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Clinical Methods > Test 2 > Flashcards

Test 2 Flashcards

1
Q
  1. Define flaccid dysarthria
A

the result of damage or impairment to the LMN of the cranial or spinal nerves (damage to the PNS)
It is characterized by:
*paralysis, weakness, hypotonicity, atrophy, and hypoactive reflexes of the involved speech subsystem musculature.
* Weakness of speech or respiratory musculature resulting in the presence of distinctive qualities

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2
Q
  1. What components of speech (muscles) does flaccid dysarthria affect?
A

respiration, phonation, articulation, prosody, and resonance.
slow labored articulation, distorted productions lingual consonants, marked degrees of hyper nasal resonance, and horse-breathy phonation

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3
Q
  1. What is the final common pathway?
A

LMN, This is because all direction for voluntary movement produced by the central nervous system (in the cortex, basal ganglia, brain stem, cerebellum and spinal cord) is transmitted via LMNs.

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4
Q
  1. What are the six pairs of cranial nerves of speech production?
A

Trigeminal (V), Facial (VII), Glossopharyngeal (IX), Vagus (X), Accessory (XI), Hypoglossal (XII)

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5
Q
  1. Discuss what damage to each of the six crainal nerves may produce if they are affected unilaterally or bilaterally.
A

Trigeminal Nerve (V)= mandibular branch important for speech and for innervating the muscles in the lower jaw and velum. bilateral damage has a severe impact on speech intelligibility. Damage can be unilateral or bilateral.

Facial (VII)= Divides into the cervicofacial and temporofacial branches.
Cervicofacial innervates the muscles of teh lower face through the lingual, labial, and mandibular subbranches.
Temporfacial innervates the muscles of the upper face through the temporal and zygomatic subbranches.
Damage to the facial nerve itself can cause weakness or paralysis in all muscles on the same side of face, resulting in drooping of the eyelid, mouth, cheek, and other structures (Bell’s Palsy)
UMN damage to one hemisphere will result in weakness of the cheek and mouth on the opposite side of the lesion, this is referred to as Unilateral UMN Dysarthria

Glossophayngeal (IX)= Can be tested by eliciting the gag reflex, damage to this nerve will also likely affect the vagus nerve.
Plays role in speech resonance and phonation by shaping pharynx into appropriate positions needed to produce specific phonemes

Vagus (X)= One of the key cranial nerves for speech production, originates at the medulla, just below the glossopharyngeal nerve. It is an extremely long nerve, serves various organs and parts of the body including the heart.
Three branches: pharyngeal, external superior laryngeal, and recurrent pharyngeal.
1. Pharyngeal= damage can affect movement of velum and resonance
2. External Superior Laryngeal= damage can affect pitch
3. Recurrent Laryngeal= damage can cause breathy phonation

Accessory Nerve (XI)= Originates in the medulla just below the vagus nerve. Works in conjunction with vagus nerve, helping innervate intrinsic muscles of velum, pharynx, and larynx.
Damage to components of accessory nerve will affect the vagus nerve and vice versa

Hypoglossal (XII)= Provides motor for all intrinsic and most extrinsic muscles of the tongue.
Damage will result in paresis or paralysis of the tongue on the same side as the damage. The tongue will deviate to the same side as the damage
Primary motor speech nerve damage are: imprecise articulation, especially with phonemes that require tongue tip elevation or the back of the tongue, phoneme distortion, and slowed lingual movements. Reduced intelligibility

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6
Q
  1. Discuss each of the six cranial nerves for speech in depth as reflected in the reading. You should be able to discuss where they arise, what they innervate, and what damage to each of the nerves might produce.
A

Trigeminal Nerve (V)=

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7
Q
  1. What is the phrenic nerve? Is it cranial or spinal? What purpose does it serve?
A

The most important nerves of respiration, provides the motor innervation of the diaphragm. It is a spinal nerve, damage will paralyze the diaphragm

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8
Q
  1. What are some causes of flaccid dysarthria?
A

physical trauma, brain stem CVA, Myasthenia gravis, Guillain-Barre’ Syndrome, Polio, Tumors, Muscular Dystrophy, Progressive bulbar palsy. Physical trauma may result from surgical trauma or may be a result of direct injury to the head and neck.

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9
Q
  1. What are some common speech characteristics of flaccid dysarthria?
A

Hypernasality, Imprecise consonants, breathiness, mono pitch, nasal emission, audible inspiration, harsh vocal quality, short phrases, and mono loudness.

