Week 1 - 7 Flashcards
(97 cards)
1
Q
Define dysarthria
A
Group of neurological speech disorders involving any/all of the basic motor speech processing, including respiration, phonation, resonance, and articulation
2
Q
Difference between AOS and dysarthria
A
AOS = planning programming issue dysarthria = muscular difficulty
3
Q
6 neuromuscular features that underlie different dysarthrias
A
- strength/force of movement
- timing/rhythm of movement
- tone of muscles
- speech/rate of movement
- range of motion
- directions/accuracy of movement
4
Q
Are perceptual properties important in the evaluation of motor speech disorder?
A
Yes able to get information on quality of vocal production including pitch, range, prosody, phonation, articulation
5
Q
Speech fine motor skill
A
accuracy and speech, motor flexibility (making adjustments on the fly), improves with practice, automatic control (the more practice the less we have to think about it)
6
Q
Theory of motor equivalence relation to speech
A
there are a variety of ways to achieve a successful outcome. the vocal tract can be different shapes to achieve the same production outcome
7
Q
What comprises the CNS? The PNS?
A
CNS = brain and spinal cord
PNS = neuronal fibers outside the CNS
- transport signals from CNS to extremities
8
Q
3 important functions of brain stem
A
brainstem = conduit function (passageway for nerve fibers), cranial nerve function (allows for movement and sensation of head and neck area) and integrative function (cardiovascular function and regulates consciousness)
9
Q
Name cranial nerves
A
Olfactory, Optic, Oculomotor, Trochlear, Trigeminal, Abducens, Facial, Vestibular, Glossopharyngeal, Vagus, Accessory, Hypoglossal
10
Q
Trigeminal
A
(V) Trigeminal: innervation of jaw movement during speech, muscles of mastication
11
Q
Facial
A
(VII) Facial: innervation of muscles of facial expression, including those that move lips and firms the cheeks
12
Q
Glossopharyngeal
A
(IX) Glossopharyngeal: innervates stylopharyngeus and upper constrictor muscles of the pharynx, gag reflex (somewhat)
13
Q
Vagus
A
(X) Vagus: forms three major branches to innervate striated muscles of soft palate, pharynx, and larynx (branches: pharyngeal, superior laryngeal, recurrent laryngeal)
14
Q
Hypoglossal
A
innervates all muscles of the tongue except the palatoglossal
15
Q
Unilateral/bilateral trigeminal damage
A
unilateral = jaw deviates to weak/damaged side bilateral = jaw remains slightly open (just hangs)
16
Q
Unilateral/bilateral facial damage
A
unilateral = weakness on one whole side of the face (damaged side) bilateral = weakness of both sides of the face
17
Q
Unilateral/bilateral glossopharyngeal damage
A
unilateral = less gag reflex on damaged side bilateral = decreased movement or no movement of gag reflex
18
Q
Unilateral/bilateral hypoglossal damage
A
unilateral = tongue deviates to the weaker/damaged side bilateral = unable to complete protrude tongue or any tongue movement significantly impaired
19
Q
Unilateral/bilateral vagus damage
A
unilateral = soft palate only elevates on one side (the weak or damage side) bilateral = the soft palate hangs down lower (weakness on both sides)
20
Q
Cranial nerve damage = damage to ipsilateral or contralateral side
A
ipsilateral (same side)
21
Q
Pharyngeal brach of vagus nerve, function, damage
A
PHARYNGEAL branch: retraction and elevation of the soft palate during VP closure during speech & swallowing and pharyngeal constriction
- unilateral damage: soft palate only elevates on one side (hypernasality)
- bilateral damage: soft palate does not elevate at all (nasal emission with more nasality)
22
Q
Superior laryngeal branch of vagus nerve, function, damage
A
SUPERIOR LARYNGEAL branch: innervates the cricothyroid muscle; lengthens and thins the vocal fold, affecting pitch
- unilateral damage: reduced ability to alter pitch, reduced loudness (less subglottic pressure)
- bilateral damage: inability to alter pitch (monotone) mild-moderate breathiness, hourseness, decreased loudness
23
Q
Recurrent laryngeal branch of vagus nerve, function, damage
A
sensory component: sensation from vocal folds and larynx
motor component: innervates all intrinsic muscles of the larynx, except for cricothyroid muscle
unilateral damage: vocal quality affected, some breathiness and harshness
bilateral damage: more significant breathiness, harshness, and reduced loudness
24
Q
High vs. low lesion of vagus nerve
A
high lesion: hypernasality
low lesion: changes in vocal quality
25
3 functions of cerebellum
voluntary movement
balance
size of muscle action
26
lobes of cerebellum and location
anterior (on the top) posterior (back part we can see) flocculonodular (tucked underneath) `
27
Importance of thalamus
nucleus and incoming sensory information
28
What comprises the basal ganglia?
