1. Neurogenic Voice Disorders

2. Innervation: Vocal Folds
Main Cranial Nerve: Vagus (X)
-Divides into left & right branches, then further divides into 3 branches,
1) Pharyngeal
2) Superior laryngeal
3) Recurrent laryngeal

3. Vagus Nerve Branches Vagus Nerve (x) Recurrent Laryngeal Nerve
Superior Pharyngeal
Constrictor Muscle
Nucleus
Ambiguus
Middle Pharyngeal
Constrictor Muscle
Jugular Foramen
Pharyngeal Branch
Inferior
Pharyngeal
Constrictor Muscle
Superior Laryngeal
Nerve
Vagus Nerve (x)
Recurrent Laryngeal
Nerve

4. Pharyngeal Branch Innervate pharyngeal middle constrictor
Subdivide & join branches from sympathetic trunk, external laryngeal & glossopharyngeal nerves= Pharyngeal plexus
Plexus supplies innervation to pharynx & muscles of velum
Lesions here result in:
adductor paralysis & velopharyngeal paralysis.

5. Superior Laryngeal Nerve Branches
Divide into internal & external branches
1) Internal laryngeal nerve:
-Divides further: upper & lower branches
Both provide afferent info (sensory)
1. Upper: Supplies mucous membranes of epiglottis & vestibule of larynx
2. Lower: Motor supply to CT
2) External laryngeal nerve:
Controls cricothyroid muscle

6. Recurrent Laryngeal Nerve Branches
Divides into right & left
1) Right & left recurrent nerves:
-Innervate all intrinsic muscles except the CT.
-Involved in sensory supply of subglottic mucous membranes

7. Branches of Vagus & Result of Lesion
Pharyngeal Branch: muscles of velum (levator & levator veli palatini) are affected one or both sides.
Superior Laryngeal Branch: CT muscle affected on one or both sides.
Recurrent Laryngeal Branch: All intrinsic laryngeal muscles are affected unilaterally or bilaterally resulting in fixed abduction position.

8. Lesions & Disorders Causing Hypoadduction
1) Lesions that damage vagal nuclei within the brainstem or “intramedullary”
-Lesion occurs after nerves leave the skull= “extracranial”
-Damage before leaving the skull but outside the brainstem itself= “extramedullary”
-All intra- & extramedullary and extracranial lesions occur before vagus separates into branches (RLN, SLN, pharyngeal)

9. Brainstem Lesions
1) Affecting nuclei of right and left vagus nerves:
-results in bilateral paresis or paralysis of pharyngeal & laryngeal muscles,
-affects sensory function,
-both folds may be involved and are abducted
-airway is without protection,
-fortunately unilateral lesions occur more than bilateral.

10. Symptoms A) Unilateral lesions: unilateral v.f. paralysis
breathiness and aphonia
tremorous vowel prolongation's
reduced loudness
reduced endurance
lowered pitch
diplophonia
hypernasal resonance
swallowing problems

11. Symptoms B) Bilateral lesions: bilat. v.f. paralysis open glottis
almost total absence of vibration
marked hypernasality
distorted pressure consonants
absent or weak cough
absent or weak gag reflex
dysphagia (nasal regurgitation on swallowing)

12. Superior & Recurrent Laryngeal Nerve Lesions
1) SLN & RLN:
-Do not create velar problems
-Result in all of the preceding laryngeal symptoms listed
-If the paralysis is complete, intracranial studies should be ordered by the physician
2) SLN alone or extracranial lesions:
-Affect CT muscle and impact on pitch
-Suspected when one fold lags in adduction

13. Symptoms: SLN Lesions Loss of high pitches
Instability in the upper range
Breathiness and weakness

14. Bilateral SLN Paralysis Symptoms
Thyroid cartilage will not tilt on the cricoid cartilage during phonation
v.f.’s appear short
v.f.’s appear bowed
Epiglottis overhangs the anterior part of the v.f.’s
Breathy or hoarse quality
Reduced loudness
Ability to alter pitch is impaired
Singing is difficult

