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Aphasia > First Test > Flashcards

First Test Flashcards

1
Q

Anomia

A

trouble with word finding
#1 difficulty presented with aphasia

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2
Q

Circumlocution

A

where the patient can describe but not identify the target word (ex. cold/white for snow)

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3
Q

Agrammatism/Telegraphic Speech

A

missing syntax, usually just getting at the content words

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4
Q

Auditory comprehension deficits

A

trouble with understanding spoken language

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5
Q

Phonological Errors (phonemic Paraphasia)

A

saying the wrong phoneme in place of another

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6
Q

Semantic Errors (Verbal paraphasia)

A

an error where there is a semantic relationship
- where a sentence can be grammatically correct but it doesn’t make sense
- ex. I cut steak with a fork

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7
Q

Perseverations

A

being stuck on something to repeating
-the word of segment will continue to come up
-sometimes can understand that they are doing it sometimes they cant

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8
Q

stereotypy

A

language that is a go to word or phrase
- can be used as a fill in word
- do not understand they are saying it

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9
Q

Alexia

A

difficulty with reading

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10
Q

Agraphia

A

difficulty with writing

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11
Q

Hempiparesis

A

one sided (unilateral) weakness

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12
Q

Hemiplegia

A

one-sided severe weakness or paralysis

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13
Q

Hemisensory Loss

A

one-sided (unilateral) loss of limitation

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14
Q

Frontal Lobe General Functions

A

-cognitive functions
- reasoning, decision making, planning
- primary motor function, including spoken language

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15
Q

INSULA General Function

A

-self-awareness, consciousness
- cognitive functions
-motor planning and control (speech articulation)

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16
Q

3 Features Necessary for Diagnosis of AOS

A
  1. Sound errors (distortions, distorted substitutions)
  2. Slowed Rate (interval between words, sound transitions, syllables)
  3. Prosodic Abnormalities (syllable segregation, equalised stress. Ex. “fer-idge)
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17
Q

Hemianopia

A

one sided visual field blindness

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18
Q

Wernicke Aphasia: auditory comprehension

A

NO

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19
Q

Wernicke Aphasia: repetition

A

NO

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20
Q

Wernicke Aphasia: fluency

A

YES

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21
Q

Wernicke Aphasia characteristics

A
  • notable anomia
  • perseverations
  • “empty speech”
  • press of speech
  • jargon, neologisms
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22
Q

Wernicke Aphasia localisations

A

Superior temporal gyrus; may involve left temporal and parietal lobes

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23
Q

Brocas Aphasia: fluency

A

NO

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24
Q

Brocas Aphasia: repetition

A

NO

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25
Q

Brocas Aphasia: auditory comprehension

A

YES

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26
Q

Brocas Aphasia characteristics

A

-apraxia of speech
- short phrase length
- agrammatism
-phonemic paraphasia
- impaired writing

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27
Q

Broca’s Aphasia Localisation

A

-large lesion involving Broca’s area and frontopartietal operculum
- May include subcortical lesions

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28
Q

Conduction Aphasia: fluency

A

YES

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29
Q

Conduction Aphasia: auditory comprehension

A

YES

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30
Q

Conduction Aphasia: repetition

A

NO

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31
Q

Conduction Aphasia characteristics

A

-repetition significantly worse than verbal output
- conduite d’approche
- conduite d’écart

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32
Q

Conduction Aphasia localisation

A
  • damage to but not destroying Wernicke’s area
  • Lesions in inferior parietal region
  • Supramarginal gyrus with or without extension to arcuate fascicules
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33
Q

Conduite d’approche

A

-repeated words come close to target with more attempts
- ex “frig-frid-friged-fridge”

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34
Q

Conduite d’ecart

A
  • repeated words move farther from target word
  • ex. “frig-freg-freeg-reek-reed?”
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35
Q

Global Aphasia characteristics

A

-virtually no speech output
- stereotypical utterances
PROFOUND anomia

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36
Q

Global aphasia: fluency

A

NO

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37
Q

Global Aphasia: auditory comprehension

A

NO

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38
Q

Global Aphasia: repetition

A

NO

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39
Q

Global Aphasia localisation

A

-lesion incorporates both Broca’s and Wernickes aphasia

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40
Q

Anomic Aphasia: fluency

A

YES

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41
Q

Anomic Aphasia: auditory comprehension

A

YES

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42
Q

Anomic Aphasia: repetition

A

YES

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43
Q

Anomic Aphasia characteristics

A

-nonspecific phrases
- word finding pauses
- circumlocution
- paraphasia rare, if present, semantic

