Disease Characteristics and Electromyographic Findings of

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1 The Laryngoscope VC 2016 The American Laryngological, Rhinological and Otological Society, Inc. Disease Characteristics and Electromyographic Findings of Nonsurgery-Related Unilateral Vocal Fold Paralysis Yu-Cheng Pei, MD, PhD; Hsueh-Yu Li, MD; Cheng-Lun Chen, MD; Alice M. K. Wong, MD; Pei-Chi Huang, MD; Tuan-Jen Fang, MD Objective: The detailed characteristics and prognosis of nonsurgery-related unilateral vocal fold paralysis (NSUVFP) are currently unclear. This study evaluated the extent of laryngeal nerve lesions and the individual characteristics for patients with NSUVFP. Study Design: Retrospective, case series. Methods: Patients with unilateral vocal fold paralysis (UVFP) were evaluated using videolaryngostroboscopy and quantitative laryngeal electromyography. The side of nerve lesions, involvement of the external branch of the superior laryngeal nerve (esln), and complete vocal fold motion recovery were evaluated after 6 month follow-up. Results: A total of 207 UVFP patients were recruited, including 153 surgery-related UVFP and 54 NSUVFP patients. Thirty-four (63%) and 20 (37%) NSUVFP patients were further assigned to idiopathic and nonsurgery-related nonidiopathic (NSNI) groups, respectively. In the idiopathic group, esln lesions occurred in all six (100%) patients with right-side paralysis, but in only six of 28 (21%) patients with left-side paralysis (P < 0.001). The turn frequency of the paralyzed thyroarytenoid lateral cricoarytenoid muscle complex is lower in the NSNI group ( ) compared with the idiopathic group ( ) (P ). The probability of complete vocal fold motion recovery did not differ among groups (P > 0.05). Conclusion: Idiopathic and NSNI UVFP have different clinical presentations defined by laryngeal electromyography. NSNI UVFP had more severe denervation changes compared with idiopathic UVFP. These results may support two pathogenic mechanisms for idiopathic UVFP: 1) neuropathy specifically involving left recurrent laryngeal nerve (RLN), and 2) neuropathy affecting nerves proximal to the RLN. Key Words: Vocal cord palsy, videolaryngostroboscopy, laryngeal electromyography, quantitative electromyography, superior laryngeal nerve. Level of Evidence: 4. Laryngoscope, 127: , 2017 INTRODUCTION Unilateral vocal fold paralysis (UVFP) has significant impacts on the patient s vocal function and quality of life 1 3 and has been an important focus of recent research. However, UVFP is not homogeneous, and a variety of disease presentations and prognoses are commonly observed. 4 6 Surgery is the most common cause of UVFP, accounting for approximately 60% of UVFP cases, and the characteristics of surgery-related UVFP From the Department of Physical Medicine and Rehabilitation (Y-C.P., C-L.C., A.M.K.W., P-C.H.), Center of Vascularized Tissue Allograft (Y-C.P.), Chang Gung Memorial Hospital at Linkou, Taoyuan, Taiwan; Department of Otolaryngology Head and Neck Surgery (H-Y.L., T-J.F.), Chang Gung Memorial Hospital at Linkou, Taoyuan, Taiwan; School of Medicine (Y-C.P., H-Y.L., T-J.F.), and the Healthy Aging Research Center (Y-C.P., A.M.K.W.), Chang Gung University, Taoyuan, Taiwan Editor s Note: This Manuscript was accepted for publication August 19, Financial Disclosure: This research was supported by grants CMRPG 3D1413 from the Chang Gung Medical Foundation and MOST B-182A-056-MY2 from the Minister of Science and Technology, Taiwan. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the article. The authors have no other funding, or financial relationships to disclose. Send correspondence to Tuan-Jen Fang, MD, Chang Gung Memorial Hospital, No. 5 Fushing St., Taoyuan 333, Taiwan. fang3109@cgmh.org.tw DOI: /lary have been carefully addressed. 7,8 However, nonsurgeryrelated unilateral vocal fold paralysis (NSUVFP) has been less well discussed, and a comprehensive assessment and therapeutic plan is required for these patients. Most NSUVFP patients referred to otolaryngology clinics initially present with UVFP without known causes. Clinicians then need to take an in-depth history and arrange the necessary evaluations to determine the etiology underlying UVFP. A diagnosis of NSUVFP may then be further subdivided into idiopathic and nonsurgeryrelated nonidiopathic (NSNI) UVFP. NSNI UVFP can be caused by a wide range of diseases, such as tumors, infection, and radiotherapy. The unique features of these patients mean that their specific disease characteristics and prognoses remain unclear, and studies with large patient populations are needed. In contrast, idiopathic UVFP has been a focus of research. Most cases of NSUVFP are idiopathic 4,9 and have unique disease presentations. 