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motor speech > benchmark 1 > Flashcards

benchmark 1 Flashcards

1
Q

What is dysarthria

A

acquired neurological motor weakness affecting changes movement; consistent mistakes; think Big 8

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2
Q

Big 8

SST SR SAC

A

symmetry, steadiness, tone (SST)

strength, ROM (SR)

speed, accuracy, coordination (SAC)

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3
Q

Volitional vs spontaneous vs reflexive speech

A

volitional: where we ask some to say something after (asking for planned speech response)
spontaneous: spontaneous speech
reflexive: saying “ouch” when hurt

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4
Q

what is anarthria

A

most severe dysarthria —> lost all ability to produce meaningful speech; all motor components breaking down; they know what they want to say but can’t get words out

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5
Q

apraxia of speech

A

neurogenic communication disorder affecting motor programming–> patient knows what they want to say but unsure how to get articulators in right position to make target speech sound; groping and inconsistent mistakes are salient feature

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6
Q

what is hypothesis

A

simple declarative statement that incorporates cause and effect and can be tested and measured

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7
Q

hypothesis guided management leads to ______

A

critical reasoning

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8
Q

what are the major differences between assumptions and hypotheses

A

assumptions are judgment and not testable (measureable)

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9
Q

T/F assessments are an ongoing process - making adjustment based on observation and client behavior

A

true

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10
Q

4 parameters of WHO model

A
  1. body function
  2. body structure
  3. activities and participation
  4. environmental factors
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11
Q

comprehensibility vs intelligibility

A

comprehensibility is the meaning of the message
intelligibility is the precision of the articulators forming target phonemes

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12
Q

3 main parts of clinical report

A

case history, direct observation, impression/recommendations

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13
Q

Restoration vs compensation

A
  • restoration of lost function
  • Compensation is the process of learning how to develop “work arounds” for a task, function, or process
  • think goals, severeity, diagnosis, treatment timeline
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14
Q

what is the indirect component of assessment

A

case history such as background info, medial history, referral, observing patient in lobby

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15
Q

define pathophysiology

A

distinctive pattern of movement disorder

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16
Q

is the patient interview direct or indirect observation of communication

A

direct; the interview is open ended and broader than client intake which is specific and narrow

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17
Q

what is the most effective way to collect perceptual speech sample

A

conversational speech

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18
Q

the formal assessment is direct observation

A

true

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19
Q

t/f slp sets up environment to help facilitate ease of patient

A

true

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20
Q

rt/f reading aloud is a great way to record and measure rate of speech

A

true

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21
Q

4 subsystems of speech

A

respiration, phonation, resonation, articulation

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22
Q

how can the subsystems affect speech

A

intelligibility, fluency, speech rate, prosody, naturalness

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23
Q

AMR vs SMR

A

AMR: alternate motion rates ex: /pa pa pa/
SMR: sequential motion rates ex /pa ta ka/

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24
Q

palpate

A

to touch or feel part of the body to examine

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25
Q

paucity of movement

A

shortening of a movement, no extra embellishments

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26
Q

fasciculations

A

slight muscle twitches; most common in tongue

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27
Q

coup de glotte

A

forcing closure of VFs; grunt

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28
Q

flaccid

A

low muscle tone, weak

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29
Q

spastic

A

high muscle tone, tense

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30
Q

stilted

A

issue with fluency

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31
Q

diplophonia

A

two vocal pitches occurring at same time

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32
Q

hypothesis

A

is something you rationalize and can easily test; to determine if you are correct or incorrect
- underlying, pathological reasoning for what is happening

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33
Q

stimulability

A

assessing if a client can attempt to do what is being ask by clinician

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34
Q

what do we look at for determining prognosis

A

restore or compensate lost function, protect/maintain current function

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35
Q

what is flaccid dysarthria

A

damage in spinal/cranial nerves; lower neuron motor dysfunction; hypotonia

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36
Q

Lower motor neuron

A

lower motor neurons begin in the spinal cord (at medulla (CNS)) and go on to innervate muscles and glands throughout the body (PNS); symptoms are more flaccid

assess indivudal cranial nerves

injury to spinal cord gray matter

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37
Q

direct vs indirect system of bulbar spinal tracts

A

direct: fewer synapses, control of movement, faster movement
indirect: many synapses, balance/posture, slower movement

