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CETP Mayu > dysarthria > Flashcards

dysarthria Flashcards

1
Q

dysarthria definition

A

Neurogenic speech sound disorder.
Characterized by abnormal strength, speed, range, steadiness, tone, and accuracy of the muscles and movements for speech production.

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2
Q

dysarthria NEUROPATHOLOGY

A

Due to stroke, infections, TBI, or progressive neurological diseases (e.g., PD, ALS, MS).
Different dysarthria types correspond to a different site of damage.

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3
Q

dysarthria COMMUNICATION DEFICITS

A

Depending on the site of damage and muscles affected, there will be different deficits.
Can happen at any or all 5 levels of speech production: respiration (RESP), phonation (PHON), resonance (RESON), articulation (ARTIC), prosody (PROS).

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4
Q

different dysarthrias chart, type, localization of damage, auditory signs & characteristic diseases

A
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5
Q

key feature of each dysarthria
if no key feature, name health condition associated

A

Ataxic - incoordination
Flaccid - Weakness
Spastic- Effortful
Hyperkinetic - Irregular
Hypokinetic- Reduction

Flaccid-Spastic - ALS
Ataxic-Spastic - MS

Unilateral UMN - weakness, incoordination & spasticity

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6
Q

differentiate between UMN damage and LMN

A
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7
Q

diff dysarthria chart with pathophysiological signs and site of lesion

A
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8
Q

ataxic dys characteristics

A

uncoordinated & cerebellum
- imprecise vowels & consonants “drunken speech”
- excessive and equal stress
- slow rate
- inappropriate silences within & between words
- gait disturbences
- monopitch, monoloud, harsh
- paradoxical breathing
- Distorted vowels
-Prolonged phonemes
- Irregular AMRs
■ telescoping/collapsing of syllables

Memory tool:
A.T.A.X.I.C.

Arhythmic speech: Irregular rhythm and inappropriate pauses.
Tone abnormalities: Voice may have a monopitch or monoloudness quality.
Articulatory imprecision: Slurred speech due to incoordination.
Xtra effort needed: Speaking may appear to be an effortful process.
Irregularities in speech rate: Might be excessively slow or, at times, too fast.
Coordination issues: This is the core issue—problems coordinating the movements of speech muscles.

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9
Q

flaccid dys

A

weakness, LMN
- weak inhalation
- breathy voice, audible inspirations, short phrases
- hypernasality, NAE
- imprecise consonants (esp. high pressure)
- imprecise AMRs, slow & slurred DDKs
- tongue fasciculations
- diminishes reflexes
- hypotonia

memory tool: spicy, breathy voice, makes you go weak (inhalation, hypotonia), cant even speak right just ooos and aahhhs (vowels), make ya quiver (fasciculations)

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10
Q

spastic dys

A

effortful, UMN
- Strangled (harsh, hyperadduction)
- Pitch breaks
- Articulatory imprecision
- Slow rate
- Tight muscles aka hypertonia
- Increased reflexes
- Cheweing/swallowing difficulty
- = excessive & equal stress
- slow & regular AMRS??

memory tool: SPASTIC + excessive & equal stress
- man doing karate and lifting weights at same time wants to strangle ya, with angry eyebrows and low pitch voice

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11
Q

hyperkinetic dysarthria characteristics

A

irregular, BG, involuntary movements:

imprecise consonants,
distorted vowels,
prolonged phonemes,
irregular articulatory breakdowns,
**slow and irregular AMRs, **
hypernasality,
variable (irregular) rate,
**strained/strangled voice, **
harsh voice,
inappropriate silences,
transient breathiness,
voice stoppages,
excess and equal stress,
loudness variation,
sudden forced inspiration/expiration*

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12
Q

memory tool for hypokinetic dysarthria characteristics

A

Reduction, BG
monopitch, monoloud
inappropriate silences
short rushes of speech
tendency for rapid/accelerated speech
rapid/blurred AMRS - fast and imprecise DDK
palilalia- delayed repetitions of words or phrases

mmory tool: hyPOPO lazy cop out of breath running for donut, mask like face, reduced lung capacity, rast rate, short rushes of speech, reduced stress, inapp. silences, C+V, mono pitch & loud

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13
Q

flaccid-spastic characteristics

A

memory tool: “FALS MIX” can remind you of the disease “ALS” and the “MIX” of flaccid and spastic characteristics.

