First Test Flashcards
1
Q
Anomia
A
trouble with word finding
#1 difficulty presented with aphasia
2
Q
Circumlocution
A
where the patient can describe but not identify the target word (ex. cold/white for snow)
3
Q
Agrammatism/Telegraphic Speech
A
missing syntax, usually just getting at the content words
4
Q
Auditory comprehension deficits
A
trouble with understanding spoken language
5
Q
Phonological Errors (phonemic Paraphasia)
A
saying the wrong phoneme in place of another
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
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
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
9
Q
Alexia
A
difficulty with reading
10
Q
Agraphia
A
difficulty with writing
11
Q
Hempiparesis
A
one sided (unilateral) weakness
12
Q
Hemiplegia
A
one-sided severe weakness or paralysis
13
Q
Hemisensory Loss
A
one-sided (unilateral) loss of limitation
14
Q
Frontal Lobe General Functions
A
-cognitive functions
- reasoning, decision making, planning
- primary motor function, including spoken language
15
Q
INSULA General Function
A
-self-awareness, consciousness
- cognitive functions
-motor planning and control (speech articulation)
16
Q
3 Features Necessary for Diagnosis of AOS
A
- Sound errors (distortions, distorted substitutions)
- Slowed Rate (interval between words, sound transitions, syllables)
- Prosodic Abnormalities (syllable segregation, equalised stress. Ex. “fer-idge)
17
Q
Hemianopia
A
one sided visual field blindness
18
Q
Wernicke Aphasia: auditory comprehension
A
NO
19
Q
Wernicke Aphasia: repetition
A
NO
20
Q
Wernicke Aphasia: fluency
A
YES
21
Q
Wernicke Aphasia characteristics
A
- notable anomia
- perseverations
- “empty speech”
- press of speech
- jargon, neologisms
22
Q
Wernicke Aphasia localisations
A
Superior temporal gyrus; may involve left temporal and parietal lobes
23
Q
Brocas Aphasia: fluency
A
NO
24
Q
Brocas Aphasia: repetition
A
NO
25
Brocas Aphasia: auditory comprehension
YES
26
Brocas Aphasia characteristics
-apraxia of speech
- short phrase length
- agrammatism
-phonemic paraphasia
- impaired writing
27
Broca's Aphasia Localisation
-large lesion involving Broca's area and frontopartietal operculum
- May include subcortical lesions
28
Conduction Aphasia: fluency
YES
29
Conduction Aphasia: auditory comprehension
YES
30
Conduction Aphasia: repetition
NO
31
Conduction Aphasia characteristics
-repetition significantly worse than verbal output
- conduite d'approche
- conduite d'écart
32
Conduction Aphasia localisation
- damage to but not destroying Wernicke's area
- Lesions in inferior parietal region
- Supramarginal gyrus with or without extension to arcuate fascicules
33
Conduite d'approche
-repeated words come close to target with more attempts
- ex "frig-frid-friged-fridge”
34
Conduite d'ecart
- repeated words move farther from target word
- ex. “frig-freg-freeg-reek-reed?”
35
Global Aphasia characteristics
-virtually no speech output
- stereotypical utterances
PROFOUND anomia
36
Global aphasia: fluency
NO
37
Global Aphasia: auditory comprehension
NO
38
Global Aphasia: repetition
NO
39
Global Aphasia localisation
-lesion incorporates both Broca's and Wernickes aphasia
40
Anomic Aphasia: fluency
YES
41
Anomic Aphasia: auditory comprehension
YES
42
Anomic Aphasia: repetition
YES
43
Anomic Aphasia characteristics
-nonspecific phrases
- word finding pauses
- circumlocution
- paraphasia rare, if present, semantic
44
Transcortical Sensory Aphasia: fluency
YES
45
Anomic Aphasia localisation
-scattered around the left hemisphere
46
Transcortical Sensory Aphasia: auditory comprehension
NO
47
Transcortical Sensory Aphasia: repetition
YES
48
Transcortical Sensory Aphasia characteristics
- frequent use on nonspecific words
- semantic paraphasia> phonemic paraphasia
- significant anomia
49
Transcortical Motor Aphasia: fluency
NO
50
Transcortical Motor Aphasia: auditory comprehension
YES
51
Transcortical Motor Aphasia: repetition
YES
52
Transcortical Motor Aphasia characteristics
- some preserved grammar
- less articulatory effort
- impaired reading and writing, especially oral reading
- inability to generate fill sentences or strings of sentences
53
Mixed Transcortical Aphasia: fluency
NO
54
Mixed Transcortical Aphasia: auditory comprehension
NO
55
Mixed Transcortical Aphasia: repetition
YES
56
Mixed Transcortical Aphasia characteristics
-echolalia
57
Purpose of Aphasia Therapy
- improve language
- improve communication
- help a person live well
58
The Continuity Hypothesis
