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07 final vocal cord paralysis
This document provides information on vocal cord paralysis, including: 1. It summarizes the anatomy of the larynx, nerves, and muscles as well as the functions of the larynx. 2. It discusses the various causes (etiologies) of vocal cord paralysis including surgical, malignant, inflammatory, traumatic, neurological and others. 3. It describes the clinical assessment and evaluation of a patient with vocal cord paralysis including history, examination findings, and surgical evaluation techniques.
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07 final vocal cord paralysis
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- 2. Topic covered underfollowing heads • Introduction • Anatomy - neural innervation and muscles of larynx • Functions of larynx • Pathology • Aetiology • Features of various paralysis • Approach to patient with VC paralysis • Surgical management 2
- 3. Introduction • It isa sign of disease and not a diagnosis. • Common problem • Potential morbidity and mortality • A sign of a disease process with multiple etiologies, necessitating thorough evaluation • Part of hypofunctional neurologic disorders • Most often the result of distal nerve injury in the neck or chest 3
- 4. • UMN -cortex to N ambiguus • LMN - N ambiguus – as vagus nerve – N ambiguus - aff – N tractus solitarius – eff – Task specific motor control – Parasympathetic - dorsal motor nucleus of vagus – Somatic sensory – sup cervical ganglion • Vagus nerve exits via the jugular foramen • Branches – Pharyngeal branch – Superior laryngeal nerve – Recurrent laryngeal nerve Anatomy of vagus nerve 4
- 5. • Superior laryngealN – 2nd major branch of vagus – External br of SLN – Internal br of SLN – Main sensory • glottic & supraglottic – Motor - cricothyroid Anatomy of Larynx - Nerves 5
- 6. • Recurrent laryngealnerve – Motor – Sensory • RLN branching patterns • RLN & inferior thyroid A • Retrothyroid segment • Laryngeal segment Anatomy of Larynx - Nerves 6
- 7. RELATIONSHIP OF INFRTHYROID ARTERY AND RECURRENT LARYNGEAL NERVE 7
- 8. 8 Anatomy of Larynx- Muscles Abductor of Larynx:
- 9. 9 Anatomy of Larynx- Muscles Adductors of the Vocal Folds
- 10. 10 Anatomy of Larynx- Muscles Adductors of the Vocal Folds: Control the tension on VC
- 11. 11 Function of Larynx •Protection of airway • Passage for Respiration • Allows Phonation • Allows Stabilization of Thorax • Physiologic sphincters – Aryepiglottic folds – Vestibular folds – Vocal folds
- 12. Voice Production • Initiation- Steps – Vocal folds rapidly abduct to allow intake of air (Pre phonatory inspiratory phase) – Tension develops in cords – Adduction of cords to midline • Phonatory attack phase – Production of airflow from lungs • Increased subglottic pressure 12
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- 14. Pathology of vocalcord palsy • Types – Unilateral / Bilateral – Incomplete / Complete • Position of vocal cord – Median - midline – Paramedian – 1.5 mm from midline – cadaveric (intermediate) – 3.5 mm – gentle abduction - 7 mm – full abduction – 9.5 mm 14
- 15. • Theories ofpalsy – Semon's law – Wagner and Grossman theory Pathology of vocal cord palsy 15
- 16. Pathology of vocalcord palsy • Semon’ s law – 1st stage abductors damaged, cords midline, mobile – 2nd stage add more damaged, cords midline, immobile – 3rd stage add paralysed, cords cadaveric • Wagner & grossman theory (1897) Most popular and widely accepted Complete palsy of RLN cord paramedian SLN also paralysed cord intermediate Chest causes of RLN cause - intermediate cord position due to retrograde atrophy of vagus 16
- 17. Site of lesion •Supra nuclear – Rare – Bilateral lesions cause paralysis – Pharyngeal and laryngeal palsy • Nuclear – Lesions of soft palate, pharynx and larynx • Posterior fossa and Jugular foramen – Vernet’s – IX,X,XI – Schmidt’s – X,XI – Hughling’s Jackson – X,XI,XII – Collet-Sicard – IX,X,XI,XII – Villaret’s – IX,X,XI,XII, Horners • Extra cranial 17