10 Idiopathic UVFP is defined as UVFP with unknown causes 4,11,12 ; however, previous studies have shown inconsistent results regarding the clinical presentation 9,12 16 and long-term prognosis 9 for patients with idiopathic UVFP. A recent case series of 17 patients with idiopathic UVFP suggested that it was associated with higher recruitment of the 1381

2 thyroarytenoid lateral cricoarytenoid (TA LCA) muscle complex and better quality of life compared with iatrogenic UVFP. 10 Laryngeal electromyography (LEMG) is necessary to confirm and identify the nerve injury responsible for UVFP, 13,17,18 with quantitative LEMG 19,20 being used to measure the severity of the nerve injury. In this study, we used quantitative LEMG to assess the TA LCA muscle complex and cricothyroid (CT) muscle to define the lesioned nerves, and videostroboscopy to measure glottal function in patients with NSUVFP. We hypothesized that NSUVFPs may have a variety of disease presentations corresponding to their etiologies. MATERIALS AND METHODS Human Subjects We recruited patients from the otolaryngology outpatient clinic at a medical center from September 2011 to December Inclusion criteria were adults (> 20 years old) diagnosed with UVFP, confirmed by laryngoscopy and LEMG, and their vocal fold motion recovery was evaluated after 6 months follow-up. Exclusion criteria were contraindications for or rejection of needle electromyography; no evidence of neurogenic vocal fold paralysis detected by LEMG; bilateral vocal fold paralysis confirmed by LEMG; or history of interventions to correct the paralyzed vocal fold position, such as intracordal injection, laryngoplasty, or laryngeal framework surgery. All aspects of the study were specifically approved by the Human Studies Research Committee of Chang Gung Medical Foundation. Written informed consent was obtained from each participant prior to recruitment. Participants were not paid for participation. durations for the TA LCA 20 muscle of 200 ms. The timing of each turn and its amplitude was localized using an automatic algorithm. Specifically, a turn was defined by a change in polarity with amplitude of at least 100 lv before and after the change, to exclude noise-related peaks. Turn frequency was computed for each epoch as the number of turns divided by the epoch duration. Turn amplitude was computed as the mean of the absolute turn-amplitude values. For each muscle, we averaged the turn frequencies for the epochs with turn frequencies that ranked among the top three epochs to yield the peak turn frequency. Videolaryngostroboscopy Patients were asked to project the vowel /e/ at their habitual pitch and intensity, and the voice and vocal fold vibration samples were recorded by videolaryngostroboscopy. The recorded movie was analyzed offline, frame by frame, using Image J 1.44 software (National Institutes of Health, Bethesda, MD) to give the normalized glottal gap area (NGGA), following the Omori et al. method 21 as described in the following equation: NGGA 5 glottal gap area = ðmembranous vocal fold lengthþ units Measurement of the NGGA has been described in detail previously. 14 Glottal gaps were measured in maximally open and closed phases during vocal fold vibration to give closed-phase and open-phase NGGAs. The magnitude of vibration was described by the difference between the open phase and closed phase of NGGA (D open closed phase NGGA): D open closed phase NGGA 5 open2phase NGGA closed2phase NGGA: Procedures Patients underwent videolaryngostroboscopy and LEMG with quantitative analysis. Videolaryngostroboscopy was performed within 2 weeks of the day of LEMG assessment. LEMG Examination The standard protocol for LEMG was performed by a board-certified otolaryngologist (T.-J.F.) and a physiatrist (Y.-C.P.). We examined the LEMG signals for bilateral TA LCA muscle complexes and CT muscles. The detailed LEMG procedure has been described previously. 