Motor Speech Exam 2

Front 1

What is the primary goal of management of motor speech disorders in adults?

Back 1

-to maximize the effectiveness, efficiency, and naturalness of communication
1. To restore lost function
2. Compensate existing speech abilities
3. Make necessary adjustments to enhance communication

Front 2

How can you restore lost function in adults with impaired motor systems?

Back 2

-not always possible (severity, etiology, etc)
-new motor learning

Front 3

How can we help adults with MSDs compensate their speech?

Back 3

-slow down rate to inc. precision
-use prosthetics (amplify voice, reduce nasality)
-modify speaking environ. (AAC, amp, etc)

Front 4

How can the environment be modified to help people with MSDs communicate?

Back 4

-reorganize work environ, responsibilities, lifestyle (reduce need for the lost function)
-counsel family and pt
-modify acoustics or speaking situations

Front 5

What are some factors influencing the decision to treat or not? (MSDs)

Back 5

-dx (progression of disease)
-other medical interventions that could fix it faster/better?
-pt's physical status (alert, stable, etc)

Front 6

Describe disability vs handicap as applies to MSDs

Back 6

dis: degree of inability to speak normally 2ndary to speech impairment

hand: effect of impairment on ability to accomplish a previous normal role

Front 7

What are some important patient factors to consider when deciding to treat (other than medical status?)

Back 7

-patient motivation (is tx a priority for them?)
-their need to communicate (age, ed. level, cog-ling factors, living situations)
-HMO coverage

Front 8

What should be the focus of tx for adults with MSDs?

Back 8

-objectives that will provide most benefit fastest
-greatest support for cog-ling functions, respiration, etc
-duration appropriate to condition

Front 9

What is the prevalence of Ataxic dysarthria (in that chart of dysarthrias)?

Back 9

10%

Front 10

Describe connections of the cerebellum to...
--(sub) cortical structures
--FCP

Back 10

-CONTRAlat cortex and thalamus

-IPSIlat FCP

Front 11

What do purkinje cells do?

Back 11

-inhibitory
-cerebellar output

Front 12

Describe the cerebellar influences on speech

Back 12

-Reciprocal connections with cerebral cortex
–Auditory + proprioceptive feedback
•muscles, tendons, joints
–Reciprocal connections with brainstem
•IDAP network
–Network with BG -->thalamus -->cerebral cortex-->IDAP

Front 13

Describe Ataxic symptoms of cerebellar lesions

Back 13

•Hypotonia:
–decrease resistance

Front 14

Describe the speech symptoms of Ataxic Dysarthria

Back 14

•Speech AMRs

Front 15

What is the prevalence of hyPOkinetic dysarthria?

Back 15

8%

Front 16

What is the BG comprised of?

Back 16

–Striatum: caudate + putamen
–Lentiform nucleus: putamen+ globus pallidus
–Substantia nigra+ subthalamic nuclei

Front 17

Describe the functions of the BG control circuits

Back 17

•Regulate muscle tone
•Regulate goal-directed movements
–Templates for redundant, over-learned tasks
•Control postural adjustments

Front 18

What are the primary influences of the BG on speech?

Back 18

•Interconnections with motor areas in cortex
•Influence is inhibitory via thalamus
•Therefore, dampens/modulates cortical output
•Maintains stable musculoskeletal environment
•Accomplishes discrete movements
•Excess or insufficient dampening of cortical output leads to -->motor control disorders

Front 19

Describe what damage to BG circuits does to speech

Back 19

•Reduces movement (hypokinesis)
•Yet, there is a failure to inhibit voluntary movement
–ie. tremor
•Speech deficits:
–an increase in rate + a decrease in ROM

Front 20

Describe the motoric symptoms of PD

Back 20

•Tremor at rest (static or resting tremor, 4-7 Hz)
•Tremor decreases with voluntary movement
•Rigidity (slowness, stiffness, cogwheel effect)
•Bradykinesia(delays/slowness

Front 21

Describe the speech symptoms of PD

Back 21

•Monoloudness, monopitch
•Reduced stress, short phrases, variable rate
•Short rushes of speech, inappropriate silences
•Breathy voice, reduced loudness
•Fast AMRs, reduce ROM, palilalia
•Mumbling, stuttering-like