- anyone can look like they have "aphasia" given the right personal (ex. fatigue) and contextual factors (ex. loud environment + multiple conversations)
59
4
Precentral gyrus (primary motor cortex)
60
6,8
Premotor Cortex
61
44,45
Inferior Frontal Gyrus (Brocas Area)
62
3.1,2
Postcentral Gyrus (Primary sensory cortex)
63
40
Supramarginal Gyrus
64
22
Sub and Post Temporal Gyrus (Wernickes area)
65
41,42
Primary auditory cortex (Heschl's gyrus)
66
9-11
Prefrontal Region (Cognitive Assoc Cortex)
67
Lesions in Frontal may result in
-contralateral paralysis
- impaired cognition (reasoning)
- judgement
- concentration
- inappropriate social aphasia
- expressive aphasia
68
Lesions in Temporal may result in
- receptive aphasia
- memory disturbances
69
Lesions in Parietal may result in
- contralateral hemisensory loss
- tactile agnosia
-inattention
- visual optical deficits
- anosagnosia (denial of impaired functioning
70
Lesions in Occipital may result in
- contralateral homonymous hemianopia
- receptive aphasia
- memory disturbances
71
Lesions in Cerebellar my result in
-reduced limb coordination and balance
72
FRAME
F: Familiarize
R: Reduce Rate
A: Assist with communication
M: Mix Communication Modalities
E: Engage Patient First
73
Anterior Cerebral Artery (ACA)
- superficial vascularisation of the frontal lobe: frontal lesions
74
Middle Cerebral Artery (MCA)
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
Posterior Cerebral Artery (PCA)
- some type of linguistic impact (depends)
- Ocular visual/spacial challenges
76
Signs and Symptoms of a Stroke (BEFAST)
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
Onset of Chronic Aphasia
- sudden
- improvement is typical
78
Primary Progressive Onset
- gradual
- related to dementia
79
Purpose of Aphasia Therapy
1. Improve Language
2. Improve Communication
3. Help a person live well
80
2 Aphasia Treatments
1. Impairment or restorative approach
2. Compensatory or functional communication approach
81
Impairment or restorative Approach Target
- specific language impairment (phonological-semantic, syntactic)
82
Impairment or restorative Approach Goal
- generalisation beyond trained items/tasks and to the communicative environment of the person
- reducing impairment> improving success of communication
83
Compensatory or Functional Communication Approach Target
- individual communication abilities with high personal relevance to daily life; eliminating barriers to communication
84
Compensatory or Functional Communication Approach Goal
Improving successful communication and quality of life> reducing impairment
85
The Continuity Hypothesis
anyone can look like they have "aphasia" given the right personal (fatigue) and contextual factors (loud environment + multiple conversations)
86
Aphasia Classification Systems
1. Fluent/Non-fluent dichotomy
2. Wernicke-Litcheim Model
87
Wernicke-Litchtheim Model
- 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
Fluent vs Nonfluent Classification
- phrase length
- pauses
-prosody
-speaking rate
-effort
-initiation and elaboration
-word finding
-telegraphic speech
89
Linguistic Impairment Features
-more specific way of describing individual's impairment for all aspects of clinical decision-making
90
Aphasia Classification System
not as clinically useful as the linguistic impairment description but need to understand these labels as its used in the clinical environment
91
Speech production
intent/conceptualisation-> linguistic-symbolic Planning-> motor planning -> motor programming-> execution
92
Aphasia in Left-Handed Individuals
- 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
Crossed Aphasia
- right handed individuals with aphasia following right hemisphere lesion
- deficits in prosody, metaphor comprehension, and abstract concepts
94
Bilingual aphasia
- NOT an aphasia classification
- Varying recovery patterns
95
cerebrovascular
-highway of the brain
- can carry nutrients and oxygen
96
Controllable Risk factors for stroke
- 87%
- obesity
- hyperglycemias
- hyperlipidemia
- renal dysfunction
- smoking
- sedentary lifestyle
- bad diet
- stress/depression
97
Non controllable risk factors for stroke
- certain medical conditions
- age and gender
- race and ethnicity
- personal family history
0 arteriovenous malformation
98
Transient Ischemic Attack (mini stroke)
- temporary stroke symptoms that resolve between minutes to hours
- once you have a TIA, 2/5 will have a stroke within 90 days
99
Stroke Diagnosis and Management
- Identify focal deficit
- Time last seen