20 In short, we initially observed insertional activity and spontaneous activity for each test. We then performed semiquantitative motor unit analysis and recruitment analysis, specifically when the rise time of a motor unit action potential was < 0.6 ls, indicating a close proximity to the recorded motor unit. A Nicolet Viking Select (Cardinal Health, Dublin, OH) was used with its band-pass filter set between 20 Hz and 10 khz. An abnormal EMG was defined as the existence of spontaneous activities (e.g., fibrillation, positive sharp wave, or complex repetitive discharge), >30% polyphasia, or decreased interference pattern (reduced, discrete, or no interference pattern). Motor unit recruitment tracings were recorded with sweep speeds of 10 ms per division and a gain of 200 lv per division. Quantitative LEMG Analysis We developed a MatLab (MathWorks, Natick, MA)-based program to analyze the raw LEMG data. The raw LEMG waveforms were first binned into nonoverlapping epochs with epoch Statistical Analysis According to disease etiology, patients were initially divided into surgery-related and nonsurgery-related groups. The nonsurgery-related group was further divided into idiopathic and NSNI groups. Specifically, surgery-related UVFP was defined as UVFP occurring following surgery. Idiopathic UVFP was diagnosed when 1) the etiology cannot be identified by clinical history, physical examination, chest X-ray, neck ultrasound, and head-and-neck computed tomography scan from skull base to upper mediastinum, 6 and 2) no known etiology was found with a follow-up period of > 6 months. Finally, NSNI was defined as UVFP with known nonsurgery-related causes. Patients in the NSNI group were further divided into NSNI patients with tumor etiology (tumor subgroup) and nontumor etiology (nontumor subgroup). For parametric data, differences between two groups were compared using Student s t tests. For categorical data, differences between groups were compared using v 2 or Fisher s exact tests. The level of significance was defined as P < RESULTS Etiology of UVFP We initially recruited 249 patients with UVFP diagnosed by laryngoscopy and/or LEMG. In total, 42 patients were excluded for lack of neurogenic vocal fold paralysis (n 5 6), bilateral laryngeal neuropathies (n 5 18), superior laryngeal neuropathies in the healthy side according to LEMG (n 5 14), and history of intracordal injection (n 5 4). The remaining 207 patients were 1382

3 Fig. 1. Flow diagram of patient characteristics, including etiology, lesion side, lesioned nerves, and status of recovery: Complete vocal fold motion recovery. esln 5 external branch of superior laryngeal nerve; LEMG 5 laryngeal electromyography; NSNI 5 nonsurgery-related nonidiopathic; UVFP 5 unilateral vocal fold paralysis. assigned to the surgery-related (n 5 153) or nonsurgeryrelated (n 5 54) groups according to their etiologies (Fig. 1). Among the 54 nonsurgery-related patients, 34 (63%) and 20 (37%) were assigned to the idiopathic and NSNI groups, respectively. Among the 20 patients in the NSNI group, 14 (70%) and six (30%) were further assigned to the tumor and nontumor subgroups, respectively. Videolaryngostroboscopy data were missing for one patient in the tumor subgroup and another patient in the nontumor subgroup. Only complete data were used for statistical analysis of each parameter. Table I lists the etiology of UVFP in patients in the NSNI group. Among the 14 patients in the tumor subgroup, five (36%) had thyroid tumors, four (29%) had lung tumors, one (7%) had esophageal tumor, and four (29%) had other tumors with mediastinal metastasis. Among patients in the nontumor subgroup, UVFP was induced by radiotherapy in three (50%) patients, herpes neuropathy in one (17%), carbon monoxide toxicityrelated neuropathy in one (17%), 22 and pulmonary tuberculosis in one (17%). Comparison Between Surgery-Related and Nonsurgery-Related Patients In terms of paralysis side, the surgery-related group had a left-to-right ratio of 1.6 (93 vs. 60), whereas the nonsurgery-related group had a much higher ratio of 6.7 (47 vs. 7) (P ) (Table II). In terms of LEMG results, the nonsurgery-related group ( ) had a higher turn frequency for the TA LCA muscle complex compared with the surgery-related group ( ) (P < 0.001), indicating less severe denervation in the nonsurgery-related group. There were no differences between the two groups in their