------------------------------------------------------------------------------- TITLE: VOCAL CORD PARALYSIS SOURCE: Dept. of Otolaryngology, UTMB, Grand Rounds DATE: September 28, 1994 RESIDENT PHYSICIAN: M. D. Bryan, M. D. FACULTY: F. B. Quinn, M. D. DATABASE ADMINISTRATOR: Melinda McCracken, M.S. ------------------------------------------------------------------------------- "This material was prepared by resident physicians in partial fulfillment of educational requirements established for the Postgraduate Training Program of the UTMB Department of Otolaryngology/Head and Neck Surgery and was not intended for clinical use in its present form. It was prepared for the purpose of stimulating group discussion in a conference setting. No warranties, either express or implied, are made with respect to its accuracy, completeness, or timeliness. The material does not necessarily reflect the current or past opinions of members of the UTMB faculty and should not be used for purposes of diagnosis or treatment without consulting appropriate literature sources and informed professional opinion." I. ANATOMY A. CENTRAL NEUROANATOMY - a knowledge of the fundamental neuroanatomy of the vagus nerve can help explain the deficits encountered in central vs. peripheral, and proximal vs distal neurologic injuries that may be seen with vocal cord paralysis. 1. Speech is thought to originate in Broca's area, but anatomic connections are not clearly understood. Injuries here result in aphasia but not paralysis. 2. Multiple bilateral supranuclear projections run through thalamus to brainstem to reach the nucleus ambiguus. The upper motor neuronal connections are to precentral gyrus of motor cortex. 3. Nucleus ambiguus is approximately 2 cm long in reticular formation of medulla. Superior portion projects fibers to CN IX, middle portion to CN X, and inferior portion to cranial part of CN XI. The nucleus ambiguus is the site of origination for the lower motor neurons projecting to the striated muscles of the larynx, pharynx, soft palate, etc. These branchiomotor ("special visceral") efferents leave the brainstem with IX, X, and cranial part of XI. The cranial portion of XI actually ends up with X. Interestingly, this means XI is really not a "cranial" nerve, but sort of a "recurrent" cervical motor nerve 4. Parasympathetics that project to the viscera and vessels with X originate in the dorsal nucleus and the of X and the nucleus ambiguus. 5. General sensory fibers from the pharynx, larynx, and esophagus travel with the main portion of X and have their cell bodies in the superior ganglion of the nerve and project to the spinal trigeminal tract and nucleus. The auricular branch of the vagus also supplies the concha, a small area postauricularly, the TM, and a portion of the EAC meatus 6. Visceral afferents have their cell bodies in the inferior ganglion and project to the tractus solitarius. Vagal input here is related to reflex control of cardiovascular, respiratory, and alimentary functions. The reflexes are mediated by connections between the tractus solitarius and the parasympathetic efferents in the nucleus ambiguus and the dorsal nucleus of X. The hypothalamus, olfactory cortex, and the reticular formation autonomic (primarily sympathetic input) centers also exert strong influences over the action of these reflex arcs. B. PERIPHERAL NEUROANATOMY 1. Just as X approaches the jugular foramen, the superior ganglion is found. The cell bodies for the auricular and meningeal branches are found here . 2. The nerve bundle leaves the cranial vault via the middle compartment of the jugular foramen, in the same sheath with the accessory nerve, penetrating the dura as it exits. 3. The inferior ganglion (nodose ganglion) is just below the jugular foramen, and the cranial component of XI blends with the fibers of X just below this landmark. The vagus is now "complete", and descends in the carotid sheath. It runs behind both the jugular vein and the carotid artery as it descends the neck. 4. The superior laryngeal nerve leaves the vagus below the nodose ganglion, passes deep to the carotids and divides into an internal and external branch as it approaches the thyroid cartilage. The internal branch penetrates the thyrohyoid membrane to supply the sensory input from the mucus membranes of the supraglottis and glottis above the TVC's. The external branch courses over the surface of the inferior constrictor to the cricothyroid muscle which it innervates. 