- Imaging
- NIG Stroke Scale
100
When the stroke happens: core
- neurone are dead
101
When the stroke happens" penumbra
- if we are able to restore function in the penumbra, functional impairment can be salvaged
102
IV tPA and TKA
- stroke intervention
- administered within 4.5 hours of time last seen normal
- only ischemic strokes
- BP under 185/110
103
Ischemic stroke
block in the artery
104
thrombotic
blood clot
105
embolic
plaque that builds up in the arteries
106
hemorrhagic
brain bleed
107
intracerebral
in the brain- within the cerebrum
108
subarachnoid
- on the surface of the brain: ventricular space outside the cerebrum but under the skill
109
Stoke Subtypes: small vessel lacunar
19%
110
Stoke Subtypes: hemorrhagic
13%
111
Stoke Subtypes: Ischemic
87%
112
Stoke Subtypes: large vessel
6%
113
Stoke Subtypes: cardio embolic
14%
114
biochemical/physiologic mechanism of recovery: primary during changes within hours after stroke
- 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
biochemical/physiologic mechanism of recovery: primary direct plastic- during first days/weeks
-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
biochemical/physiologic mechanism of recovery: secondary- indirect changes over subsequent weeks and months
- transneuronal degeneration
- denervation supersensitivity
- development of diaschisis
117
transneuronal degeneration
- 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
denervation supersensitivity
neurone who have lost input become super sensitive to any input
119
development of diathesis
- 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
biochemical/physiologic mechanism of recovery: secondary- indirect PLASTIC changes over weeks and months
- collateral sprouting
- regenerative sprouting
- collateral regenerative sprouting
121
collateral sprouting
-axons from nearby neutrons grow new connections with sites previously innervated by dead cells
122
regenerative sprouting
axonal or dendritic, creates new synapses
123
collateral regenerative sprouting
intact cells grow new synaptic connections to attempt to increase connections in the penumbra
124
Stroke recovery behavioural
capacity to perform previously impaired task in the same manner as before the injury
125
stroke compensation behavioural
use of a new strategy to perform that same task
126
stroke recovery neural level
restoration of function within an area that was initially lost
127
stroke compensation neural level
different neural tissue takes over functions after injury
128
Neurological Factors for recovery without treatment
- 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
Personal Factors for Recovery without treatment
-age
- baseline linguistic abilities
- satisfaction with life participation and self-perceived aphasia severity
- social suppor
130
Aphasia Biopsychosocial Approach
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
Distributed langue models (connectionist)
-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
verbal paraphasia
degree of semantic relatedness
133
phonemic aphasia
additions, substitutions, anticipatory, perseverative
134
mixed paraphasia
both semantic and phonological
135
neologistic paraphrases (neologisms)
- response -> "chith" (<50 phonemes shared with target
136
characteristics that cannot be used to diagnose apraxia of speech
- limb or oral non speech aphasia
- expressive- receptive speech/language gap
137
Wernicke associated signs
-possible right hemianopia
-usually no motor or sensory abnormalities
138
Wernicke vascular distribution
- MCA and posterior cerebral artery (PCA)
139
conduction associated signs
- right hemiparesis, right hemisensory loss, right hemianopia
140
conduction vascular distribution
MCA, parietal branches of the PCA
141
brocas associated signs
- right hemiparesis, right hemisensory loss
142
brocas vascular distribution
-anterior branches of the MCA
143
global aphasia associated signs
- right hemiparesis, right hemisensory loss, right hemianopia
144
global aphasia vascular distribution
most of MCA
145
anomic aphasia associated signs
variable, often absent
146
anomic aphasia vascular distribution
variable
147
subcortical aphasia lesion site
subcortical lesions
148
subcortical aphasia symptoms
hypophonia- weak voice
149
PPA Subtypes
-PPA confluent/agramatic varient: effortful speech
-PPA semantic varient (semantic dementia)
- PPA logopenic varient (wrod retreiual deficits
150
Brodmann Area
region of the cortex defined by its cytoarchitecture (organization of neurons)
