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Motor Speech Disorders > Week 8 - 14 > Flashcards

Week 8 - 14 Flashcards

1
Q

Salient features of flaccid dysarthria

A
  • LMN damage
  • weakness
  • breathiness
  • looks different depending on cranial nerve
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2
Q

Ataxia = individual muscle movements or movement patterns

A

movement patterns

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3
Q

Salient features of spastic dysarthria

A
  • UMN damage
  • slow speech
  • slow but regular AMRs
  • strained/strangled vocal quality
  • emotional lability
  • suck/snout reflexes
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4
Q

Salient features of ataxic dysarthria

A
  • cerebellar control circuit
  • irregular articulatory breakdowns
  • irregular AMR rhythm
  • excess/equal stress (scanning speech)
  • distorted vowels
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5
Q

Salient features of hypokinetic dysarthria

A
  • basal ganglia control circuit
  • short rushes of speech
  • fast or accelerated AMRs
  • monopitch/monoloudness
  • harsh/breathy vocal quality
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6
Q

Salient features of hyperkinetic dysarthria

A
  • variability
  • prolonged intervals and phonemes
  • inappropriate silences
  • variable stress
  • extraneous non-speech sounds
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7
Q

Salient features of AOS

A
  • planning and programming issue (not linguistic)
  • consonants and vowels distorted
  • sound prolongation distorted
  • voicing distinction distorted
  • inconsistent trial to trial errors
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8
Q

Lesion area for ataxia

A

bilateral cerebellum lesions or lesions in the vermis (midline).

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9
Q

Dysmetria

A

overshooting or undershooting where your articulators are supposed to be to produce a specific speech sound
(related to ataxia)

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10
Q

Decomposition of movement

A

we have coordinated movement, and then all of the sudden something goes awry, and it decomposes (related to ataxia)

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11
Q

Dysdiacochokinesia

A

decomposition of skilled and unskilled movements (related to ataxia)

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12
Q

What do dysmetria, decomposition of movement and dysdiadochokinesia have to do with ataxia

A

ataxia = lack of movement coordination
cerebellar control circuit damage = ataxia (responsible for timing, scaling size of movement, and coordination)
three things all relate to movement or movement errors

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13
Q

Name and explain underlying neuromuscular features of ataxic dysarthria
(5)

A
  1. reduced tone –> pedulousness (more arm swinging then expected)
  2. slowness of movement –> slow to start/stop movement and reach target
  3. impaired check and excessive rebound (push on a persons outstretched arm = super slow to return to original position)
  4. irregular timing of repetitive movements
  5. inaccurate direction and range of motion
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14
Q

Confirmatory signs of ataxia (4)

A

nystagmus (Rapid eye movement at rest. Can be L/R or up/down)
jerkiness of movement/incoordination
wide-based lurching gait
tremors

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15
Q

Lesion area for hypokinetic dysarthria and depletion or insufficiency of what neurotransmitter

A

basal ganglia control circuit

dopamine

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16
Q

Neuromuscular features of hypokinetic dysarthria (3)

A
  1. rigidity - increased resistance of muscle movement in any direction (cogwheel rigidity)
  2. reduced range of movement (mouth doesn’t open/move much)
  3. increased rate of repetition or movement
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17
Q

Distinctive features of hypokinetic speech

A
  • short rushes of speech
  • increased rate
  • monopitch/monoloudness
  • diminished stress patterns
  • palilalia (compulsive reiteration of word or short phrase)
  • harsh/breathy voice
  • rapid AMRs (blurred)
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18
Q

Difference between flaccid and hypokinetic breathy voice

A 
hypokinetic = harsh and breathy 
flaccid = breathy
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19
Q

Confirmatory signs of hypokinetic dysarthria (7)

A
  • infrequent eye-blinking and swallowing
  • minimal facial expression
  • lips might appear tight
  • trenulousness of jaw/lips
  • AMRs accelerate
  • lack of movement that accompanies speech
  • reduced chest wall movement during quiet breathing
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20
Q