5. The right vagus continues its descent, passes anterior to the right subclavian artery, where it gives off the right recurrent laryngeal nerve (RLN), which loops below and behind the subclavian to ascend behind the carotid sheath, angling toward the tracheoesophageal groove. It typically courses close to the inferior thyroid artery and reaches the larynx by passing beneath the lower border of the inferior constrictor. It may or may not branch before it enters the larynx behind the cricothyroid joint. The branching is functional, with sensory branches supplying the underside of the cords and subglottis, and motor branches to all laryngeal muscles except the cricothyroid. The average adult right RLN is 32 cm. long. 6. The left RLN is a branch off the vagus that arises as the main trunk of the nerve passes the aortic arch. The RLN swings below the ductus arteriosis (which can tether it in the chest) and ascends parallel to the TE groove to the larynx. The average adult left RLN is 43 cm. long. C. LARYNGEAL ANATOMY - There are 9 cartilaginous structures ( 3 pairs and 3 unpaired), 11 intrinsic muscles (5 paired and 1 unpaired), and 4 extrinsic muscles (2 pair) that make up the functional larynx. See table 1 to correlate their anatomic function and innervation. There are two synovial joints that facilitate the intercartilaginous movements that allow the larynx to function normally. 1. Synovial joints - a. cricothyroid - the flat articular surface is between the inferior cornu of the thyroid cartilage and the posterolateral surface of the cricoid ring i. the movement is limited by the posterior and lateral cricothyroid ligaments. ii. the motion about the joint is rotational rather than sliding, allowing anteroinferior tilt of the thyroid cartilage which lengthens or tenses the vocal cords b. cricoarytenoid - a concave (arytenoid)/convex (cricoid) articular surface allows a joy-stick like motion of the arytenoid cartilage relative to the cricoid i. the posterior cricoarytenoid ligament limits anterior rotation ii. primary motion appears to be "rocking " around the long axis of the joint that coincides with the superior surface of the cricoid ring under the arytenoid; this in itself would allow abduction and adduction of the vocal cords II. PATHOPHYSIOLOGY - Specific injury sites should coincide with predictable anatomic or functional deficits that can aid in etiologic diagnosis and management of vocal cord paralysis A. Cord Position: Wagner - Grossman theory explains rationale behind the characteristic position of paralyzed cords 1. RLN lesion - should result in a paramedian cord position by virtue of loss of all active ipsilateral abduction, with intact cricothyroid adduction, and some interarytenoid action (bilateral innervation of interarytenoid) 2. SLN lesion - the cord should be shortened & bowed, lower than the intact side, and the larynx , and the posterior larynx should be rotated slightly to the paralyzed side secondary to the intact and unbalanced action of the opposite cricothyroid muscle. Ab- and adduction are intact. 3. Combined RLN/SLN injury - intermediate cord position, usually flaccid, bowed, and lower than intact side. B. Specific lesions and clinical features 1. Unilateral SLN injury - a. anesthesia of hemilarynx above cords; may see some pooling of secretions and occasionally slight aspiration (usually temporary) b. voice will be lower, slightly weak, with decreased range of pitch; most notable with attempt at singing 2. Unilateral external branch SLN injury a. almost always a surgical lesion; relevant because of risk during thyroid surgery b. no anesthesia, so no aspiration c. exam will still show the lower, bowed, shortened, but mobile cord; voice will be as with complete SLN injury 3. Bilateral SLN injury a. uncommon, but usually a result of surgical injury b. initially the voice is breathy and low, over time the voice will improve, but the singing voice will not; cough is intact usually c. both cords are bowed but mobile; if internal branches are affected there will likely be pooling and aspiration seen secondary to anesthetic larynx; if only external branches involved can be difficult to detect on routine exam (see below) d. abduction and adduction intact; loss of bilateral cricothyroid function causes absence of anterior tilting of thyroid cartilage (and therefore less TVC tension), and this makes the epiglottis overhang or "hood" the anterior glottic inlet - difficult to see 4. Unilateral RLN injury a. the most common injury seen b. paramedian (2 mm from ML typical), tense, non-mobile cord c. voice is just slightly breathy initially, compensation usually occurs fairly quickly, but voice will not become "normal" d. airway is adequate; compromise possible with exercise or marked edema 5. Bilateral RLN injury a. both cords are paramedian; airway may seem stable clinically, but stridor and distress more common b. voice may remarkably good given the degree of abnormality c. tracheotomy is usually indicated 6. Unilateral SLN/RLN lesion a. unless a result of thyroid surgery this is suggestive of high (at or above nodose ganglion) vagal or brainstem lesion if the internal branch of the SLN is involved; brainstem lesion should have other findings (e.g. see Wallenberg syndrome below) b. intermediate position; flaccid cord lower than intact side; rotation of posterior commissure to the lesion side; motionless cord c. breathy poor voice; inadequate compensation even over time d. aspiration will occur if the internal branch of the SLN is involved; preservation of the internal branch (as would expect in post thyroidectomy patients) would prevent the aspiration syndrome 7. Bilateral SLN/RLN paralysis a. the most severe