1.  What are the characteristics of Flaccid D?
2.  What are the cranial nerves of Speech productions and why are they important?
3.  What are common causes for cranial nerve damage
4.  Know each of the nerves.
 Where in the brain stem does the N. originate? What muscles are innervated? If it branches, what are the branches and effects of damage for each branch.  What happens with unilateral damage and with bilateral damage? Where does the muscle deviate (weak or strong side)? Is there a “test” that cues us as to which N is damaged?  Give speech characteristics of the damaged N if provided.
5.  Be able to explain the etiologies. Know the speech characteristics if given.
6.  Variations in speech characteristics occur in individuals with dysarthria.  Explain how we can go about identifying the dysarthria?
7.  Describe the speech characteristics of flaccid dysarthria. What causes the error?
8.  What is a confirmatory sign for flaccid dysarthria?
9.  How do you determine whether a person with flaccid dysarthria who has air wastage is due to a problem with weakened respiration or poor laryngeal valving?
10.  What is the disagreement regarding oral strengthening exercises for flaccid dysarthria?  What are some oral strengthening exercise for damage to each of the nerves? What are treatment options to improve speech for damage to the various nerves?

Flaccid Dysarthria

1.  What are the characteristics of Flaccid D?
Characteristics:
Caused by impairments of the lower motor neurons in the cranial or spinal nerves or sometimes called the final common pathway (Damage to the peripheral nervous system)
Weakness in the speech or respiratory musculature

2.  What are the cranial nerves of Speech productions and why are they important?
Trigeminal, facial, glossopharyngeal, vagus, accessory, and hypoglossal  The lower motor neurons inside these nerves transmit motor impulses from the upper motor neurons to the muscles used in speech production.  If a cranial nerve is damaged, the motor impulses it sends to the muscles may be distorted or stopped completely and will affect the accurate production of speech.

3.  What are common causes for cranial nerve damage:  brainstem stoke (disrupting blood flow to the cell bodies of its LMN, tumors, viral or bacterial infection, physical trauma, surgical accidents.

4.  Know each of the nerves.
 Where in the brain stem does the N. originate? What muscles are innervated? If it branches, what are the branches and effects of damage for each branch.  What happens with unilateral damage and with bilateral damage? Where does the muscle deviate (weak or strong side)? Is there a “test” that cues us as to which N is damaged?  Give speech characteristics of the damaged N if provided.
Nerves:
Trigeminal N.
Pons
 Ophthalmic
 Maxillary
 Mandibular:innervates masseter, pterygoid, mylohyoid (elevate and lower jaw)
   Tensor veli palatine: elevates velum

 Unilateral damage: weakness of jaw/velum on the same side as the damage.
 Jaw deviates toward the affected side when opened.  Unilateral damage usually  doesn’t cause speech problems because the unaffected side is strong enough to  compensate
 Bilateral damage: can’t raise jaw to produce consonant and vowel phonemes   (bilabial, linuadental or linguapalatal) rate of speech is slowed; Hypernasality  may occur if the veli palatine is damaged

Facial Nerve (VII) Pons right below the Trigeminal N
 Two branches
  Cervico facial (lower face: buccal, lingual, mandibular
  Temporofacial: upper face:  temporal and zygomatic brance
 Damage before the split into the two branches—entire face on the same side as  the lesion.  All muscles on the same side of the face as the damage will have some  weakness/paresis (facial drooping)
 Damage to just one branch: only that part will be affected, i.e,. only bilabials  labiodentals, and muscles of the lips

 Upper motor neuron
 Upper motor neuron innervation of the facial nerve:
 Unilateral damage:  upper face in tact because it is innervated by both sides of the  brain.  Lower face is damaged however because it only receives information from  the opposite side of the brain.  If lower face is notably weak (cheek and mouth)  then that means unilateral upper motor damage of the opposite side. (Upper motor  neuron dysarthria)
 Bilateral damage:  upper face will not be able to wrinkle.

Glossopharyngeal nerve IX
 Medulla to pharynx to innervate stylopharynx and superior pharyngeal constrictor (elevation and opening of upper pharynx) .  Gag reflex is one way of assessing this nerve. Probably affects speech production simply because it affects the shaping of the pharynx into various positions when producing speech sounds.