Describe features of disease typically caused by hypokinetic dysarthria

A 
Parkinson's disease 
- resting tremors 
- rigidity 
- bradykinesia or hypokinesia/akinesia 
- loss/diminishment of postural reflexes
can manifest as festations, micrographic writing, masked face, and reduced arm swing while walking
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21
Q

Define bradykinesia and akinesia

A 
bradykinesia = hypokinesia or slowness of movement
- false starts 
- slowness once movement starts
- difficulty stopping movement 
akinesia = no movement
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22
Q

Define parkinsonism vs. Parkinson’s

A

parkinsonism used when person has Parkinson’s like symptoms but they are caused by something else like toxic metabolic issue or trauma

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23
Q

Common vascular, toxic-metabolic, infectious conditions and traumas that cause parkinsonism

A

Progressive supranuclear palsy (PSP), Diffuse Lewy body disease, Pick’s disease, dopamine antagonistic drugs, chronic exposure to heavy metals or some chemicals, chronic traumatic encephalopathy (CTE), neurosurgery

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24
Q

What is progressive supranuclear palsy? What are some symptoms?

A 
parkinsonism caused by cell loss in many areas of the brain (unknown etiology) 
Symptoms include: 
- paralysis of vertical gaze 
- signs of parkinsonism 
- dysarthria and dysphasia 
- personality and cognitive changes 
(not responsive to PD drugs)
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25
Q

What is Lewy body disease? Early signs?

A 
disease similar to Parkinson's 
symptoms include: 
- severe cognitive impairment (dementia) 
- visual hallucinations 
- paranoid delusions
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26
Q

Can exposure to heavy metals/chemicals cause parkinsonism?

A
  • causes Wilson’s disease which is a parkinsonism (truncal rigidity, masked face, slow movement, dystonia, dysarthria and drooling)
  • can cause hypokinetic dysarthria (symptom of PD but not all with PD have hypokinetic dysarthria)
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27
Q

What is deep brain stimulation?

A
  • used to reduce tremors or dyskinesias in Parkinson’s or Parkinsonism
  • pacemaker is implanted under skin of chest wall and electrical wire connects it to brain
  • sends currents to particular parts of brain (thalamus, globus pallidus)
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28
Q

Side effects of PD medication

A
  • dyskinesia: any generalized involuntary movements
  • dystonia: slow-building contraction of muscles = painful but gets better (e.g. foot cramping)
  • confusion
    on-off effect (it works until it doesn’t)
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29
Q

Define hyperkinetic dysarthrias

A
  • group of speech disorders characterized by involuntary extraneous movements that affect any/all components of speech production
  • type of involuntary movement helps define what kind of hyperkinetic dysarthria
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30
Q

Lesion causing hyperkinetic dysarthrias

A

basal ganglia control circuit

- disruption in excitatory or inhibitory neurotransmitters

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31
Q

What are the two major movement disorders?

A

chorea (quick or choreiform)

dystonia (slow or dystonic)

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32
Q

Huntington’s disease inheritance

A

autosomal dominant degenerative CNS disorder

1/2 of offspring will inherit disease

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33
Q

Define chorea

A
  • rapid/abrupt involuntary unsistaned muscle contraction that move body part
  • can be interrupted by voluntary movement
  • occur randomly
  • muscle tone varies
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34
Q

Define dystonia

A
  • involuntary sustained muscle movements that are painful
  • build slowly and gradually recede over time
  • can involve one or more body part
  • voluntary movement = delayed
  • repetitive movement = restricted in range
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35
Q

What are the different types of spasmodic dysphonia? Symptoms

A

Adductor (common) = spasms that cause vocal folds to stiffen and slam together
Abductor = spasm that cause vocal folds to stay open
Symptoms:
- voice arrests, strained/strangled/effortful voice, tremor, inappropriate silences, slow rate

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36
Q

Essential voice tremor: confirmatory signs/speech characteristics

A

confirmatory signs: Rhythmic laryngeal movement, adductor/abductor oscillation of cords in sync with tremor
speech characteristics: 4 to 7 Hz tremor, voice arrests possible, articulation WNL, slow rate, restricted pitch/loudness variability

37
Q

Tardive dyskinesia signs/symptoms

A
  • lip smacking/pursing
  • lip retraction
  • tongue protrusion
  • opening and closing of the jaw
  • lateral tongue movements
    • side effect of potent antipsychotic medication
38
Q

What is the Guillain-Mollaret triangle?