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10
Q
  1. What types of treatments are available for flaccid dyarthria?
A

Treatments are grouped according to which cranial nerve or combination of nerves are damaged.

Trigeminal (V)= unilateral damage typically has a negligible effect on speech production.
Bilateral damage: rare diagnosis, can leave jaw muscles on each side of the face very weak or in severe cases, causes inability to close jaw.
Treatment: jaw sling, splinting, or Kinesio Taping to improve placement of jaw and bring articulators into contact with each other for speech production

Vagus (X)= damage to this nerve also affects glossopharyngeal and accessory cranial nerves due to their close proximity to each other. Damage may result in disorders or resonance, phonation, and prosody.
Treatment for Resonance: surgical treatments (flap, augmentation), palatal lifts, velar strength-training via CPAP, modifications of speech via reduced rate, more open position mouth during speech, and increasing loudness.
Treatment for Phonation: pushing and pulling exercises, holding breath, head turn to weak side, lateral pressure on the larynx, ENT referrals for vocal fold injections/augmentation
Treatments for Prosodic Events: pitch range exercises, contrastive stress drills, chunking utterances into syntactic units (breathe when normal pauses would occur)

Facial (VII) and Hypoglossal (XII)= damage often impacts speech production by decreasing labial strength and range of movement. Traditional articulation drills are often recommended
Treatment for Respiratory Weakness= correct posture, speaking immediately on exhalation (breath curve), complete inhalation via diaphragmatic breathing, EMST150(Expiratory Muscle Strength Trainer)

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11
Q
  1. What percent of their maximum forces do the tongue and lips use for speech?
A

10-30

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12
Q
  1. What two symptoms, when combined, are a strong confirmatory sign that flaccid dysarthria is the correct diagnosis?
A

hypernasality and phonatory incompetence

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13
Q
  1. What are some surgical treatment options available for damage to the vagus nerve?
A

Pharyngeal Flap Procedure- a flap of tissue from the pharynx is surgically attached to the velum. As a result much of the velopharyngeal port is closed by this attached flap of tissue. The sides of the flap are left loose to provide an opening between the oral and nasal cavities for nasal breathing and nasal speech sounds.

Posterior Pharyngeal Wall Augmentation- teflon paste or hyaluronic acid is injected into the pharynx at the point where the velum normally makes contact when it is elevated. The injection creates a bulge at the point on the pharynx and lessens the distance the velum must elevate before velopharyngeal closure is completed

Palatal Lift- essentially a dental retainer that has a rear extension that helps push upward on the velum, it can aid in the elevation of the velum during speech

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14
Q
  1. Describe Mysathenia Gravis?
A

Disease process that affects the neuromuscular junction (point where the nerves meet the muscle tissue) Caused by antibodies that block/damage muscle tissue. Characteristic symptom is rapid fatigue of muscular contractions over short period of time with a recover after rest.

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15
Q
  1. What is a feature that distinguishes flaccid from spastic dysarthria? Consider site of lesion.
A

Flaccid is lower motor neurons and spastic is upper motor neurons. Spastic is BILATERAL damage to the upper motor neurons

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16
Q
  1. What causes spastic dysarthria?
A

bilateral damage to the UMN

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17
Q
  1. Name some possible causes of spastic dysarthria
A

stroke, ALS, TBI, MS

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18
Q
  1. Which of the five components of speech is typically not as affected in spastic dysarthria?
A

respiration

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19
Q
  1. What is the most common articulation disorder in spastic dysarthria?
A

Imprecise consonant production is the most common due to abnormally short vocal onset time for voiceless consonants, incomplete articulatory contact and incomplete consonant clusters/blends

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20
Q
  1. What is pseudobulbar affect?
A

uncontrollable laughing or crying that can accompany damage to the UMNs of the brain

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21
Q
  1. What is bulbar palsy?
A

atrophy and weakness in the muscles innervated through the medulla. Caused by damage to the LMN

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22
Q
  1. What is pseudobulbar palsy?
A

means weakness and slowness in the same muscle, caused by the UMN

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23
Q
  1. Would one expect hypernasality to be more severe in spastic or flaccid dysarthria? Why?
A

More severe in Flaccid, NOT DONE

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24
Q
  1. What might effective treatment of spastic dysarthria include?
A

Should target phonation, articulation, prosody and resonance.

