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MA-SLP BootCamp Exam > Day 5 > Flashcards

Day 5 Flashcards

1
Q

In the 18th century it was

believed that aphasia was caused by a ________________ (Johann Gesner 1738-1801)

A

congestion of the nerve ducts

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2
Q

__________ was practiced in the 19th century

A

Phrenology

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3
Q

20th century –___________ believed language is localized to specific areas in the brain.

A

localizationists

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4
Q

Define: aphasia

A

impairment of language affecting the production or comprehension of speech and the ability to read or write

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5
Q

(More, less) people have aphasia than other common conditions, including cerebral palsy, multiple sclerosis, Parkinson’s disease, or muscular
dystrophy.

A

More

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6
Q

_________ is a leading cause of long-term disability.

A

Stroke

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7
Q

There are at least __________ people in the USA with aphasia.

A

1,000,000

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8
Q

2 fathers of aphasia

A

Paul Broca and Carl Wernicke

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9
Q

Paul Broca

A

French neurologist who, worked with a patient with limited speech and impaired language due to
brain damage to a specific area. These clinical features are now identified with Broca’s aphasia.

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10
Q

Carl Wernicke

A

Such as Broca’s area and Wernicke’s area

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11
Q

2 structures in the specific :eloquent cortex”

A

Broca’s area and Wernicke’s area

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12
Q

Many now believe (mostly from fMRI and PET data) that language should be viewed as __________. Why?

A

Neural networks. During imaging studies, many areas light up when
performing language tasks

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13
Q

White matter pathways carry information to/from ____________.

A

the “eloquent” cortex

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14
Q

Cognitive areas impact what 4 cognitive-linguistic functions?

A

attention, memory, impulse control, initiation

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15
Q

Blue lobe (largest) at forehead/front region

A

frontal

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16
Q

Pink lobe at bottom middle region

A

temporal

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17
Q

Green lobe at top middle region

A

parietal

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18
Q

Orange/red small lobe in back

A

occipital

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19
Q

10 primary structures of the cerebral cortex

A
  • Central sulcus (Fissure of Rolando)
  • Lateral sulcus (Sylvian fissure)
  • Primary Motor cortex • Primary Sensory Cortex • Broca’s area • Wernicke’s area • Supramarginal gyrus • Angular gyrus • Primary visual cortex • Primary auditory cortex
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20
Q

Central Sulcus (Fissure of Rolando)

A

divides frontal and parietal lobes.

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21
Q

Lateral Sulcus (Sylvian Fissure)

A

divides frontal and temporal

lobes.

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22
Q

Primary Motor Cortex- define and location

A

AKA precentral gyrus Sends motor information to contralateral body (in frontal lobe)

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23
Q

Primary Sensory Cortex - define and location

A 
AKA postcentral gyrus Receives sensory information from
contralateral body (in parietal lobe)
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24
Q

Broca’s Area- define and location

A

Motor programming for speech production (in frontal lobe)

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25
Q

Wernicke’s Area- define and location

A

Comprehension of oral

language (in temporal lobe)

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26
Q

Supramarginal gyrus- define and location

A

Symbolic integration for writing (in parietal lobe)

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27
Q

Angular gyrus- define and location

A

Symbolic integration for reading (in

parietal lobe)

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28
Q

Primary visual cortex (define and location)

A

Receives visual information for seeing (in occipital lobe)

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29
Q

Primary auditory cortex (define and location)

A

Receives auditory information for hearing (in temporal lobe)

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30
Q

Perisylvian Zone- aka, lesion implications

A

aka Lateral fissure, lesions in this area can result in language disturbances

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31
Q

Largest cortical vascular territory- most important implications for speech/language

A

Middle cerebral artery

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32
Q

Wernicke-Geschwind process of reading aloud

A

Primary visual cortex –> angular gyrus –> Wernicke’s area –> Broca’s area –> Primary motor cortex