problem; severe aspiration; near aphonia b. bilateral intermediate flaccid motionless cords c. isolation of airway to survive; chronic aspiration procedure such as TL and permanent diversion tracheostome if no recovery III. DIAGNOSIS A. Laryngoscopy 1. IDL vs Machida ==> Machida 2. Videostroboscopy - best documentation and analysis method 3. DL - the last step in the evaluation; must palpate the arytenoid to evaluate the cricoarytenoid joint for fixation B. Other diagnostic methods 1. H&P - history and physical including best method of laryngoscopy available for an awake patient 2. Radiology - if no obvious source is found, patients should undergo a. CXR and C-spine (all should get this regardless) b. barium swallow c. CT of head, neck, and thorax d. thyroid scan/USG as indicated 3. Laboratory a. Infectious - VDRL or FTA-ABS, PPD, fungal immunodiffusion, Lyme titers, CBC, ?LP? b. Inflammatory - ESR, rheumatoid factor c. Metabolic - Calcium, blood glucose,TFTs, parathormone 4. Electromyography a. topical and local anesthesia; external approach is standard b. tracheotomy causes decreased PCA activity, so occlude trach at time of testing to stimulate increased PCA activity c. can be done endoscopically with precise placement of electrodes at time of DL IV. ETIOLOGIES - classification is arbitrary; some use central vs peripheral, although probably better classified as neurogenic vs non-neurogenic; A. NEUROGENIC - only about 5% to 10% of cases where cause is found 1. Supranuclear ALS (affects upper and lower motor neurons) CVA - rarely a cause of vocal cord paralysis MS Parkinson's disease 2. Bulbar Wallenberg syndrome (lateral medullary stroke) Syringomyelia Progressive bulbar palsy Poliomyelitis Syphilis MS 3. Peripheral neuropathy - wasting, fasciculation Lead poisoning Guillian - Barre Diabetes mellitus Arsenic Vincristine neuritis 4. Neuromuscular junction myasthenia gravis pesticide exposure botulinum toxin Eaton-Lambert syndrome B. NON-NEUROGENIC - 90% to 95% of cases where cause is identified 1. Inflammatory RA (not really paralysis) 2. Infectious Syphilis Histoplasmosis Tuberculosis Thyroiditis Pneumonia Viral (EBV - mononucleosis) Meningitis 3. Neoplastic Laryngeal lesion Bronchogenic or mediastinal lesion Esophageal Thyroid Parathyroid Glomus tumors Lymphoma Posterior fossa tumor Intermedullary tumor Vagal neurilemoma 4. Traumatic Penetrating neck or chest trauma Skull fracture Blunt chest or neck trauma Acceleration-deceleration injury Birth trauma 5. Iatrogenic Thyroid or parathyroid surgery Post intubation Neck dissection Larynx preserving resections of CA CABG Carotid endarterectomy Temporal bone resection Posterior fossa surgery Anterior approaches to cervical vertebrae 6. Primary muscle disorders - little documentation with respect to laryngeal involvement Toxic and metabolic myopathies Poly- and dermato-myositis muscular dystrophies 7. Idiopathic disease processes Sarcoidosis Ortners syndrome - left atrial hypertrophy SLE Polyarteritis nodosa C. IDIOPATHIC - 1. 20 to 25% of all cases, the cause will not be identified 2. Unilateral >> bilateral cases 3. Close follow-up is important as may be a sign of occult malignancy 4. Recovery - a. reports of up to 50% spontaneous recovery b. early partial functional return best prognosis; if no return by 6 months, the prognosis is poor; if no return by 12 months can consider it permanent 5. Treat conservatively for at least 6 months if possible V. INCIDENCE A. Bilateral - Paparella, et. al., and K. J. Lee, et. al., state that surgery is the most frequent cause of bilateral paralysis; Cummings, et. al., state that thyroidectomy used to be the #1 cause, but blunt and penetrating trauma is replacing this as the most frequent etiology; overall bilateral RLN is much more common than any other form of bilateral paralysis, but bilateral paralysis makes up only 6% abductor paralysis cases (see next item) B. Unilateral - Bailey, et. al., and K. J. Lee, et. al., identify surgical injury as the most common cause of any kind of unilateral paralysis; Paparella, et. al., place malignant tumors as the #1 cause, with surgical injury just behind; the discrepancy relates to the specificity of Paparella, et. al. to RLN paralysis; both agree that unilateral paralysis cases (any kind) far outnumber bilateral cases 1. In adults, left side paralysis seen much more often than right side (from 2:1 to 5:1 ratios reported); attributed to the increased length (and thus chances of injury) and the path around aorta C. Age - two subpopulations: pediatrics and adults 1. Pediatrics - actual incidence not well known; 50% congenital and 50% "acquired" a. Congenital - vocal cord paralysis accounts for 10 % of congenital laryngeal anomalies, is more often on the right when unilateral and is probably related to birth trauma and stretching the nerve; about 50% of pediatric cases are congenital in nature; bilateral paralysis is most commonly related to a central cause, and the most common association is Arnold-Chiari malformation b. Acquired - about half of pediatric vocal cord paralysis cases are considered