Flaccid qualities: Weakness, atrophy, and fasciculations of the speech muscles.
Articulatory imprecision
Low muscle tone (initially): From the flaccid component.
Strained-strangled voice quality: From the spastic component.
Monopitch and monoloudness: Reduced prosodic variation.
Increased muscle tone (as it progresses): From the spastic component.
Xtra effort: Speaking may appear effortful due to muscle weakness and spasticity.

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14
Q

ataxic-spastic dysarthria

A

memory tool: P.H.A.R.M.S.

-Pitch & loudness problems
-HHarsh or breathy voice
-Articulatory imprecision:
-Reduced vital capacity: Limited breath affecting sustained speech.
-Misplaced emphasis: Impaired stress patterns in speech.
-Significant hypernasality

Or PHHARM: and put hypernasality with harsh & breathy

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15
Q

Flaccid (LMN)
- Lesion location:

A

LMN (cell, axon, NMJ, or muscle)

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16
Q

Common etiologies for LMN

A

: trauma, motor neuron disease, muscular dystrophy, myasthenia gravis, Guillain-Barré Degenerative disease, Brainstem stroke (CVA)

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17
Q

Spastic (UMN)
- Lesion location:

A

UMN (bilateral; pyramidal or extrapyramidal)

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18
Q

Common etiologies UMN lesion spastic d

A

: stroke, TBI, motor neuron disease (ALP, PLS), unknown etiology (10%)

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19
Q

Unilateral UMN ____ subset of spastic)

A

(milder

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20
Q
  • Common perceptual features of Unilateral UMN:
A

slow rate, imprecise articulation, irregular articulatory breakdowns, harsh voice, reduced loudness

  • Common perceptual features: imprecise consonants, rapid “blurred” AMRs, variable rate of speech, short rushes of speech, harsh voice, breathy voice, monopitch, low pitch, reduced stress, inappropriate silences, monoloud
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21
Q
  • Common etiologies for U UMN
A

: Parkinson’s disease/Parkinsonism, progressive supranuclear palsy, stroke, unknown etiology (4%), TBI

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22
Q

hyperkinesias

A

Chorea: rapid, random movements of body part(s)
o Dystonia: co-contraction of antagonistic muscles – “frozen”
o Myoclonus: involuntary, repetitive jerks of a body part
o Voice tremors, spasmodic dysphonia

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23
Q

common etilogolies hyperkinetic

A

unknown (67%), toxic/drug-induced, Huntington’s chorea, Tourette’s syndrome

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24
Q

ataxic cerebellum pathophysiology

A
  • Pathophysiology: incoordination, reduced range of motion, inaccuracy in force/timing/direction of movements, hypotonia, dysmetria (the inability to control the distance, speed, and range of motion necessary to perform smoothly coordinated movements), sequencing errors
    o Size, strength, and symmetry may be WNL at rest
    o During movement/speech, over- or under-shoot targets
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25
Q

ataxic perceptual features

A
  • Common perceptual features: imprecise consonant, irregular articulatory breakdowns, prolonged phonemes, distorted vowels, irregular AMRs, slow rate, prolonged intervals, harsh voice, monopitch, excess and equal stress, loudness variation*
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26
Q

common etiology for ataxia

A
  • Common etiologies: cerebellar degeneration, multiple systems atrophy, multiple sclerosis, stroke/trauma, tumour
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27
Q
A

Manifestation of two or more dysarthrias in a single individual
o Encountered more often than any other individual type of dysarthria (~30-35% of all dysarthrias)