15. Inferior RLN Lesions
Result in paralysis of all intrinsic laryngeal muscles of the larynx with the exception of the CT
CT assumes a compensatory function and adducts
Folds may be positioned at midline or paramedian position rather than in an adducted position

16. Unilateral RLN Paralysis Symptoms
Reduced airway
Weak cough
Reduced loudness
Diplophonia
Pitch breaks
Breathy, hoarse quality

17. Bilateral RLN Involvement
Major concern is maintenance of airway, not phonation
Folds approximate at midline
Voice may sound normal
Abductor muscles are paralyzed, serious respiratory distress occurs
Stridor during inhalation is common
Requires tracheotomy

18. Lower Motor Neuron Disease: Bilateral muscle weakness
Incomplete adduction of the folds
Bowing of folds
Inhalation stridor (as condition worsens)
Hypernasality
Nasal emission
Reduced loudness
Restricted pitch range
Breathy, hoarse quality
Tremor on prolonged vowels
Phonemic distortions

19. LMN Disease: Respiratory Disorders
May coexist with flaccid dysphonia
Lesions of cervical, thoracic or lumbar spinal nerves may result in weakness & atrophy of speech muscles & flaccid dysarthria
Lesions may result from: trauma, tumors, & myoneural junction disease

20. LMN Disease: Respiratory Disorders
Weakness in respiratory muscles results in:
-Reduced lung volume
-Reduced expiratory force
-Limitations in subglottic air pressure

21. LMN Disease: Voice Related Symptoms
Increased number of breaths per minute
Diminished tidal volume
Breathiness because of weak vocal fold adductors
Short breath groups
Inhalatory stridor if abductors can’t open glottis wide enough
Decreased loudness because of hypofunctional laryngeal valving
Dysphagia
Minimal intonation, stress, loudness variation

22. Management Strategies
Postural changes and support
Family counseling
Physical therapy
Respiratory therapy
Mechanical ventilation
Palatal lift prosthesis if VP inadequacy/flaccidity
Voice therapy to improve speech breathing and laryngeal adduction
Alternative communication strategies

23. Spasmodic Dysphonia Primary Voice Symptom: Strain/Struggle
Description & Etiology:
Focal dystonia affecting laryngeal muscle control
Occurs equally in women & men
Onset in middle aged
Onset: related to URI, traumatic emotional event, begins as mild hoarseness (may be rapid or take many years
Etiologies include: Psyhcogenic, neurological (basal ganglia)

24. Spasmodic Dysphonia Perceptual Voice Signs & Symptoms: Adductor-
Struggle & strain with intermittent voice stoppage
Hoarseness, harshness & tremor
Creaky, tense, choked
Perceptual- Strain/struggle, sudden interruption of voicing, loudness & pitch variation
Abductor-
Intermittent episodes of breathy phonation
Drops in pitch & vowel prolongation's
Perceptual- Delay of voice onset following voiceless consonant

25. Spasmodic Dysphonia Acoustic Signs: Measurable Physiological Signs:
Fundamental Frequency-
Adductor (women-162 Hz; men-134Hz)
Greater variation of fundamental frequency
Vocal Intensity-
Variation of amplitude
Reduced in conversation
Measurable Physiological Signs:
Airflow low & within normal limits (different studies)
Abductor-High
Adductor-Low
Pressure higher (13-14 cm H20)

26. Spasmodic Dysphonia Observable Physiological Signs: Laryngoscopy-
Larynx appears normal
During phonation, hyperadduction(adductor), Inefficient closure (abductor), bowed vocal folds
True & ventricular fold tremor
Stroboscopy-
Hard to visualize due to not being able to sustain phonation

27. Spasmodic Dysphonia Other Considerations: Other neurological signs-
Voice tremor
Jaw
Facial jerks
Hand or limb tremor
Hyperflexia
Sucking reflex
Asymmetries in the face or palate
Possible etiologies-
Brainstem abnormalities due to organic CNS disease which slows conduction within brainstem auditory pathway-
Patients show abnormal ABR (capacity of brainstem to conduct impulses is impaired)