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44
Q

Transcortical Sensory Aphasia: fluency

A

YES

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45
Q

Anomic Aphasia localisation

A

-scattered around the left hemisphere

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46
Q

Transcortical Sensory Aphasia: auditory comprehension

A

NO

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47
Q

Transcortical Sensory Aphasia: repetition

A

YES

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48
Q

Transcortical Sensory Aphasia characteristics

A
  • frequent use on nonspecific words
  • semantic paraphasia> phonemic paraphasia
  • significant anomia
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49
Q

Transcortical Motor Aphasia: fluency

A

NO

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50
Q

Transcortical Motor Aphasia: auditory comprehension

A

YES

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51
Q

Transcortical Motor Aphasia: repetition

A

YES

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52
Q

Transcortical Motor Aphasia characteristics

A
  • some preserved grammar
  • less articulatory effort
  • impaired reading and writing, especially oral reading
  • inability to generate fill sentences or strings of sentences
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53
Q

Mixed Transcortical Aphasia: fluency

A

NO

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54
Q

Mixed Transcortical Aphasia: auditory comprehension

A

NO

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55
Q

Mixed Transcortical Aphasia: repetition

A

YES

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56
Q

Mixed Transcortical Aphasia characteristics

A

-echolalia

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57
Q

Purpose of Aphasia Therapy

A
  • improve language
  • improve communication
  • help a person live well
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58
Q

The Continuity Hypothesis

A
  • anyone can look like they have “aphasia” given the right personal (ex. fatigue) and contextual factors (ex. loud environment + multiple conversations)
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59
Q

4

A

Precentral gyrus (primary motor cortex)

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60
Q

6,8

A

Premotor Cortex

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61
Q

44,45

A

Inferior Frontal Gyrus (Brocas Area)

62
Q

3.1,2

A

Postcentral Gyrus (Primary sensory cortex)

63
Q

40

A

Supramarginal Gyrus

64
Q

22

A

Sub and Post Temporal Gyrus (Wernickes area)

65
Q

41,42

A

Primary auditory cortex (Heschl’s gyrus)

66
Q

9-11

A

Prefrontal Region (Cognitive Assoc Cortex)

67
Q

Lesions in Frontal may result in

A

-contralateral paralysis
- impaired cognition (reasoning)
- judgement
- concentration
- inappropriate social aphasia
- expressive aphasia

68
Q

Lesions in Temporal may result in

A
  • receptive aphasia
  • memory disturbances
69
Q

Lesions in Parietal may result in

A
  • contralateral hemisensory loss
  • tactile agnosia
    -inattention
  • visual optical deficits
  • anosagnosia (denial of impaired functioning
70
Q

Lesions in Occipital may result in

A
  • contralateral homonymous hemianopia
  • receptive aphasia
  • memory disturbances
71
Q

Lesions in Cerebellar my result in

A

-reduced limb coordination and balance

72
Q

FRAME

A

F: Familiarize
R: Reduce Rate
A: Assist with communication
M: Mix Communication Modalities
E: Engage Patient First

73
Q

Anterior Cerebral Artery (ACA)

A
  • superficial vascularisation of the frontal lobe: frontal lesions
74
Q

Middle Cerebral Artery (MCA)

A

Most often implicated in aphasia post stroke from an MCA blockage or decreased bloodflow
- superficial cortical structures and the INSULA
- language impact; wernickes and brocas

75
Q

Posterior Cerebral Artery (PCA)

A
  • some type of linguistic impact (depends)
  • Ocular visual/spacial challenges
76
Q

Signs and Symptoms of a Stroke (BEFAST)

A

B: Balance - dizziness, loss of balance
E: Eyes- vision changes
F: Face- facial dropping, headache
A: Arms- weakness, numbness
S: Speech- trouble speaking, confusion
T: Time: call 911

77
Q

Onset of Chronic Aphasia

A
  • sudden
  • improvement is typical
78
Q

Primary Progressive Onset

A
  • gradual
  • related to dementia
79
Q

Purpose of Aphasia Therapy

A
  1. Improve Language
  2. Improve Communication
  3. Help a person live well
80
Q

2 Aphasia Treatments

A
  1. Impairment or restorative approach
  2. Compensatory or functional communication approach
81
Q