A
  • the G-M triangle is a feedback loop that includes the dentate nucleus, red nucleus and inferior olive
  • damage = palatopharyngeal myoclonus a hyperkinetic disorder
39
Q

Treatment options for hyperkinetic dysarthria

A
  • pharmacological (reduce symptoms)
  • surgical ablation (destroys neurons in certain area of the nervous system not used much)
  • Deep brain stimulation (doesn’t improve speech but stimulating the BG can improve movement disorders which improves quality of life)
40
Q

SLP role in treating spasmodic dysphonia

A
  • voice evaluation
  • therapy for improving perceptual features
  • recommend additional treatments like botox (may not do injections)
41
Q

Important characteristics of Friedreich’s ataxia? What causes it? Do people recover from it? Is dysarthria the only symptom?

A
  • limb and gait ataxia, absent muscle stretch reflexes in lower limbs, sensory loss, signs of corticospinal tract involvement (UMN), dysarthria (mixed, with ataxic and spastic components)
  • dysarthria not the only symptom
  • most common recessively inherited dysarthria
  • cannot recover from it: leads to incapacitation followed by death (course: 20 years)
42
Q

Which form of ataxia can resemble Friedreich’s ataxia? Why is this important to be aware of?

A
  • ataxia with vitamin E deficiency

- it is important to be aware of vitamin E deficiency because it can be treated

43
Q

Where do 16% of metastatic brain tumors develop?

A

in the cerebellum

44
Q

What are the signs of normal pressure hydrocephalus (NPH)? How does this relate to ataxic dysarthria/ what does it lead to?

A
  • ventricles may be enlarged while CSF pressure is normal
  • associated with trauma, meningitis, and subarachnoid hemorrhage
  • may lead to: progressive gait disorder, impaired mental function, urinary incontinence, possible dysarthria, dementia
45
Q

Is it possible to have intermittent ataxia dysarthria?

A
  • possible to have intermittent ataxia dysarthria
  • known as episodic ataxias and are caused by autosomal dominant etiologies
  • can last seconds to minutes
46
Q

How would you distinguish between rigid rate control and self-determined rate control?

A
  • rigid rate control: rate is externally determined (speaker does not choose rate e.i. pacing board)
  • self-determined rate control: determined interactively between the client and the clinician
47
Q

What are the major trade offs a client should be aware of when using rigid rate control?

A
  • trade off between natural speech and intelligible speech

- clinician may slow down speech to improve intelligibility but it sounds less natural

48
Q

Why would rate control lead to improve articulation and/or an improved communication interaction?

A
  • increases time for individual to coordinate their articulatory movements = more precise articulation
  • gives listener time to presses each word
49
Q

Difference between hypokinetic dysarthria AMRs and others

A
  • accelerated rate or blurred speech rate
50
Q

Name typical complaints of patients with hypokinetic dysarthria

A
  • weak/quiet voice
  • trouble getting started
  • rate of speech is too fast
  • speech gets worse with fatigue
  • upper lip feels stiff
51
Q

Palato-pharyngo-laryngeal myoclonus etiology, Guillain mollaret triangle =, speech characteristics, confirmatory signs

A

etiology - brainstem or cerebral stroke
GM triangle - dentate nucleus, red nucleus, inferior olive
speech characteristics: myoclonic “beats” at 1 - 4 Hz, occasional hypernasality
confirmatory signs: rhythmic/semirhythmic myoclonus, unilateral or bilateral movement of the soft palate, pharynx and larynx (heard during prolonged /a/)

52
Q

Define mixed dysarthria

A
  • any combination of two or more dysarthrias
  • the result of involvement of two or more components of the motor control system
  • often times seen in MS, ALS, Wilson’s disease
53
Q

How do you name a mixed dysarthria?

A
  • name component that is more prominent first
54
Q

What causes ALS?

A
  • unknown etiology result of loss motor neuron in either the pre central cortex, corticospinal tract, motor nuclei of cranial nerves, and/or anterior horn of spinal cord
55
Q

What areas change in the nervous system that characterize ALS?