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28
Q

Common etiologies:
for. mixed dys

A

o Motor neuron disease (ALS): flaccid-spastic
o Multiple sclerosis: spastic-ataxic
o Progressive supranuclear palsy: hypokinetic-spastic-ataxic
o Friedrich’s ataxia: ataxic-spastic

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29
Q

another dysarthria +apraxia chart

A
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30
Q

AOS differential diagnosis

A
  • Speech errors unrelated to muscle weakness, tone, range of motion, cognitive-linguistic difficulties
  • Predominantly articulatory and prosodic effects
  • Errors variable across trials/utterances
    o Automatic speech > volitional speech
  • Substitution/addition errors, dysfluencies (start/restart patterns)
  • Trial-and-error groping for correct articulatory postures; frequent attempts to self-correct
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31
Q

AOS vs. ataxic dysarthria

A

Differences:
o AMRs are usually irregular in ataxic dysarthria but regular in AOS (reverse for SMRs)
o “Islands of effort free speech” (bypass planning mechanism) are unusual in ataxic dysarthria and very usual in AOS
o Automatic speech is no better than volitional speech in ataxic dysarthria
o Ataxic speakers rarely grope for articulatory postures and do not usually attempt to correct articulatory errors
o Perceived substitutions are not as frequent in ataxic dysarthria as AOS

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32
Q

Speech subsystems

A
  • Respiratory
  • Phonatory/laryngeal
  • Resonatory
  • Articulatory
  • *Prosodic (doesn’t just live in one system – is a combination of all systems together)
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33
Q

dysarthria is commonly found in…

A
  • HD
  • MS
  • neuromuscular disease (e.g. myasthenia gravis, amyotrophic lateral sclerosis, muscular dystrophy)
  • Nonfluent variant primary progressive aphasia (nfvPPA)
  • PD
  • Stroke
  • TBI
  • Down syndrome
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34
Q

Psychosocial Impacts

A

Communication demands effort and may need assistance.
Time constraints can lead patients to abbreviate their messages.
Interruptions can make patients feel rushed.
Communication partners differ in their willingness to accommodate.

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35
Q

Components of MSD assessment

A
  • Medical history/clinical interview
  • Patient observations
  • Non-speech examination
    o Oral mechanism exam
  • Motor speech tasks
  • Evaluation of speech production (instrumental and non-instrumental)
    o Tasks by speech subsystem + prosody
    § Quantifiable measures!
    o Passage reading
    o Picture description
    o Spontaneous conversation
    o Intelligibility, comprehensibility, efficiency
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36
Q

ways to test respiratory subsystem

A
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37
Q

Motor control hierarchy (top down)

A

Primary motor cortex →
motor association cortex (pre-motor cortex, supplementary motor area) →
basal ganglia →
cerebellum →
lower motor neurons in brainstem/spinal cord →
peripheral nerves →
smooth/striated/cardiac muscles and glands

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38
Q

DDK - AMR SMR

A

Diadochokinesis (DDKs): movement repetitions
o Alternating Motion Rates (AMR): repetition of the same syllable /pa/, /ta/, /ka/
o Sequential Motion Rates (SMR): repetition of a movement sequence /pataka/ “buttercut”

39
Q

Principles of neuroplasticity

A

10 principles:
1. Use it or lose it (cortical loss from lack of activity) – failure to drive specific brain functions can lead to functional decline
2. Use it and improve it – training that drives a specific brain function can lead to enhancement of that function
3. Experience Specificity (changes occur only in the specific behaviour that you’re practicing) – the nature of the training experience dictates the nature of plasticity
4. Repetition matters – induction of plasticity requires specific repetition
5. Intensity matters (balance between enough stimulation to create change without overwhelming the system) – sufficient training intensity is required for the induction of plasticity
6. Time matters (and duration of practice – consolidation requires continuous, uninterrupted practice) – different forms of plasticity occur at different times in training
7. Salience matters (how important something is to the individual) – a training experience must be salient to induce plasticity
8. Age matters (neuroplastic ability is higher when we’re younger vs. when we’re older) – training induced in plasticity occurs more readily in younger brains
9. Transference (plasticity in one area can prime for plasticity in another area) – plasticity in response to one training experience can enhance the acquisition of similar behaviours
10. Interference (plasticity in one area can interfere with plasticity in another area) – plasticity in response to one experience can interfere with the acquisition of other behaviours