age, gender, esln involvement, complete vocal fold motion recovery, or glottal area (open-phase NGGA, closed-phase NGGA, or D open closed phase NGGA) (all P > 0.05). Disease Presentation of NonSurgery-Related UVFP Patient Characteristics. Patient characteristics, including age, sex, paralysis side, duration from disease onset to LEMG (disease-onset duration), external branch of superior laryngeal nerve (esln) involvement, and complete vocal fold motion recovery assessments, are shown in Table III. Patients in the NSNI group ( ) were significantly older than those in the idiopathic group ( ) (P ). Among the NSNI group, the tumor ( ) and nontumor ( ) subgroups were comparable in terms of age (P ). The sex distributions were similar in the idiopathic and 1383

4 TABLE I. Disease Characteristics of Patients in Nonsurgery-Related Nonidiopathic Group. Sex Age (Year) Pathogenesis Paralysis Side esln lesion Complete Vocal Fold Motion Recovery Tumor Subgroup F 48 Thyroid tumor L 1 2 M 67 Lung tumor L 2 2 F 56 Thyroid tumor L 2 2 M 68 Lung tumor L 2 2 F 53 Breast tumor L 2 2 F 79 Thyroid tumor L 2 2 M 58 Mediastinal metastatic cancer, unknown primary L 2 2 F 55 Ovary tumor with paraaortic lymph node L 2 2 and pleural metastases F 62 Lung tumor L 2 2 F 58 Thyroid tumor L 2 2 M 41 Mediastinum tumor L 2 2 F 52 Thyroid tumor L 2 2 M 70 Lung tumor L 2 2 M 56 Esophageal tumor R 2 2 Nontumor Subgroup M 74 Herpes neuropathy L 1 2 M 66 Radiotherapy fibrosis L 1 2 F 56 Radiotherapy fibrosis L 2 2 M 51 Carbon monoxide toxicity-induced neuropathy L 2 2 F 38 Radiotherapy for lung cancer L 2 2 F 68 Pulmonary tuberculosis, involving left upper lobe L 2 1 esln 5 external branch of superior laryngeal nerve; F 5 female; L 5 left; M 5 male; R 5 right. TABLE II. Comparison of Disease Presentation Between Surgery-Related and Nonsurgery-Related Groups. Item Surgery-Related Group Nonsurgery-Related Group P Value n Demographics Age (year) Gender (male/female) 69/84 24/ Paralysis side (right/left) 60/93 7/ * esln involvement (yes/no) 31/122 15/ Complete vocal fold motion recovery (n/%) 10(6%) 5(9%) 0.55 Glottal area n Open-phase NGGA Closed-phase NGGA D open closed phase NGGA LEMG n TA LCA turn lesion side (Hz) < 0.001* *P < esln 5 external branch of superior laryngeal nerve; LEMG 5 laryngeal electromyography; NGGA 5 normalized glottal gap area; TA LCA 5 thyroarytenoid lateral cricoarytenoid. 1384

5 TABLE III. Disease Presentation of Patients With Nonsurgery-Related Unilateral Vocal Fold Palsy. Item Idiopathic Group All NSNI Group Tumor Subgroup Nontumor Subgroup P Value Between Idiopathic and NSNI Groups P Value Between Tumor and Nontumor Subgroups n vs vs. 6 Demographics Age (year) * 0.99 Gender (male/female) 15/19 9/11 6/8 3/ Paralysis side (right/left) 6/28 1/19 1/13 0/ esln involvement (yes/no) 12/22 3/17 1/13 2/ Complete vocal fold motion 4(12%) 1(5%) 0(0%) 1(17%) recovery (n/%) Glottal area n vs vs. 5 Open-phase NGGA Closed-phase NGGA D open closed phase NGGA LEMG n vs vs. 6 TA LCA turn lesion side (Hz) * 0.20 *P < esln 5 external branch of superior laryngeal nerve; LEMG 5 laryngeal electromyography; NGGA 5 normalized glottal gap area; NSNI 5 nonsurgeryrelated nonidiopathic; TA LCA 5 thyroarytenoid lateral cricoarytenoid. NSNI groups (P ) and in the tumor and nontumor subgroups (P ) (Table III). Paralysis Side. In terms of paralysis side, the idiopathic and NSNI groups did not differ in their side distribution (Table III and Fig. 1), and among the NSNI group, there was no significant difference between the tumor and nontumor subgroups (all P > 0.05). Lesioned Nerves. The interaction between lesion side and esln involvement showed that, among the 34 patients in the idiopathic group, esln lesions occurred in all six (100%) of right-side paralysis patients but only in six out of 28 (21%) left-side paralysis patients (P < 0.001) (Fig. 1). Vocal Fold Motion Recovery and Glottal Gap. The proportion of patients with complete vocal fold motion recovery was comparable between the idiopathic (4 patients, 12%) and NSNI groups (1 patient, 5%) (P ) and between the tumor (0 patients, 0%) and nontumor subgroups (1 patient, 17%) (P ) (Table III and Fig. 1). Open-phase and closed-phase NGGAs, which reflected the size of the glottal gap as measured by videolaryngostroboscopy, did not differ between the idiopathic and NSNI groups or between the tumor and nontumor