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Motor Speech Disorders > Motor Speech Exam 3 > Flashcards

Motor Speech Exam 3 Flashcards

1
Q

What is the neurological basis for ataxic dysarthria?

A

cerebellar damage or it’s pathway

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2
Q

ataxia

A

a lack of coordination

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3
Q

cerebellum

A

coordinates timing and force of muscular contractions

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4
Q

symptoms of cerebellar ataxia

A

disequilibrium, nystagmus, intention tremor, hypotonia, problems with motor learning

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5
Q

what are the etiologies of ataxic dysarthria

A

degenerative diseases, stroke, toxic conditions, TBI, tumors

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6
Q

what is a degenerative disease for ataxic dysarthria

A

friedreich’s ataxia

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7
Q

what are the characteristics of friedreich’s ataxia

A

progressive, hereditary, symptoms appear in the late 20s

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8
Q

what are the components of the etiology of a stroke in ataxic dysarthria

A

occlusions, ruptured aneurysms, and cerebellar arteries

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9
Q

what are the components of the etiology of toxic conditions in ataxic dysarthria

A

lead, mercury, cyanide with history of ethanol, phenytoin, and metabolic conditions such as vitamin deficiencies and hypothyroidism

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10
Q

what are the components of the etiology of a TBI in ataxic dysarthria

A

cerebellum and cerebellar control circuit

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11
Q

ataxic dysarthria speech characteristics

A

movements of speech mechanisms are poorly coordinated, timing and force of muscular contractions for clearly articulated speech, “drunken speech”, and “scanning speech”

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12
Q

ataxic dysarthria articulation

A

imprecise consonants and vowel distortions

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13
Q

what are the type of imprecise consonants for ataxic dysarthria

A

slurred, irregular, and inconsistent errors

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14
Q

ataxic dysarthria prosody

A

equal and excess stress, prolonged phonemes, prolonged intervals between phonemes, slow speech rate with increased pause time/articulation time and “choppy speech”, monopitch, and monoloudness

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15
Q

ataxic dysarthria phonation

A

harsh voice quality with decreased muscle tone in laryngeal and respiratory structures

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16
Q

ataxic dysarthria respiration

A

exaggerated or paradoxical movements including excessive loudness variations, reduced vital capacity, speaking on residual air, decreased loudness, and harsh voice quality

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17
Q

what are the key evaluation tasks for ataxic dysarthria

A

AMRs, conversational speech and reading, and sentence repetition

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18
Q

how do you treat respiration for those with ataxic dysarthria

A

speak immediately on exhalation with visi-pitch for visual feedback, stop phonation early, optimal breath group

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19
Q

how do you treat prosody for those with ataxic dysarthria

A

pitch range exercises, intonation profiles, contrastive stress drills, and chunking utterances into syntactic units

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20
Q

what is intonation profiles

A

written sentences and protocol on visi-pitch

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21
Q

how do you treat articulation for those with ataxic dysarthria

A

over articulation of consonants and minimal contrast pairs

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22
Q

is hypokinesis the same as hypotonia?

A

no

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23
Q

hypokinesis

A

less movement, but more muscle tone

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24
Q

the vast majority of cases of hypokinetic dysarthria are due to

A

parkinsonism

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25
Q

parkinsonism

A

umbrella term for brain conditions that cause slow movements, rigidity and tremors

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26
Q

Parkinsonism neurologists’s diagnosis is based on

A

TRAP - tremor, rigidity, akinesia, postural instability

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27
Q

parkinson’s disease is an idiopathic (unknown cause) form of

A

parkinsonism

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28
Q

parkinson’s disease have a high prevalence of

A

speech deficits 60-80%

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29
Q

WHO: wrote an account of his patients in 1817, described a “shaking palsy”, not all PD patients have a tremor, tremor dominant or rigid dominate, speech symptoms clearly resembled what is known today as hypokinetic dysarthria

A

James Parkinson

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30
Q

medical treatment for parkinson’s disease is usually

A

treated pharmacologically, deep brain stimulation to send current to thalamus, and surgeries

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31
Q

what are the two types of surgeries for medical treatment of parkinson’s

A

thalamotomy and pallidotomy

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32
Q

thalamotomy surgery

A

lesion on thalamus, less input from basal ganglia goes through

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33
Q

pallidotomy

A

lesion in globus pallidus - terrific for tremor and akinesia

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34
Q

what is the second most common form of parkinsonism

A

neuroleptic-induced parkinsonism

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35
Q

what are the side effects of antipsychotic drugs in neuroleptic-induced parkinsonism

A

chlorpromazine and schizophrenia; (tardive diskenesia - weird jerking movements after years of drugs)

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36
Q

schizophrenia is often associated with

A

excess dopamine

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37
Q

post encephalic parkinsonism

A

caused by viral encephalitis and can also affect children

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38
Q

traumatic brain injury

A

cerebral anoxia (if it affects BG), “punch drunk” encephalopathy (pugilism - caused by fighting)

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39
Q

CVA when it affects

A

basal ganglia, substantia nigra, BG control circuit

40
Q

hypokinetic dysarthria prosody

A

monopitch, reduced stress, mono loudness, inappropriate silences, short rushes of speech, variable speech rate

41
Q

hypokinetic dysarthria articulation

A

imprecise consonants, repeated phonemes, and palilalia

42
Q

what are the characteristics of imprecise consonants in hypokinetic dysarthria

A

reduced ROM, distortions, spirantization, articulatory undershoot

43
Q

hypokinetic dysarthria phonation

A

harsh voice, breathy, reduced vocal loudness

44
Q

hypokinetic dysarthria respiration

A

faster breathing rates, paradoxical movements (when the agonist and antagonist are co-contracting - tug of war), reduced ROM, may result in shallow breath support, poorly controlled exhalations, short breathing cycles, short rushes, breathy