- 18. Aetiology Congenital Acquired (Lt-78%,Rt-16%,Both-6%) (Male: Female 8-10:1) Stell & Maran (1978) • Malignant 25% - Lung(50%), oesophagus (25%),Thyroid (10%), Others • Surgical 20% - Thyroid, Lung, Heart, Oesophagus, Mediastinum 18
- 19. Aetiology • Idiopathic 13%- Viral, Smokers • Inflammatory 13% - Tuberculosis (95%) • Non Surgical trauma 11% - # skull, penetrating injuries neck, cardiomegaly, aneurysm. • Neurological 7% - CVA, Parkinson’s, MS, Alcoholic and diabetic neuropathy. • Miscellaneous 11% - Haemolytic anaemia, RA, Collagen disease 19
- 20. Etiology: Malignancy • Thyroid •Esophagus • Lung • Skull base – temporal lobe malignancies, – posterior fossa tumors, – paraganglioma 20
- 21. Etiology: Surgical Rosenthal etal. showed that surgical causes of unilateral vocal cord immobility were the result of 1. Non-thyroid surgeries (67%) • Anterior cervical spine (15%) • Carotid endarterectomy (11%) • Cardiac (9%) 1. Thyroid surgeries (33%) • Thyroid (26%) • Parathyroid (6%) • Thyroid and parathyroid (1%) Rosenthal et al. Vocal Fold Immobility: A Longitudinal analysis of Etiology Over 20 Years. Laryngoscope. 2007 Oct;117(10): 1864-1870. 21
- 22. Etiology thyroid surgery •Single most common cause • High risk following – thyroiditis, previous surgery, radiation • Mechanical – thermal, stretch, cutting, vascular compromise, compression • Prior to Surgery – 0.7% • After surgery 2.6 – 5.9% temporary 0.5 – 2.4% permanent 22
- 23. Etiology: Idiopathic • Notwell understood • Possible infectious cause – Lyme disease – Tertiary syphilis – Epstein-Barr virus – Herpes simplex virus Type I • Diagnosis of exclusion – Urquhart et al. showed that 26% of patients with a diagnosis of idiopathic VCP had a preexisting neurologic condition and 20% developed a subsequent CNS condition. Urquhart et al. Idiopathic vocal cord palsies and associated neurological conditions. Arch Otolaryngol Head Neck Surg. 2005 Dec;131(12):1086-9. 23
- 24. Etiology: Inflammatory • Tuberculosis –This could be due to apical scarring of the mediastinum or enlargement of hilar nodes. • Jugular vein thrombophlebitis • Subacute thryoiditis, • Meningitis both viral and bacterial. 24
- 25. Etiology: Traumatic • Iatrogenic:Non-surgical – Endotracheal intubation • Arytenoid dislocation, subluxation • Tapia’s syndrome (combination of recurrent laryngeal and hypoglossal palsy. It has been reported afterinterscalene brachial plexus block) – Nasogastric tube placement • Cardiomegaly, aneurysm • Non-iatrogenic – Blunt or penetrating trauma to the neck 25
- 26. Etiology: Neurologic • Stroke •CNS tumor • Diabetic neuropathy • Amyotrophic lateral sclerosis (ALS) • Arnold chiari malformation • Myasthenia gravis • Post polio palsy 26
- 27. Etiology: Systemic disease •Systemic lupus erythematosus • Sarcoidosis • Amyloidosis • Charcot-Marie-Tooth • Hemolytic anaemia • Porphyria • Polyarteritis nodosa • Silicosis 27
- 28. Etiology: Medications • Vincaalkaloids – Vincristine and vinblastine – Unilateral or bilateral – Dose related neurotoxicity effect – Resolves with dose adjustment or cessation 28
- 29. Congenital vocal cordpalsy • Very common cause of stridor • Infants with stridor may have congenital paralysis of vocal cords • Occurs with or without other associated abnormalities - neurologic, laryngeal and cardiac defects • Most common anomaly is hydrocephalus. • The mechanism of vocal cord palsy in these children not clear. – could be due to stretching of the vagus nerve, due to complicated delivery etc. 29
- 30. • 1st examination isflexible laryngoscopy – Nasal or oral – videorecording • Laryngeal ultrasound • Laryngoscopy under anaesthesia 30 Congenital vocal cord palsy
- 31. Superior Laryngeal NervePalsy Unilateral • More rarely recognised • Symmetry maintained during phonation • Ipsilateral bowed and flabby vocal cord • Voice not severely affected • Arytenoid movements unimpaired • Fails to regain its original strength, though quality returns 31