subgroups (all P > 0.05) (Table III). However, the D open closed phase NGGA, which reflects vocal fold vibration, tended to be higher in the idiopathic group ( ) compared with the NSNI group ( ) (P ), implying better vocal fold vibration in the idiopathic group. Among the NSNI group, the D open closed phase NGGA did not differ between the tumor ( ) and nontumor subgroups ( ) (P ). LEMG and Quantitative Analysis. The idiopathic group ( ) had a higher turn frequency for the TA LCA muscle complex in the lesion side compared with the NSNI group ( ) (P ), indicating less severe denervation in the idiopathic group. The turn frequency for the TA LCA muscle complex did not differ between the tumor ( ) and nontumor subgroups ( ) (P ) (Table III). DISCUSSION NSUVFP comprises a wide variety of etiologies. It may be the first sign of malignancy, or the cause may remain unknown even after evaluation. This study provides the first comprehensive description of the characteristics of NSUVFP. We categorized patients with NSUVFP as idiopathic or NSNI, and further subdivided NSNI UVFP into tumor-related and nontumor-related NSNI. The relatively large sample size in this case series provided enough power to characterize the differences between these subgroups. Finally, we used quantitative LEMG to provide valuable information on the severity and location of nerve involvement, yielding quantitative measurements corresponding to different NSUVFP etiologies. 5,13,17,19,23 From our results, two independent pathophysiological hypotheses for idiopathic UVFP could be constructed. First, for patients without esln involvement, the overwhelmingly higher prevalence of left-sided involvement compared with right-sided (22 vs. 0) indicates a mechanism that specifically occurs in left RLN (Fig. 2, red 1385

6 known etiologies that occurred below the neck, such as mediastinal or lung lesions, which were associated with UVFP without esln involvement. In those cases, UVFP may be caused by entrapment neuropathy or nerve injury of the RLN within the chest cage or mediastinum. Compared with patients with idiopathic UVFP, patients with NSNI UVFP were older and had poorer vocal fold vibration. This finding could be accounted for by the fact that most NSNI patients had tumors, and nerve insults induced by tumors and tumor-related therapies tend to be more severe. 35,36 This study had two limitations. First, it was not a prospective study, and the patients were recruited from laryngology outpatient clinics in a medical center. Second, the variety of disease etiologies in the NSNI group ranged from mediastinal tumors to radiotherapy, making classification difficult. Further larger case series with adequate samples for each specific etiology are needed. Fig. 2. The two hypotheses for idiopathic UVFP. 1) Neuropathy specifically in left RLN. 2) Neuropathy proximal to the RLN that occurs equally on both sides. CT 5 cricothyroid muscle; RLN 5 recurrent laryngeal nerve; SLN 5 superior laryngeal nerve; TA LCA 5 thyroarytenoid lateral cricoarytenoid muscle complex. [Color figure can be viewed in the online issue, which is available at segment) (hypothesis 1). Second, the identical numbers of patients with combined RLN and esln involvement among left- and right-sided involvement (6 vs. 6) UVFP imply a pathophysiological cause occurring equally on both sides and involving a location proximal to the bifurcation of the laryngeal nerve and superior laryngeal nerve (Fig. 2, blue segments) (hypothesis 2). We suppose that a majority of idiopathic UVFP could be accounted for by these two hypotheses. Indeed, idiopathic UVFP is a cluster of diagnoses when known etiologies are not yet found, given that diagnostic tools such as image studies and laboratory examinations have been performed. For hypothesis 1, additional span of the left RLN, which travels lower and around the aortic arch, might make it more susceptible to entrapment neuropathy or other local lesions Possible causes underlying this could include fibrosis, 27,28 mass lesions, 29 inflammation, or infection. 11,30 33 For hypothesis 2, one possible cause for this is neuritis occurring in the proximal part of the laryngeal nerve. 