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final exam 485 > motor speech disorders > Flashcards

motor speech disorders Flashcards

1
Q

where is the primary motor cortex found?

A

frontal lobe

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2
Q

what are the 3 motor processes to produce speech?

A

planning
programming
execution

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3
Q

what happens in the “planning” process when producing speech?

A

sequencing of articulatory goals

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4
Q

what happens in the “programming” to produce speech?

A

preparing the flow of motor info across muscle, control timing, and force of movement.

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5
Q

what happens during the “execution” to produce speech?

A

activating the relevant muscles.

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6
Q

what are two major speech disorders?

A

apraxia

dysarthria

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7
Q

do people with apraxia and dysarthria have problems with writing?

A

no. these are only issues with motor processes.

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8
Q

What is the cause of motor speech disorders?

A

Neuromuscular and /or motor control system.

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9
Q

Where is the issue for apraxia ?

A

Planning and sequencing

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10
Q

Where is the issue for dysarthria?

A

Execution

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11
Q

Where is the disconnect for dysarthria?

A

Damage is on nervous system pathways. Disconnect between cerebellum and muscles

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12
Q

What can be affected from dysarthria?

A

Respiration
Phonation
Resonance
Articulation.

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13
Q

What is the cause of motor speech disorders?

A

Stroke
Head trauma
Progressive diseases

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14
Q

How is the hearing abilities of motor speech disorders?

A

Fine

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15
Q

Spastic:
Damage where?
Major symptom:
Other signs:

A

Upper motor neurons
Spasticity
Weakness, increases muscle tone, gagging, drooling, involuntary crying

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16
Q

Ataxic:
Damage where?
Major symptom:
Other signs:

A

Cerebellum
In coordination
Reduced muscle tone, “intoxicated speech”, wide based gait, tremors

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17
Q

Difficulty with properly planning, programming, and executing motor movements for speech

A

motor speech disorders.

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18
Q

what are the stages of word production (4)

A

concept/message
lexical-concept
phonological encoding
articulation

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19
Q

broca’s aphasia does not have writing impairments. t/f

A

false!

their writing matches their speech.

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20
Q

MSD has writing impairments. t/f

A

false. Their writing is fine.

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21
Q

MSD have deficits that result from impairment of ___________ and/or motor control system.

A

neuromuscular

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22
Q

MSD may co-occur with other language impairments, t/f

A

t

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23
Q

other oral movements (besides speech) may be impaired, including chewing and smiling. t/f

A

t

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24
Q

is MSD/s common among adults or children? what type?

A

adults.

46% dysarthria

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25
Q

What are the impaired mechanisms in MSDs?

A

planning/programming

execution

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26
Q

Apraxics have issues with what motor processes?

A

planning and programming

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27
Q

dysarthrics have issues with what motor processes?

A

execution

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28
Q

in general what does dysarthria impact? (4)

A

respiration
phonation
resonance
articulation

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29
Q

Speech disorder due to dysfunctional motor execution resulting in incoordinated, weak, and slow articulatory movements

A

dysarthria

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30
Q

what is the cause of dysarthria?

A

Damage to nervous system pathways results in inability to send proper message from brain to the muscles involved in speech

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31
Q

Typically occurs because of a progressive disease, stroke, or trauma

A

acquired dysarthria

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32
Q

what imposes control on movement initiated in primary motor cortex?

A

cerebellum

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33
Q

Group of cell nuclei in the medial part of the brain

A

Basal Ganglia

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34
Q

where do upper motor neurons originate?

A

primary motor cortex

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35
Q

where do lower motor neurons originate?

A

brainstem and spinal cord.

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36
Q

what receives information from upper motor neurons?

A

lower motor neurons

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37
Q

what part of the body is responsible for phonation?

A

vocal cords

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38
Q 
what type of dysarthria;
LMN damage
weakness
reduced muscle tone
reduced reflexes
atrophy
fasiculations
A

flaccid

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39
Q 
what type of dysarthria:
UMN damage
spasticity
weakness
reduced range of movement
increased muscle tone
hypertonia
A

spastic

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40
Q 
what type of dysarthria:
Non-speech deficits:
		Paresis/spasticity of other body parts
		Hyperactive reflexes (e.g., gag)
		Dysphagia, drooling
		Pseudobulbar affect 
					(involuntary crying)
A

spastic

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41
Q 
what type of dysarthria:
Cerebellum damage
Errors in force, speed, timing, range, & direction of movements 
	i.e., incoordination
Reduced muscle tone
“intoxicated speech”
A

ataxic

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42
Q

what are the primary deficits of basal ganglia dysarthrias?