Front 22

What is the prevalence of hyPERkinetic dysarthria

Back 22

18%

Front 23

Describe what destruction of the subthalamic nucleus does

Back 23

•Reduced inhibitory output from BG
•Increased thalamic and cortical firing
•Uninhibited (abnormal firing) is released
–via corticobulbar+ corticospinaltracks (DAP)
•When there is a disruption of excitatory (Ach) and inhibitory (dopamine) neurotransmitters
–it produces hyperkinesia
•Damage to dentate, red nucleus, inferior olive
–also produce hyperkinesia

Front 24

Describe symptoms of Hyperkinesia

Back 24

–Slow or fast abnormal movements
–Regular or irregular movements
•The presence of involuntary movement suggests that the location of lesion is in the BG control circuits

Front 25

Describe the various types of hyPERkinesia with effects and location of lesion

Back 25

•Dyskinesia: fast/slow, irreg/rhythmic, BG
•Myoclonus: fast/slow, irreg/rhythmic, Cortex-Spinal
•Tics: fast, irregw/pattern, BG
•Chorea: fast, irreg, BG
•Ballism: fast, reg, Subthalamic nucleus
•Athetosis: slow, irreg, BG
•Dystonia: slow, irreg/sustained, BG
•Spasm: slow/fast, irreg, BG
•Essential voice tremor: slow/fast, rhythmic, striatum

Front 26

What is the (approximate) prevelance of Unilat UMN dysarthria?

Back 26

8%-8.5%

Front 27

Compare "central" and "peripheral" weakness

Back 27

•Contralateral lower facial weakness
–Corticobulbar involvement
–“central”weakness (UnilUMN)
–below the eye on one side
-can smile reflexively
•Ipsilateral upper + lower facial weakness
–On one side of the face is due to:
–“peripheral”weakness (LMN)

Front 28

Describe the etiology of Unilat UMN dysarthria

Back 28

•Lacunarinfarcts: occlusion of small penetrating arteries of large cerebral arteries
–ACA and MCA and lenticulostriatearteries
•Most often involve:
–putamen, caudate nucleus, thalamus
–pons, IC, cerebral cortex white matter
•No associated aphasia, neglect, visual field and memory deficits, unconsciousness

Front 29

Describe the non-speech symptoms of unilat UMN lesions

Back 29

•Contralateral Hemiplegia/hemiparesis
•Loss of skilled movement on contralateral side relative to cortical lesion
•Absent abdominal reflexes/hyperactive stretch reflexes
•Central facial weakness (lower face)
•Lingual weakness
•Spasticity, increased muscle tone
•+ Babinskion effected side

Front 30

Describe the speech symptoms of unilat UMN lesions

Back 30

•Imprecise consonants
•Irregular articulatory breakdowns
•Slower AMRs, slower rate
•Harshness
•Hypernasality, nasal emission (some)

Front 31

Describe some examples of mixed dysarthrias

Back 31

•Examples:
–ALS (Flaccid + Spastic)
–MS (Ataxic + Spastic)
–Parkinson’s (Hypokinetic+ Hyperkinetic)
–Wilson’s Disease (Hypokinetic+ Ataxic + Spastic)
–Progressive Supranuclear Palsy (Hypokinetic+ Spastic)

Front 32

What is the prevalence of AOS?

Back 32

8%

Front 33

Describe the Motor Speech Programmer (MSP)

Back 33

•Motor speech interacts with these activities: conceptualization

Front 34

Describe the L and R functions of the Motor Speech Programmer

Back 34

•Organizes motor commands
–Sequences of phonemes, syllables, words, phrases with rate + prosody.
•L-hemisphere -->linguistic aspects
–Left perisylvian area
–temperoparietal cortex and,
–posterior-inferior frontal cortex
•R-hemisphere + limbic system + amydala+ BG + thalamus -->emotional + affective components