40
Q

But first (before practicing feedback conditions; pre-practice targets):
o
- If no, direct practice will not be effective
o Consider:

A

Is the client motivated to learn?
o Does the client understand the task?
o Is the client stimulable for the desired response?
- If no, direct practice will not be effective
o Consider as “pre-practice” targets

41
Q

Practice conditions that are optimal for neuroplasticity

A

Practice conditions:
1. Practice amount (less vs. more)
2. Practice distribution (massed vs. distributed)
3. Practice variability (constant vs. variable)
4. Practice schedule (blocked vs. random)
5. Attentional focus (internal vs. external) aka focus of effects of movements like the sound not the bodily movement itself like placement
6. Target complexity (simple vs. complex)
o Bold = ideal conditions for long-term retention; however, some of these things, in an earlier acquisition phase, may be better (e.g., stimulability and shaping the exact response you want)

42
Q

feedback conditions for neruoplasticity

A
  • Feedback conditions:
    1. Feedback type (performance vs. results)
    2. Feedback frequency (high vs. low)
    3. Feedback timing (immediate vs. delayed)
    4. Feedback control (other vs. self)
43
Q

In rehabilitation, our goal is to use principles of neuroplasticity and motor learning to our advantage
o Example:

A

In rehabilitation, our goal is to use principles of neuroplasticity and motor learning to our advantage
o Example: regain lost functions, following stroke or injury
o Use it or lose it risk assessment when recommending NPO or limited PO intake – dysphagia therapy providing ample opportunities to practice swallowing tasks may promote improved neuroplastic recovery compared to therapy that focuses on non-swallowing tasks
o Use it and improve it maximizing opportunities for patients to use the skill/behaviour
o Specificity how is training mirroring the desired outcomes (i.e., swallowing tasks vs. non-swallowing tasks)
o Intensity consider the patient’s medical status and etiology – high intensity can sometimes result in greater harm than healing – integrating rest to reduce risk of overstimulation and/or overtraining
o Time matters initiating high-quality therapy as soon as medically appropriate
o Salience matters incorporating patient priorities into therapy goals
o Age matters an older patient may have a longer recovery time and may need more repetitions of exercises or frequency of therapy sessions
o Transference to what degree is the therapy plan relying on generalization (e.g., non-swallowing exercises) – integrating tasks more specific to swallowing may enhance recovery outcomes
o Interference the patient may need to “un-learn” compensatory maladaptive behaviours

44
Q

Primary goal (aim) is to ___
- Start by ensuring the patient has ___
- Next, target what has the___
- Overarching aim: __

A

maximize the client’s ability to communicate

some form of functional communication

greatest effect on speech intelligibility/comprehensibility/naturalness

increased participation

45
Q

The principles that support motor acquisition are ___ as those that support motor learning

examples:

A

not the same as
o The application of specific principles may be more appropriate at different times in the rehabilitation process

ex 1. High (blocked) task repetitions with **specific, frequent feedback and consistent ** practice conditions support the acquisition of a task/skill
pt 2. As a skill becomes more automatic, shifting the practice and feedback conditions to be more variable will support learning

46
Q

Relating the Principles of Neuroplasticity to Treatment of MSDs:

A

Relating the Principles of Neuroplasticity to Treatment of MSDs:
- Improve speech by speaking
o Use it or lose it
o Use it and improve it
o Task specificity
- Many opportunities for practice
o Repetition matters
o Time (of practice) matters
- Early treatment is ideal (pending medical status)
o Time (since injury) matters

47
Q

Association cortex

A

Main function: programming movements that are appropriate to
the context
■ Includes: somatosensory association cortex, supplementary
motor area, premotor area
■ Damage can result in difficulty selecting movements for
speech

48
Q

Cerebellum

■ Main function: trajectory of movement
■ Lesions to cerebellum may cause ataxic dysarthria
● Ataxia is ipsilateral to side of lesion

A
49
Q

Basal Ganglia

■ Main function: initiation and speed of movement
■ Lesions to basal ganglia (e.g. due to Parkinson’s) can lead to slow
movements → can cause slowed speech

A
50
Q

Cranial nerves involved in speech

A
51
Q

As spontaneous oral movements are apparently intact in apraxia, gross motor support and muscle weakness are not at issue.