A

hypokinetic (parkinsons)

hyperkinetic (huntingtons)

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43
Q

symptoms associated with ?:
Chorea

Dystonias

Tremor

Palatopharyngolaryngeal myoclonustics (muscles spasms of vocal folds)

A

hyperkinetic

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44
Q

Relatively slow waxing/waning involuntary postures resulting from excessive muscles contracting

A

dystonia

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45
Q

Area of damage: primary motor cortex, white matter in frontal lobe, or brainstem

Major symptoms:
Weakness
Incoordination
Spasticity
central face weakness
hemiparesis/plegia
A

unilateral upper motor neuron dysarthria

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46
Q

upper motor neuron damage will lead to :

A

spastic dysarthria

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47
Q

what are three ways to measure Dysarthria symptoms?

A

perceptual
acoustic
physiological (measuring muscle strength)

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48
Q

problems with apraxia deal mainly with?

A

sequencing

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49
Q

the main problem with dysarthria is?

A

execution

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50
Q

do apraxics have writing impairments?

A

no

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51
Q

what does an apraxic person sound similar to?

A

broca’s

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52
Q 
dysarthria or apraxia?
Speech distortions
Consistent errors
Little/no groping for sounds
All speech affected
Muscle weakness/rigidity
A

dysarthria

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53
Q 
dysarthria or apraxia?
Speech substitutions
Inconsistent errors
groping for sounds
“Island of fluency”
Automatic speech = ok
No muscle weakness/rigidity
A

apraxia

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54
Q

Speech disorder or neurological origin characterized by inability to program or sequence articulatory movements for speech production

A

apraxia

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55
Q

what is the cause of apraxia?

A

Can be developmental or acquired

No known cause for developmental

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56
Q

acquired AOS means there is damage where?

A

only to Broca’s area. (left frontal corex)

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57
Q

Acquired AOS is due to :

A

stroke, brain injuries, illness, infections

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58
Q

Inability to transform an intact linguistic representation(idea in their head) into coordinated movements of the articulators(words)

A

acquired AOS

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59
Q

what does speech sound like for acquired AOS?

A 
sound substitutions
sound distortions
prolonged durations of sounds
reduced prosody
difficulties initiating speech
groping of articulators
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60
Q

what is the most common error type for AOS?

A

anticipation

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61
Q

what are three common error in AOS?

A

anticipations:(felephone)
perseverations (gave the goy)
exchanges (with this wing I do red)

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62
Q

if someone could not stick out their tongue or puff their cheeks they may have?

A

acquired AOS

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63
Q

2 non language symptoms of acquired AOS are:

A

oral motor apraxia

impaired oral sensation

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64
Q

treatment of apraxia includes?

A 
speech therapy (awareness of articulators/exercises)
AAC
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65
Q

what disorder involves deficits with processing and using language? including reading, writing, speaking, auditory.

A

aphasia

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66
Q

what disorder involves inability to execute speech movements, sequencing, disconnect between brain and articulators?

A

apraxia

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67
Q

inability to activate volitional movements for speech

A

apraxia

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68
Q

if a client has difficulty moving their tongue when given directions, this is an example of

A

apraxia

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69
Q

someone who drools or has poor speech due to facial weakness

A

dysarthria

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70
Q

someone that may have other weakness’ other than just speak may be

A

ataxic dysarthria

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71
Q

errors are consistent and predictable

A

dysarthria

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72
Q

errors are inconsistent and unpredicatable

A

apraxia

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73
Q

errors are many distortions and omissions

A

dysarthria

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74
Q

substitutions are most common type of error

A

apraxia

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75
Q

all aspects of speech are affected

A

dysarthria

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76
Q

mainly an articulation issue

A

apraxia

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77
Q

apraxia and dysarthria both may have swallowing issues. t/f

A

t

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78
Q

what is always a result from damage to the broca’s area?