acquired even though a significant number are secondary to some congenital anomaly that doesn't manifest as vocal cord paralysis at birth; most are related in some way to hydrocephalus or a meningomyelocele. c. males >> females d. 60% to 70% resolve without or don't require treatment (avoid irreversible treatments) 2. Adults - all acquired; difficult to interpret because of the difference in SLN vs RLN injuries; in SLN injury, the most common cause is thyroid surgery, and for RLN injury the number of cases due to malignancy (mostly lung, and only 10% thyroid CA) about equals those due to surgical trauma (mainly thyroid surgery), and is not much more than the incidence of idiopathic cases a. RLN - most cases in sixth and seventh decades, with lung CA being a major contributor b. SLN - probably most common in third and fourth decades due to the increased incidence of papillary thyroid CA, and benign thyroid disease treated surgically in this age group. D. Sex - males >> females; ratios reported in large series vary from 2:1 to 8:1 VI. MANAGEMENT - A. General considerations - principles of airway management are employed; early management depends on the airway status of the patient; definitive management depends on the degree of clinical problem, the time elapsed from onset, and the prospect for return of function 1. intubation and/or tracheotomy usually indicated in bilateral paralysis 2. if functional recovery expected or possible, but the airway is compromised, a reversible procedure to stabilize the airway and possibly improve the voice is desirable; keep in mind that spontaneous resolution is the rule rather than the exception: a. > 50% of idiopathic cases resolve b. 75% of post thyroidectomy paralysis cases resolve in 4 to 7 months 3. if no return of function is anticipated definitive surgical treatment is not delayed 4. particularly important to carefully evaluate and keep follow-up on "idiopathic" cases for extended periods 5. in general, pre-operative studies should include stroboscopy, and if available spectrographic voice analysis; maximum phonation time (MPT), mean air flow rate (MFR), measurements of subglottic pressure during phonation, and glottic resistance are sometimes used to assess the post- vs pre-op results A. Non-surgical treatment - this can be anticipated in cases where the airway is stable and adequate, with voice and cough not significantly compromised; where function may be expected to return, surgery is avoided if possible for 6 months; B. Surgical treatment of unilateral paralysis - medialization is the usual goal 1. Isshiki thyroplasty type I - probably the most popular technique today; introduced in 1970's, but not popularized in U.S. until last few years; really a modification of technique introduced by Sawashima in 1968; Sawashima in turn used elements of Meurman procedure (1952), and Opheim's procedure (1955) a. technique - i. local and topical anesthesia in awake patient ii. continuous fiberoptic laryngoscopy iii. incision and dissection to expose thyroid ala iv. 12 x 7 mm window in ala at level of true cord (slightly smaller window in females) v. subperichondrial elevation of endolarynx vi. vocalization by patient indicates best position vii. Silastic implant tailored to fill defect is inserted through window; secured by friction fit usually; window cartilage may or may not be left in situ viii. use perioperative antibiotics; steroids optional for control of edema b. complications - there is a low incidence of complications with this procedure, but the potential exists for serious problems i. airway obstruction ii. hematoma iii. infection/chondritis iv. migration of implant c. Advantages - i. neutral head position & minimal anatomic distortion ii. reversible iii. retention of mucosal wave iv. can be performed after failed injection medialization v. outpatient procedure d. Disadvantages - i. external incision ii. results variable iii. limited time to perform procedure because of local edema iv. subsequent endotracheal intubation may dislodge or traumatize corrected side 2. Intralaryngeal injection medialization - until recently, the mainstay of medialization treatments; first performed by Brunings in 1911 using paraffin (unsuccessful because of granuloma formation); reintroduced by Arnold in 1962 utilizing PTFE (Teflon); subsequently Schramm introduced Gelfoam, and later Ford reported the use of collagen (bovine) and autologous fat for the same procedure a. technique - can inject perorally with Brunings syringe, or percutaneously through the cricothyroid membrane or thyroid ala i. larynx and pharynx anesthetized with pontocaine ii. anterior commissure scope used to visualize the larynx iii. first injection lateral to vocalis muscle (between vocalis and thyroid ala), at middle third of TVC; insert needle about 5mm, and inject just enough to see midcord approach midline iv. patient phonates after removal of scope; if further improvement is needed, further injections preformed, usually more anteriorly v. antibiotics and steroids not indicated b. complications - i. injection too medial