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25
Q
  1. What might phonation treatments in spastic dysarthria include?
A

musculoskeletal relaxation exercises, easy onset of phonation rather than hard glottal attack and yawn-sigh exercises

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26
Q
  1. Describe tongue stretching exercises.
A

the clinician gently grasps the patients tongue with a gauze pad and carefully pulls it straight forward until resistance is felt. This position is held for 10 seconds. The tongue is then gently pulled to the left or right side of the mouth and again held for 10 seconds. These stretches are good for increasing strength, speed, and accuracy of tongue movements . More examples include: elevating the tongue tip up to the nose, lower the tongue tip toward the chin, and hold the tongue at the corners of the mouth
pg. 157-8

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27
Q
  1. Is drooling a non speech finding in spastic dysarthria? Why or why not?
A

yes, caused by impaired oral control of saliva and/or a less frequent trigger of the swallow

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28
Q
  1. What are some exercises that might be helpful in monopitch/monoloudness?
A

pitch range exercises, contrastive drills, chunking utterances into syntactic units (breathing when normal pauses would occur)

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29
Q
  1. Discuss how a single brainstem stroke may cause spastic dysarthria.
A
  1. when two or more CVA’s occur in certain combinations in the cerebrum
  2. a single CVA occurs in the brain stem where the neural fibers of each pathway are extremely close in proximity
  3. a single CVA occurs in one hemisphere and a preexisting condition has previously damaged the pyramidal and extrapyramidal tracts of the opposite hemisphere
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30
Q
  1. When was UUMN dysarthria “discovered”
A

researched in the 1980s

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31
Q
  1. Define UUMN dysarthria.
A

a MSD caused by damage to the UMNs on a single side of the brain that supply the cranial and spinal nerves involved in speech production

32
Q
  1. What is the neurological bases of UUMN dysarthria?
A
  1. most cranial nerves serving the speech muscles, except the lower face and tongue, receive bilateral innervation from UMNs.
  2. Thus motor speech deficits after unilateral UMN damage are typically less severe than when bilateral damage occurs.
    The affected side will demonstrate:
    paresis or paralysis with facial asymmetry/facial droop
    slowed movements
    reduced range of motion of lower face and tongue
    tongue may deviate to the affected side
  3. unilateral UMN damage appears to impact the function of bilaterally inervated structures
33
Q
  1. What is the most common cause of UUMN dysarthria?
A

CVA/stroke, brain tumors, and traumatic brain injury

34
Q
  1. Discuss brain tumors in relation to causing UUMN. Be able to read scenarios and identify if the tumor would cause UUMN or not.
A

Not a common cause, brain tumors can cause focal, unilateral UMN damage resulting in this type of dysarthria
1. tumors may themselves destroy the UMN
2. tumors may cause pressure or edema (swelling)
3. tumors may cut off the arterial blood supply to portions of the brain

35
Q
  1. What serverity is typically ascribed to UUMN dysarthria?
A

mild to moderately impaired.

36
Q
  1. What does UUMN typically co-occur with?
A

dysphagia, aphasia, apraxia, limb hemiparesis, visual deficits, or cognitive-linguistic impairments

37
Q
  1. Why might UUMN with a co-occuring language deficit be difficult to diagnose?
A

patient output may be limited, the dysarthria may take a “back seat” to other deficits.

38
Q
  1. Which of the speech components is most often affected with UUMN?
A

articulation

39
Q
  1. What does UUMN damage typically affect in terms of the face, tongue, etc.
A

tongue and lower face

40
Q
  1. What articulation deficit is the most common in UUMN?
A

imprecise consonant production

41
Q
  1. What is the reason for the harsh vocal quality in UUMN?
A

the larynx can be affected by unilateral UMN damage, despite being bilaterally innervated by the Vagus (X) nerve

42
Q
  1. What is the likely cause of prosodic deficits in UUMN?
A

not usually impacted, when prosody is affected the most likely cause is a slowed rate of speech

43
Q
  1. What are some tasks that provide valuable diagnositic information for UUMN?
A

oral mech exam, AMR tasks, prolonged vowels, sentence repetition or reading, conversational speech, picture description, and passage reading

