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Motor Speech and Cranio-facial > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q
  • rate and rhythm control approach to treating AOS
  • speech produced in time to a metronome
  • usually about 1 syllable per beat
  • rate initially slow, gradually increased
A

metronome pacing

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2
Q
  • Due to damage to cerebellum
  • Impairment affects:
    • coordination
    • decreased muscle tone
  • Impairment results in slowness and inaccuracy of aspects of movement
A

Ataxic dysarthria

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3
Q
  • articulatory and kinematic approach to treating AOS
  • client consciously focuses on production in a word s/he can say
  • clinician tries to generalize this correct production to other words
A

key word approach

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4
Q

vascular problems that could cause spastic dysarthria

A
  • stroke- most likely brainstem, not unilateral cerebral
  • vascular dementia
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5
Q

True or false apraxia of speech rarely occurs without an accompanying aphasia

A

True

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6
Q

Unilateral Upper Motor Neuron Dysarthria

Clinical characteristics (4)

A
  • hemiplegia or hemiparesis
  • early-weakness, hyporeflexia, hypotonia
  • later- spasticity, hypertonia
  • contralatral lower face weakness
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7
Q
  • inflammatory demyelinating disease
  • destruction of white matter in brain or spinal cord
  • possible etiology of spastic dysarthria
A

leukoencephalitis

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8
Q

Unilateral Upper Motor Neuron Dysarthria

Etiologies (3)

A
  • stroke- most common
  • tumors
  • trauma
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9
Q
  • prolonged or continuous spasms
A

tonic spasm

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10
Q

Types of Neuromotor speech disorders (2)

A
  • dysarthria
  • apraxia of speech
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11
Q

Etiologies of Hyperkinetic dysarthria (5)

A
  • toxic- metabolic conditions
  • degenerative diseases
  • infectious disease
  • stroke
  • tumors
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12
Q

errors in sequence and speed of parts of movement

A

decomposition of movement

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13
Q

How many types of dysarthria?

A

7

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14
Q

rhythmic tremor of body or head

A

titubation

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15
Q

Ways to evaluate speech (3)

A
  • perceptually
  • acoustically
  • physiologically
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16
Q

neuromotor speech disorders management goals (2)

A
  • restore lost function
  • promote the use of residual function
  • reduce the need for lost function
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17
Q
  • rapid, stereotyped movements
  • often irresistible urge to make the movements
A

tics

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18
Q
  • most often due to impairment of basal ganglia indirect pathway
  • often prominent effects on prosody
  • different kinds of involuntary movements cause hyperkinetic dysarthrias
  • orofacial dyskinesia
  • tardive dyskinesia
  • myoclonus
  • tics
  • chorea
  • ballismus
  • athetosis
  • dystonia
  • spasm
  • tremor
A

Hyperkinetic dysarthrias

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19
Q
  • rate and rhythm control approach to treating AOS
  • model two syllable words, accenting the stressed syllable, client imitates
  • gradually increase word length
A

stress patterning

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20
Q
  • a combination of two or more types of dysarthria
  • more common than single dysarthrias
A

mixed dysarthrias

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21
Q

Hypokinetic dysarthria impairment produces: (4)

A
  • rigidity
  • reduced force
  • reduced range
  • slow individual, but sometimes fast repetitive movements
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22
Q
  • repetitive and brief spasms
A

clonic spasm

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23
Q
  • biofeedback
    • mirror under the nose
    • nasal flow transucer (if available)
  • resistance treatment during speech continuous positive airway pressure (CPAP)
  • produce words containing pressure sounds with nares pinched closed
  • modification of speaking (over articulation)
  • no evidence for NSOMEs
  • no evidence for inhibition techniques
A

treating velopharyngeal dysfunction associated with dysarthria

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24
Q

distrubance in trajectory or inability to control range

A

dysmetria

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25
Q
  • electrodes surgically implanted, most often in subthalamic nucleus
  • may be unilateral or bilateral
  • electrical impulses sent to electrodes via stiumulator implanted implanted under the skin
  • stimulator connected to electrodes via wires
  • electrical impulses disrupt tremors and other motor problems
  • limb movement problems respond better to drugs and DBS than speech problems
  • speech may worsen with drugs or DBS
A

