosomes 21, 14,1, ( trisomy 21)
  • effects language and memory function
86
Q

Late-onset for Alzheimer’s Disease

A
  • age over 65
  • mixture of genetic and environmental causes
    “susceptibility genes,” including ApoE (shared with heart disease and high cholesterol)
  • ApoE, chromosome 19
  • ApoE 4: Risk factor
  • ApoE 2: Protective
87
Q

Mild Alzheimer’s Disease

A

Frontal Lobes
* Trouble naming common items (language & memory)
* Less interest in things they once liked to do
* Personality changes (irritability, anger, withdrawal) Hippocampus
* Memory loss, especially with recent events
* Repetition of questions or actions
* Getting lost easily (visuo-spatial memory)
* Lose things more often than normal
Subcortical
* Depression and/or anxiety
* Sleep disturbances
- anomia
- good syntactic structure
good content with some tangential addition
- last 2-10 years

88
Q

Moderate Alzheimer’s Disease

A

Greater ADL involvement, require supervision
* Frontal
* Difficulty dressing for the weather or occasion
* Poor judgment and insight
* Argumentative/violent
Hippocampus
* Difficulty with formulaic tasks like washing dishes
* Forget to shave or shower
Parietal/integrative, occipital
* Hallucinations and illusions
Subcortical
* Wander, often at night
- worse anomia
- neologisms
- loss of coherence and cohesion
- last 2-10 years

89
Q

Severe Alzheimer’s disease

A

Global deficits, loss of independence
* Difficulty eating/dysphagia
* Problems with speech or no speech
* Inability to recognize loved ones
* Inability to control bowels or bladder
* Physical difficulties, including walking
- only stereotypic phrases/utterances
- no topic maintenance
- ultimately mute
- last 1-5 years

90
Q

Alzheimer progression

A

live as long as 8-20 years
- depends when on diagnosis

91
Q

More likely to be Lewy bodies when…

A

they score high in motor function test (not AD)

92
Q

Hachinski Ischemia index

A

looks at different kinds of deterioration processes and historical data
- score is higher (9-18), more likely to be a vascular dementia
- score is lower (0-4) is more likely to be AD

93
Q

mostly like to be lewy body when…

A

if there’s data of moment to moment fluctuations in cognitive functions
- if there is greater involvement of motor function

94
Q

Most likely to be frontotemporal dementia when…

A
  • if there’s greater involvement initially of personality changes

Cognitive Communication Disorders (1 decks)

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