44
Q
  1. What are some treatments for UUMN?
A

traditional arctic drills:
recommended for imprecise consonant productions
focus is on increasing the patients awareness of their articulation errors and practicing best phoneme productions
may include intelligibility drills, training of phonemic placement, exaggeration of consonants, and minimal contrast drills
Treatment for phonation:
weakness of the vocal folds
pushing and pulling exercises
holding breath to facilitate greater adduction
head turn to weak side
chunking utterances into syntactic units (breath when normal pauses would occur)
ENT referrals for vocal fold injections/augmentation
Treatment for Spasticity:
musculoskeletal relaxation exercises
easy onset of phonation rather than hard glottal attack
yawn-sigh exercise

45
Q
  1. What are some treatments for UUMN?
A
46
Q
  1. What is the neurological site of lesion for ataxic dysathria?
A

the cerebellum

47
Q

What is the neurological site of lesion for ataxic dysathria?

A
48
Q
  1. What speech components are most affected with ataxic dysarthria?
A

articulation and prosody, often sounds like “drinken speech”

49
Q
  1. What part of the nervous system is the cerebellum typically assigned to? Motor? Sensory?
A

motor

50
Q
  1. Differentiate between the inferior, middle, and superior cerebellar peduncles.
A

inferior: allows the cerebellum receive sensory information from the entire body about position of its body parts in space, recognize what the body is doing during movement, and whether a motor impulse to the muscles is accomplishing the intended result, monitoring timing and force of movements while performed, transmits sensory information from the body to the cerebellum

middle: the largest of the peduncles, allows the cerebellum to receive preliminary information from the cortex regarding planned movements, coordinate planned movements by integrating sensory information from the body with am individuals experience of what appropriate movement should be, smoothing and refining according to current conditions, transmits planned movements from association cortex to the cerebellum

Superior: allows the cerebellum to provide output through one main channel to the PNS, send its processed motor impulses to motor areas of cortex, completing corticocerebellar control circuit, transmits commands to the cortex and extrapyramidal system

51
Q
  1. What are the cerebellar control circuits?
A

neurons that course through these 3 cerebellar pathways, they often synapse with the true UMNs or interneurons of the brain stem and spinal cord

52
Q
  1. How does the cerebellum influence speech production?
A
  1. the corticocerebellar speech movements are sent from the cortex to the cerebellum
  2. the cerebellum then coordinates and refines preliminary movements based on sensory information received from the body and prior knowledge
  3. coordinated motor impulses are then sent to the thalamus to be refined further before being sent to motor the cortex and the muscles
  4. Cerebellar connections to the extrapyramidal system, makes rapid adjustments in the timing and force of movements to compensate for unexpected changes in circumstances of movement
53
Q
  1. Name some causes of the ataxic dysarthria.
A

damage to the cerebellum or its control circuits can result in a variety of movement disorders that are accompanied by dysarthria

the coordination of speech movement is highly dependent on the midpoint of the cerebellum between the 2 hemispheres, known as the vermis

most often a result of generalized damage to the cerebellum, though some studies have suggested that focal damage may also cause the motor speech disorder.

Degenertive diseases: Autosomal dominate cerebral dysfunction of late onset, Idiopathic sporadic late-onset cerebral ataxia, Friedrich’s ataxia, Olivopontocerebellar degeneration

CVA/stroke, toxic conditions, TBI, tumors, viral infections, bacterial abscess

54
Q
  1. What is the most prevalent speech error in ataxic dysarthria?*** this question’s wording is wrong (question #58)
A

primarily a disorder of articulation and prosody
Artic: imprecise constant production is the main prevalent speech error. Distorted vowels are the second most frequent error. Irregular articulatory breakdowns are imprecise constant and vowel productions which vary from utterance to utterance

55
Q
  1. What are the prosodic deficits present in ataxic dysarthrias?
A

6 prominent prosodic errors

  1. equal or excess stress: a predominate and distinguishing characteristic of ataxic dysarthria
  2. Prolonged phonemes and prolonged intervals between phonemes: seen in slowed production of both single and repetitive motion tasks; secondary to hypotonia of speech musculature
  3. Monopitch and mono loudness: secondary to hypotonia of the speech musculature
56
Q
  1. Discuss phonation of individuals with ataxic dysarthria.
A

harsh vocal quality caused by decreased muscle tone in the laryngeal and respiratory structure which prevents the full contraction of these muscle groups

vocal tremor: far less common, though has been observed within some cases

57
Q
  1. What are some key evaluation tasks for ataxic dysarthria?
A

AMR tasks, sentence completion or reading, conversational speech, picture description, passage reading, each of the tasks will contain multisllabic words and will allow for the symptomolgy associated with ataxic dysarthria to come to the forefront