- 32. Superior Laryngeal NervePalsy Bilateral • Rare condition • Professional Voice • Epiglottis hangs over endolarynx • Flaccid, bowed and hyperemic vocal cord • Voice lower, weaker, breathy • Good compensation; speaking voice returns, but singing voice compromised 32
- 33. Recurrent Laryngeal NervePalsy Abductor palsy Adductor palsy 33 Unilateral Bilateral BnilateralUnilateral
- 34. Unilateral Abductor Palsy •Asymptomatic, or only hoarseness - improves with time • Single paralysed cord in paramedian position • Compensation occurs • In some patients, disordered protective mechanism • Pts with less severe cause, dysphonia persists or voice tires • Management Speech therapy Surgical management Vocal fold injection( Medialisation) Arytenoid rotation Nerve muscle pedicle reinnervation RLN reinnervation 34
- 35. Bilateral Abductor Palsy •VC in paramedian position • Voice is good but degree of stridor variable • Good voice; poor airway • If after thyroidectomy; reopen • Management Tracheostomy (Speaking valve) Others Cordectomy Laterofixation of cord Arytenoidectomy and arytenoidopexy Reinnervation 35
- 36. Unilateral Adductor Palsy •Flaccid paralysed VC in lateral position • Weak husky Voice, sometimes no more than whisper • Lesion of Vagus or both RLN and SLN • Aspiration • Management Type and timing depends on aetiology. If Ca, immediate VC injection. Teflon injection for adductor – poorer results than abductor due to posterior glottic insufficiency Others Speech therapy Medialisation laryngoplasty and arytenoid adduction 36
- 37. Bilateral Adductor Palsy •Rare, cental nervous system disease or neoplasm • Involving medulla, skull base or upper neck • Both VC in lateral position • Aphonic • Laryngeal incompetence • Psychiatric disturbance ‘Hysterical aphonia’ • Management Total Laryngectomy Epiglottopexy Others Teflon injection Suturing of cords 37
- 38. Evaluation of Vocalpalsy – History • Symptoms – Voice changes • Hoarseness to aphonia • Compensatory voice changes – Hyperfunctional supraglottic voice – Paralytic falsetto • Vocal fatigue, neck pain – Aspiration – Weak, ineffective cough • Past medical and surgical history • Social history 38
- 39. Evaluation - Examination •Complete Head and Neck Examination – Cranial nerve exam • Flexible Fiberoptic Laryngoscopy (Nasopharyngolaryngoscopy) – Vocal cord asymmetry – Horizontal and vertical position • Median, Paramedian, Lateral – Glottic gap – Pooled secretions – Aspiration – Supraglottic hyperfunction – Adequacy of Airway, Gross Aspiration – Posterior Glottic Gap on Phonation • 90 degree Hopkins Rod-lens Telescope 39
- 40. Surgical Evaluation • Lateralmanual compression test – To determine if patient will benefit from medialization thyroplasty – Pressure applied at level of vocal cords – If quality of speech improves with pressure, patient will benefit from procedure – Limitations: older patients, scarred vocal cords 40
- 41. Evaluation • Assess swallowfunction and aspiration – Modified barium swallow – Functional endoscopic evaluation of swallowing (FEES) • No additional work up required if clear cut etiology 41
- 42. 42 Evaluation - Videostroboscopy •Demonstrates small mucosal motion abnormalities • Video-documentation
- 43. 43 Evaluation - Electromyography •Miller et al in 1982 • Assesses integrity of laryngeal nerves • Analysis of the electrical activity generated by a motor unit. • It is performed percutaneously, under local anesthesia • Electrode on the cricothyroid muscles and thyroarytenoid muscles • Miller, et al claims that laryngeal EMG is the most accurate method of determining superior laryngeal nerve paralysis. • Differentiates denervation from mechanical obstruction of vocal cord movement
- 44. 44 Evaluation - Electromyography •Normal – Joint Fixation – Post. Scar • Fibrillation – Denervation • Polyphasic – Synkinesis – Reinnervation
- 45. 45 Evaluation - Imaging •Chest X-ray – Screen for intrathoracic lesions • MRI of Brain – Screen for CNS disorders • CT Skull Base to Mediastinum • Direct Laryngoscopy – Palpate arytenoids, especially when no L-EMG