A

apraxia

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79
Q

what is the result of damage to either the CNS or PNS?

A

dysarthria

80
Q

dysarthria or apraxia?

speech substitutions

A

apraxia

81
Q

dysarthria or apraxia?

speech distortions

A

dysarthria

82
Q

dysarthria or apraxia?Little/no groping for sounds

A

dysarthria

83
Q

dysarthria or apraxia?

Automatic speech = ok

A

apraxia

84
Q

dysarthria or apraxia?All speech affected

A

dysarthria

85
Q

dysarthria or apraxia?“Island of fluency”

A

apraxia

86
Q

treatment for apraxia includes? (2)

A

speech therapy

aac

87
Q

the patient has subcortical damage. What is most likely the outcome?

A

dysarthria

if cortical damage, it will be bilateral

88
Q

the patients speech behavior has sound level distortions.

A

dysartharia

89
Q

The patient’s speech has abnormal prosody.

A

aos

90
Q

this patient has problems initiating speech and has phoneme substitutions.

A

aos

91
Q

the patient has phoneme substitutions.

A

aos

92
Q

the patient has infrequent metathetic errors.

A

aos

93
Q

presence of paralysis, paresis, ataxia, involuntary movements. apraxia or dysarthria?

A

dysarthria

94
Q

the longer the utterance the more errors are made. apraxia or dysarthria?

A

aos

95
Q

prolonged durations of sound is typical for apraxia or dysarthria?

A

aos

96
Q

where is the damage for flaccid?

A

lower motor neurons

97
Q

where is the damage for spastic?

A

upper motor neurons

98
Q

where is the damage for ataxic?

A

cerebellum

99
Q

where is the damage for hypokinetic/hyperkinetic?

A

basal ganglia

100
Q

what are the 2 control circuits relating to the motor system?

A

basal ganglia

cerebellar

101
Q

what are the 2 execution pathways relating to the motor system?

A

upper

lower motor neurons.

102
Q

what control circuit imposes control on movement initiated in primary motor cortex?

A

cerebellum

103
Q

what part of the brain plays a major role in error correction based feedback?

A

cerebellum

104
Q

group of cell nuclei in the medial part of the brain is the?

A

basal ganglia

105
Q

where do upper motor neuron axons synapse?

A

cell bodies of lower motor neurons in the brainstem and spinal cord.

106
Q

where do lower motor neurons originate where?

A

brain stem and spinal cord.

107
Q

lower motor neuron axons synapse where?

A

muscle fibers

108
Q

a patients primary deficit is weakness. what type of dysarthria and where is damage?

A

flaccid

lower motor

109
Q

a patients primary deficit is spasticity. what type of dysarthria and where is damage?

A

spastic

upper motor

110
Q

a patients primary deficit is incoordination. what type of dysarthria and where is damage?

A

ataxic

111
Q

a patients primary deficit is involuntary movements. what type of dysarthria and where is damage?

A

basal ganglia

hyperkinetic

112
Q

a patients primary deficit is rigidity. what type of dysarthria and where is damage?

A

hypokinetic

basal ganglia

113
Q

a patient has weakness; incoordination; spasticity. what type of dysarthria and where is damage?

A

unilateral UMN

UMN

114
Q 
major deficit is: weakness other signs of this type of dysarthria:
reduced muscle tone
reduced reflexes
atrophy
fasciculations
A

flaccid

115
Q

people with conduction aphasia make what type of errors with their speech?

A

phonological paraphasias

116
Q

where is brain damage when the result is conduction aphasia?

A

cortex in the posterior superior temporal lobe.

117
Q

why do conduction aphasics have a hard time repeating non-words?

A

this would require intact phonological processing; which they do not have.

118
Q

harry has a large amount of right hemisphere damage. What would be a difficult task for him?

A

summarizing a paragraph that he read or summarizing a conversation he heard.
also, paying attention to information in their left visual field.

119
Q

paying attention to information in the left visual field would be difficult for someone with …?

A

right hemisphere damage

120
Q

t/f people with apraxia and dysarthria make the same errors consistently.

A

false

dysarthria makes consistent, but not apraxia

121
Q

why does someone with apraxia have difficulty with saying fairly long words but does not have difficulty with simple sounds, such as “tatatata”?