Impairment or restorative Approach Target

A
  • specific language impairment (phonological-semantic, syntactic)
82
Q

Impairment or restorative Approach Goal

A
  • generalisation beyond trained items/tasks and to the communicative environment of the person
  • reducing impairment> improving success of communication
83
Q

Compensatory or Functional Communication Approach Target

A
  • individual communication abilities with high personal relevance to daily life; eliminating barriers to communication
84
Q

Compensatory or Functional Communication Approach Goal

A

Improving successful communication and quality of life> reducing impairment

85
Q

The Continuity Hypothesis

A

anyone can look like they have “aphasia” given the right personal (fatigue) and contextual factors (loud environment + multiple conversations)

86
Q

Aphasia Classification Systems

A
  1. Fluent/Non-fluent dichotomy
  2. Wernicke-Litcheim Model
87
Q

Wernicke-Litchtheim Model

A
  • an early neuroanatomically based model of language and its impairment
  • all aphasia types step from where the lesion is located
  • “classic” classifications of aphasia
  • Parameters: fluency, auditory comprehension, repetition, naming
88
Q

Fluent vs Nonfluent Classification

A
  • phrase length
  • pauses
    -prosody
    -speaking rate
    -effort
    -initiation and elaboration
    -word finding
    -telegraphic speech
89
Q

Linguistic Impairment Features

A

-more specific way of describing individual’s impairment for all aspects of clinical decision-making

90
Q

Aphasia Classification System

A

not as clinically useful as the linguistic impairment description but need to understand these labels as its used in the clinical environment

91
Q

Speech production

A

intent/conceptualisation-> linguistic-symbolic Planning-> motor planning -> motor programming-> execution

92
Q

Aphasia in Left-Handed Individuals

A
  • Language is left lateralized about 96% of right-handers and about 70% in non-right handers
  • we previously believed more cases of transient aphasia reported for non-right handed individuals (now believed incorrect)
93
Q

Crossed Aphasia

A
  • right handed individuals with aphasia following right hemisphere lesion
  • deficits in prosody, metaphor comprehension, and abstract concepts
94
Q

Bilingual aphasia

A
  • NOT an aphasia classification
  • Varying recovery patterns
95
Q

cerebrovascular

A

-highway of the brain
- can carry nutrients and oxygen

96
Q

Controllable Risk factors for stroke

A
  • 87%
  • obesity
  • hyperglycemias
  • hyperlipidemia
  • renal dysfunction
  • smoking
  • sedentary lifestyle
  • bad diet
  • stress/depression
97
Q

Non controllable risk factors for stroke

A
  • certain medical conditions
  • age and gender
  • race and ethnicity
  • personal family history
    0 arteriovenous malformation
98
Q

Transient Ischemic Attack (mini stroke)

A
  • temporary stroke symptoms that resolve between minutes to hours
  • once you have a TIA, 2/5 will have a stroke within 90 days
99
Q

Stroke Diagnosis and Management

A
  • Identify focal deficit
  • Time last seen
  • Imaging
  • NIG Stroke Scale
100
Q

When the stroke happens: core

A
  • neurone are dead
101
Q

When the stroke happens” penumbra

A
  • if we are able to restore function in the penumbra, functional impairment can be salvaged
102
Q

IV tPA and TKA

A
  • stroke intervention
  • administered within 4.5 hours of time last seen normal
  • only ischemic strokes
  • BP under 185/110
103
Q

Ischemic stroke

A

block in the artery

104
Q

thrombotic

A

blood clot

105
Q

embolic

A

plaque that builds up in the arteries

106
Q

hemorrhagic

A

brain bleed

107
Q

intracerebral

A

in the brain- within the cerebrum

108
Q

subarachnoid

A
  • on the surface of the brain: ventricular space outside the cerebrum but under the skill
109
Q

Stoke Subtypes: small vessel lacunar

A

19%

110
Q

Stoke Subtypes: hemorrhagic

A

13%

111
Q

Stoke Subtypes: Ischemic

A

87%

112
Q

Stoke Subtypes: large vessel

A

6%

113
Q

Stoke Subtypes: cardio embolic

A

14%

114
Q

biochemical/physiologic mechanism of recovery: primary during changes within hours after stroke

A
  • necrosis: core
  • cellular inflammation: penumbra area
  • retrograde and intergrade cell degeneration
  • there is a dead neural cell not getting normal inputs and they begin to die- goal is to reproduce/save those areas
115
Q

biochemical/physiologic mechanism of recovery: primary direct plastic- during first days/weeks

