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Published byLauren Lynn Quinn Modified over 9 years ago
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Neurogenic dysphonia
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Neurogenic Dysphonia: Topics Neurology of the larynx Organizational Framework Selected Disorders Vocal fold paresis/paralysis Essential Tremor Spasmodic Dysphonia Selected Central Nervous System Disorders
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UW-Madison Neuro Website
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Nerve supply to Larynx
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Relation of nerves to thyroid gland
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Neurologic Voice Disorders: A Classification Scheme Hypoadduction Hyperadduction Phonatory Stability Short term Long term Phonatory Incoordination/Voiced-voiceless Mixed Miscellaneous (Ramig & Scherer, 1992)
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Vocal Fold Paresis/paralysis
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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
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Degree of involvement Anatomical level Pharyngeal n. Superior laryngeal n. Recurrent laryngeal n.
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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
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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
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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
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Unilateral Right Recurrent N. paralysis: Inspiration
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Unilateral Right Recurrent N. paralysis: Phonation
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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*
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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
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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
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Videoendoscopic evaluation Phonatory Maneuvers Tensor: glissando/pitch gliding Asymmetries often revealed during repetitive & alternating activities
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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
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Video Examples
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Diagnosis: Additional tests Electromyography (EMG)
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Treatment Issues Voice Quality Aspiration Airway
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Treatment Behavioral Surgical Recovery can occur up to 6-12 months post- insult Permanent procedures need to be delayed
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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
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Surgical Management: Medialization procedures Reinnervation Experimental procedures Laryngeal pacing
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Surgical Management: Medialization procedures Intrafold injections Implantation (Isshiki Type I thyroplasty) Arytenoid Adduction
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Intrafold Injection
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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
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Intrafold Injection Surgical Approaches Peroral Direct Indirect Percutaneous (through cricothyroid space)
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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
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Arytenoid Adduction
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Reinnervation Prevent atrophy and unfavorable reinnervation Possibilities Ansa cervicalis phrenic n. hypoglossal n. sympathetics
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Bilateral Involvement When airway problems are an issue Options Tracheotomy Cordotomy Arytenoidectomy Thryoplasty (Lateralization) Dennervation/Reinnervation
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Bilateral Involvement When airway is OK and voice is an issue Options Medialization procedures Unilateral or bilateral
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