REVIEW URRENT C OPINION
Vocal fold paresis: etiology, clinical diagnosis and clinical management Sheila V. Stager
Purpose of review Recent papers on incidence of unilateral paresis in general and for specific causes; techniques to assist clinical diagnosis; computer and animal modeling leading to new assessment tools; and studies on the effectiveness of clinical management. Recent findings There is much interest in being able to assess unilateral paresis in patients both pre and post-thyroidectomy. Because the gold standard for defining the presence of paresis is by laryngeal electromyography, which is not routinely available, much interest has been placed in finding other measures that correlate with electromyographic findings, including use of ultrasound imaging and high-speed videoendoscopy. Paresis is also being seen as an underlying factor in other voice disorders, such as reflux and presence of granulomas. Animal modeling is providing insights into the mechanisms that will help our understanding of vocal fold asymmetry. The development of trial injections to determine if more permanent interventions will provide good outcomes is an important step in good patient care. Summary Randomized clinical trials need to be completed to provide level 1 evidence for the efficacy of treatments. Centers that have access to laryngeal electromyography need to lead the way in developing assessment tools and treatment trials for patients with paresis. Keywords animal models, asymmetry, injection medialization, paresis, translaryngeal airflow
INTRODUCTION The standard definition of unilateral vocal fold paralysis is immobility of the arytenoid cartilage on the recurrent laryngeal nerve (RLN)-injured side [1–5]. In our clinic, in a subset of patients with unilateral nerve injury confirmed by laryngeal electromyography (EMG) with an onset of 9 months or less who sought treatment between 1999 and 2009, only 15% (13/88) demonstrated no mobility of the arytenoid cartilage. The assumption, then, is that the remainder of the patients with EMG-confirmed unilateral nerve injury will be diagnosed with paresis. Unilateral vocal fold paresis (UVFP), then, is defined in terms of results from EMG assessment, rather than endoscopic assessment. A decrease in motor unit recruitment due to fewer normal motor units and reduced volitional activity (as evidenced by a reduced interference pattern of motor neurons during modal voice or high-pitched voice) and/or evidence of fibrillations or insertional fibrillations and/or nascent or spontaneous activity suggest paresis, if present, in recordings from either the www.co-otolaryngology.com
thyroarytenoid and/or cricothyroid muscles [6]. Paresis patients also demonstrate a constellation of signs or symptoms, although not all are present in every patient [6]. These include: reports of vocal fatigue; changes in pitch range, especially the higher pitches; lack of projection; subtle vocal fold asymmetry (lag) of mucosal wave; incomplete glottal closure; and impaired mobility of the arytenoid cartilage [7–9, 10 ,11]. This review will discuss research papers written from 2011 to the present in the areas of cause and incidence, clinical assessment and clinical management, specifically for UVFP. &
Voice Treatment Center, Medical Faculty Associates, Division of Otolaryngology, Department of Surgery, The George Washington University Medical Center, Washington, District of Columbia, USA Correspondence to Sheila V. Stager, PhD, CCC-SLP, Voice Treatment Center, Medical Faculty, Associates, 2021K Street NW, Suite 206, Washington, DC 20006, USA. Tel: +1 202 741 3265; fax: +1 202 741 3218; e-mail: sstager@mfa,gwu.edu Curr Opin Otolaryngol Head Neck Surg 2014, 22:444–449 DOI:10.1097/MOO.0000000000000112 Volume 22 Number 6 December 2014
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KEY POINTS The gold standard for diagnosing unilateral paresis is either RLN or SLN injury as assessed by laryngeal electromyography.