Deep brain stimulation (DBS)

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26
Q
  • most often due to impairment of basal ganglia indirect pathway
A

hyperkinetic dysarthrias

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27
Q
  • Impairment affects
    • muscle strength
    • muscle tone
    • speed, range, and accuracy
A

flaccid dysarthria

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28
Q

Formal perceptual assessments for speech (4)

A
  • Frenchay Dysarthria Assessment
  • Assessment of Intelligibility in Dysarthric Speech (AIDS)
  • Speech Intelligibility Test (SIT)
  • Apraxia Battery for Adults
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29
Q

Clinical characteristics of ataxic dysarthria (8)

A
  • problems in standing and walking
  • titubation
  • nystagmus
  • dysmetria
  • dysdiadochokinesis
  • decomposition of movement
  • possible intention tremor
  • cognitive disturbances
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30
Q
  • traditional approaches
    • phonetic placement
    • phonetic derivation
    • integral stimulation-watch and listen tasks
  • rate modification-slowing
  • exaggeration of articulation
A

treatment of articulatory dysfunction associated with dysarthria

31
Q
  • articulatory and kinematic approach to treating AOS
  • tactile cues are used to facilitate correct production
  • requires extensive training to learn cues
A

PROMPT

32
Q

face looks like they’re wearing a mask, lacks facial expression

A

masked facies/ hypomimia

33
Q

degenerative diseases that are possible etiologies of mixed dysarthria (4)

A
  • progressive bulbar palsy
  • pseudobulbar palsy
  • ALS
  • MS
34
Q

rate and rhythm control approaches to treating Apraxia of Speech (2)

A
  • metronome pacing
  • stress patterning
35
Q

What is the most common cuase of hypokinetic dysarthria?

A

Parkinson’s Disease

36
Q

Due to bilateral impairments of direct and/or indirect activation pathways

A

spastic dysarthria

37
Q
  • Parkinson’s Disease
  • Parkinson-plus or atypical parkinsonism
  • dementing diseases (Lewy body, Pick’s)
  • Toxic/metabolic conditions
  • trauma
  • Infections
A

Etiologies of Hypokinetic Dysarthria (6)

38
Q

What is the type of dysarthria based on?

A

the site of the lesion

39
Q
  • used to increase loudness
  • think “loud and big”
  • increase effort
  • intensive treatment (4xs a week for 4 weeks)
  • certification required
  • work from short (single words) to longer material
  • use of objective measures to monitor loudness (e.g., sound level meter)
  • provide home practice materials (1 hour/day, 5 days)
  • provide a lot of trials (15/item)
A

Lee Silverman Voice Therapy (LSVT)

40
Q

Informal perceptual tools for speech assessment

A
  • Mayo tests of motor programming
  • Motor Speech Examination (Wertz et al. 1984)
41
Q
  • most common involuntary movement
    *
A

tremor

42
Q

Prosthetic options for neuromotor speech disorders (2)

A
  • palatal lift prosthesis
  • voice amplifier
43
Q

What are the types of dysarthria? (7)

A
  • flaccid
  • spastic
  • ataxic
  • hypokinetic
  • hyperkinetic
  • unilateral upper motor neuron
  • mixed
44
Q

Assessments of non-speech movements (2)

A
  • cranial nerve exam
  • Duffy’s (2013) examination
45
Q

Impairment of basal ganglia direct pathway

A

hypokinetic dysarthria

46
Q
  • postural adjustments
  • try to incorporate respiration activities into speech tasks
  • sustaining phonation with feedback (e.g. Visipitch)
  • some non-speech tasks may be beneficial for improving respiratory support
    • maximum inhalation and exhalation tasks
    • breathing against resistance (masked or pused lips)
A

treatment for respiratory dysfunction associated with dysarthria

47
Q
  • involuntary single repetitive brief jerks
  • may be rhythmic or non-rhythmic
  • palatal or palatopharyngeal
A

myoclonus

48
Q

Clinical characteristics Flaccid dysarthria (6)