34 These findings indicate that in-depth patient evaluation is needed for patients with idiopathic UVFP, especially for those specifically involving left RLN. The incidence of esln involvement was lower in patients with tumor-related compared with nontumorrelated NSUVFP. Only one patient with tumor-related UVFP had esln involvement, and the patient had thyroid cancer with neck metastasis. This suggests that esln involvement is rare in tumor-related NSNI UVFP, and its occurrence may imply the existence of neck or high vagal lesions. Most patients in the NSNI group had 1386 CONCLUSION NSUVFP has a wide range of etiologies corresponding to different clinical presentations. Patients with NSNI UVFP are relatively older, have poorer vocal fold vibration, and tend to have left-sided paralysis compared with patients with idiopathic UVFP. Among patients with NSNI UVFP, nontumor patients are more prone to have esln lesions. Finally, esln lesions occurred in all patients with right-sided idiopathic UVFP, supporting the existence of two pathophysiological hypotheses: 1) Neuropathy specifically in left RLN, and 2) neuropathy proximal to the RLN. BIBLIOGRAPHY 1. Benninger MS, Ahuja AS, Gardner G, Grywalski C. Assessing outcomes for dysphonic patients. J Voice 1998;12: Fang TJ, Li HY, Gliklich RE, Chen YH, Wang PC, Chuang HF. 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7 16. Ward PH, Berci G. Observations on so-called idiopathic vocal cord paralysis. Ann Otol Rhinol Laryngol 1982;91: Lindestad PA, Persson A. Quantitative analysis of EMG interference pattern in patients with laryngeal paresis. Acta Otolaryngol 1994;114: Smith LJ, Rosen CA, Niyonkuru C, Munin MC. Quantitative electromyography improves prediction in vocal fold paralysis. Laryngoscope 2012; 122: Statham MM, Rosen CA, Nandedkar SD, Munin MC. Quantitative laryngeal electromyography: turns and amplitude analysis. Laryngoscope 2010;120: Pei YC, Fang TJ, Li HY, Wong AM. Cricothyroid muscle dysfunction impairs vocal fold vibration in unilateral vocal fold paralysis. Laryngoscope 2014;124: Omori K, Slavit DH, Kacker A, Blaugrund SM. Quantitative videostroboscopic measurement of glottal gap and vocal function: an analysis of thyroplasty type I. Ann Otol Rhinol Laryngol 1996;105: Pulst SM, Walshe TM, Romero JA. Carbon monoxide poisoning with features of Gilles de la Tourette s syndrome. Arch Neurol 1983;40: Fang TJ, Pei YC, Hsin LJ et al. Quantitative laryngeal electromyography assessment of cricothyroid function in patients with unilateral vocal fold paralysis. Laryngoscope 2015;125: Glazer HS, Aronberg DJ, Lee JK, Sagel SS. Extralaryngeal causes of vocal cord paralysis: CT evaluation. AJR Am J Roentgenol 1983;141: Myssiorek D. Recurrent laryngeal nerve paralysis: anatomy and etiology. Otolaryngol Clin North Am 2004;37:25 44, v. 26. Williams MJ, Ayylasomayajula A, Behkam R, et al. A computational study of the role of the aortic arch in idiopathic unilateral vocal-fold paralysis. J Appl Physiol (1985) 2015;118: Jaruchinda P, Jindavijak S, Singhavarach N. Radiation-related vocal fold palsy in patients with head and neck carcinoma. J Med Assoc Thai 2012;95(suppl 5):S23 S Lin YS, Jen YM, Lin JC. Radiation-related cranial nerve palsy in patients with nasopharyngeal carcinoma. Cancer 2002;95: Heikkinen J, Milger K, Alejandre-Lafont E, et al. Cardiovocal syndrome (Ortner s syndrome) associated with chronic thromboembolic pulmonary hypertension and giant pulmonary artery aneurysm: case report and review of the literature. Case Rep Med 2012; 2012: Yew WW, Chau CH, Lee J, Wong PC, Leung CK. Hoarseness due to recurrent laryngeal nerve palsy from intrathoracic mycobacteriosis. Int J Tuberc Lung Dis 2001;5: Amin MR, Koufman JA. Vagal neuropathy after upper respiratory infection: a viral etiology? Am J Otolaryngol 2001;22: Dabrowska A, Tarnowska C, Jalowinski R, Amernik K, Stankiewicz J, Grzelec H. [Paresis of the vagus and accessory nerve in the course of the herpes zoster]. [Article in Polish]. Otolaryngol Pol 2006;60: Vyravanathan S. Hoarseness in tuberculosis. J Laryngol Otol 1983;97: Jacobs CJ, Harnsberger HR, Lufkin RB, Osborn AG, Smoker WR, Parkin JL. Vagal neuropathy: evaluation with CT and MR imaging. Radiology 1987;164: Mehlum CS, Faber CE, Grontved AM. [Vocal fold palsy etiology and outcome]. [Article in Danish]. Ugeskr Laeger 2009;171: Takimoto T, Saito Y, Suzuki M, Nishimura T. Radiation-induced cranial nerve palsy: hypoglossal nerve and vocal cord palsies. J Laryngol Otol 1991;105:

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