amygdala, caudate nucleus, putamen, globus pallidus
29
Function of basal ganglia
regulating tone, maintaining normal posture, maintaining static muscle contraction
30
What is the internal capsule? Why is it important?
it is where the motor fibers are bundled together in the brainstem in same order as homunculus
31
Where do UMN originate?
cerebral cortex
32
name 3 gyri/cortex in cerebral cortex and their primary function
precentral gyrus: primary motor cortex
premotor strip/premotor cortex: initiation of speech
postcentral gyrus: primary sensory cortex
33
What is LMN? What is another name for LMN?
LMN innervate muscles to contract and produce movement
| another name = final common pathway (includes spinal and cranial nerves
34
effect of LMN damage on the muscles they innervate
Depends on individual nerves that are damage and muscles they innervate
ipsilateral - damage to LMNs affect the same sides of the face (both upper and lower portions of face)
paresis or paralysis - partial or total weakness
atrophy - only with paresis or paralysis
fasciculations - small muscle contractions or twitches
diminished or absent normal reflexes
35
What are UMN where do start/end
- upper motor neurons regulate lower motor neurons for muscle movement
- contained within the CNS (brain and spinal cord)
- originate in cerebral cortex and descend to brainstem or spinal cord
36
Direct activation pathway: originate, function, damage
originates: in primary motor cortex or premotor cortex, descends and there is only 1 synapse, ends in brainstem (corticobulbar tract) or spinal cord (corticospinal tract)
function: mediating voluntary, skilled motor activity
unilateral damage: weakness or reduced/total loss of skilled voluntary movement
reflexes: simple reflexes are not affected
37
Indirect activation pathway: origin, function, damage
- aka extrapyramidal tract/system
- has multiple synapses to final common pathway (FCP) [reticular formation, vestibular nuclei, red nucleus]
- does not have much effect on speech
- starts in cerebral cortex, descends multiple pathways, ends cranial and spinal nerve nuclei and cerebellum
- function: maintain tone, posture, and movements that support voluntary movement
- damage ABOVE midbrain and red nuclues: decorticate posturing (e.g. arms hyperexcited)
- damage AT midbrain and below red nucleus: decerebrate posturing
- damage BELOW medulla: general flaccidity (low muscle tone)
- damage AT reticular formation: death
38
Cranial nerve contralateral or bilateral UMN innervation
bilaterally innervated: V trigeminal, VII facial, IX glossopharyngeal, X vagus, XII hypoglossal (some)
contralaterally innervated: VII facial (lower face only) & XII hypoglossal
39
What is the effect of damage to the direct activation pathway?
- weakness for any movement
- loss of reduction of skilled movement
- hyporeflexia
- decreased muscle tone
- Babinski sign
* * reflexes will be intact **
40
What is the effect of damage to the indirect activation pathway?
lesions ABOVE midbrain and red nucleus - decorticate posturing
lesions AT midbrain below red nucleus - decerebrate posturing
lesions BELOW medulla - generalized flaccidity
lesions of brainstem that damage reticular formation - death
41
Significance of term circuit control
a control circuit exerts influence over movement but it does not directly influence the final common pathway (aka LMN which directly innervates muscles)
42
Basal ganglia control circuit function
helps regulate muscle tone, maintain normal posture and static muscle contract and to regulate amplitude and velocity of movement
43
Cerebellar control circuit function
has inhibitory function that helps us scale size of movement and maintain steadiness
44
Components of basal ganglia
striatum (caudate nucleus and putamen), lentiform nucleus (putamen and globus pallidus), substantia nigra and subthalamic nuclei in the midbrain are also functionally related
45
Function of basal ganglia
regulating tone, maintaining normal posture, maintaining static muscle contraction
46
Movement disorders that occur because of damage to basal ganglia or basal ganglia control circuit
hypokinesia: reduction of movement, the more tone, the more rigidity
hyperkinesia: too much movement, involuntary extraneous movement
47
Primary functions of cerebellar control circuit
loop 1: planning and programming learned movement
loop 2: inhibitory, coordination of voluntary skilled movement, scaling size of movement, maintaining steadiness
scales the magnitude of muscle action, timing of movement, coordinates sequences of agonist and antagonistic muscle groups necessary for speech production
48
Symptoms if damage of cerebellar control circuit
ataxic dysarthria - gait, disturbance, rigid staccato speech with stress on every syllable or "sloshy" speech, intention tremors, nystagmus
49
How do the motor pathways and control circuits influence each other
work together to give each other feedback and based on that feedback they send signals to different pathways to help with coordinating and ensuring that planning and production is smooth. The direct and indirect pathways are made of UMN.