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33
Q

Wernicke-Geschwind process of Verbal repetition

A

Primary auditory cortex –> Wernicke’s area –> Broca’s Area –> Primary motor cortex

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34
Q

What stroke location/cerebrovascular artery has most implies aphasia

A

Left hemisphere, MCA

35
Q

Define: White matter

A

bundles of myelinated axons that are interconnected

36
Q

Define: Arcuate fasciculus

A

white matter pathway that connects Broca and Wernicke’s areas

37
Q

Clinical features of Broca’s aphasia

A

Relatively good auditory comprehension ▫ Nonfluent speech with short sentence length ▫ Increased effort in speaking ▫ Agrammatism (lack of “little words”) ▫ Poor repetition and naming

38
Q

Neurological location often associated with Broca’s aphasia

A

Broca’s area AND surrounding white/gray matter

39
Q

Clinical features of Wernicke’s aphasia

A

Poor auditory comprehension ▫ Fluent speech/normal sentence length ▫ Lack of meaning in speech ▫ Paraphasias (jargon) ▫ Poor repetition and naming

40
Q

Neurological location often associated with Wernicke’s aphasia

A

Wernicke’s area in the temporal lobe

41
Q

Clinical features of global aphasia

A

▫ Poor auditory comprehension ▫ Nonfluent/limited speech
▫ Poor naming and repetition
▫ Comprehension of pictures and gestures are typically better than auditory comprehension

42
Q

Neurological location often associated with global aphasia

A

Larger area of damage including both Broca and Wernicke areas

43
Q

Which types of aphasia have poor auditory comprehension?

A

Wernicke’s and Global

44
Q

Which types of aphasia have non-fluent speech?

A

Broca’s and Global

45
Q

Commonality between Global, Wernicke, and Broca

A

Poor naming and repetition

46
Q

Which type of aphasia involves more awareness of their deficits?

A

Broca’s aphasia

47
Q

Which type of aphasia is the most severe in characteristics and implications?

A

Global aphasia

48
Q

Are lesion sizes/locations variable between patients?

A

YES!

49
Q

Define: Conduction aphasia

A

repetition is primary impairment

50
Q

Define: transcortical aphasia

A

repetition is intact

51
Q

Define: subcortical aphasia

A

damage is in subcortical structures such as thalamus, internal capsule, basal ganglia

52
Q

Define: crossed aphasia

A

Right handed with right hemisphere stroke

resulting in aphasia

53
Q

Define: primary progressive aphasia

A

Focal dementia impacting language functions first

54
Q

2 important aphasia clinical resources

A

Aphasia simulation, ASHA practice portal

55
Q

Movement over the past decade to focus on the ______, or _____ model.

A

Person, social.

56
Q

4 considerations of social model

A

Life participation is the ultimate goal
▫ Important to assure treatment generalizes to real life
▫ Social supports are important
▫ Communication partner training is included in treatment

57
Q

6 communication tips for clinicians

A

• Minimize background noise when speaking • Make sure you have the person’s full attention
before you start
• Get on the person’s level and communicate face to face
• Acknowledge that this person is smart and has something to contribute to the conversation
• Speak slower but in a natural way
• Give the person time to speak

58
Q

4 cognitive constructs

A

speed of processing, memory, executive functions, attention

59
Q

2 types of memory- define each

A 
Episodic memory (long-term, autobiographical) 
Working memory (simultaneous storage and manipulation)
60
Q

3 types of executive functions

A

Resistance to interference, Inhibition of distractions
Manipulating information, Planning & strategizing
Multi-‐tasking

61
Q

2 types of attention- define

A

Sustained- focus on one activity for a long period of time

Selective- ability to focus on one thing when other distractions are present

62
Q

Impacts of speed and memory on assessment and treatment

A

Introduce yourself and tell them why you are there every single time. make a lot of lists, be direct of split into 2 sentences

63
Q

Function of hippocampus

A

central switchboard where all aspects (taste, smell, sight, sounds, etc). come together and are integrated into one mental representation.

