Neurogenic dysphonia

Neurogenic Dysphonia: Topics Neurology of the larynx Organizational Framework Selected Disorders Vocal fold paresis/paralysis Essential Tremor Spasmodic Dysphonia Selected Central Nervous System Disorders

UW-MadisonNeuro Website

Nerve supply to Larynx

Nerve supply to Larynx

Relation of nerves to thyroid gland

Neurologic Voice Disorders: A Classification Scheme Hypoadduction Hyperadduction Phonatory Stability

Short term Long term

Phonatory Incoordination/Voiced-voiceless Mixed Miscellaneous

(Ramig & Scherer, 1992)

Vocal Fold Paresis/paralysis

Causes of vocal fold paralysis/paresisCentral Medullary lesions affecting nucleus ambiguus

Peripheral (Vagus nerve lesions) Disease (tumors of lung, esophageal, thyroid) Surgical trauma (thyroid, anterior cervical spine, lung resection, carotid

artery Sx) Nonsurgical trauma (penetrating wounds, blunt trauma) Neurological disease (Guillain-Barre, ALS) Peripheral neuropathy

Idiopathic Diagnosis of exclusion Often presumed viral

Degree of involvement

Anatomical level Pharyngeal n. Superior laryngeal n. Recurrent laryngeal n.

Degree of involvementLaterality Unilateral Bilateral

Degree of mobility Paresis

Weakness Hypomobility

Paralysis Immobility

Degree of Nerve Injury

(Rubin & Sataloff, 2007)

1°: Neurapraxia and full recovery

2°: Wallerian degeneration but full recovery

3°: Misdirected neural regeneration

4°: Scarring which may block regeneration

5°: Complete nerve transection

Breathy voice Hoarse voice Low volume Limited pitch range & pitch control problems Increased effort and frequent vocal fatigue Weak cough Aspiration of liquids during swallowing

Signs and symptoms

Vocal fold positionRecurrent laryngeal nerve Typically affects ad/abductors Paramedian position common Bilateral impairment can cause airway

problems

Superior laryngeal nerve Deceptively normal position

Superior + Recurrent laryngeal nerve Vocal fold(s) may be more abducted than in

recurrent only May affect vertical position of vocal fold

making compensation more difficult

*Reinnervation pattern will influence vocal fold position

Paramedian

Abduction

Median

Unilateral Right Recurrent N. paralysis: Inspiration

Unilateral Right Recurrent N. paralysis: Phonation

Videoendoscopic evaluationGoals Assess vocal fold mobility Determine degree of glottic closure Relate mobility to voice production Differentiate level of involvement Identify/rule out compensatory behaviors

supraglottic compression Differentiate paresis/paralysis from CA joint

immobility*

CA joint immobility Ankylosis (fixation)/Dislocation Presumed etiology

arthritis trauma joint disease

Appearance Similar to vocal fold paralysis

Differentiating paralysis from ankylosis/dislocation Can be difficult to differentiate with indirect laryngoscopy Reduced passive mobility under direct laryngoscopy Paralysis

Mobility normal during passive movement Affected side “jostles” when contralateral arytenoid hits it

Ankylosis/dislocation Reduced mobility during passive movement Affected side does not “jostle” when contralateral arytenoid hits it

Videoendoscopic evaluationPhonatory Maneuvers Seek to isolate adductors, abductors, tensors Abduction:

sniffing/quick inhalation on/off voicing

Adduction: voicing at various levels on/off voicing Sharp cough

Videoendoscopic evaluationPhonatory Maneuvers Tensor:

glissando/pitch gliding Asymmetries often revealed during repetitive

& alternating activities

Superior laryngeal nerve damage Tricky to identify Controversial list of laryngoscopic signs

Sluggish adduction Asymmetry during glissando Laryngeal tilt toward weak side with voluntary increase in pitch Posterior commissure rotates toward weak side Obliquely shaped glottis due to rotation Lower vocal fold height on involved side Bowed, thin and shortened vocal fold Recent evidence: “movement” of petiole of epiglottis toward

affected side during phonation

Video Examples

Diagnosis: Additional tests Electromyography (EMG)

Treatment Issues Voice Quality Aspiration Airway

Treatment Behavioral Surgical

Recovery can occur up to 6-12 months post-insult

Permanent procedures need to be delayed

Behavioral Management Optimizing voice production and reduce maladaptive

behaviors Tension reduction Facilitating techniques

Treatment for “hypofunction”* Half swallow Pushing Head turn Manual compression

*need to be very careful not to create hyperfunction

Surgical Management:

Medialization procedures Reinnervation

Experimental procedures Laryngeal pacing

Surgical Management:Medialization procedures Intrafold injections Implantation (Isshiki Type I thyroplasty) Arytenoid Adduction

Intrafold Injection

Intrafold Injection Injection of material to increase vocal fold

bulk ~ increase glottic closure Materials include

Gelfoam (temporary) Teflon (problems with fibrosis and migration) Autologous fat (will resorb) Autologous & bovine collagen (slower to resorb) Dermis, fascia etc

Intrafold InjectionSurgical Approaches Peroral

Direct Indirect

Percutaneous (through cricothyroid space)

Implantation Placing/implanting solid material just medial

to thyroid cartilage thus pushing the vocal fold medially

Type I thyroplasty Materials include

Silicone Gore-Tex Cartilage

Arytenoid Adduction

Reinnervation Prevent atrophy and unfavorable

reinnervation Possibilities Ansa cervicalis phrenic n. hypoglossal n. sympathetics

Bilateral Involvement When airway problems are an issue

Options Tracheotomy Cordotomy Arytenoidectomy Thryoplasty (Lateralization) Dennervation/Reinnervation

Bilateral Involvement When airway is OK and voice is an issue

Options Medialization procedures Unilateral or bilateral