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motor speech > final exam > Flashcards

final exam Flashcards

1
Q

flaccid dysarthria

A

impairments of lmns in cranial or spinal nerves (pns damage)

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2
Q

flaccid dysarthria causes

A

caused by any disorder that disrupts flow of neural impulses along lmns travel to reach muscles

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3
Q

location of damage flaccid

A

final common pathway

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4
Q

final common pathway

A

last and only road nueral impulses from umns travel to reach muscles

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5
Q

flaccid injuries

A

brainstem stroke, growing tumor, viral or bacterial infections, physical trauma, surgical accidents, mysathenia gravis, guillain-barre syndrome, polio, muscular dystrophy, progressive bulbar palsy

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6
Q

speech charateristics flaccid

A
  • May NOT demonstrate deficits in all areas; severity level will vary
  • Hallmarks: slow-labored articulation, marked degrees of hypernasal resonance, hoarse-breathy phonation
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7
Q

resonance characteristcs flaccid

A
  • Hypernasality most common
  • Nasal emission
  • Weak pressure consonants
  • Shortened phrases
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8
Q

articulation characteristics flaccid

A

imprecise consonant production

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9
Q

phonation characteristics flaccid

A

Phonatory incompetence (incomplete adduction of VFs during phonation) giving hoarse-breathy voice

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10
Q

respiration characteristics flaccid

A
  • May not be affected
  • If it is, you would see reduced loudness and speaking on residual air
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11
Q

prosody characteristics flaccid

A
  • Monopitch, monoloudness
  • Not unique to flaccid so not a diagnostic marker
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12
Q

evaluation tasks

A
  • Look for clusters of symptoms when trying to diagnose
  • Conversational speech and reading: Can evoke errors of resonance, arctic, respiration, and prosody
  • AMR: /puh puh puh/ /tuh tuh tuh/ /kuh kuh kuh/. Will highlight a slowed rate of phoneme production
  • Prolonged vowel: Will elicit breathy voice quality heard in phonatory incompetence
  • Speech stress test: Necessary IF myasthenia gravis is suspected
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13
Q

treatment flaccid

A
  • Treatments are according to which cranial nerve
  • Needs and abilities vary greatly
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14
Q

resonance treatment flaccid

A

Velar strength-training procedure; modification of speech; reduce rate

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15
Q

phonation treatment flaccid

A

Pushing and pulling procedures, hard glottal attack

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16
Q

prosody treatment flaccid

A

Pitch range exercises, intonation profiles, contrastive stress drills

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17
Q

respiratory treatment flaccid

A

Correct posture, prosthetics, speaking immediately on exhalation

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18
Q

spastic dysarthria

A

bilateral damage to umn tracts

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19
Q

pyramidal system spastic

A

damage = weak/slow skilled movements

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20
Q

extrapyramidal system spastic

A

damage = weakness, increased muscle tone (spasticity), and abnormal reflexes

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21
Q

injuries spastic dysarthria

A
  • stroke - most common; only occurs in LH and RH as a combo OR single in brainstem
  • degenerative diseases: ALS, multiple sclerosis
  • TBI
    -infection
    -tumors
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22
Q

speech characteristics spastic

A

-imprecise consonants, monopitch, monoloudness, reduced stress, harsh vocal quality
- Errors result bc of spasticity, slowness, weakness in vocal-tract muscles

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23
Q

articulation characteristics spastic

A

Imprecise consonant productions, vowel distortions

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24
Q

phonation characteristics spastic

A

Harsh vocal quality, Strained-strangled, Low pitch

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25
Q

resonance characteristics spastic

A

hypernasality

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26
Q

prosody characteristics spastic

A

Monopitch, monoloudness, short phrases, short rate of speech

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27
Q

evaluation tasks spastic

A
  • Conversational speech and reading
  • AMR (ppp, ttt, kkk)
  • Vowel prolongations
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28
Q