A

because apraxia is a deficit in the planning and sequencing of motor sequences.

122
Q

would an apraxic have difficulty with “tatatata” or “ta ba ka da”?

A

ta ba ka da

this requires motor sequencing which is impaired.

123
Q

apraxia is a deficit in the processing that occurs before the motor movements are made. t/f

A

t

124
Q

if the basal ganglia is not active enough, the patient might have….

A

hypokinetic dysarthria

125
Q

what is an example of hypokinetic dysarthria?

A

parkinson

126
Q

what is an example of hyperkinetic dysarthria

A

huntingtons

127
Q

what is the one thing that all types of aphasia have in common ?

A

anomia

128
Q

main symptom of hyperkinetic dysarthria.

A

involuntary movements

129
Q

main symptom of hypokinetic dysarthria

A

rigidity, stiffness, and tightness

130
Q

main symptom of spastic dysarthria

A

increased muscle tone, lack of inhibitory signals

131
Q

main symptom of flaccid dysarthria

A

weakness

132
Q

main symptom of ataxic dysarthria

A

“druken speech”, due to cerebellum damage

133
Q

how is transcortical motor aphasia’s speech comprehension

A

good, no major deficits

134
Q

how is broca’s aphasia speech comprehension?

A

good ,but difficulties with some complex syntactic constructions

135
Q

how is wernickes aphasia speech comprehension?

A

very poor

136
Q

how is global aphasia speech comprehension?

A

very poor

137
Q

how is anomic aphasia speech comprehension?

A

good, no major deficits

138
Q

Transcortical motor and Broca’s aphasias are mainly problems of speech production, not comprehension. One exception to this though is that Broca’s aphasics’ comprehension is ____________

A

agrammatic, meaning that they have difficulty understanding phrases or sentences in which the grammatical structure is needed to understand the sentence

139
Q

which neurons are the neurons that have synapses with the muscles?

A

lower motor

140
Q

where do UMN and LMN connect?

A

brain stem and spinal cord

141
Q

do conduction aphasics have speech comprehension problems?

A

no

142
Q

what is alexia?

A

ACQUIRED (dyslexia) inability to comprehend written language

143
Q

what are the 3 routes used in reading?

A
  1. Grapheme to phoneme conversion (sound it out)
  2. whole word to phonology conversion (words activate the appropriate sound based representation, which then activates meaning)
  3. whole word meaning route (familiar words activate appropriate visual word form, which activates meaning)
144
Q

Can you use the grapheme to phoneme conversion for irregular words?

A

no, only works for regular words.

145
Q

why is grapheme to phoneme conversion not a route to depend on?

A
  1. it would take forever to read!

2. doesn’t work for irregular words.

146
Q

which word route takes care of irregular word issues?

A

whole word to phonology conversion.

147
Q

whole words activate the appropriate sound representation, which then activates meaning. However, what type of words still present a problem?

A

him vs. hymn
write vs. right

homophones

148
Q

how would someone use the whole word to meaning route?

A

Words activate the appropriate visual representation which in turn activates meaning

149
Q

why do people not use the whole word to meaning route all the time?

A

the words must be familiar!

150
Q

what are the 3 routes needed in order to read normally?

A
  1. grapheme to phoneme
  2. whole word to phonology
  3. whole word to meaning
151
Q

when reading is disrupted, what is it called?

A

acquired alexia

152
Q

what are two ways to describe deficits with reading?

A
  1. neurological model

2. cognitive model

153
Q

which model is used to explain the different types of alexia with agraphia a clinician might see?

A

cognitive model

154
Q

when using the neurological model for pure alexia, what is the diagnosis?

A

a ‘disconnection’ syndrome, from left hemisphere word-recognition system

155
Q

according to the neurological model, alexia with agraphia, has what deficits?

A

pure reading and writing

156
Q

according to the neurological model, aphasic alexia, has what type of deficits?

A

reading deficits mirror language deficits

157
Q

A patient with pure alexia would be able to do what?

A

write

read letter-by-letter

158
Q

can a person with pure alexia read individual words?

A

sometimes, however when combining words they cannot access meaning.