A

-physical repair of penumbra cells(repair) : neuro cells are rewiring what they normal do with different cells
- reorganise impaired areas (adaptation): body finding new ways to access information
- Retraining to perform a specific skill (new learning): reconsider how to do things again because a group of cells has stopped doing things

116
Q

biochemical/physiologic mechanism of recovery: secondary- indirect changes over subsequent weeks and months

A
  • transneuronal degeneration
  • denervation supersensitivity
  • development of diaschisis
117
Q

transneuronal degeneration

A
  • areas receiving or sending neural input to impacted areas degenerate
  • any of the connecting neural pathways that were getting information from the core begin to die off
118
Q

denervation supersensitivity

A

neurone who have lost input become super sensitive to any input

119
Q

development of diathesis

A
  • development of a temporary disability or injury
  • the body has shut down so it will not do things that you used to do so they can focus on other things
120
Q

biochemical/physiologic mechanism of recovery: secondary- indirect PLASTIC changes over weeks and months

A
  • collateral sprouting
  • regenerative sprouting
  • collateral regenerative sprouting
121
Q

collateral sprouting

A

-axons from nearby neutrons grow new connections with sites previously innervated by dead cells

122
Q

regenerative sprouting

A

axonal or dendritic, creates new synapses

123
Q

collateral regenerative sprouting

A

intact cells grow new synaptic connections to attempt to increase connections in the penumbra

124
Q

Stroke recovery behavioural

A

capacity to perform previously impaired task in the same manner as before the injury

125
Q

stroke compensation behavioural

A

use of a new strategy to perform that same task

126
Q

stroke recovery neural level

A

restoration of function within an area that was initially lost

127
Q

stroke compensation neural level

A

different neural tissue takes over functions after injury

128
Q

Neurological Factors for recovery without treatment

A
  • severity of aphasia
  • size and side of lesion
  • vascular perfusion and white matter integrity
  • fluent vs non-fluent: fluent recover faster
  • cognitive skills at baseline
129
Q

Personal Factors for Recovery without treatment

A

-age
- baseline linguistic abilities
- satisfaction with life participation and self-perceived aphasia severity
- social suppor

130
Q

Aphasia Biopsychosocial Approach

A

therapy should take into account:
- biological impairment based factors
- psycholinguistic and cognitive processes or languid and social communication within the social context of a person with aphasia

131
Q

Distributed langue models (connectionist)

A

-representation: language is represented by learned patterns of activation networks between different knowledge units
- Processing: knowledge (word retrieval) is processed in an interactive manner, not sequentially/serially
- more neutrally plausible

132
Q

verbal paraphasia

A

degree of semantic relatedness

133
Q

phonemic aphasia

A

additions, substitutions, anticipatory, perseverative

134
Q

mixed paraphasia

A

both semantic and phonological

135
Q

neologistic paraphrases (neologisms)

A
  • response -> “chith” (<50 phonemes shared with target
136
Q

characteristics that cannot be used to diagnose apraxia of speech

A
  • limb or oral non speech aphasia
  • expressive- receptive speech/language gap
137
Q

Wernicke associated signs

A

-possible right hemianopia
-usually no motor or sensory abnormalities

138
Q

Wernicke vascular distribution

A
  • MCA and posterior cerebral artery (PCA)
139
Q

conduction associated signs

A
  • right hemiparesis, right hemisensory loss, right hemianopia
140
Q

conduction vascular distribution

A

MCA, parietal branches of the PCA

141
Q

brocas associated signs

A
  • right hemiparesis, right hemisensory loss
142
Q

brocas vascular distribution

A

-anterior branches of the MCA

143
Q

global aphasia associated signs

A
  • right hemiparesis, right hemisensory loss, right hemianopia
144
Q

global aphasia vascular distribution

A

most of MCA

145
Q

anomic aphasia associated signs

A

variable, often absent

146
Q

anomic aphasia vascular distribution

A

variable

147
Q

subcortical aphasia lesion site

A

subcortical lesions

148
Q

subcortical aphasia symptoms

A

hypophonia- weak voice

149
Q

PPA Subtypes

A

-PPA confluent/agramatic varient: effortful speech
-PPA semantic varient (semantic dementia)
- PPA logopenic varient (wrod retreiual deficits

150
Q

Brodmann Area

A

region of the cortex defined by its cytoarchitecture (organization of neurons)

Aphasia (2 decks)

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