Iatrogenic Incidence data for iatrogenic cause are primarily from studies following thyroid surgery. In one study, the incidence of RLN injury resulting in vocal fold weakness following thyroidectomy was 6.6% in 320 patients [15]. In a Danish study [16 ], after a median of 7 months after surgery, 142 of the 6859 individuals (2%) were found to have unilateral ‘permanent’ palsy (permanent palsy defined as any partial or complete immobility). Of these 142 patients, 76 (54%) were from surgeries with benign histology. Another study reported that 17/26 individuals with EMG data before and after surgery were found to have unilateral or bilateral paresis prior to thyroidectomy surgery, but only seven reported any vocal symptoms. Following surgery, only five reported voice complaints [17]. Incidence data have also been reported for surgical resection of cerebellopontine angle tumors. Among 181 patients, 10% were found to have unilateral palsy (defined as unilateral vocal fold motion impairment) [18]. &
The glottal function index may prove to be a valuable subjective rating scale for demonstrating improvement following treatment. Aerodynamic measure of translaryngeal mid-vowel flow provides useful information to diagnosis and evaluating treatment effects. Patients with idiopathic unilateral paresis may not require a CT work-up, whereas those with idiopathic unilateral paralysis should be followed up with a CT work-up. Trial injections are a good way to determine if more permanent augmentation will improve voice outcomes.
ETIOLOGY Incidence
Intubation
A review of 739 patients over 4 years from a tertiary care practice produced 195 who were thought to have paralysis or paresis [7]. Six were found to have paresis due to RLN damage, one due to superior laryngeal nerve (SLN) damage and two had evidence of combined RLN/SLN nerve damage. No information on the etiology of these cases was provided. An early study reported 31% of the 22 patients with iatrogenic etiology, 23% with viral, 18% with idiopathic, 14% with trauma and another 14% with accompanying muscle tension dysphonia [12]. In our clinic, over a 15-year period, using the criterion of decreased recruitment [6,7] in patients whose onset of symptoms was 9 months or less from the time of initial evaluation, 238 patients were found to have unilateral RLN paresis, 121 had combined unilateral RLN/SLN paresis and eight had unilateral SLN paresis. As far as etiologies were concerned, for those with RLN paresis, 36% were iatrogenic, 32% idiopathic, 13% intubation, 11% malignant and 8% viral. For those with combined RLN/SLN paresis, 44% were iatrogenic, 40% idiopathic, 11% viral, 4% intubation and 2% malignant. For those with SLN paresis, 63% were iatrogenic, 25% idiopathic and 12% viral. To compare, the following percentages have been reported for etiologies of unilateral paralysis: surgical (iatrogenic), 55.6%; malignancy, 17.8%; idiopathic, 13.2%; intubation, 6.2% and central, 1.9% [13]. In a study specifically of elderly patients (65–89 years), the incidence of paresis was found to be 72% (126/175), based on EMG assessment [14].
Normal or limited arytenoid movement and impaired vocal fold movement were documented in 11% (7/60) individuals following arytenoid dislocation due to endotracheal intubation. EMG studies revealed unilateral nerve injury in these individuals [19].
Association of paresis with other disorders Patients with paresis frequently complain of vocal fatigue. It has been thought that part of that percept of fatigue may be due to using vocally hyperfunctional behaviors, as they try to compensate for deficits resulting from nerve injury [6,20]. Granulomas have been also associated with vocal hyperfunction. One study demonstrated 53% of patients with granuloma may have had underlying glottal insufficiency, and one possible cause of that glottal insufficiency was decreased mobility of the arytenoid [21]. An earlier study also reported granulomas on the contralateral vocal process in three patients with unilateral SLN injury [22]. Paresis has been associated with not only development of granuloma but also with reflux disease. A third of the patients with an original diagnosis of reflux disease that proved recalcitrant to proton pump inhibitor therapy were subsequently found to have paresis [23 ]. Two studies have listed other voice disorders that co-occurred in patients with unilateral or bilateral paresis involving injury to RLN and/or SLN [6,12].
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CLINICAL ASSESSMENT Assessment of paresis currently is based on patient report, followed by endoscopic examination, followed by EMG assessment for confirmation of nerve injury. Very few objective measures have been used. Finding sensitive-enough measures may be difficult, given the subtlety of the symptoms and the other voice disorders that can co-occur with paresis. The following section offers some suggestions.