45
Q

what are the key evaluation tasks in hypokinetic dysarthria

A

conversational speech, AMRs, and vowel prolongation

46
Q

what are the conversational speech/reading tasks in hypokinetic dysarthria

A

rate problems and intelligibility

47
Q

what are the AMR tasks in hypokinetic dysarthria

A

imprecise consonants, variable rate, and “blurring” of syllables

48
Q

what are the vowel prolongations in hypokinetic dysarthria

A

breathy voice quality

49
Q

treatment of hypokinetic dysarthria for rate reduction

A

can improve articulation, give articulators more time to reach target positions, give listener more processing time

50
Q

treatment of hypokientic dysarthria for DAF

A

speech is amplified, delayed, then “fed back” to the speaker’s ears, speech prolongs syllable until the delayed signal is perceived, then begins next syllable, and slow, fluent speech with prolonged vowels, connected syllables

51
Q

DAF and normal speakers

A

delay indicated that speech sound has not completed, repetition or prolongations of syllables, “artificial stuttering” (lee 1951), responses vary with attention paid to delayed signal and helps to explain variability in responding

52
Q

frequency - altered feedback (FAF)

A

shifts pitch up or down, might increase activity in left auditory cortex, alter pitch change VF tension, increase/decrease VF tension

53
Q

increase VF tension is better for

A

Parkinson’s

54
Q

decrease VF tension is better for

A

person who stutters

55
Q

what are the ways to asses phonation

A

pushing/pulling, HGA, instrumental biofeedback, LSVT, and SpeakOut

56
Q

LSVT (think Loud)

A

the voice issues were caused by Parkinson’s by a lack of respiratory effect

57
Q

what are the procedures of LSVT

A

daily AHs

58
Q

Speak Out (Parkinson’s Voice Project)

A

Samantha Elandary saying with “intent” and “throw the sound over my head”

59
Q

Speak Out is based on

A

“intent” - Dr. Daniel Boone

60
Q

what are the components of Speak Out

A
  1. warm up: MAY ME MY MOE MOO
  2. Sustained “ah”
  3. Glides
  4. Counting
  5. Reading activities
  6. Cognitive activities
61
Q

Masking auditory feedback

A

applies lombard effect, kayPentax facilitator, speechvive

62
Q

hyperkinesis

A

excessive involuntary movements

63
Q

what are the two neurological basis for those with hyperkinetic dysarthria

A

damage to basal ganglia and imbalance of dopamine and ACH

64
Q

____ and ____ smooth and coordinate rough motor impulses from the associated cortex then send them to the PMC via the thalamus

A

basal ganglia and cerebellum

65
Q

what are the three parts of the basal ganglia

A

caudate nucleus, putamen, globus pallidus

66
Q

what are the subdivisions of the basal ganglia

A

striatum, lenticular nucleus, and pallidus

67
Q

striatum is made up of

A

caudate and putamen

68
Q

lenticular nucleus is made up of

A

putamen and globus pallidus

69
Q

pallidum is made up of

A

globus pallidus

70
Q

substantial nigra contains

A

dopaminergic neurons

71
Q

reduced dopamine in stratum leads to

A

TRAP and hypokinetic dysarthria

72
Q

TRAP

A

tremor, rigidity, akinesia, postural instability

73
Q

loss of neurons in the striatum leads to

A

involuntary movements and hyperkinetic dysarthria

74
Q

chorea

A

rapid, dance-like involuntary movements

75
Q

chorea effects

A

limbs, trunk, head and neck

76
Q

sydenham’s chorea

A

rare, idiopathic, childhood

77
Q

huntington’s diease

A

progressive degeneration of basal ganglia and cerebral cortex, onset in middle age

78
Q

hemiballism

A

contralateral to the lesion

79
Q

stroke

A

rarely causes chorea, basal ganglia or nearby structures, hemiballism

80
Q

hyperkinetic dysarthria prosody

A

prolonged intervals, variable speech rate, mono-itch, inappropriate silences, monoloudness

81
Q

hyperkinetic dysarthria articulation

A

imprecise consonants, distorted vowels, prolonged phonemes

82
Q

hyperkinetic dysarthria phonation

A

harsh voice quality, excess loudness variations, strained-struggled voice, breathy voice, voice stoppages

83
Q

hyperkinetic dysarthria respiration

A

unexpected inhalations and exhalations

84
Q

hyperkinetic dysarthria resonance

A

intermittent hyper nasality in some patients

85
Q

essential (organic) tremor

A

idiopathic, faster than tremor in parkinson’s, action/intention tremor, no other neurological signs, essential voice tremor

86
Q

essential voice tremor

A

contractions of laryngeal muscles

87
Q

dystonic

A

disorder of muscle tone, slow, sustained, “waxing and waning”, can by constant or fixed

88
Q

spasmodic dysphonia

A

many features of a focal dystonia, involuntary VF movements during phonation, contractions are vigorous and active

89
Q

AD spasmodic dysphonia

A

most common type -strained-strangled

90
Q

AB spasmodic dysphonia

A

breathy and aphonia

91
Q

key evaluation tasks for hyperkinetic dysarthria

A

vowel prolongation, AMRs, conversational speech/reading, observation of involuntary movements

92
Q

medical treatment for hyperkinetic dysarthria

A

usually pharmacological to suppress involuntary movements and botox

93
Q

botox interferes with

A

ACH transmission

94
Q

treatments for hyperkinetic dysarthria

A

voice therapy for SD, sensory tricks, and bite blocks

95
Q

treatments for spasmodic dystonia

A

counseling, /h/ onset (AD type) and continuous voicing (AB type)

Motor Speech Disorders (2 decks)

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