A
  • degeneration in the precentral cortex (motor area), the corticospinal tract, and the motor nuclei of the cranial nerves, including the anterior horns of the spinal cord
56
Q

Age of onset, common gender, and early signs for ALS

A
  • 50’s and 60’s
  • men are more likely
  • early signs include: fatigue or cramping typically in limbs and in the head and neck area
57
Q

What are the neuromuscular features of ALS?

A
  • weakness or muscle atrophy
  • hyperactive reflexes with spasticity
  • fasciculations
58
Q

Describe effects of ALS on motor speech production: Early on? When more severely impaired?

A
  • early on: vowel distortion, slowed rate, reduced loudness, reduced stress contrasts, short phrases, consonant imprecision
  • severely impaired: hypernasality, strained/strangled voice, groaning voice, mono-pitch, mono-loudness
59
Q

What kind of disease is MS? What changes in the nervous system characterize MS?

A
  • autoimmune demilenating disease

- death of oligodendrocytes within the lesions and sclerosis in patch areas in subcorticol white matter

60
Q

What is the average age onset of MS?

A

20 - 40 years

61
Q

Why is MS difficult to diagnose? Are there symptoms that help confirm a diagnosis?

A

Symptomatology and severity can vary based on the individual, some can experience symptoms for years prior to obtaining a diagnosis

62
Q

What symptoms might you expect early on in MS? Later?

A
  • problems with gait, visual and/or other sensory difficulties, cerebellar dysfunction
  • progressive MS can include cognitive difficulties, cranial nerve abnormalities
63
Q

Describe the possible courses of MS?

A
  • benign: 1 or more attack of symptoms
  • relapsing-remitting: episodes of symptoms occur
  • remitting-progressive: periods of remission, getting worse over time
  • malignant-progressive: symptoms persist and get worst over time
64
Q

Common type of dysarthria for MS? Common symptom?

A
  • spastic
  • dysarthria symptom = impaired loudness control
    • severity depends on extent of neurologic involvement
65
Q

What types of treatment are available for MS?

A

pharmacological and symptomatic

  • reduce pain, spasticity and fatigue
  • reduce inflammation
  • promote remission
  • shorten attacks
  • fight infections
66
Q

What type of disease is Wilson’s disease? How is it diagnosed?

A
  • progressive degenerative disease

- diagnosis by person having abdominal pain, jaundice, ring around cornea

67
Q

Age and ethic group associated with Wilson’s disease

A
  • begins in early adolescence

- more common with Eastern Europeans, Sicilians, and Southern Italians (reasons unknown)

68
Q

Is dysarthria common in Wilson’s disease? If so what kind?

A
  • yes; mixed dysarthria
69
Q

Symptoms of Wilson’s disease? Treatment options?

A
  • ataxia, intention tremors, extremity and truncal rigidity, dystonia, dysarthria, dysphasia, drooling, masked facies
  • pharmaceutical treatments to reduce copper absorption and increase zinc levels; reduced food intake of foods w/copper in them; liver transplant for extreme cases
70
Q

What is apraxia of speech, dysarthria and aphasia-AOS? Is there nonverbal apraxia (NVOA)? Is there hemiparesis?

A

AOS
- impairment in planning or programming the movements of speech, oral mech generally normal, aphasia frequently co-occurs, NVOA often present, right hemiparesis common
Dysarthria
- disturbed execution of movement due to muscle weakness, slowness, in coordination and/or alteration in muscle tone, oral mech may be abnormal
Aphasia-AOS
- may or may not be present, NVOA less often present, right hemiparesis common

71
Q

What is the most significant etiology of AOS?

A
  • stroke is the most common but can also be caused by degenerative diseases, trauma or tumor
72
Q

Why is variability of articulation considered to be a hallmark feature AOS?