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38
Q

final common pathway

A

the motor route (efferent signals) a neural signal takes from the CNS and travels OUT until it reaches endpoint like the hand muscle or larynx; innervate individual strcutres or muscles

damage to FCP affects individual muscles or muscle groups

all nerves that have to do with movement (contracting muscles) pass along FCP

  • message is sent out, no way of getting it back
  • last chunk of neurons firing on that pathway
  • flaccid dysarthria: damage to FCP affects individual muscles of muscle groups
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39
Q

efferent signals

A

motor only
- voluntary, reflexive, autonomic movements

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40
Q

damage to SPINAL nerves C3-C5 =

A

Phrenic nerve innervates diaphragm

41
Q

Upper motor neuron

A

upper motor neurons originate in the cerebral cortex and travel down to the brain stem; damage is more spastic

assess each subsystem of speech separately (LMN assess individual cranial nerves)

injury to brain and injury to white matter in spinal cord

42
Q

bulbar spinal tract

A

the nerves and tracts connected to the medulla, and also by association to the muscles thus innervated, those of the tongue, pharynx and larynx
- brainstem and medulla (CNS)

43
Q

name the 4 CN passing through medulla

A

CN 9, 10, 11, 12

  • not CN V or CN VII (because these innervate the face)
44
Q

CN V

A

Trigeminal - sensory of face and motor innervation to the muscles of mastication

45
Q

CN VII

A

Facial Nerve - motor innervation of facial muscles and sensory of anterior 2/3 tongue
Bell palsy is an idiopathic form of facial nerve palsy

46
Q

CN IX

A

Glossopharyngeal - motor innervation to the stylopharyngeus muscle. This muscle is responsible for elevating the larynx and pharynx, especially during speaking and swallowing
sensory - posterior third of the tongue

47
Q

CN X

A

SLN - innervates cricothyriod muscle, sensory above glottis
RLN - below the cord; sensory below glottis

The cricothyroid muscle is the only tensor muscle of the larynx aiding with phonation. It is innervated by the superior laryngeal nerve. Its action tilts the thyroid forward to help tense the vocal cords, thus increasing the pitch of the voice.

48
Q

CN XII

A

Hypoglossal: motor only for tongue

49
Q

Phases of muscle contraction:

A
  1. latent period
  2. contraction period
  3. relaxation period
50
Q

Components of a Nerve

A

Neuron generates and conducts impulses
Neuron consists of cell body, dendrites, axon

Glia cells: myelination
astrocyte cells, oligiodendroglia cells, schwann cells

51
Q

Synaptic cleft:

A

space between an axon terminal and muscle fiber or dendrite

acetycholine releases into the synaptic cleft, where the neurotransmitter is free to bind with receptors; all or nothing

(ie mysenthia gravis)

52
Q

Myoneural junction

aka neuromuscular junction

A

space between an axon and a muscle

(MYO = muscle)

53
Q

Myotonic

A

prolonged muscle contraction; delayed relaxation

54
Q

flaccid dysartheia aka Bulbar palsy

A

signal hits muscle in a weakened way; doesn’t reach muscle as accurately as intended

55
Q

signs of flaccid dysartheria/bulbar palsy

A

hypotonia (low muscle tone), hyporeflexia (reduced reflexes), limited ROM, changes in symmetry, lack of steadiness, atrophy, akinesia, flaccidity, reduced strength

56
Q

unilateral bulbar palsy

A

damage to PNS is often unilateral and impairs individual muscles on one side

LMN polyneuropathies can be bilateral and affect more than 1 nerve (ie Guillain-Barre, muscular dystrophy, mysenthia gravis)