159
Q

what type of alexia is a disconnection of visual information from left hemisphere word-recognition system?

A

pure alexia

160
Q

A patient is able to write normally, however they cannot read what they just wrote. This is an example of what type of alexia?

A

Pure alexia.

161
Q

a patient is able to tell you what you spelled out. for example, “C-A-T”. they can tell you it says ‘cat”. this is an example of what type of alexia?

A

pure alexia

162
Q

other symptoms of pure alexia are: (3)

A
  1. impaired ability to copy words.
  2. acalculia
  3. hemianopsia (blind in one visual field; usually the right)
163
Q

what type of speech comprehension and production does a person with pure alexia have?

A

normal

164
Q

what two parts of the brain must be damaged to cause Pure Alexia?

A
  1. left primary visual cortex

2. splenium

165
Q

part of the corpus callosum that connects the right visual cortex to the left hemisphere.

A

splenium

166
Q

where is the calcarine sulcus?

A

primary visual cortex

167
Q

what is the etiology of pure alexia?

A

blocked splenium

168
Q

why does a blocked splenium cause pure alexia?

A

Because visual information cannot get to the regions in the left hemisphere that process word forms

169
Q

where is the splenium?

A

posterior part of the corpus callosum

170
Q

which type of alexia is not affected by orthographical regularity?

A

pure alexia

171
Q

what type of alexia has relatively pure reading/writing deficits, with no aphasia?

A

alexia with agraphia

172
Q

a patient has a brain lesion on the angular gyrus in the left hemisphere. What type of alexia would they most likely suffer from?

A

alexia with agraphia

173
Q

according to the neurological model, what two types of alexia do not have aphasia?

A

pure alexia

alexia with agraphia

174
Q

the cognitive model, describes what 3 types of reading deficits?

A

surface dyslexia
phonological dyslexia
deep dyslexia

175
Q

when the only route left is to “sound it out”, it is known as what type of dyslexia?

A

surface (visual form)

176
Q

what patients typically exhibit surface dyslexia?

A

dementia

alzheimer

177
Q

a patient cannot read non-words or new words and is unable to “sound it out”. what type of dyslexia?

A

phonological dyslexia (sound form)

178
Q

where is there brain lesions when the result is phonological dyslexia?

A

superior temporal lobe, angular gyrus, and other nearby areas.

179
Q

A patient is making semantic errors, has difficulty with abstract and function words. What type of dyslexia?

A

deep dyslexia

180
Q

where is damage when the result is deep dyslexia?

A

large left hemisphere perisylvian lesion.

181
Q

what type of patients typically have surface dyslexia?

A

dementia

182
Q

what part of the brain is thought to be the central area involved in the processing of orthographic word forms?

A

angular gyrus

183
Q

lesions to what part of the brain will result in alexia with agraphia?

A

angular gyrus

184
Q

a patient is able to read and comprehend words, however cannot read pseudowords. What type of alexia?

A

phonological

185
Q

a patient with phonological alexia might have damage to what areas of the brain?

A

temporal lobe and surrounding areas, as well as angular and supramarginal gyri

186
Q

a patient is able to read words and pseudowords but has profound impairments with comprehension. What type of alexia?

A

semanti

187
Q

a patient is supposed to read the word “soft” but verbalizes the word “hard”. The next word is “vegetable” and their response is “broccoli”. This is an example of what type of alexia?

A

deep

188
Q

the disconnection between orthographical units and phonological units is representative of what type of alexia?

A

phonological

189
Q

is the reading and comprehension preserved with phonological alexia?

A

yes

190
Q

which type of alexia has problems with pseudo words?

A

phonological

191
Q

a patient is a not able to use visual input to activate the orthographic unit therefore unable to read, although can recognize individual letters. What type of alexia?

A

pure

192
Q

“groping” is a common characteristic for what type of patient?

A

apraxic

193
Q

a patient is making inconsistent errors, such as substitutions, additions, repetitions and prolongation. What is the deficit?

A

apraxia

194
Q

inability to transform graphemes into phonemes, and thus non-words are often read as real words they resemble.

A

phonological alexia

195
Q

This type of dyslexia is similar to phonological dyslexia but in addition makes numerous semantic errors.

A

deep

final exam 485 (2 decks)

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