treatment spastic

A
  • Phonation deficits: work on relaxation, easy onset of phonation, yawn-sigh, tongue and lip stretching
  • Articulation deficits: intelligibility drills, phonemic placement, minimal contrast drills
  • Prosody deficits: pitch range exercises, contrastive stress drills, chunking utterances
  • Resonance deficits: pharyngeal flap, palatal lift
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29
Q

special spastic

A
  • Pseudobulbar affect- uncontrollable crying or laughing
  • Drooling and swallowing issues
  • Pseudobulbar palsy- weakness and slowness in same muscle
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30
Q

uumn dysarthria

A
  • caused by damage to upper motor neurons one side of the brain that supply cranial and spinal nerves involved in speech production
  • usually less severe than with bilateral damage
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31
Q

location of damage uumn

A
  • Lower face and tongue
  • Any condition that damages upper motor neurons on one side of brain after damage to either left or right hemisphere
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32
Q

injuries uumn

A
  • Most frequent cause is stroke; specifically stokes involving frontal lobe
  • Tumors and TBI can be a cause, but they are uncommon
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33
Q

speech characteristics uumn

A
  • Weakness in lower face, lips, and tongue on opposite side of lesion
  • Mild or moderate speech production errors - often short term with recovery after days or weeks
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34
Q

articulation uumn

A

-primary deficit
- Imprecise consonant production, articulatory breakdowns, slow and irregular AMRs

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35
Q

phonation uumn

A

Mild to harsh vocal quality

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36
Q

resonance uumn

A

Hypernasality

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37
Q

prosody and respiration uumn

A

Rarely impaired

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38
Q

evaluation tasks uumn

A
  • Medical records
  • Conversational speech or reading paragraph
  • AMR tasks
  • Prolonged vowel
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39
Q

treatment uumn

A
  • Coexciting deficits are usually treated
  • Artic may be so minor that SLP may decide not to treat
  • Intelligibility drills, phonetic placement, exaggerating consonants, minimal contrast drills
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40
Q

ataxic dysarthria

A

due to damage to cerebellum or its neural pathways

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41
Q

location of damage ataxic

A

cerebellum, inferior peduncles, middle peduncle, superior pedunle, cerebellar control circuits

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42
Q

cerebellum ataxic

A

coordinate timing and force of muscular contractions; attached to brainstem; communicates with rest of CNS through 3 bundles of neural tracts called cerebellar peduncles

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43
Q

inferior peduncles ataxic

A

receives sensory info

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44
Q

middle peduncle ataxic

A

smooths and refines the planned movement

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45
Q

superior peduncle ataxic

A

Sends out the motor impulses

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46
Q

cerebellar control circuits ataxic

A

neurons that course through 3 cerebellar pathways

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47
Q

injuries ataxic

A
  • Stroke
  • Toxic conditions
  • Metabolic conditions
  • Traumatic head injury
  • Tumors
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48
Q

speech characteristics ataxic

A
  • Movements appear poorly coordinated, problems controlling timing/force for speech, slurred, monotonous arctic, primarily disorder of artic and prosody
  • Scanning speech - slow, deliberate production of syllables with each syllable in a word receiving equal stress
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49
Q

articulation ataxic

A
  • Imprecise consonant production
  • Distorted vowels
  • Irregular articulatory breakdowns
  • Decomposition of movement: manifestations of cerebellar dysfunction, where instead of smooth coordinated movements, they are distinct and jerky
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50
Q

prosody ataxic

A
  • Equal and excess stress
  • Prolonged phonemes and prolonged intervals between phonemes
  • Monopitch and monoloudness
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51
Q

phonation ataxic

A
  • Harsh vocal quality
  • Voice tremor
52
Q

resonance ataxic

A
  • Hyponasality
53
Q

respiration ataxic

A
  • Uncoordinated movements in respiratory muscles, contributing to speech deficits
  • Paradoxical movements: movements that occur when muscles work against each other rather than in coordination
54
Q