- 46. Differential Diagnosis • Cricoarytenoidfixation – Caused by • Joint subluxation/dislocation with ankylosis • Joint fixation by rheumatoid arthritis or gout – Normal EMG – Direct laryngoscopy • Laryngeal malignancy 47
- 47. Treatment - goal •Improve voice and prevent aspiration • Patient factors affect treatment strategies. –Presence of aspiration –Nature of nerve injury –Vocal demands –Medical comorbidities –LEMG findings 48
- 48. Treatment • Strategies: –Observation for6-12 months –Speech and swallow therapy • Provides voice therapy • Teaches vocal hygiene and compensatory strategies • Identifies and eliminates counterproductive compensatory strategies • Pre-operative and post-operative assessment 49
- 49. Treatment -Surgical –Surgical intervention •Temporary: – Injection laryngoplasty • Permanent: Vocal fold injection with durable material, –medialization thyroplasty – arytenoid adduction – laryngeal reinnervation 50
- 50. VOCAL FOLD INJECTION • Aim: Medialization Restoring vibratory surface • Procedure Bruening Arnold syringe Piston grip, Ratchet handle UNILATERAL VOCAL CORD PARALYSIS 51
- 51. THYROPLASTY Type I •Aim of the procedure • Technique Preservation of the inner perichondrium Implant kept out of the body of the vocal fold 52
- 52.
- 53. Thyroplasty Type I •Advantages – LA, Minimal discomfort to patient – Assess voice during procedure – Structural integrity of VC maintained • Disadvantages – Open procedure – Technically more difficult – Intubation later may cause displacement of prosthesis • Complications – Wound infection – Chondritis – Implant migration or extrusion – Airway obstruction 54
- 54. Arytenoid Adduction • Twomain indications – Large posterior glottic chink – Paralysed Vocal cord at different vertical levels • Rotation of arytenoid with downward displacement of vocal process and closure of gap • Ipsilateral SLN and RLN injury • Sutures around muscular process and tied to thyroid lamina. Pull in direction of thyroarytenoid and lat cricoarytenoid muscle • Separately or in combination with Type I thyroplasty 55
- 55. Arytenoid Adduction • Disadvantages Technical difficulty Risk to RLN Edema Irreversibility Future intubation • Contra-indication Spontaneous recovery VC bowed/atrophic 56
- 56. Laryngeal reinnervation procedures •Goal: Increase bulk and tone • Indications: Poor chance of spontaneous recovery • Nerve characteristics – RLN – Ansa cervicalis • Types – Neuromuscular pedicle – Nerve-nerve anastamosis • May be combined with temporary injection laryngoplasty until reinnervation 57
- 57. Laryngeal Reinnervation • Ansacervicalis to RLN – Provides weak tonic innervation to intrinsic laryngeal muscles – Adv: Extralaryngeal, no permanent implant material, does not affect subsequent procedures – Disadv: Deeper dissection, requires intact nerves , delay in voice improvement • Crumley reported improved vocal quality and restoration of the mucosal wave. • Lorenz et al. reported improved vocal quality as well as glottic closure and vocal fold edge straightening. 58
- 58. Laryngeal Reinnervation • Nervemuscle pedicle (NMP) – Nerve with portion of motor units transferred to a denervated muscle. – Thyrotomy performed to place the NMP to the lateral cricoarytenoid muscle. – Tucker et al. reported improvement in voice quality and restoration of adduction. 59
- 59. Bilateral Vocal cordlesions. Vocal fold Lateralization Tracheostomy Transcervical approach Arytenoidectomy Cordopexy Woodman’s operation – 1946 Lateral open approach Arytenoidectomy Endoscopic approaches Arytenoidectomy Thornell 1948 LASER : Cordectomy / arytenoidectomy – Ossoff 1984 Cordotomy Traditional method Kashima’s method of transverse LASER cordotomy 60
- 60. Bibliography 61 • Scott BrownOtorhinolaryngology, Head and Neck surgery, 6th & 7th edition • Stell Maran’s H&N Surgery • Otorhinolaryngology Head & Neck Surgery, Ballenger (17th edition)
- 61.