Vagus X
One of he most important Origin in the medulla just below the glossopharyngeal N.
From the medulla …long with branches serving the larynx, intestines, hear, velum.
For speech, the pharyngeal branch, the external superior laryngeal branch and the recurrent N
 Paryngeal Branch: motor innervation to the uvulae, levator veli palatine,  salpigopharyngeus, palatopharyngeus, and superior and middle pharyngeal
 constrictor.
 Unilateral Damage: affects velum, unilateral damage usually doesn’t hurt speech  because the other side will compensate.  Bilateral damage: significant  hypernasality because nearly all the muscles of the velum will demonstrate  weakness.  Pressure consonants may be distorted with nasal emissions.

 External Superior Laryngeal Branch: Innervates the cricothyroid muscle of the  larynx which stretches and tenses the VF affecting pitch. Unilateral damage  produces minimal difficulty in varying pitch. Bilateral damage: decreased  loudness, increased breathiness and notable difficulty in changing pitch.
 Recurrent Nerve branch:  supplies innervation to all the intrinsic muscles of  adduction/abduction of the larynx except the cricothyroid.  Unilateral damage will  cause one focal fold to be paralyzed in the paramedian position.  Will have  breathy phonation and decreased loudness.  Bilateral damage: phonation on  inhalation: stridor, paresis of both folds in the paramedian position.  The voice  will be breathy and hoarse.

 Accessory N. (XI) not a pure cranial nerve. Originates in the medula below the  vagus. Helps innervate the intrinsic muscles of the velum, pharynx, and larynx.  Spinal components of the accessory supply innervation for the  sternocleidomastoid and trapezius  Very integrated with Vagus N.

 Hypoglossal Nerve (Xii)  Originates in the medulla and courses to the tongue. Provides motor innervation for he intrinsic and most of the extrinsic muscles o the tongue.
 Unilateral damage of hypoglossal cranial nerve: weakness in half of the tongue on the same side as the damage.  When the tongue is protruded, it will deviate toward the affected side. Bilateral damage: overall weakness, the range of the tongue will be reduced.
Damage to upper motor neurons: will result in weakness in the opposite of the tongue (receives unilateral innervations).  Characteristics:  imprecise articulation.  With unilateral damage: distortion will be mild, because the unaffected sides can compensate.  With bilateral: significant articulation problems.  Difficulty elevation of tip or back of the tongue, notable distortion, Slow lingual movements.

Spinal nerves:  provide innervation to muscles of respiration
Phrenic nerve provides innervation to the diaphragm.
Damage to cervical and thoracic spinal nerves can affect respiration and therefore speech.
Impaired respiration: decreased loudness (reduced subglottal air pressure).  Shortened phrasing that can affect prosody producing a breathy or stained vocal quality (speaking on residual air)

5.  Be able to explain the etiologies. Know the speech characteristics if given.
Etiologies
Flaccid dysarthria can be caused by anything that disrupts the flow of motor impulses along the cranial or spinal nerves that innervate the muscles of speech production.  Can occur anywhere along the course of lower motor neurons, from the cell bodies in the brainstem to the neuromuscular junction

Physical Trauma:
Surgical trauma, head injury and neck injury (34%)
 Surgical:  carotid endarterectomy (removal of plaque in the carotid artery),  cardiac surgery; removal of head and neck tumors, and dental surgery.
 Motor vehicle accidents (broken bones may compress or cut one of the cranial  nerves; rotational forces can twist or stretch a nerve enough to cause damage

Brainstem stroke:
CVA (occurs when the blood flow to the brain is interrupted because an artery breaks or is blocked).  When a stroke occurs in one of the brainstem arteries, the neurons serving that artery can be destroyed.  The cell bodies of lower motor neurons are located within the brainstem. The degree of impairment depends on the number of lower motor neurons that are lost to a stroke.  If many of the cranial nerve’s motor neurons are affected, numerous muscles innervated by that cranial nerve will be weakened or paralyzed.
A single brainstem stroke can damage more than one cranial nerve (the cranial nerve nuclei of the glossopharyngeal, vagus, and accessory nerves are close.)