Front 35

Describe non-speech symptoms of AOS

Back 35

•Reflect damage

Front 36

Describe a DDX of AOS vs Brocas vs Wernikes

Back 36

•AOS-->motor level deficits

Front 37

Describe speech symptoms of AOS

Back 37

•Articulation distorted:
–vowels, consonants, additions, substitutions
•Fluency unsuccessful: trial + error, groping speech
–Frustration due to poor attempt, false starts
•Impaired Rate + Prosody:
–Slow rate esp. for multisyllabic utterances
–Prolonged + variable rate
•Prolonged, decreased, altered stress
•Poor sequencing of AMRs (and speech)

Front 38

Describe the DAB model of AOS, with implication for lesion site

Back 38

•A central language processor (CLP) unit
•A motor speech programmer (MSP) that activates sensorimotor programs to transmit the verbo-motoric message, and
•The final common pathway (FCP) for motor execution.
-->Breakdown would be in the MSP

Front 39

Describe the Whiteside and Varyley model of AOS with implications for lesion site

Back 39

2 "routes:
-Direct route: automatic, for high freq. words
-Indirect route: conscious, letter-to-sound conversion
-->Breakdown is in direct route, requiring all speech to be indirect

Front 40

Describe mutism (in general)

Back 40

•Lack of speech, yet alert + conscious
•+/-cognitive deficits
•+/-motor deficits
•+/-locked in syndrome
•+/-deliberate = psychogenic
•+/-hearing loss, laryngectomy
•absence of speech
•may have multiple origins

Front 41

What is an Anarthria?

Back 41

-severe dysarthria
"an"= lack of
"arthria" = motor speech ability
-NOT an AOS
-Bilateral damage, usually spastic (sometimes flaccid)

Front 42

Describe Locked-in Syndrome

Back 42

-spared ability to blink and move eyes vert.
-spared cognition
-spastic or spas-flac.
-87% mort. in 1st 4 mos
-provision of AAC helps reduce depression

Front 43

Describe aboulia

Back 43

-aka akinetic mutism
-lack of initiation for cog. or motor execution
-occurs with bi-anterior frontal lesions (like smashed head on windshield)

Front 44

Describe possible etiologies of Neurogenic stuttering

Back 44

–word finding prob, verbal information (aphasia)
–incorrect articulatory movement (AOS)
–festination, freezing movement (hypokinetic)
–drug-related neurogenicstuttering

Front 45

What are some possible etiologies of pseudo-foreign accent?

Back 45

-psych
-part of a Broca's aphasia
-part of an AOS

Front 46

What are the primary goals of tx with adults with MSDs?

Back 46

1.Restore lost function
2.Compensate existing speech abilities
3.Make necessary adjustments to enhance communication

Front 47

What are some ways adults with MSDs can modify their speech or environment to enhance their communication?

Back 47

•Modify rate + prosody of speech
•Use of prosthetic devices
–amplify voice
–reduce nasal emission: obturator
•modify speaking environment
–Supplemental speaking devices
–Alternative communication devices
*reduce need for lost function by altering environment (work, noise level, acoustics, etc)

Front 48

What are some factors influencing the decision to treat adults with MSDs?

Back 48

•Medical diagnosis:
–Etiology, course, progression of disease
•Medical interventions:
–Surgical, systemic (available to try first?)
–Pre-op assessment, counseling, post-op tx.
•Patient’s physical status:
–Alert, somnolent, unstable, fluctuating

Front 49

Describe disability vs handicap as applies to speech

Back 49

disability: inability to speak normally due to an impairment

handicap: how this inability affects daily life (job, etc)

Front 50

Describe the three general fields of tx approaches for adults with MSDs

Back 50

•Medical Management (Botox, surgery, L-dopa)
•Prosthetic and instrumental management (palatal lift, voice amp, AAC)
•Behavioral Management (breath support coaching, speak in normal range, etc)

Front 51

Describe the stages of motor learning

Back 51

•Cognitive stage (understand what prob. is and how to fix it)
•Associative stage (move form consc. to auto. control, use feedback)
•Automatic or autonomous stage (skill becomes auto., FB less crucial)

Front 52

Describe possible causes for neurogenic mutism:

Back 52

-anarthria (from severe spas. dsyarth, sev. flac. dysarth, hypo/per kinetic dysarth, cerebelar mutism, biopercular synd)
-sev. AOS
-asphasia
-diffuse cog. deficits