A
  • weakness
  • hypotonia
  • diminished reflexes
  • fasiculations
  • atrophy
  • progressive weakness with use
49
Q
  • may affect a single muscle group
  • may affect only one speech subgroup
  • subtypes based on site of lesion
A

Flaccid dysarthria

50
Q

Etiologies of flaccid dysarthria (7)

A
  • trauma
  • degenerative diseases
  • muscle disease
  • neuromuscular junction
  • brainstem stroke
  • demyelinating disease
  • infectious diseases
51
Q

parts of a case history (7)

A
  • basic data
  • onset and course of the problem
  • associated deficits
  • patient’s perception
  • consequences
  • management
  • patient awareness of medical diagnosis and prognosis
52
Q
  • Due to impairment of the final common pathway (lower motor neuron)
A

Flaccid dysarthria

53
Q

treatments that have supporting evidence for treating AOS (2)

A
  • eight step continuum/integral stimulation
  • PROMPT
54
Q

slow initiation of movements

A

brodykinesia

55
Q

Degenerative diseases that could cause flaccid dysarthria (2)

A
  • amyotrophic lateral sclerosis (ALS)
  • Progressive bulbar palsy
56
Q
  • for hypoadduction-effort closure techniques
  • LSVT
  • Resonant Voice Exercies
  • Sirening
A

treatment of phonatory dysfunction associated with dysarthria

57
Q

slow, writhing movements

A

athetosis

58
Q

involuntary orofacial movements

A

orofacial dyskinesia

59
Q

Neuromotor speech disorders

approaches to management (4)

A
  • medical intervention
  • prosthetic
  • behavior management- patient and significant other(s)
  • speech management
60
Q

Articulatory and kinematic approaches (3)

A
  • phonetic placement/derivation
  • key word approach
  • PROMPT
61
Q
  • due to damage to UMNs that innervate cranial or spinal nerves important for speech
  • often mild and short lived
A

Unilateral Upper Motor Neuron Dysarthria

62
Q

forceful, sustained closure of the eyes

A

blepharospasm

63
Q

flailing movements

A

ballismus

64
Q
  • involuntary rapid, random, purposeless movements
  • can be subtle or very obvious
A

chorea

65
Q
  • idiopathic and hereditary forms
  • progressive loss of cells in the substantia nigra
  • decreased dopamine the basal ganglia
  • imbalance between ACh and dopamine in the basal ganglia
  • treated with drugs that increase dopamine
  • when drugs fail, may be treated with deep brain stimulation (DBS)
A

Parkinson’s Disease

66
Q

short, rapid, shuffling steps

A

festination

67
Q

intermittant freezing

A

akinesia

68
Q
  • resting tremor (about 3-8 Hz)
  • brodykinesia
  • intermittent freezing
  • pill-rolling movement
  • masked facies (hypomimia)
  • reduced arm swing
  • micrographic writing
  • festination
  • impaired sensory function
A

Clinical Characteristics Parkinsonism (9)

69
Q

FAST

A

Face, Arm, Speech, Time

70
Q
  • degenerative motor neuron disease
  • corticobulbar, corticospinal signs
  • if dysphagia and dysarthria major components, it is called progressive pseudobulbar palsy
  • possible etiology of spastic dysarthria
A

primary lateral sclerosis

71
Q

Neuromuscular junction diseases that could cause flaccid dysarthria (2)

A
  • myasthenia gravis
  • botulinum toxin exposure (botulism)
71
Q

clinical characteristics of spastic dysarthria (4)

A
  • spasticity
  • weakness (especially distal)
  • reduced range of movement
  • slow movement
71
Q

Etiologies of spastic dysarthria

A
  • vascular problems
  • primary lateral sclerosis
  • leukoencephalitis

Motor Speech and Cranio-facial (3 decks)

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