Myasthenia Gravis:
Affects the neuromuscular junction which is the point where lower motor neurons meat muscle tissue. Symptom of MG is rapid fatigue of muscular contractions over a short period of time, with recovery occurring after rest.
Cause:  antibodies that cause damage to the muscle tissue that receive the neurotransmitter acetylcholine (which triggers a muscular contraction) from the lower motor neurons. With the loss of too many acetylcholine receptors, the muscle is not able to use all of the acetylcholine being produced by the motor neuron: result: fatigue and weakness but with rest the muscle can again make efficient use of the acetylcholine and stronger contractions occur.
Speech characteristics:  hypernasality, decreased loudness, breathy voice quality and decrease articulatory imprecision during prolonged speaking.  Use stress test to diagnose

Guillain-Barre Syndrome
Results in the progressive inflammatory loss of the myelin sheath around axons (demyelination).  Frequently occurs after certain kinds of infections and immunizations.  Usually in the PNS and tends to affect motor rather than sensory neurons. Progression is rapid(days/weeks). Complaints of weakness and numbness in the limbs (early symptom).  Flaccid dysarthria and dysphagia occur once demyelization affects the cranial nerves.  Recover good.  5% die in acute stages.

Polio
Infectious viral disease that attacks the cell bodies of the lower motor neurons.  Unvaccinated individuals can become infected after close contact with a recently vaccinated child. It affects cervical and thoracic spinal nerves which often results in isolated respiratory weakness causing labored inhalations during speech, shortened speech phrases, speaking on residual air and decreased loudness. Polio can also affect cranial nerves and can damage the lower motor neurons in the V, VII, XII, and X nerve.(10-15%) causing weakness in the muscles innervated by those nerves.

Tumors- growing in the neck or any oralfacial structure can affect functioning

Muscular dystrophy: progressive degeneration of muscle tissue can result in weakness in the muscles served by the cranial nerves (tongue face, and pharynx)

Progressive bulbar palsy: affects both upper and lower motor neurons, although it often is present only in LMN.  If only in LMN Faccid dysarthia if both upper and lower Mixed Dysarthria of Flaccid-spastic type.

6.  Variations in speech characteristics occur in individuals with dysarthria.  Explain how we can go about identifying the dysarthria?  It is important to look for clusters of symptoms.  Once a cluster has been identified determine the type of dysarthria it most closely represents.

7.  Describe the speech characteristics of flaccid dysarthria. What causes the error?
See table 4-1

Resonance: Primarily reflects bilateral damage to the pharyngeal branch of the Vagus N. because it innervates most of the muscles of the velum
What is the most noticeable speech error?  Hypernasality is an important diagnostic marker for flaccid dysarthria.  It is more noticeable in Flaccid d. than in other types of D.
Nasal emissions due to incomplete velopharyngeal closure
Weak pressure consonants caused by decreased intraoral air pressure
Shortened phrases: wasted air that escapes through the nasal cavity
Question: A person exhibits pronounced hypernasality.  What dysarthria and what nerve is probably damaged?

Articulation:
Imprecise consonant production caused by damage to facial nerve and hypoglossal nerves.  Bilateral damage to the face can have significant effect on the production of bilabial and labiodental phonemes as well as with consonant and vowels requiring lip rounding.  Bilateral damage to the hypoglossal nerve will result in misarticulations of the phonemes requiring the elevation of the tongue, especially the tongue tip. Can affect lingupalatal phonemes and in severe cases linguavelar phonemes. /l, j, and in severe cases).
Questions:
A person exhibits articulatory imprecision in producing the /l and j/.  What nerve is affected?
A person exhibits difficulty producing /p,b, and f,v/ what nerve is affected?

Phonation
Phonatory incompetence: incomplete adduction of VF due to damage to the recurrent branch of the Vagus N. which innevervates all the intrinsic muscles of the larynx.
Result: paralysis of adductor and abductor muscles
 Adductor: breathy voice quality; Abductor:  can’t open all the way so audible  inhalation.
8.  What is a confirmatory sign for flaccid dysarthria?
***Prominent Hypernasality or phonatory incompetence is a confirmatory sign for flaccid dysarthria.  But together (hypernasality with phonatory incompetence) is the strongest sign.

Respiration: may or may not be a component.  If the cervical and thoracic spinal nerves (diaphragm or intercostals) are affected, result can be decreased inhalation or impaired control of exhalation causing insufficient amts of subglottal air pressure for speech—reduced loudness and shortened phrase length.  If speaking on residual air—strained vocal quality.  This affects prosody.  In addition, weak respiratory:  can produce monoloudness and monopitch.