50
What part of the nervous system is involved in flaccid dysarthria
specific nerves in PNS and or cranial nerve issues (LMN) important for speech production
51
Why do those with flaccid dysarthria sound different?
speech differences depend on which cranial nerve has damage
52
Confirmatory signs/neuromuscular features of LMN involvement
atrophy, fasciculations/fibrillations, and diminished or absent normal reflexes such as gag reflexes
muscle weakness or hypotonia (low tone/flaccidity/floppiness)
53
Primitive reflexes or normal reflexes with flaccid dysarthria?
primitive reflexes: no (UMN only)
| normal reflexes: no because of damage to nervous system
54
Describe damage to cranial nerves effect on speech
hypoglossal nerve - imprecise articulation
vagus nerve, recurrent branch - breathy vocal quality
bilateral glossopharyngeal nerve - no real effect on speech
vagus nerve, pharyngeal branch - hypernasality
trigeminal nerve - inability to elevate jaw
55
If hypoglossal nerve is damaged on the right side, where would you expect to see the effect of the damage?
- when the person sticks out their tongue, it deviates/points toward the side that is damaged
- eventual muscle atrophy on tongue
56
Why is myasthenia gravis considered an autoimmune disease
MG is an autoimmune response to acetylcholine (ACh) receptors in the motor endplate of the neuromuscular junction. There is a decreased number of functioning receptors so muscles are less responsive to ACh so muscle contractions are diminished
57
How to identify myasthenia gravis
- stress test on motor speech system
- how long a person can talk before unintelligible
- droopy eyelid, weakened facial muscles, dysphagia
58
What is Bell's palsy?
unilateral damage to the facial nerve
59
Is bulbar palsy the result of upper motor neuron damage? why is it called "bulbar palsy?"
no, LMN damage
called BP because the site of lesion is typically in brainstem (brainstem strokes/tumors located here)
can damage multiple LMN at one time
extensive BP can lead to ALS
60
Can you develop flaccid dysarthria from TBI
damage to cerebellum or brainstem could occur = damage to LMN
61
What factors other than speech diagnosis itself are important to consider in recommending/planning treatment
- environment and communication partners such as the setting, people and how they interact
- client's motivation and goals for therapy
- other motor/cognitive impairments may effect performance in intervention
- nature and discourse of their disease
- any planned medical/surgical intervention that may need to occur before treatment begins
62
How to determine a starting point for treatment
- determine the patient's communication needs and goals, environment etc.
- establish a hierarchy of symptoms to be treated
- begin with whatever components will have the greatest beneficial effect on other components
- identify features of speech production that are readily modifiable
- treatment should usually begin by improving functions that improve speech
- make speech highly conscious
63
When to end treatment
- plateau
- mastery of all goals
- patient decides they no longer want to seek treatment
- patient is no longer making progress
64
Role of hierarchy of symptoms in planning treatment
use bottom-up approach treating most severe symptoms first
65
Role of SLP in medical management of motor speech
- assess potential/establish need for medical intervention
- assess likelihood the patient will benefit from medical intervention and management
- determine specific benefits to the patient
- determine the need for post-procedure management
- communicate this info
- follow up treatment
66
Are oral-motor exercises important in speech
they have been proven ineffective in treating motor speech disorders as they are irrelevant to the motor planning individual sounds require
67
Traditional approaches to motor speech treatment
integral stimulation (repeat after me), phonetic placement, minimal contrast work, intelligibility drills
68
What are the Rosenbek's motor learning guidlines for treatment of MSDs?
- physical and cognitive work are essential
- patients must speak to important their speech
- treatment tasks should be relevant to speech
- training should be specific as possible, patients need instruction and demonstration
- drill is essential
- increasing task variability tends to lead to better retention and generalization
- accuracy should be emphasized initially for most patients (60-80%)
69
blocked vs. random presentation in treatment exercises
- blocked: beneficial in the beginning
| - random: mimics real-life speaking scenarios
70
Communication oriented approach
altering the environment around the speaker/patient instead of the speech itself
- identifying the topic
- prepare the listener
- signaling a topic shift
- checking to make sure message has been understood
71
When would you focus on respiration. in treatment of someone with flaccid
- to maximize consistent respiratory support for someone
- to ensure responsible breath group lengths (not speaking or limited respiration)
- to ensure flexibility for speech
72
What is inspiratory checking
barking activity in which inspiratory thoracic muscles must be engaged to hold the elastic recoil forces in check to sustain phonation. Speech typically involves a checking action during exhalation. The inspiratory muscles are used to control the rate of lung deflation. This technique allows individuals to have enough respiratory capacity for speech and helps strengthen the muscles needed to respiration.