A
  • disorder involves programming and planning
  • damage that occurs affects the brain capacity to program and plan movements made by speech musculature for volitional production of phonemes and the sequencing of muscle movements for production of words
  • no because of weakness, slowness or incoordination disturbances
73
Q

Name the different features of AOS (4)

A
  • perceptual features
  • articulatory features
  • rate and prosodic features
  • fluency features
74
Q

Perceptual features of AOS

A
  • effortful visible and audible trail-and-error groping for articulatory postures
  • obvious difficulty in initiating speech
  • unrelieved dysprosody
75
Q

Articulatory features of AOS

A
  • consonants and vowels distortions
  • distorted substitutions
  • distorted additions
  • distorted sound prolongations
  • distorted voicing distinctions
  • inconsistent trail-to-trial errors
76
Q

Rate and prosodic features of AOS

A
  • slow overall rate
  • decreases phonemic accuracy as rate increases
  • prolonged but variable vowel duration in multisyllabic words or words in sentences
  • prolonged but variable inter word intervals (regardless of phonemic accuracy)
77
Q

Fluency features of AOS

A
  • false starts and restarts
  • sound and syllable repetitions
  • successful and unsuccessful attempts to self-correct
78
Q

What are common co-occurring conditions of AOS

A
  • Broca’s aphasia

- dysarthria

79
Q

Why is AOS considered not to be the result of phonological impairment?

A
  • AOS is an articulatory/movement based disorder that is linguistic in nature
  • impairs the ability to plan and program the muscles for volitional production of phonemes and the sequencing of muscles movements for vowel production
80
Q

What are common lesions sites that produce AOS?

A
  • lesions in left cerebral hemisphere (specifically “Broca’s Area”), the SMA, parietal lobe, somatosensory cortex, and supramarginal gyrus, insula, and basal ganglia
81
Q

Assuming we have a “network” within the language zone that we refer to as a “motor speech programmer,” what is its function thought to be?

A
  • leading role in establishing the plans and programs for cognitive and linguistic goals of spoken language
  • planning and programming the motor movements required to produce the target sound
82
Q

If you are going to do an informal assessment for possible AOS, what tasks would you include? Why?

A

Spontaneous speech sample to look at diversity in word errors, words of varying motor syllable complexity

83
Q

What pattern of performance would you expect from a person with AOS?

A
  • look for speech difficulties
    • most substitutions are close to target
    • more trouble with blends and consonant clusters than single consonants (more complex motoric task)
    • more trouble with consonants than vowels
    • better with plosives than fricatives
    • lost of trouble with /l/
84
Q

Easier and harder tasks for AOS

A
  • easier tasks: automatic tasks, AMRs, isolated sounds or single words, CVCs with same phoneme at beginning and end of word
  • more difficult: SMRs, multisyllabic words with unstressed initial syllable, words/sentences of increasing length, conversation/narrative
85
Q

Is it appropriate to diagnose AOS using a standardized test score? Explain

A
  • there is no standardize test for diagnose AOS
  • AOS diagnosis is rarely done by single standardized test
  • clinician obtain additional information through collecting medical history
  • have them perform different tasks (e.i. conversational speech sample, vowel prolongation, AMRs)
86
Q

What is the difference between intersystemic and intrasystemic reorganization in treatment for AOS? Give examples

A
  • intersystemic: pairs speech with something else; uses non-speech to facilitate speech
    • Ex: using signs from ASL to pair gestures with speech to help improve speech
  • intrasystemic: focused on improving the person’s performance by emphasizing either a more automatic level of function or a higher level of control; working within the system to reorganize things to restore function
    • Ex: integral stimulation (watch and listen then imitate)
87
Q

What is integral stimulation?

A
  • it’s imitation

- “watch and listen” method by Rosenbek that is performed by clinician in which there are no cues given to client

88
Q

Why might it by beneficial to try MIT with a client who has AOS?

A

MIT uses repetition that gradually fades as the client makes progress, verbal and gestural cues are used during this treatment, high-probability phrases are utilized

89
Q

What strategies for producing speech could you try for client who has little or no speech (presumably as the result of AOS)

A
  • targeting words chosen by the client to increase buy-in
  • pairing gestures with speech
  • pairing highly used symbolic gesture with its word or sound
  • minimal pairs
  • utilize high frequency words that are common in their day to day routine (wife’s name, words for their previous employment)

Motor Speech Disorders (2 decks)

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