evaluation tasks ataxic

A
  • Speech alternate motor tasks: slower than normal, difficulty maintaining steady rhythm with repetition
  • Reading, conversational speech, and repeating sentences containing numerous multisyllabic words
55
Q

respiration treatment ataxic

A
  • Do not need to address strengthening
  • Concentrate on controlling airflow more accurately during speech, as uncoordinated movements of respiratory muscles cause speech on residual air, affecting prosody and phonation
  • Slow and controlled exhalation
  • Speak immediately on exhalation
  • Stop phonation early
  • Optimal breath group - teaching how many syllables or words can be said clearly on one full inhalation
56
Q

prosody treatment ataxic

A
  • Slow rate
  • Incorporating more typical stress and intonation into utterances
  • Rate control: Reciting syllables to a metronome, Finger or hand tapping, Cued reading material
  • Stress and intonation: Contrastive stress drills, Pitch range exercises, Intonation profiles, Chunking utterances into syntactic units
57
Q

articulation treatment ataxic

A
  • Intelligibility drills
  • Phonetic placement
  • Exaggerating consonants
  • Minimal contrast drills
58
Q

hypokinetic

A

any process that damages basal ganglia (extrapyramidal system)

59
Q

main cause of hypokinetic

A
  • Parkinsonism - collective term for different disorders sharing many similar symptoms
  • Causes:
    Idiopathic parkinson’s disease
    Neuroleptic-induced parkinsonism
    Postencephaltic parkinsonism
    Traumatic head injury
    Toxic metal poisoning
    Stroke
60
Q

symptoms hypokinetic

A
  • Resting tremor
  • Bradykinesia: slow, reduced range of movement
  • Rigidity
  • Spasticity
  • Akinesia: delay in initiation of movements
  • Postural reflexes
61
Q

location of damage hypokinetic

A

dysfunction in basal ganglia; depends on balanced interaction of dopamine and acetylcholine

62
Q

speech characteristics hypokinetic

A

harsh vocal quality, reduced stress, monoloudness, imprecise consonants; significant indvidual differences

63
Q

prosody hypokinetic

A

monopitch, reduced stress, and monoloudness most common

64
Q

articulation hypokinetic

A

imprecise consonants, repeated phonemes, palilalia

65
Q

phonation hypokinetic

A

harsh/breathy quality, aphonia, low pitch

66
Q

respiration hypokinetic

A

sometimes noted

67
Q

evaluation tasks hypokinetic

A

-conversational speech and reading: evoke errors of prosody
-AMRs: highlight artic errors
-vowel prolongations: assess vocal quality

68
Q

pharamcologic treatment hypokinetic

A

-L-dopa
-replacing dopamine in striatum
-correct neurotransmitter imbalance by decreasing acetylcholine activity in striatum

69
Q

surgical treatments hypokinetic

A

-ablative surgery
-deep brain stimulation
-stem cell implantation

70
Q

articulation treatment hypo

A
  • Most common deficit: imprecise consonants due to reduced range of motion in arctic
  • Compounded by increased ate
  • Rate reduction, stretching, traditional artic tasks
71
Q

phonation treatment hypo

A
  • Adduct VFs only partially or have harsh or breathy voice quality
  • Pushing and pulling procedure, hard glottal attack, LSVT
72
Q

respiration treatment hypo

A
  • Speaking immediately on exhalation
  • Stop phonation early
  • Optimal breath group
73
Q

prosody treatment hypo

A
  • Intonation profiles
  • Contrastive stress drills
  • Chunking utterances into syntactic units
  • All used to Slow rate
74
Q

hyperkientic dysarthria

A

caused by damage to the basal ganglia

75
Q

causes of hyperkinetic dysarthria

A
  • Myoclonus - involuntary and brief contractions of part, whole, or group of muscles in same area
  • Tics
  • Essential tremor - benign hyperkinetic movement disorder that causes tremulous movements in affected body parts
  • Dystonia
  • Degenerative diseases
  • Traumatic head injury
  • Stroke
  • Infections
76
Q

evaluation tasks hyper

A

-Vowel prolongation
- AMRs
- Conversational speech and reading
- Careful observation of associated involuntary movements