73
Effortful closure techniques
- grunting controlled coughing, pushing, pulling, lifting and hard glottal attack
- can improve vocal fold strength by maximizing vocal fold adduction
- for patients with unilateral or bilateral vocal fold weakness or paralysis
74
What is medial laryngoplasty? Arytenoid adduction surgery?
- medial laryngoplasty is a surgical procedure to medialize the vocal folds
- arytenoid adduction is repositioning of paralyzed vocal folds by rotating the vocal process of the arytenoid medially
75
Benefit of over articulating on resonance? What is "clear speech"
over exaggeration of jaw = more resonance in oral cavity over nasal cavity and it can be increase overall loudness
- "clear speech" = over articulated speech intelligible
76
CPAP as a treatment for VPI
hypernasality is likely because of weak soft palate not closing when it should be closed. CPAP introduces positive pressure
77
Role of contrastive stress drills
- using minimal contrast pairs clinician can see if client is hearing and producing the correct minimal pair
- used to improve intelligibility
78
Spastic dysarthria results from damage to what part(s) of the nervous system? Does damage effect individual muscles or muscle groups
- bilateral UMN
| - muscle groups
79
Functions of direct and indirect activation pathways
direct - mediates voluntary skills discrete movement
| indirect - maintains posture and tone, provides framework for skilled movement
80
Underlying neuromuscular features of spastic dysarthria
- spasticity, hear it at the level of the larynx strained effortful production
- generalized weakness
- slowness (person cannot overcome no mater how much you ask them to speak faster)
- reduced range of motion
81
slowed speech in spastic dysarthria
increased word and syllable duration, prolonged phonemes, slow transition from phoneme to phoneme, increased intersyllabic pauses, prosodic alteration
82
Distinctive features of of speech in spastic dysarthria
- slow rate
- strained/strangled voice
- slow and regular AMRs
83
Confirmatory signs for bilateral UMN damage
- positive primitive/pathological reflexes
- emotional lability
- hyperactive gag
- dysphagia
- drooling
84
Confirmatory signs of LMN damage
- specific muscle weakness
- hypotonia
- fasciculations
- atrophy
- diminished or absent normal reflexes
85
What are lacunes and what do they have to do with spastic dysarthria
- multiple small subcortical lesions in the arteries of brainstorm and what matter
- may cause bilateral damage to the UMN
86
How can brain-stem stroke result in spastic dysarthria
The brain stem is where cranial nerves emerge
87
What is leukoencephalitis?
an inflammatory disease where demyelination occurs, it causes bilateral and multifocal UMN damage = spastic dysarthria
88
What is primary lateral sclerosis (PLS)? What is slower PLS or ALS
PLS = degenerative disease also known as progressive pseudobulbar palsy
- UMN dying and leading to generalized weakness and spastic dysarthria
- PLS is slower
89
Define inspiratory checking. Why is respiratory control important
- holding back the breath as we exhale to practice controlled exhalation
- results in longer breath during speech production
- teaches when in the breathing cycle to initiate speech or phonation and knowing when/how to efficiently use breaths
90
Why might breathy onset reduce the strained, strangled vocal quality characteristic of spastic dysarthria
breathy onset would help air the vocal folds to abduct which will allow for forced air to produce speech with the idea of reducing the strained and strangled vocal quality
91
What is a pharyngeal flap? Why is it used?
a prosthetic used to close off air from going into the nasal cavity, reduces hypernasality
92
What is the yawn-sigh approach?
teaches when in the breathing cycle to initiate speech/phonation
93
What aspect of communication does alphabet supplementation address?
- speaker oriented treatment for rate of speech
- alphabet supplementation is a rate control technique that can be used to transition from non-augmented to augmented speech
- speaker points to the first letter of each spoken word on an alphabet board
94
Which 2 cranial nerves are in close proximity to each other and may overlap somewhat in function?
Glossopharyngeal and vagus pharyngeal branch
95
Which cranial nerve is responsible for elevation and retraction of the soft palate during phonation
CN X: Vagus nerve
96
Which cranial nerves enable us to seal our lips for bilabial production
Facial nerve
97
If you damage this cranial nerve, one could expect imprecise articulation
Hypoglossal nerve
