Neurogenic dysphonia Neurogenic Dysphonia: Topics  Neurology of the larynx  Organizational Framework  Selected Disorders  Vocal fold paresis/paralysis.

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Presentation transcript:

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-Madison Neuro Website

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/paresis Central  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 involvement Laterality  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 position Recurrent 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 evaluation Goals  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 evaluation Phonatory 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 evaluation Phonatory 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

 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 Injection Surgical 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