Editor's Notes
- #5 Corticobulbar fibers from cerebral cortex travel through the internal capsule to synapse on motor neurons in the nucleus ambiguus in the medulla Lower motor neurons leave the nucleus ambiguus and exit the medulla between the olive and pyramid as a series of 8-10 rootlets which coalesce into a single nerve root, the vagus nerve. The vagus nerve exits the skull base via the jugular foramen The vagus nerve descends in the carotid sheath giving off 3 major branches: pharyngeal branch, superior laryngeal nerve and the recurrent laryngeal nerve
- #12 The muscles controlling these sphincters are derived from the intrinsic muscles of larynx. These sphincters can contract together or independently. All these sphincteric components act in unison during the act of swallowing thus preventing effectively any aspiration of food into the airway.
- #16 Peripehral damage to the laryngeal innervation may be of three types:1. Damage to the vagus trunk above the nodose ganglion, the origin of superior laryngeal nerve2. Damage to the vagus nerve below the level or to the recurrent laryngeal nerve3. Damage to the superior laryngeal nerve alone.
- #17 Semon’s law - " In the course of a gradually progressing organic lesion involving the recurrent laryngeal nerve three stages can be observed. In the first stage only the abductor fibers are damaged, the vocal folds approximate in the midline and adduction is still possible. In the second stage the additional contracture of adductors occur so that the vocal folds are immobilized in the median position. In the third stage the adductors become paralysed and the vocal folds assume a cadaveric position". Differential innervation theory: This theory was based on the anatomic fact that the recurrent laryngeal nerve often branched outside the larynx. Injury to individual branches could cause paralysis of specific groups of muscles accounting for the varying positions assumed by the paralysed cord. Changes in the cricoarytenoid joint and paralysed muscles: These changes have been proposed to explain the position of the cord in vocal fold paralysis. This theory of progressive fibrosis of muscles has no anatomical proof. Disturbance of autonomic supply: This theory has no experimental evidence. It suggests that the vocal cord position is determined by the laryngeal muscle tone due to autonomic innervation. Wagner and Grossman theory: This is the most popular and widely accepted theory which could account for the varying positions assumed by a paralysed vocal cord. This theory was first proposed by Wagner and Grossman (1897). This theory states that in complete paralysis of recurrent laryngeal nerve the cord lies in the paramedian position because the intact cricothyroid muscle adducts the cord. (Because the superior laryngeal nerve is intact). If the superior laryngeal nerve is also paralysed the cord will assume an intermediate position because of the loss of adductive force.
- #18 Extra cranial- -- Vagal trunk above nodose ganglion (RLN+SLN) -- Below nodose ganglion (RLN)—Neck and thorax -- SLN only
- #21 Skull base, such as paraganglioma, temporal lobe malignancies, posterior fossa tumors, Thyroid: Thyroid malignancy, benign lesion, goiter Esophageal or lung malignancy
- #22 In the same study, Rosenthal et al. analyzed all surgical causes of unilateral vocal cord paralysis and showed that the most common cause were non-thyroid surgeries at 67%. These included cervical spine procedures, CEA and cardiac procedures. Thyroid and parathyroid surgeries comprised the remaining 33%.