57
Q

Flaccid dysartheria/Bulbar Palsy etiology

A
  • idiopathic
  • tumor
  • TBI
  • brain stem stroke
  • infection
58
Q

T/F all CNs are PNS

A

true

59
Q

Bulbar Palsy : damage to Spinal Nerves

A

only changes seen in respiration/chest during motor assessment
- rapid shallow breathing
- reduced VC
-short MPT
- inadequate checking action
- weak cough

60
Q

Bulbar Palsy: essential assessment for respiration (spinal nerves)

A

conversational speech
- reduced loudness
- short breath groups
- fade at end of sentence
- speak on residual air
- AMR/SMR: limited reperions
- Prolonged vowels: short duration

61
Q

Flaccid Dysarthria: CN V Trigeminal

A

rarely occurs independently

damage must be bilateral for symptoms to emerge

62
Q

Motor assessment of CN V

A

changes only seen in jaw
- weak mandibular valve
- jaw sags open
- reduced ROM

63
Q

Essential assessment of CN V

A

conversational speech (artic) –> greatest difficulty
- severely reduced intelligibility
- imprecise consonants and vowels
- can be slow

AMR/SMR:
- limited ROM
- imprecise
- slow

64
Q

Flaccid Dysarthria: CN VII Facial –> Bell’s Palsy

A

Facial paralysis from dysfunction/inflammation of CN VII
- unilateral weak unresponsive on affected side
- decreased facial expression
- food pocketing
- inability to close eye
- rapid onset of partial or complete paralysis
- can occur bilaterally –> total facial paralysis
- spontaneous recovery –> 75% have complete recovery w/i 2-3 weeks

65
Q

Motor Assessment of CN VII –> Bell’s Palsy

A
  • decreased facial expression
  • changes only seen in lips –> weak pursing, rounding/retraction, weak labial seal for holding air in cheeks

AMR/SMR: imprecise

66
Q

Essential assessment of CN VII –> Bell’s Palsy

A

Conversational Speech (Artic)
- imprecise bilabials/labiodentals/Labial vowels
- flutter of cheeks during speech

67
Q

Absence of CN VII Facial –> Moebius Syndrome

A
  • congenital neurological disorder
  • complete facial paralysis
  • no facial expression
  • normal intelligence
68
Q

Flaccid Dysarthria CN X Vagus - Motor assessment of 2 branches

A

Velopharynx: Velopharyngeal
- decreased elevation of soft palate
- uvula points to strong side

Larynx: Laryngeal
- weak cough/glottal coup
- paralysis of VFs (RLN)

69
Q

Flaccid Dysarthria CN X Vagus - essential assessment of Velopharyngeal Branch

A

Conversational speech

-Resonance: HYPERnasal/nasal emission
- Artic: weak pressure consonants
AMR/SMR: weak artic of stops
Prolonger Vowels: short duration

70
Q

Flaccid Dysarthria CN X Vagus - essential assessment of Recurrent Laryngeal Branch

A

Conversational speech

  • Respiration: reduced loudness/stridor
  • Phonation: breathy, rough, diplophonia (voice is perceived as being produced with two concurrent pitches)
  • AMR/SMR: diplophonia
  • Prolonged Vowels: short duration
71
Q

Flaccid Dysarthria CN X Vagus - essential assessment of Superior Laryngeal Branch

A

conversational speech

  • Phonation: monopitch, limited pitch range
  • SLN responsible for lengthening VFs
72
Q

Flaccid Dysarthria: CN XII Hypoglossal –> motor assessment

A

Tongue

  • atrophy
  • fasciculation (involnert mvmt)
  • weak protrusion/lateralization/elevation/resistance
73
Q