results in granuloma and possible extrusion/rejection of injected material ii. airway edema or obstruction iii. non-uniform surface of cord if injection too much or too deep in one area and not enough in another; results in weak voice iv. perichondritis/infection c. Advantages i. fairly low risk; ii. outpatient procedure iii. no external incision d. Disadvantages i. not reversible with PTFE (Gelfoam is potentially reversible as the material is absorbed over several weeks) ii. difficult for patient; anatomy distorted by position iii. precise control of bolus not possible; difficult to tell how deep injection is if there is any edema iv. must work quickly because of fairly rapid onset of true cord edema that will make interpretation of result difficult e. Percutaneous injection method - introduced by Ward in 1985 for patients who were not candidates for endoscopy; needle is inserted through the cricothyroid membrane or laterally through the thyroid ala; flexible laryngoscopy used throughout; comparable results to endolaryngeal injections 3. Nerve Muscle Transfer - Tucker (1977) described reinnervation attempt utilizing nerve-muscle pedicle consisting of 2 x 2 mm block of omohyhoid with attached branch of ansa hypoglossi; approximated to the ipsilateral paralyzed thyroarytenoid; reserved for unilateral SLN/RLN injury with large posterior glottic chink and cord bowing; rationale based on the function of strap muscles as accessory muscles of inspiration and phonation, thus the synchronous input by ansa with these activities a. technique - i. local or general ansthesia ii. horizontal incision, level of thyroid cartilage, midline to anterior SCM iii. identify jugular vein, ansa, omohyoid; expose thyroid ala and elevate muscles as needed iv. 2 - 3 mm block of ansa cut out, preserving the ansa supply v. create window in thyroid ala and an inner perichondrial flap door vi. attach pedicle to thyroarytenoid muscle and close perichondrium vii. close and place drain; use antibiotics perioperatively b. complications - no significant complications reported; routine operative risks c. Advantages - (per Tucker) i. no need for nerve section & neurorrhaphy ii. selective reinnervation of cord tensor and adductor d. Disadvantages - i. inconsistent results ii. external incision e. Results - Tucker originally reported 7 of 9 patients achieving significant improvement within weeks of surgery; subsequent report (1989) of 73 patients with 88% achieving marked improvement and no complications; May and Berry (1986) also reported 19 of 20 patients were improved, although in their patients, they observed no vocal cord motion to explain this Although Tucker asserts that the reinnervation establishes tension and bulk of the cord, the lack of consistent detectable motion of the cord has led some to assert that the effect of the surgery is really a result of edema and scarring after the operation 4. Nerve Anastamosis - Crumley and Izdebski (1986) described the treatmentof a high vagal lesion with anastamosis of the ipsilateral ansa hypoglossi to the RLN, and contralateral ansa hypoglossi to the paralyzed cricothyroid; they claimed excellent results; however vocal fold motion was not noted even 4 months post-op; theory behind procedure is improvement in tone and bulk related to reinnervation; a. technique - i. approach and incision same as for nerve-muscle pedicle procedure ii. transect branch of ansa hypoglossi to sternothyroid muscle iii. identify and transect RLN iv. anastamose ansa to RLN stump using 10-0 nylon b. complications - none reported c. Advantages i. no entry into or direct manipulation of larynx ii. can combine with Gelfoam injection to provide interim medialization while awaiting reinnervation effects iii. dennervation of sternothyroid actually helps by reducing tension on ipsilateral thyroid ala, allowing slight medialization of thyroid lamina and thus the vocal cord d. Disadvantages i. long (about 12 weeks) delay before improvement expected ii. technical difficulty iii. inconsistent results between surgeons iv. limited numbers of patients to derive results from 5. Combined thyroplasty and nerve-muscle transfer - proposed by Tucker in 1990; offers the immediated results and reversibility of thyroplasty type I and the potential for recovery of dynamic function; early results very good with 100% of 29 patients reporting marked improvement in voice quality C. Surgical treatment of bilateral abductor paralysis - restoration of stable airway with voice preservation is the goal; all of the procedures have reported "success" rates between 70% to 90%; 1. Arytenoidectomy - the body and all or a portion of one arytenoid is removed to create a posterior glottic chink of sufficient size to allow adequate ventilation; an opening of 4 mm is considered to be adequate for normal adults, but 6 mm or more will likely result in severe breathiness and problems with aspiration; the procedure can be done endoscopically with conventional instruments or CO2 laser, or can be done open via an anterior thyrotomy or lateral (Woodman procedure) approach; endoscopic