- #24 Idiopathic unilateral VCP is not well understand. A possible infectious cause has been proposed because many patients report an antecedent URI before the onset of vocal symptoms. However, there is no data to suggest that steroids or antivirals affect the course of the disease. In a retrospective analysis, Urquhart et al. showed that of 193 patients diagnosed with VCP, 18% (35) were idiopathic. Of these 35 patients, 26% (9) had a preexisting neurologic condition and 20% (7) developed a subsequent CNS condition (CVA, post polio syndome, polyneuorpathy associated with a paraneoplastic syndrome). 23% (8) resolved within 5 months. Thus careful neurological evaluation of patients with a diagnosis of idiopathic VCP is recommended.
- #26 Traumatic injury is the most common cause of unilateral VCP. Traumatic causes are iatrogenic and non iatrogenic. Surgical causes are the most common in this category, and this includes thyroidectomy, anterior cervical spine procedures, esophagectomy, thymectomy, CEA, and CT surgeries. Non surgical causes include -Tapia syndrome: This is a recurrent laryngeal and hypoglossal nerve paralysis caused by cuff of the endotracheal tube on the thyroid cartilage. -NGT syndrome: Triad of NGT placement, throat pain and vocal cord paralysis. A rare syndrome that is usually associated with bilateral VCP. Pressure phenomenon causes local irritation, edema and ulceration of laryngeal tissues causing vocal cord injury. Caused by rubbing of laryngeal structures against a fixed NGT, cricoid compression against the spine while in the supine position and tonic contraction of the CP muscle against a fixed NGT injuring the posterior cricoid mucosa. Finally, non iatrogenic traumatic causes include blunt or penetrating trauma to the neck.
- #28 Poor fear ee ah
- #29 Vinca alkaloids: Used in hematologic malignancies and head and neck sarcoma. It has a known neurotoxicity effect that may result in unilateral or bilateral vocal cord paralysis. This is a dose related effect that resolves with dose adjustment or cessation.
- #32 Unilateral Superior Laryngeal Nerve Injury: Isolated palsy rare and clinically unrecognised Post thyroid Sx, tumors, diphtheria Normal vocal fold position - quiet respiration. Deviation of posterior commissure to paralyzed side during phonatory effort Vocal fold on paralyzed side is slightly shortened and bowed - rest Singers pitch difference Loss of sensation - frequent throat clearing, paroxysmal coughing, voice fatigue, vague foreign body sensations
- #33 Fortunately this condition is very rare Surgery, trauma, neuritis, pressure by cervical nodes, tumor Symmetry maintained during phonation Epiglottis hangs over endolarynx Result in fatal aspiration and pneumonia Difficult to diagnose as there is no asymmetry between the vocal folds due to compensation
- #39 Evaluation of unilateral VCP includes a thorough history and physical exam. Symptoms Voice change: Patients may report symptoms ranging from hoarseness to complete aphonia. A breathy, weak voice is due to incomplete glottic closure and subsequent “air wasting” during speech, which may give the patient a sensation of “shortness of breath”. A “watery” or “gurgly” quality to the voice is due to pooled secretions in the pyriform sinus. Patients may compensate with increased respiratory effort and a hyperfunctional supraglottic voice, contracting the supraglottis laterally to appose the false cords or in the anterior-posterior dimension to appose the epiglottis to the arytenoids or the arytenoids to the contralateral false folds. This will produce a voice not dissimilar to muscle tension dysphonia, causing a rough, pitch-locked low frequency voice. Other patients may compensate with a high pitched voice, referred to as a “paralytic falsetto”. This is an 85 Hz increase in fundamental frequency caused by compensatory contraction of the ipsilateral cricothyroid muscle, which remains innervated. These compensatory changes causes an increase in paralaryngeal contractions and subsequently will result in vocal fatigue and neck pain. Incomplete glottic closure may also result in aspiration of liquids. High vagal injuries can cause dysphagia to solids due to denervation of the pharyngeal constrictors. High vagal injuries can also exacerbate aspiration due to SLN involvement and loss of sensation. Incomplete glottic closure also results in a weak and ineffective cough due to the inability to create positive end expiratory pressure (PEEP). This loss of auto-PEEP may even affect pulmonary function as well as maneuvers that require a strong Valsava. PMH: One must assess any history of neurologic or rheumatologic disease to explain an idiopathic unilateral VCP, previous surgeries, prolonged intubations, or trauma. In addition, significant cardiopulmonary cormorbidites may affect the patient’s surgical options. Social history: One must also assess risk factors for malignancy as well as a good voice history, specifically the patient’s vocal habits and needs.
