Neurogenic Voice Disorders
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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
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Vagus Nerve Branches
Superior Pharyngeal
Constrictor Muscle
Nucleus
Middle Pharyngeal
Ambiguus
Constrictor Muscle
Jugular
Foramen Pharyngeal Branch
Vagus Nerve
(x)
Superior
Laryngeal
Nerve
Inferior
Pharyngeal
Constrictor
Muscle
Recurrent
Laryngeal
Nerve
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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.
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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
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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
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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.
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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)
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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.
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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
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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)11
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
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Symptoms: SLN Lesions
• Loss of high pitches
• Instability in the upper range
• Breathiness and weakness
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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
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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
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Unilateral RLN Paralysis Symptoms
• Reduced airway
• Weak cough
• Reduced loudness
• Diplophonia
• Pitch breaks
• Breathy, hoarse quality
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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
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Lower Motor Neuron Disease: Bilateral
muscle weakness
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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
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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
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LMN Disease: Respiratory Disorders
• Weakness in respiratory muscles
results in:
-Reduced lung volume
-Reduced expiratory force
-Limitations in subglottic air
pressure
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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
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Management Strategies
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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
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• Alternative communication strategies
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)
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Spasmodic Dysphonia
• Perceptual Voice Signs & Symptoms:
– Adductor•
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•
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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
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Spasmodic Dysphonia
• Acoustic 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)
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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
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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)
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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
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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
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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
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Case # 3 (CD 1; Track 3)
– Aerodynamic findings•
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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: ?
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Case # 3: Adductor Spasmodic Dysphonia with Tremor
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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
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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
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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
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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
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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
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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)
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Pseudobulbar Palsy
• Acoustic Signs:
– Fundamental frequency= 124.1 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
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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
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Parkinson’s
• Primary Voice Symptom:
– Monopitch
• Description & Etiology:
– 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
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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:
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•
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Unknown
Linked to encephalitis lethargica
Slow-growing virus
Head trauma
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Parkinson’s
• Perceptual Voice Signs & Symptoms:
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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
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• Lower SNR
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
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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
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Masklike face
Hand tremor
Shuffling gait
Stooped posture
– Speech articulation was mildly imprecise
• Moderate decrease of prosodic quality
• Slow rate
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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
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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
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Case 9: Hypokinetic Dysarthria Secondary to Parkinson’s Disease
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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
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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, 30-47.
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