58
Q
  1. What do patients needing work on respiration deficits due to ataxic dysarthria benefit from?
A

focus on controlling airflow more accurately during speech tasks, as uncoordinated/paradoxical movements of the respiratory muscles cause the patient to speak on residual air

treatment interventions to improve breath control during speech
1. slow and controlled exhalation
2. speak at peak of inhalation/immediatly on exhalation
3. cease phonation early to prevent speaking on residual air
4. optimizing the breath-teaching how many syllables or words can be said clearly on one full inhalation

59
Q
  1. What do patients with ataxic dysarthria need work on regarding prodosy?
A

rate, stress, and intonation.

60
Q
  1. What do patients with ataxic dysarthria need work on regarding prodosy?
A
61
Q
  1. How is hypokinetic dysarthria unique?
A

it is the only dysarthria that displays increased rate as a symptom,
it is mainly attributed to one causative factor: Parkinsonism

62
Q
  1. What are some parkinsonism symptoms that have the greatest affect on speech?
A

most errors are in prosody and articulation
most errors are due to bradykinesia (reduced range and speed) amnesia (delayed initiation), and muscle rigidity. In severe cases, tremors may cause tremulous phonations

63
Q
  1. What causes parkinsonism sysmptoms (where is the site of lesion)?
A

damage to the basal ganglia control circuit of the extrapyramidal system.

64
Q
  1. Discuss rigidity and spasticity.
A

rigidity: resistance to passive movement
spasticity: increased tone of muscle fibers

65
Q
  1. What are some primary symptoms of parkinsonism?
A

resting tremors primarily of fingers and hands “pill rolling”
bradykinesia: slowed speed of movement
rigidity: resistance to passive movement
spasticity: increased tone of muscle fibers
akinesia: delayed initiation of movements, under activity of movement “freezing”
disturbed postural reflexes of balances and movement
masked faces
festering gate
micrographia

66
Q
  1. What makes up the striatum?
A

the putamen and the caudate nucleus

67
Q
  1. What are two neurotransmitters that the basal ganglia depend upon for balanced interaction?
A

dopamine (inhibitory) and acetylcholine (excitatory)

68
Q
  1. What is the primary cause of hypokinetic dysarthria?
A

dysfunction of the basal ganglia, dopamine is produced in the substancia nigra, a grouping of gray matter cells that are located adjacent to the striatum.
the dopamine is then used by the stratum to refine and slow neural activity
a reduction of dopamine in the striatum causes a neurotransmitter imbalance
too much acetylcholine (excitatory) is believed to be the primary cause cause of rigidity, bradykinesia, and other various symptoms of Parkinsonism

the reduction of dopamine is secondary to multiple causes/factors

69
Q
  1. What percentage of cases are L-dopa treatments successful for?
A

pg. 220

70
Q
  1. In what percentage of cases does idiopathic Parkinson’s disease does dementia occur?
A

present in 8% to 30% of cases

71
Q
  1. What form of parkinsonism is most likely to be present in children?
A

post encephalitic Parkinsonism, it is caused by viral encephalitis

72
Q
  1. Discuss stroke and parkinsonism.
A

a single stroke can affect the basal ganglia and cause the sudden onset of Parkinsonian symptoms, but it is rare. Such a stroke would results on symptoms on the side of the body opposite the lesion with the majority of cases showing improvement over time. More likely to be seen in a person that has had multiple strokes

73
Q
  1. List some of the common speech characteristics of hypokinetic dysarthria.
A

mono pitch, reduced stress, mono loudness, imprecise constants, inappropriate silences, short rushes, harsh voice quality, breathy voice, pitch level and variable rate

74
Q
  1. What are the three categories of treatment for hypokinetic dysarthria?
A

pharmacological, surgical, and behavioral

75
Q
  1. Discuss L-Dopa and its impacts on speech.
A

has the least effect on the speech disturbances associated with this disorder.

76
Q
  1. What is Delayed Auditory Feedback
A

“feeds” the patient their own voice after a short delay, the literature is mixed on the usage oof such a device

77
Q
  1. What is Deep Brain Stimulation?
A

Clinical Methods (3 decks)

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