- #40 The physical exam includes a full head and neck exam with particular attention to the cranial nerves. Evaluate the gag reflex and palatal elevation, as a high vagal injury will cause palatal deviation to the intact side. NPL is performed with an evaluation of voice during various phonatory tasks and at several frequencies. (CLICK) Attention to asymmetry, vocal fold bowing and lesions. Horizontal position: Cadaveric (lateral), paramedian, median. Vertical position Maximal abduction and adduction may be achieved with the “ee-sniff” maneuver. It is important to note that any ad-duction of the affected cord does not represent partial innervation as the interarytenoid muscle has bilateral innervation. Glottic gap on phonation. Pooling of secretions in the pyriform sinus on the affected side, aspiration of secretions Maximal phonation time (MPT) is measured by having the patient take a deep breath and phonate /i/ for as long as possible. A normal MPT is 25 sec. Patients with VCP are usually less than 10 sec. Shorter times indicate severe glottic incompetence, worse voice and increased vocal fatigue. However, it is important to note that MPT is affected by pulmonary disease. In long standing unilateral VCP, supraglottic hyperfunction (CLICK) may obscure visualization of the vocal folds. Asking the patient to “sigh” or “hum through the nose” may remove this compensatory muscle contractions.
- #41 Most valuable in incomplete glottic closure Unilateral RLNP Vocal Fold atrophy Sulcus vocalis Sulcus vergeture Sustain phonation using /o/ Type I thyroplasty
- #42 Aspiration is assessed with a MBS or FEES (CLICK) If there is a clear cut temporal relation between surgical or iatrogenic trauma and VCP, no additional workup is necessary. However, if the etiology is unclear, imaging studies are required.
- #48 The differential of unilateral VC immobility includes CA joint dislocation/subluxation caused by intubation trauma or blunt trauma to the neck leading to joint ankylosis or by joint fixation by rheumatoid arthritis or gout EMG is normal and direct laryngoscopy with palpation of the CA joint shows no passive mobility. Laryngeal malignancy with involvement of the joint or the thyroartyenoid muscle is also included in the differential. EMG may show decreased amplitude and recruitment of the TA muscle. However, EMG findings of other muscles were normal. NPL will also show a laryngeal lesion.
- #49 The goal of treatment is to improve the voice and prevent aspiration. However, patient factors affect treatment strategies. The presence of aspiration favors early treatment Nerve transection and thus poor prognosis for spontaneous recovery favors early treatment Vocal professionals, such as salespeople, teachers or attorneys, favor early treatment, nonvocal professionals and those with limited voice use favors observation Significant medical comorbidities, such as cardiopulmonary disease, may make general anesthesia unsuitable and thus favor in-office treatment Good prognosis according to LEMG findings favors observation or temporary vocal fold injection Stategies include Observation for 6-12 months if there is good prognosis for spontaneous recovery and no sign of aspiration Speech and swallow therapy Surgical intervention. Temporary surgical intervention includes vocal cord injection with shorter duration material. Permanent surgical intervention includes vocal cord injection with durable material, medialization thyroplasty, arytenoid adduction, and laryngeal reinnervation.
- #50 Speech therapy provides several important functions. Provides voice therapy with attention to vocal exercises, head and neck muscle relaxation, intrinsic laryngeal muscle strength and agility and abdominal and thoracic muscle strength for optimal breathing. Teaches vocal hygiene (smoking cessation, hydration) and compensatory strategies, such as pitch modification Identifies counterproductive compensatory strategies which produce voice strain, voice fatigue and neck discomfort Pre-operative assessment to document and quantitate vocal fold dysfunction, to determine the appropriate treatment modality, to prepare the patient psychologically for surgery, and to provide training for optimal post operative phonation. Post-operative assessment to determine efficacy of treatment and to provide post operative training for optimal phonation. With excellent speech therapy, some patients, especially those with VC in the median position with equal tonicity, may compensate well and avoid surgery altogether.