A
52
Q

Anarthria

A
53
Q

Flaccid dysarthria is effectively treated with pushing and pulling exercises to help strengthen muscles and increase tone.

A
54
Q

People with spastic dysarthria need to practice relaxation exercises to
reduce muscle tone and increase flexibility.

A
55
Q

UUMN

A
56
Q

Speech characteristics-unilateral UMN

■ Slow rate
■ Imprecise articulation
■ Irregular articulatory breakdowns
■ Strained voice
■ Reduced loudness
■ Unilateral facial weakness
■ Harsh voice

A
57
Q

Those with ataxic dysarthria benefit from rhythmic or metered
cueing due to inability to adequately pace their speech
production.

A
58
Q

Hyperkinetic dysarthria

A

○ Due to damage to the basal ganglia (excess dopamine)
○ Consequence: hyperkinesias (extra and involuntary
movements) that interfere with speech production; impact
varies with the type and severity and location of hyperkinesias
○ Etiology
■ Huntington’s, Tourettes
○ Involuntary movements
○ People with hyperkinetic dysarthria benefit from sensory tricks
to reduce involuntary movements.

59
Q

Hypokinetic ○ Due to damage to basal ganglia (dopamine depletion)
○ Consequence: rigidity, reduced amounts of volitional
movement, reduced range of motion present in remaining
movements
○ Etiology- parkinson’s disease and repeated head trauma
○ Rigidity and decreased ROM

A
60
Q

treatment goals ○ Modifying respiratory, phonatory, articulatory, resonatory, and
prosodic problems
○ Increasing efficiency, effectiveness, and naturalness of
communication
○ Increasing physiological support
○ Teaching compensatory behaviours
■ AAC

A
61
Q

Some treatment strategies that are helpful for 1 dysarthria
are counterproductive for another
■ E.g., relaxation techniques that are appropriate for
treating spasticity should not be used for treating flaccid
because muscles are already too loose and relaxed

A
62
Q

monopitch is common in

A

spastic, hypokinetic and may be in flaccid

63
Q

myoclonus aka __ is common in

A

involuntary twitching ; hyperk

64
Q

pitch breaks is known in

A

flaccid??

65
Q

diplophonia is in

A

flaccidd

66
Q

breathiness & flutter in

A

flasccid hypokinetic

67
Q

specifiic characteristic of imprecise consonants in diff dysarthrias

A
  • weakness (flaccid, spastic)
  • slow (spastic)
    discoordinated (ataxic)
    reduced ROM (hypok)
    involuntary movements (hyper
68
Q

irregular artic breakdowns

A

artic

69
Q

normal rate

A

flaccid

70
Q

Apraxia articulatory characteristics

A

○ Groping to find the correct articulatory postures and sequences
○ Facial grimaces, moments of silence, phonated movements
○ Consonant phonemes involved more often than vowel phonemes
○ Errors are inconsistent and highly variable
○ Errors are primarily substitutions, additions, repetitions, prolongations
○ Attempts at self-correction

71
Q
A
71
Q

Treatment of AOS

○ Behavioural treatment most effective
○ Easily produced words - need not be initial targets
■ More difficult words when taught successfully may promote better
generalization

○ Speech movements as opposed to non-speech movements
○ Practice with variety of sound combinations and sounds
■ Repeated trials on same target response (drill) is essential for initial learning
○ Positive reinforcement and correct feedback
○ Articulatory accuracy, slower rate, systematic practice, gradual increase in rate,
normal prosody
○ Instructions, demonstrations, modeling, shaping, phonetic placement, frequent
cueing, rhythm, immediate positive/corrective feedback
○ Total communication
○ Teaching accurate/improved sound productions in conversational speech
○ Self-monitoring and self-correction of errors
○ Severe AOS - ask fam members to speak slowly, use shorter sentences, and
talk only when client is focused