28. Spasmodic Dysphonia Differentiating SD:
Similar features- SD, psychogenic dysphonia, musculoskeletal tension
History important & reveals differences
Psychogenic- stress, dysphonia clearly defined during stressful periods, variable (normal sometimes), respond well to voice therapy
SD- report increased stress since onset of dysphonia, minimal variability in normal productions, spasmodic not constant, do not respond well to voice therapy
Hyperfunction- consistent symptoms, do not vary phonemically, consistent vocal tension (not episodic), responds well to therapy

29. Case # 3 (CD 1; Track 3) History: 70 year old female
1 year history of progressive worsening dysphonia
Intermittent periods of voice arrest & a “Squeezing” sensation during conversational speech
Active participant in a family owned business
No smoking

30. Case # 3 (CD 1; Track 3) Examination Findings:
Oriented, no signs of language or cognitive impairment
Cranial nerve exam was unremarkable
Perceptually breathy voice quality
When asked to increase loudness- moderate-severe tremor and strain/strangled quality ensued
Acoustic Analysis-
Maximum phonation time= less than 5 seconds
Fundamental frequency= 165 Hz
Jitter= 1.3%
Shimmer= 0.84 dB
Harmonic-to-noise ratio= 6.5 dB

31. Case # 3 (CD 1; Track 3) Aerodynamic findings- Stroboscopic-
Mean airflow rate= 685 cc/sec (whispered)
Mean airflow rate= 23 cc/sec (when urged to phonate)
Subglottal pressure= 16 cm H20 (whispered)
Subglottal pressure= 22 cm H20 (when urged to phonate)
Glottal resistance= 20 cm H20 /lps (whispering)
Glottal resistance= 92 cm H20 /lps (when urged to phonate)
Stroboscopic-
small nodules on middle 1/3
Persistent chink in posterior glottis
Prolonged closure time
Diagnosis: ?

32. Case # 3: Adductor Spasmodic Dysphonia with Tremor

33. Case # 3 (CD 1; Track 3) Treatment Results-
10 sessions of voice therapy
Easy onset voice production
Increasing pitch
Humming
Sing song
Manual stabilization of the larynx
Visipitch for biofeedback
Unilateral Botox injections were recommended

34. Myasthenia Gravis Progressive neurological disease
Manifests itself in the muscles supplied by vagus nerve
Progressive flaccid weakness or paralysis elated to muscular effort
Initially when a patient reads or speaks for a long time, gradual decrease in control of muscles of the velum and larynx
Change from normal quality to hypernasal, breathy or hoarse

35. Management of Myasthenia Gravis
Corticosteroids
anticholinesterase drugs to improve the action of the neurotransmitter chemical acetylcholine
removal of thymus gland
adrenocorticotrophic hormone therapy
palatal lift prosthesis to compensate for velar inadequacy
voice therapy to increase hyperadduction if medical treatment does not work

36. Upper Motor Neuron Disorders: Supra or Pseudobulbar Palsy
Primary Voice Symptom:
Hoarseness or harshness
Description & Etiology:
Pyramidal & extrapyramidal tracts
2 major pathway systems that converge on lower motor neurons that control muscles of voice & speech
1) Damage to extrapyramidal (indirect pathway) results in spasticity & increased muscle reflexes
2) Damage to pyramidal (direct pathway) results in loss of function or skilled movements
Lesions may occur in both tracts as they are close in proximity
Effects to voluntary movement:
Spasticity, weakness, limitation of range, slowing movement

37. Pseudobulbar Palsy Description & Etiology (cont.):
Results from progressive lesions that occur bilaterally in the corticobulbar tracts
Lesions usually result of stroke, cerebral palsy, brain injury, multiple sclerosis & arteriosclerosis
Symptoms:
Difficulty with speech & swallowing
Emotional lability
Bursts of laughter or crying

38. Pseudobulbar Palsy Perceptual voice signs & symptoms:
Dysarthria of speech
Prosodic excess (excess rate & stress)
Prosodic insufficiency (monopitch, monoloudness, reduced stress, short phrases)
Articulatory-resonatory incompetence (imprecise consonants, distorted vowels, hypernasality)
Phonatory stenosis (harsh voice, strain/struggle, pitch breaks)