77
Q

treatment hyper

A

-Pharamacologic - drugs that suppress involuntary movements that cause speech deficits
- Botox
- Deep brain stimulation

78
Q

treatment for huntingtons disease

A
  • Early stages - maintain normal prosody and optimal rate
  • Middle stages - rate of speech, rhythmic breathing and relaxation, speaking on exhalation
  • Progressive dementia - work closely with caregivers
79
Q

treatment for tic disorders

A

Behavioral treatments:
- Habit reversal training
- Relaxation therapy may be helpful when combined with other treatment procedures
- Exposure response prevention
- Comprehensive behavioral intervention for tics

80
Q

dystonia (part of hyper)

A
  • Causes involuntary, prolonged muscle contractions
81
Q

dystonia artic hyper

A

imprecise consonants, distorted vowels, irregular articulatory breakdowns, prolonged phonemes

82
Q

prosody dystonia

A

monopitch, monoloudness, inappropriate silences, shortened phrases

83
Q

phonation dystonia

A

harsh vocal quality, strained-strangled quality, excess loudness variation

84
Q

respiration and resonance dystonia

A

less impacted

85
Q

treatment dystonia

A
  • Sensory tricks - idiosyncratic strategies that can suppress involuntary movement for a time
  • Bite blocks - to stabilize jaw during speech
  • Easy onset of phonation
86
Q

chorea (part of hyper)

A
  • Sydenham’s chorea - rare disorder affecting children after rheumatic fever
  • Huntington’s disease - progressive inherited disorder
  • Tardive dyskinesia - caused by taking certain antipsychotics
  • Stroke - rare to cause chorea
87
Q

speech characteristics chorea

A

Prolonged intervals between syllables and words, inappropriate silences, prolonged phonemes, intermittent breathy voice quality

88
Q

mixed dysarthria

A
  • when neurologic damage extends into two or more parts of motor system; any combo of pure dysarthrias
  • Prominence of each pure dysarthria within mixed dysarthria within mixed dysarthria varies significantly among individuals
89
Q

injuries mixed dysarthria

A
  • Single or multiple strokes
  • Brain tumors
  • Traumatic head injuries
  • Degenerative diseases
  • Infectious diseases
  • Multiple sclerosis
  • multisystems atrophy
  • amyotrophic lateral sclerosis
  • wilson’s disease
    -friedreich’s ataxia
90
Q

multiple sclerosis

A
  • Progressive demyelinating disease
  • Can occur in brainstem, cerebellum, cerebral hemispheres, and spinal cord
  • Can cause any pure or any combo of mixed dysarthria
  • Ataxic-spastic most common
91
Q

multisystems atrophy

A
  • Collective term for group of degenerative disorders, many including parkinsonian symptoms:
  • Shy-drager syndrome
  • Progressive supranuclear palsy
  • Olivopontocerebellar atrophy
92
Q

amyotrophic lateral sclerosis

A
  • Progressive degeneration of any four areas of motor neurons
  • Often progresses from affecting two motor neuron groups to all four
  • Mixed dysarthria predominates throughout much of this disorder
93
Q

wilson’s disease

A
  • Very rare hereditary disease preventing normal metabolism of dietary copper
  • Penicillamine successful in treating most patients
  • Dysarthria of earliest signs
  • ataxic-spastic -hypokinetic present in many
94
Q

friedreich’s ataxia

A
  • Rare, inherited, progressive disorder
  • Causes neuron degeneration in cerebellum, brainstem, and spinal cord
  • Untreatable, fatal
  • Ataxic-spastic most prevalent
95
Q

treatment mixed

A
  • General rule: first treat component most severely affecting speech production
  • When all are equally affected: respiration, resonation, phonation, articulation, prosody (RRPAP)
  • AAC for ALS
96
Q

apraxia of speech

A

disorder of motor timing and sequencing

97
Q

ideational apraxia

A

uncommon; disturbance in conception of object or gesture

98
Q

ideomotor apraxia

A

disturbance in performance of movements needed to use object, make gesture, sequence movements