A

Ataxia

Muscular incoordination and irregular movements

72
Q

Features of Childhood Apraxia of
Speech

○ Inconsistent errors on consonants and vowels in repeated productions
of syllables or words
○ Lengthened and disrupted coarticulatory transitions between sounds and
syllables
○ Inappropriate prosody, especially in the realization of lexical or phrasal
stress

○ Vowel and consonant distortions
○ Inconsistent voicing errors
○ Prosodic errors, especially equal stress and segmentation
○ Awkward and/or imprecise movement transitions
○ Groping and/or trial and error behaviour

A
73
Q

CAS vs dysarthria vs motor speech NOS

A
74
Q

Dysarthria/apraxia may co-occur with aphasia
○ Client has difficulty with speech as well as language
○ Communication may be especially difficult in this instance

Dysarthria/apraxia may occur with cognitive-communication difficulties
● Client may have difficulty producing speech as well as language
difficulties

A
75
Q

Childhood apraxia of speech may co-
occur with

○ Delayed language development
○ Expressive language difficulties (e.g. grammatical errors)
○ Problems with learning to read, spell, and write
○ Problems with social language/pragmatics
○ May also have non-speech sensory and motor problems
■ Gross and fine motor delays
■ Motor clumsiness
■ Oral apraxia
■ Limb apraxia
■ Feeding difficulties
■ Abnormal orosensory perception

A
76
Q

Assess phonation, resonance,
articulation, and prosody, using
perceptual and acoustic measures
ADD ACTIVITIES FOR EACH

A

Articulation - Evaluating consonant production, duration of speech sounds,
phoneme repetition, and irregular breakdowns in articulation
Resonance - Clinical observations regarding hyponasality, hypernasality, and NAE
Prosody - Evaluating the rate of speech, phrase lengths, stress patterns, and
pauses in speech
Respiratory - Observations of forced inspiration/expiration, audible or breathy
inspiration, and grunting at the end of expiration
Phonatory - abnormal pitch, pitch breaks, abrupt variations, mono pitch, and
diplophonia

77
Q

Members must make sure the word disorder is being used to describe
symptoms
● Examples of terms that describe symptoms include:
○ Aphasias, dysarthrias, apraxias, including childhood apraxia of
speech

A
78
Q

Restorative strategies

A

Therapy techniques that have the goal of restoring lost function by
reducing the severity of the underlying deficits
○ See an improvement
○ Example- expiratory muscle strength training

79
Q

Compensatory strategies

○ Therapy strategies that have the goal of restoring lost function by
compensating for underlying deficits
○ Example- AAC, amplification
○ only see improvement with restorative

A
80
Q

Expiratory muscle strength training

A
81
Q

Inspiratory muscle strength training

A
82
Q

Diaphragmatic breathing

A
83
Q

phrase grouping

A
84
Q

resonatory treatments

A
85
Q

Resistance Training for the Velum
During Speech

A
86
Q

Nonspeech Velopharyngeal Exercises

A
87
Q

Palatal lift

A
88
Q

pharyngeal flap

A
89
Q

phonatory treatment

A

multiple

90
Q

Articulatory treatments

A
91
Q

Prosody treatments

A
92
Q
A

Strategies for severe AOS

● To elicit vocalizations:
○ Shape phonation from a cough, yawn (relax VF), laugh
○ Push gently on stomach during the exhalation phase of breathing
○ Use automatic speech tasks, social response situations, singing
● Shape syllables from phonation
○ Humming → nasal context
● Shape words based on the existing sound repertoire (fine → fire, five)
● Shape words from stereotypic utterances (as in Multiple Input Phoneme
Therapy)
● Use cues: auditory, visual, including written, tactile

CETP Mayu (11 decks)

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