procedures depend partially upon scar contracture to maintain posterior cord lateralization, while the external approaches usually incorporate direct suture of the vocal process remnant of the arytenoid to the thyroid cartilage to ensure permanent latralization 2. Arytenoidopexy - not a popular procedure today; introduced by Montgomery in 1961; endoscopic application of stainless steel pin through the arytenoid into the cricoid cartilage while the arytenoid is held in lateralized position 3. Cordotomy - Kashima and Dennis (1989) described the use of the CO2 laser to create a transverse incision just in front of the vocal process of the arytenoid, through the vocal cord and medial false cord, including the thyroarytenoid muscle; postoperative contracture of the cut thyroarytenoid maintains the airway adequacy, while the release of the anterior cord from the vocal process minimizes dysphonia 4. Cordopexy - Kirchner (1979) and Ejnell (1984) described basically same idea: Kirchner's version is done endoscopically, this procedure involves making an incision along the lateral margin of the midlde 2/3 of one cord and excising a small wedge of thyroarytenoid muscle; needles are inserted above and below the cord percutaneously from the lateral aspect and heavy nylon suture is passed through the needles; tension is adjusted while viewing the cords endoscopically and the sutures are tied over buttons on the external skin; sutures are removed in 6 weeks; scarring creates a permanent mid-posterior cord lateralization; Ejnell's version does not require excision of thyroarytenoid muscle because the suture is left in place permanently 5. Nerve-muscle transposition - Introduced by Tucker in 1976; a neuromuscular pedicle is grafted to the PCA in order to attempt recovery of abduction. Same technique as used in unilateral cases except that the approach is via the inferior constrictor which is separated to expose the PCA. Tucker' success rate of over 80% has not been duplicated by other investigators. Critics of the procedure claim that the real mechanism of the improvement seen in these patients is that postoperative scarring provides a rigid enough framework through which extralaryngeal musculature moves the arytenoid. D. Surgical treatment of bilateral total laryngeal paralysis - prevention of severe aspiration and death requires surgical intervention 1. Tracheotomy with or without bilateral Gelfoam injection - offers immediate stabilization of the airway; Gelfoam can be used to improve the patient's voice until recovery can begin if desired; reversible 2. Epiglottic flap oversew - can be done as a permanent, reversible, or even an adjustable procedure; usually performed through an open approach 3. Glottic closure - theoretically reversible, but likely to result in signiicant vocal cord scarring 4. Tracheal separation and diversion - complete anatomic separation of airway and digestive tract; potentially reversible; technically easier than TL 5. Total laryngectomy and permanent tracheostome - obviously only for those with no hope of recovering laryngeal function ------------------------------------------------------------------------------- BIBLIOGRAPHY 1. Alfredsunder P; Hochman MC; Kaplan BH Low-dose vincristine-associated bilateral vocal cord paralysis. Division of Critical Care Medicine, Booth Memorial Medical Center, Flushing, NY 11355. N Y State J Med 1992 Jun;92(6):268-9 2. Annino DJ Jr; MacArthur CJ; Friedman EM Vincristine-induced recurrent laryngeal nerve paralysis. Children's Hospital, Boston, MA. REVIEW ARTICLE: 10 REFS. Laryngoscope 1992 Nov;102(11):1260-2 3. Bawa R; Ramadan HH; Wetmore SJ Bilateral vocal cord paralysis with Shy-Drager syndrome. 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Center for Voice Disorders, Wake Forest University, Winston- Salem, North Carolina. Otolaryngol Clin North Am 1991 Oct;24(5):1151-77 22. Levine HL and Tucker HM Surgical management of the paralyzed larynx in Surgery of the Larynx, BJ Bailey and HF Biller, eds. W. B. Saunders 1985 Philadelphia, PA. pp 117-134. 23. Maddern BR; Werkhaven J; Wessel HB; Yunis E Infectious mononucleosis with airway obstruction and multiple cranial nerve paresis. Department of Pediatric Otolaryngology, Children's Hospital of Pittsburgh, University of Pittsburgh School of Medicine, PA 15213. REVIEW ARTICLE: 22 REFS. Otolaryngol Head Neck Surg 1991 Apr;104(4):529-32 24. Montgomery WW; Blaugrund SM; Varvares MA Thyroplasty: a new approach. Department of Otolaryngology, Massachusetts Eye and Ear Infirmary, Boston. Ann Otol Rhinol Laryngol 1993 Aug;102(8 Pt 1):571-9 25. Moralee SJ; Reilly PG Metabolic stridor: bilateral vocal cord abductor paralysis secondary to hypokalaemia? Department of Otolaryngology, Melbourne University, Victoria Australia. J Laryngol Otol 1992 Jan;106(1):56-7 26. Nonomura M; Kojima H; Omori K; Kanaji M; Honjo I Anticus-lateralis muscle suturing. Treatment of recurrent nerve paralysis. Department of Otolaryngology, Faculty of Medicine, Kyoto University, Japan. Arch Otolaryngol Head Neck Surg 1993 Mar;119(3):343-6 27. Nonomura M; Kojima