64
Q

Speed relationship with pathology and age

A

Speed much worse with pathology and worse with age

65
Q

Episodic memory- details vs. larger picture, locations that cause worse damage to episodic memory

A

Gist memory is good, details may be hazy

– VERY impaired if damage to hippocampus or white matter leading to hippocampus

66
Q

Working memory- aging, locations that cause worse damage to working memory

A

Somewhat limited in healthy aging – Even worse if significant frontal lobe damage

67
Q

Executive function- aging, locations that cause worse damage to executive function

A

Somewhat impaired in aging
• Active inhibition of distractions
• Multi-‐tasking • Much worse with frontal & parietal lobe damage
– Mostly intact in aging: Planning & strategizing, understanding cause & effect

68
Q

2 other disorders that cause impaired executive function in at least some patients- explain

A

ALL get impaired with TBI
• Diffuse damage to white matter, especially connections within frontal lobe and to/from frontal lobe
– Impaired in dementia (but different types of dementia will affect different abilities at different times)

69
Q

Attention relies on integrity of _______________ that go from frontal lobes to parietal lobes to basal ganglia
(bidirectionally)

A

large cortical networks (loops)

70
Q

Aging has minor effects on sustained attention, but may impact __________ a bit more . Why?

A

selective attention. Related to inhibition, but inhibition is active suppression of distraction, selective attention is more basic FOCUSing ability.

71
Q

Attention is Seriously impaired in ______, with any kind of _______ or ________ damage.

A

TBI, frontal lobe or basal ganglia

72
Q

Impacts of attention on assessment and treatment

A

Make sure TV is off and no other distractions before you ask them to concentrate. Make a lot of lists. Shorter more varied assessment. More frequent breaks. Positive reinforcement. Physical activity.

73
Q

3 mitigating factors

A

education, pain and infection, sensory impairment

74
Q

Education effects, considerations

A

Education & learning experiences build neural connections, give a buffer so that normal function can be maintained .
• Every day performance used to be much higher, but can still perform “within normal limits” even with age-‐related changes • Greater education has been found to predict better recovery (and sometimes amount of functional deficits) in some studies.
Hard to see if highly educated have memory issues because were so incredibly well-performing before that they still may perform normally on memory tests.

75
Q

Pain and infection effects

A

Can magnify apparent cognitive impairment. – Normal function returns when condition is resolved

76
Q

Visual impairment effects, considerations, solutions

A

Considerations: glass, macular degeneration; do as many auditory tasks as possible, has effects on written or picture-based assessment

77
Q

Define- cognitive reserve

A

how much more you have beyond the required functioning for everyday tasks

78
Q

Hearing impairment effects, considerations, solutions

A

Hearing aids on, and batteries properly installed/functioning? Use written or picture based communication.

79
Q

Hypothesis about visual and hearing impairments

A

Long-term uncorrected visual and hearing impairments may have effects on cognition- less input to that cortex, those parts of the brain get taken over by other functions

80
Q

6 parts of a bedside exam or general assessment

A 
Introductions
Item naming 
Orientation questions 
Multi-‐step Commands 
Oral-‐Mech exam
Swallowing Exam
81
Q

10 primary considerations in thinking about changes in neural bases of communication throughout the lifespan

A
  • Speed of processing • Episodic memory
  • Working Memory • Inhibition • Multi-‐‐tasking • Attention • Education
  • Pain • Visual impairment • Hearing impairment
82
Q

6 populations that demonstrate possible cognitive impairment as compared to normal adults

A 
Mild Cognitive  Impairment 
Alzheimer & other  dementias
Parkinson’s disease
Following Stroke 
Young Adult with TBI
Children
83
Q

6 things that individual differences in cognitive abilities and history
(education, sensory impairments, pain levels) can impact

A

Cognition at assessment
Ability to understand instructions Response to treatment
Probability of completing “homework” Expectations of improvement
Awareness of their own deficits

MA-SLP BootCamp Exam (5 decks)

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