99
Q

location of damage apraxia

A

Motor speech programmer - neural network in the brain that sequences motor movements needed to produce speech.
- first analyzes linguistic, motor, sensory, and emotional info
- Near perisylvian area of left hemisphere

100
Q

injuries apraxia

A
  • Stroke
  • Degenerative disease
  • Trauma
  • tumor
101
Q

speech characteristics apraxia

A
  • Primarily disorder of articulation and prosody
  • Slow, labored, halting speech
  • Instances of groping
102
Q

articulation apraxia

A

most common errors

103
Q

prosody apraxia

A

frequently abnormal

104
Q

respiration apraxia

A

may have difficulty taking deep breath on command

105
Q

resonance and phonation apraxia

A

seldom issues

106
Q

assessment strategies apraxia

A
  • SMRs - sensitive assessment
  • Conversational speech and reading aloud - determine effects of prosody
  • Repeating words of increasing length
  • Reading or repeatin low-frequency, multisyllabic words in isolation or sentences
107
Q

categories to determine correct diagnosis apraxia

A
  • Primary clinical characteristics
  • Non Discriminative clinical characteristics
  • Behaviors usually found in disorders other than apraxia
  • Behaviors that rule out presence of apraxia
108
Q

treatment apraxia

A

Goal: help patient relearn motor sequences to produce phonemes accurately

109
Q

sequencing treatment apraxia

A
  • Repetitive and intensive drill
  • Patients learn to self-monitor
  • Concentrate on functional words
110
Q

articulatory kinematic treatments apraxia

A

Concentrate on improving timing and placement of articulatory movements through modeling, positioning of articulators, and repetition

111
Q

rate and rhythm procedues apraxia

A

Assume apraxia primarily result of timing errors

112
Q

AAC apraxia

A

Recommended with limited verbal communication

113
Q

interystemic facilitation and reorganization treatment apraxia

A

Patient’s communicative strengths used to assist verbal speech

114
Q

parkinsonism

A

known cause

115
Q

parkson;s disease

A

unknown etiology

116
Q

important to know parkinsonism

A
  • Basal ganglia damage
  • Festinating speech: same as gait just speech related
  • Festinating gait: walking starts slow → fast, quick, short
117
Q

features of CAS

A
  • inconsistent errors
  • inappropriate prosody
    -groping
    -vowel errors
118
Q

treatments CAS

A

-prompt
-rest
-dttc
-NDP3
-cycles

119
Q

prompt

A

-tactile-kinetshetic-propriocetive based tx
-emphasizes normalization of speech movement patterns in an age-appropriate, functional lexicon of words

120
Q

ReST

A

-high intensity practice of randomly presented pseudowords with varying phonetic structure and lexical stress

121
Q

dttc

A

-cueing hierarchy
-never in isolation, start with the easiest and work it up

122
Q

NDP3

A

-bottom-up approach builds from single sounds to syllables and syllable sequencing

123
Q
  1. primary clinical characteristics
A

-prosody
-slow speech rate
-slow speech rate w/pauses
-distorted phonemes with substitutions
-consonants and vowels are distorted
-inconsistent articulation errors

124
Q
  1. nondiscriminitive clinical characteristics
A

-self-corrects and shows signs of awareness
-difficulty initiating speech
-speech errors increase as word length increases
-artic groping

125
Q
  1. behaviors usually found in disorders other than AOS
A

-demonstrates difference between expressive and receptive speech and language skills
-has transposition errors
-anticipatory articulation errors
-presence of limb or oral apraxia

126
Q
  1. Behaviors that rule out presence of AOS
A

-fast speech rate
-normal speech rate
-normal prosody

motor speech (12 decks)

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