Flaccid Dysarthria: CN XII Hypoglossal –> essential assessment

A

conversational speech

  • imprecise lingual consonants
  • tense vowels (i, o, u)
  • slow rate

AMR/SMR: imprecise, slow

74
Q

Flaccid Dysarthria: Damage to Multiple Nerves –> 3 types

A

guillian-barre
muscular dystrophy
Myasthenia gravis

75
Q

Flaccid Dysarthria: Damage to Multiple Nerves –> guillian-Barre

A
  • quick onset; distal –> proximal
  • can go away just as quick
  • infection/autoimmune/idiopathic
    everything shuts down; progressive paralysis
  • generalized flaccidity of entire body
  • CNs and SNs are involved
  • nerves loses myelin sheath
76
Q

Flaccid Dysarthria: Damage to Multiple Nerves –> Muscular Dystrophy

A
  • expressionless face - flat affect
  • weakness of CNs and SNs
  • AMR/SMR: pervasive bulbar weakness
  • short breath groups
    -rough breathy voice
  • mild hypernasality
  • air leakage thru Velopharyngeal port
77
Q

Flaccid Dysarthria: Damage to Multiple Nerves –> Myasthenia Gravis

A
  • issue @ synaptic cleft and neuromuscular junction (acetylcholine issues)
  • fatigue, fluctuating muscle weakness –> improves with rest (no drill practice)
  • diminished facial expression
  • waves of symptoms
  • progressive fatigue from prolonged speaking
  • reduced loudness, short breath groups
  • weak breathy voice
  • imprecise Consonants
78
Q

therapy for flaccid dysarthria

A
  • provide supports to reduce effort in the speech subsystems
  • avoid fatigue
79
Q

compensatory strategies for CN V and VII

A

jaw bra and hand support

80
Q

compensatory strategies for CN XII

A
  • thermal stimulation
  • stroking
  • increase awareness and reflexive movements
  • increase ROM and strength
  • functional speech/swallowing therapy
81
Q

compensatory strategies for CN X

A
  • surgery –> thyroplasty, injections, nerve transfer
  • amplifiers
  • SOVT exercises
  • turn head to weak side
  • palatal prosthesis
  • thermal stimulation
  • blowing exercises
  • open mouth wider for oral resonance
82
Q

palialia

A

occurs in PD –> repeating phrase over and over with increased speed and decreased intelligbility

Mostly occurs at end of sentence

83
Q

motor physiology of speech –> 3 subsystems

A

motor control
sensation
reflexes

84
Q

CN X Vagus RLN innervates muscles of larynx wcept cricothryoid

A

true

85
Q

when looking at motor control start at symmetry

A

true

86
Q

when to use sniff test

A

sniffinf cuases diaphragm to descend and flatten the most

use the sniff to observe how much air the indivial can inhale; also tests ROM

87
Q

spirometer measures vital capacity

A

true

88
Q

phonation quotient tells us how efffectivly patient is using the iar that they are moving

A

true

89
Q

prognositc statement include excellent, good, or poor potential for improvement

A

true

90
Q

the most logical way to oganize data from an assessment into a clinical report is based on he speech subsystems

A

true

91
Q

spinal nerves: spinal intercostal, phrenic and thoracic control respiration

A

true

92
Q

components of functional motor unit

A

cell body
axon
dendrite
myoneural junction
muscle fibers innervated by that cell body

93
Q

goal of therapy: fatigue

A

to structure enviroment, communication so that client is using little effort to reduce fatigue

94
Q

gray matter vs white matter

A

gray is made up of cell bodies -> functions to receive information and regulate outgoing information

white matter is made up of axons –> serves to transmit signals to other regions of the brain, spinal cord, and body

95
Q

sensory function drives motor function

A

true –> increase sensory awareness to aid motor function

96
Q

CN VII damage and AMR/SMR

A

/puh/ would be most damaged because of lip closure

97
Q

What happens in RLN is damage during heart durgery

A

pt will have left VF paralysis

breathy rough voice

diplophonia

stridor

98
Q

if velopharyngeal branch is damaged

A

damage seen in uvula –> points to strong

motor speech (3 decks)

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