- #58 The goal of laryngeal reinnervation procedures is to prevent denervation atrophy of the vocal fold and to provide bulk and tone to the denervated muscles, resulting in less asymmetry between the normal and reinnervated vocal fold. It is indicated in unilateral VCP where these is a poor chance of spontaneous recovery. The recommended waiting time is at least 12 months. In the case of ansa to RLN anastamosis, this may be done sooner in the setting of a known transected nerve. Nerve characteristics The RLN has 500-1000 motor fibers which are intermixed before branching within the larynx. Thus selective reinnervation of the RLN is impractical. Reinnervation instead produces laryngeal synkinesis, with adductor and abductor nerve fibers nonselectively innervating the laryngeal muscles. Thus all muscles innervated by the RLN are stimulated with no resulting functional movement of the vocal fold. The ansa cervicalis is a purely motor nerve derived from the ventral rami of the cervical plexus that is readily accessible near the laryngeal complex. It has an ideal diameter for nerve to nerve anastamosis and its sacrifice produces little morbidity. Types of laryngeal reinnervation include Neuromuscular pedicle Nerve-nerve anastamosis These may be combined with injection laryngoplasty until reinnervation takes place.
- #59 Although other reinnervation techniques, including from the phrenic, preganglionic sympathetics, and hypoglossal nerves have been described, the ansa cervicalis to RLN reinnervation has been most described. Ipsilateral or contralateral ansa may be used. Provides weak tonic innervation to intrinsic laryngeal muscles to increase bulk and tone. Reinnervation of the TA restores tension resulting in a more normal mucosal wave. Reinnervation of PCA and LCA stabilizes the arytenoid and prevents inferior displacement of the vocal process, thus providing a more symmetric position relative to the opposite side. Procedure: Incision made below level of cricoid usually at level of thyroidectomy incision. After both nerves are identified and the distal RLN is confirmed to be intact, the ansa and RLN are transected. Each nerve should be divided inferiorly enough to allow a tension-free anastomosis. A tunnel deep to the sternohyoid and sternothyroid muscles connects the two operative sites and facilitates the anastomosis. Advantages of this procedures is that it provides bulk and tone to the denervated cord and improves position of the paralyzed vocal cord without placement of any permanent implant material. In addition, the procedure is extralaryngeal and does not affect subsequent use of injection or thyroplasty. Disadvantages are that It requires a deeper level of dissection in the neck, with increased OR time compared to thyroplasty or vocal fold injection. It requires intact ansa and RLN distal stump which may be difficult in a previously operated neck. In addition, the possibility of spontaneous recovery is eliminated with the division of the RLN before anastamosis, thus necessitating at least a 12 month waiting period from the onset of paralysis. Finally, there is a delay of 6-9 months before substantial improvement in voice occurs. As a result, injection laryngoplasty with a temporary material may be combined with this procedure until reinnervation takes place. Crumley reported improved vocal quality and restoration of the mucosal wave.1 More recently, in a retrospective review, Lorenz et al. found an improvement in voice quality, specifically improved severity, roughness, breathiness, and strain and improvement in glottic closure and vocal fold edge up to 18 months post op.
- #60 In the nerve muscle pedicle procedure, the nerve is transferred with a portion of its intact motor units. Reinnervation depends partly on the ability of the transplanted axons to reach receptive sites on the recipient muscle fibers and partly on the ability of the muscle fibers to accept innervation from foreign nerves. In this procedure, NMP harvested using branch of ansa cervicalis and 2-3 mm block of omohyoid and placed into the LCA via a thyrotomy. The thyroid cartilage on the denervated side is exposed, and the lower half of the perichondrium of the thyroid cartilage is incised in the midline. A posteriorly based perichondrial flap exposing the lower half of the thyroid ala is created. A block of thyroid cartilage is removed from this area, leaving the underlying perichondrium and the inferior margin of the thyroid cartilage intact. The inner perichondrium is incised to expose the denervated LCA muscle and the NMP sutured in place. Although Tucker et al. reported improvement in voice quality and restoration of adduction, the widespread use of NMP is limited. Benefits Allows for preservation of vocal cord bulk Provides tone to vocal fold Used well with medialization procedures