H; Omori K; Kanaji M; and others Remobilization of paralyzed vocal cord by anticus-lateralis muscle suturing. Department of Otolaryngology, Faculty of Medicine, Kyoto University, Japan. Arch Otolaryngol Head Neck Surg 1993 May;119(5):498-503 28. Panosian MS; Quatela VC Guillain-Barre syndrome presenting as acute bilateral vocal cord paralysis. Division of Otolaryngology, Head and Neck Surgery, University of Rochester School of Medicine and Dentistry, NY. Otolaryngol Head Neck Surg 1993 Feb;108(2):171-3 29. Rinne J Late results of laterofixation in the treatment of bilateral abductor paralysis of the vocal cords: a clinical study with long- term follow-up. Department of Otorhinolaryngology, University of Helsinki, Finland. Clin Otolaryngol 1991 Oct;16(5):436-41 39. Rontal E; Rontal M; Silverman B; Kileny PR The clinical differentiation between vocal cord paralysis and vocal cord fixation using electromyography. Department of Otolaryngology-Head and Neck Surgery, University of Michigan Medical School, Ann Arbor. Laryngoscope 1993 Feb;103(2):133-7 31. Saltzman LS; Rosenberg CH; Wolf RH Brainstem infarct with pharyngeal dysmotility and paralyzed vocal cord: management with a multidisciplinary approach. Department of Physical Medicine and Rehabilitation, Jamaica Hospital, New York. Arch Phys Med Rehabil 1993 Feb;74(2):214-6 32. Scott B and Quinn FB Vocal cord paralysis Grand Rounds Presentation, May 23, 1990 University of Texas Medical Branch 33. Simon NP Evaluation and management of stridor in the newborn [see comments] Department of Pediatrics, University of South Alabama, Mobile. REVIEW ARTICLE: 10 REFS. Clin Pediatr (Phila) 1991 Apr;30(4):211-6 34. Takimoto T; Saito Y; Suzuki M; Nishimura T Radiation-induced cranial nerve palsy: hypoglossal nerve and vocal cord palsies. Department of Otolaryngology, School of Medicine, Kanazawa University, Japan. J Laryngol Otol 1991 Jan;105(1):44-5 35. Tanaka S; Hirano M; Umeno H Laryngeal behavior in unilateral superior laryngeal nerve paralysis. Department of Otolaryngology-Head and Neck Surgery, Kurume University, School of Medicine, Japan. Ann Otol Rhinol Laryngol 1994 Feb;103(2):93-7 36. Terris DJ; Arnstein DP; Nguyen HH Contemporary evaluation of unilateral vocal cord paralysis. Division of Otolaryngology-Head and Neck Surgery, Stanford University Medical Center, CA 94305. REVIEW ARTICLE: 16 REFS. Otolaryngol Head Neck Surg 1992 Jul;107(1):84-90 37. Tucker HM; Wanamaker J; Trott M; Hicks D Complications of laryngeal framework surgery (phonosurgery). Department of Otolaryngology and Communicative Disorders, Cleveland Clinic Foundation, OH 44195. Laryngoscope 1993 May;103(5):525-8 38. Willatt DJ and Stell PM Vocal cord paralysis in Otolaryngology, MM Paparella and K Shumrick, eds., 3rd edition, W.B. Saunders Co., 1991 Philadelphia, PA. pp 2289-2306. 39. Zitsch RP 3d Continuous positive airway pressure. Use in bilateral vocal cord paralysis. Division of Otolaryngology, University of Missouri-Columbia School of Medicine. Arch Otolaryngol Head Neck Surg 1992 Aug;118(8):875-6 -------------------------------END------------------------------------------- TEST QUESTIONS - The following test questions are intended to provide proof to accrediting agencies that you have read and understood the entire Grand Rounds element. Your answers should be based on the text of the Grand Rounds element. Answers should be sent by e-mail addressed to fbquinn@utmb.edu. Answers can be sent by U.S Postal Service mail, using a plain sheet of paper on which the Grand Rounds element and the subscriber are fully identified. Correct answers will be transmitted to the subscriber via e-mail. Comments and alternative points of view should be expressed at the end of the list of the subscriber's answers. The University of Texas Medical Branch (UTMB) is accredited by the Accreditation Council For Continuing Medical Education (ACCME) to sponsor continuing medical education for physicians. UTME designates this continuing medical education activity for 1 credit hour in Category 1 of the Physicians's Recognition Award of the American Medical Association. TEST QUESTIONS - VOCAL CORD PARALYSIS The following test questions are intended to provide proof to accrediting agencies that you have read and understood the entire Grand Rounds element. Your answers should be based on the text of the Grand Rounds element. Answers should be sent by e-mail addressed to either psanty@utmb.edu or to fbquinn@phil.utmb.edu. Answers can be sent by U.S Postal Service mail, using a plain sheet of paper on which the Grand Rounds element and the subscriber are fully identified. Correct answers will be transmitted to the subscriber via e-mail. Comments and alternative points of view should be expressed at the end of the list of the subscriber's answers Question 1: A young salesman was in excellent health until he was struck in the throat by an elbow during a basketball game last night. He indicates that the elbow hit him exactly on the left thyroid ala. Since the injury he has noticed that his voice is lower, slightly weak, and with decreased range especially