39. Pseudobulbar Palsy Acoustic Signs: Measurable Physiological Signs:
Fundamental frequency= Hz in men
equal or slightly higher than normal
Reduced variability of fundamental frequency
Reduced intensity variation
Measurable Physiological Signs:
Higher than normal subglottal pressure
Hypertonicity, strain/struggle
If breathy- Higher than normal airflow's
Slow opening & closing times, short closed time
inability to maintain sufficient muscle forces

40. Pseudobulbar Palsy Observable Physiological Signs: Laryngoscopy-
No laryngeal abnormalities
Vocal fold hyperadduction may be visible
Stroboscopy-
Reduced vocal fold amplitude
Diminished mucosal wave
Excessive glottal closure
Asymmetry, aperiodicity

41. Parkinson’s Primary Voice Symptom: Description & Etiology: Monopitch
Progressive, degenerative disease of the central nervous system affecting basal ganglia (substantia nigra)
Decrease in dopamine in caudate nucleus & putamen
Results in rigidity, resting tremor & reduced range of movement in the limbs, neck & head
Absence of facial expression
Decreased initiating movement of command

42. Parkinson’s Description & Etiology (cont.):
Muscles not paralyzed but hypokinetic
Respiratory movements impaired- Shallow, irregular breathing cycle
Limited vital & inspiratory capacity
Affect the ability to produce normal loudness & length speech
Causes:
Unknown
Linked to encephalitis lethargica
Slow-growing virus
Head trauma

43. Parkinson’s Perceptual Voice Signs & Symptoms: Acoustic Signs:
Monopitch
Excessively low pitch
Harshness
Variability of loudness & rate
Caused by muscle rigidity & hypokinesia
Acoustic Signs:
Fundamental frequency within the normal range
Greater variation of fundamental frequency in sustained vowels
Higher jitter values
Lower SNR

44. Parkinson’s Measurable Physiological Signs:
Higher activity in the interarytenoid & posterior cricoarytenoid muscles
Greater activity in lip muscles
Observable Physiological Signs:
Laryngoscopy-
Diminished vocal fold movement
Bowed vocal folds
Greater amplitude
Stroboscopy-
Mild glottal incompetence
Tremor
Abnormal phase closure & phase symmetry

45. Case 9 (CD 1; Track 9) History: 72 year old male
12 month history of progressive dysphonia
18 months ago he was diagnosed as having Parkinson’s disease
Masklike face
Hand tremor
Shuffling gait
Stooped posture
Speech articulation was mildly imprecise
Moderate decrease of prosodic quality
Slow rate

46. Case 9 (CD 1; Track 9) Examination Findings:
Perceptually: Moderately hoarse-breathy quality & volume was markedly reduced, pitch variations were undetectable
Maximum phonation time was WNL
Acoustic-
Fundamental Frequency= 244 Hz
Jitter= .87%
Shimmer= .65 dB
Harmonic to noise= 6.9 dB
Aerodynamic-
Mean airflow rate= 336 cc/sec
Subglottal pressure= 9 cm H20
Glottal resistance= 7.6 cm H20/lps

47. Case 9 (CD 1; Track 9) Stroboscopic-
Mild atrophy of left vocal fold
Persistent glottal incompetence
Elliptical shaped chink in middle third of vocal folds
Moderate stiffness
Diagnosis: Hypokinetic dysarthria secondary to Parkinson’s
Voice therapy 2 x per week was recommended

48. Case 9: Hypokinetic Dysarthria Secondary to Parkinson’s Disease

49. Case 9 (CD 1; Track 9) Treatment Results: 15 voice sessions
Increasing laryngeal resistance & loudness control utilizing various vocal fold medialization techniques
Pushing on arms of chair, pulling up on bottom of chair, squeezing palms of hands together and simultaneously producing voice
Visipitch- Vocal loudness biofeedback
Isolated vowel efforts, single words, phrases, sentences & conversational speech

50. Readings Colton & Casper: Ch. 5 Next Directed Reading (For:10/21/99):
Verdolini-Martson, K., Sandage, M., & Titze, I. (1994). Effect of Hydration Treatments on Laryngeal Nodules and Polyps and Related Voice Measures, Journal of Voice, 8,