9.  How do you determine whether a person with flaccid dysarthria who has air wastage is due to a problem with weakened respiration or poor laryngeal valving?

When you have reduced loudness, shortened phrase length and strained vocal quality, frequent inhalations determine the cause.
 1.  coughing  and glottal stop.
Feeble cough may indicate either poor respiration or poor valving.
Poor cough strong glottal stop: respiration because producing a sharp glottal stop doesn’t take that much air.

Prosody:
Monoloudness and monopitch are a result of weakened laryngeal muscles. (cricothyroid/superior laryngeal N damage).  Monoloudness and pitch do not help make a definite diagnosis.

Keys:
1. Conversation: hypernasality, articulation, respiration and prosody affected
2.  AMR- slowed
3.  Prolonged vowel breathy (phonatory or respiratory)
4.  Stress test- myasthenia gravis

Treatment:

10.  What is the disagreement regarding oral strengthening exercises for flaccid dysarthria?  What are some oral strengthening exercise for damage to each of the nerves? What are treatment options to improve speech for damage to the various nerves

Trigeminal N.
Therapy probably needed only for bilateral damage
 Jaw strengthening
  1.  opening and closing the mouth fully
  2.  increasing strength of the closure using a resistance wedge
 Jaw sling
  A prosthetic device that supports the jaw and lifts it close to the maxilla to    achieve appropriate articulatory contact for the lower lip and tongue.

Facial N.
Decreasing lip strength and ROM for bilabial and labiodental phonemes.

 Lip strengthing:
  1.  Lip strengthening exercises using button and string.
 Lip puckering
  1. hold lips in that position
  2. move the pucker from side to side
 Holding a smile and resist forcing into a pucker

Vagus N./glossopharyngeal/accessory (very close together and difficult to separate the functions)
 Pharyngeal branch: velum (resonance deficits)
  Surgical
   1.  pharayngeal flap or
   2.  injection of material (gelfoam) that will causes a bulging of the      pharynx for the velum to contact
  Prosthetic:
   1.  Palatal lift (most used)
   Best candidates:  see pg 123
  Velar strengthening exercises:
   1.  questionable?
  Modification of Speech (reduces the perception of hypernasality)
   1.  increase loudness
   2.  reduce rate of speech (gives velum more time to reach target)
   3.  more open mouth position (sound comes out the mouth
    a.  increase awareness of hypernasality
    b.  read sentences with nasals and w/o nasals
    c.  look in mirror for jaw opening
    d.  use negative practice to see effects of open mouth on       hypernasality

 Recurrent laryngeal branch (phonation- intrinsic muscles of the larynx)
  Harsh breathy, because of inefficient vf adduction

  1.  Pushing/pulling procedures when speaking
  2.  Holding breath ?
  3.  Hard glottal attack when speaking
  4.  Head turning and sideways pressure on the larynx (head should be turned to the affected side or pushed toward the unaffected side. (either turn to or push the affected side) The weakened fold is brought to the strong fold.

 Superior laryngeal n damage- (prosody-cricothyroid muscle (pitch)
  1.  Pitch range exercises?
  2.  Contrastive stress drills (increasing loudness)
  3.  Chunking utterances into syntactic units for phrasing—inhalation    points

Hypoglossal N. (imprecise consonant production)
 1.  nonspeech strengthening exercises—no evidence of effectiveness
  a.  Tongue strengthening
   while looking in mirror:  push against tongue tip, sides of tongue     top of tongue and back of tongue with tongue blade while client     resists
 2.  Articulation
  a.  Intelligibility corrective feedback
  b.  Phonetic placement:
  *c.  Exaggerating consonants in medial and final position
  *d.  Minimal contrast drills

Treatments for respiratory weakness in Flaccid D.
 1.  Correct posture (may need prosthetic devices)
 2.  Compensatory – abdominal girdle and wraps—warning against continued use    (pneumonia); lap trays to lean on to help compress abdomen for forceful    exhalation.
 3.  Speaking immediately on exhalation to prevent air wastage
 4.  Cueing for complete inhalation for deeper inhalations;
 5.  To maximize the efficient use of subglottic air, do #3 and 4.