on attempting to sing. Last night he seemed to choke briefly when swallowing a drink of water. This morning, however, this has not reappeared. He has not experienced diffulty breathing, nor has he coughed up any blood-streaked sputum. You find no bruising, edema, or abrasion of his neck. His voice is unremarkable. Flexible fiberoptic laryngoscopy shows that both cords move normally on abduction and adduction, but the right true vocal cord seems a little shorter and lower than the left, and appears a slightly concave on phonation. There is neither ecchymosis nor free blood in the larynx or upper trachea. What is your diagnosis? Question 1: A middle-aged salesman is brought to you by relatives because of sudden onset of hoarseness and choking on drinking liquids. While in your examining room he begins to complain of severe dizziness and nausea, and diminished hearing in the left ear. You observe a diminished gag reflex, a deviation of the uvula to the right, normal eardrums and ear canals, with the Weber test lateralizing to the right and the Rinne test positive in each ear. He has nystag mus with quick phase to the right, and his voice is breathy. Fiberoptic laryngoscopy shows the larynx to be slightly rotated with the posterior commissure more towards the left, the left true vocal cord to be slightly flaccid, immobile in the partly abducted position on phonation, and a little lower than its mate, which is normal in all respects. When he attempts to rise from the examination table he stumbles and nearly falls, and is unable to walk in a coordinated fashion. Finally, he indicates that his right hand feels numb, as does the left side of his face. What is your diagnosis? Question 3: A saleslady of a indeterminate age was operated upon in your hospital this morning. You are on call for the hospital Emergency Room and are making your rounds when you are summoned to the patient's bedside and informed that she is having increasingly difficult respirations. She has a bandage on her neck. Her breathing is labored, with inspiratory stridor but her voice is normal and reasonably strong. She has taken sips of water by mouth without difficulty. What operation was performed upon her that morning? Question 4: An elderly saleslady is brought in by her daughter, because of progressive hoarseness, really simply a weakening of her voice, over the past several weeks. She denies difficulty swallowing or breathing. She has a peculiar transient inspiratory sibilant stridor which apparently does not concern her. She has a long history of cigarette smoking, adult onset diabetes controlled on antiglycosurics, and had a single episode of symptoms consistent with a demyelinating disorder many years ago. Her daughter, an avid horsewoman, employed as an assistant to a veterinarian, mentions that when she spoke with her employer this morning, he stated that it sounded like something that horses get. a. What was the veterinarian thinking of? b. What is the laryngoscopic appearance of your patient's larynx? c. What ancillary studies would you obtain? In order for the sponsors of this CME activity to monitor its usefulness and appropriateness to subscribers, we ask that your supply answers to the following questions concerning the accompanying Grand Rounds Online CME segment: 1. Was the presentation organized in an acceptable manner? yes no opinion no 2. Was the material adequate to your continuing education needs with respect to content? yes no opinion no 3. Was the material appropriate to your clinical practice needs? yes no opinion no 4. Did you feel that the discussants' remarks were responsive to the issues presented in the body of the Grand Rounds segment? yes no opinion no 5. Do you consider the presentation to be timely with regard to current information available in both the lay press and the professional literature? yes no opinion no 6. Are the questions submitted with the Grand Rounds element meaningful in that they stimulate thought and perhaps further inquiry? yes no opinion no 7. Is the method of submitting the subscriber's answers to these questions expeditious and convenient? yes no opinion no 8. Would you recommend this method of completing the general requirment for Continuing Education Activity to your colleagues? yes no opinion no 10. How much money (U.S. dollars) would you be willing to pay for each award of 10 or more CME Category I credits earrned through this type of online CME activity? $100 $50 $25 $12.50 $6.25 $3.00 $1.50 $0.75 $0.35 $0.15 Please submit any comments, criticisms and suggestions which you may have in the space below. They will be given thoughtful consideration, especially if they are favorable comments, gentle criticisms, or constructive suggestions. 8-) /s/ The Editor. ================================================================== Francis B. Quinn, Jr., M.D. University of Texas Medical Branch Dept. of Otolaryngology Galveston, TX 77555-0521 Internet addresses: 409-772-2706, 772-2701 fbquinn@UTMB.edu 409-772-1715 FAX fbquinn@phil.utmb.edu ==================================================================