Self-rating scales The diagnosis of paresis is suspected when patients report vocal fatigue, an inability to project, and loss of their higher register. For example, in a survey of frequency of voice symptoms in thyroid cancer patients following surgery, the largest percentages of complaints were inability to get loud (52.5%), inability to sing (54%), and pain while speaking (29.2%) [10 ]. The glottal function index is a 4-question 6-point Likert self-rating scale of severity of patient symptoms, specifically vocal effort, vocal fatigue, throat pain after talking, and voice cracking or sounding different [24]. It has been validated with the degree of glottal insufficiency [24]. Changes in patients’ responses to this index may provide a mechanism to track perceived change following treatment. &
Endoscopy and high-speed videoendoscopy Endoscopic findings from patients with paresis can include the following: asymmetry between left and right vocal fold mucosal waves (also known as lag or ‘chasing wave’); incomplete glottal closure; and impaired mobility of the arytenoid cartilage. However, there are several issues that preclude using endoscopic examination as the gold standard for diagnosis. Because of the subtlety of the asymmetry, several studies have focused on ways to accentuate it during the endoscopic examination. Repetitive phonatory tasks have been used for patients with SLN paresis [25]. These tasks are meant to ‘fatigue’ the system, thereby making asymmetry more obvious. While these tasks did improve the ability to assess mild asymmetry, looking at the whole endoscopic examination was most helpful in identifying the injured side. Asking the patient to whistle has also been used to make the asymmetry more pronounced [8]. Asymmetry has also been studied using high-speed videoendoscopy. In a case study, analyzing the cycle by cycle vocal fold vibration using high-speed videoendoscopy brought out asymmetry not visible during the traditional endoscopic and stroboscopic techniques [26]. Another study also 446
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used a technique called Fourier image to quantify phase relations between parts of the vocal folds from high-speed videoendoscopy recordings. Asymmetries were found in normophonic speakers, suggesting that this methodology may be sensitive to the subtle asymmetries of unilateral paresis patients [27]. A second endoscopic finding – incomplete glottal closure – has been studied using a frame-byframe determination of percentage of closure duration. The number of frames in which the vocal folds are closing or are closed is calculated, and this is divided by the total number of frames in a vibratory cycle [28]. Patients with paresis had a shorter percentage of closure duration (34% compared to 50% in normal). Another study had looked at the size of the glottal gap to compare RLN and SLN injury. Glottal gap was larger in those with SLN injury during the closed phase and smaller during the open phase, which was interpreted to mean that there were poorer vibration dynamics during vibration with SLN injury [29 ]. Several studies have demonstrated lack of agreement between raters asked to determine the side of the nerve injury, especially if both arytenoids demonstrate full extent of movement, closure is good, and hyperfunctional compensatory behaviors are present [9,30]. The interarytenoid spatial relationship was developed to see if improvements could be made in residents’ abilities to determine the correct side of paresis, the side demonstrating EMG abnormality recorded from the lateral cricoarytenoid (LCA) muscle [30]. The spatial relationship between the cuneiform and corniculate cartilages is different on the nerve-injured side compared to the normal side. With training on visualizing these differences, residents were able to improve their accuracy [30]. &&
Ultrasound Colleagues in Asia have been examining the usefulness of pre and postoperative ultrasound recordings in determining which patients have paresis following thyroidectomy. One study claims good sensitivity and specificity of ultrasound in determining those who may have unilateral paresis following surgery when compared with laryngoscopic images [31 ]. &
Computed tomography and other imaging This was one area in which the diagnosis of paresis or paralysis was important. A review article summarizing results from five studies suggested that computed tomography (CT) testing should be completed following a diagnosis of idiopathic paralysis (not paresis), as an average of 81% were found to Volume 22 Number 6 December 2014
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Vocal fold paresis Stager
have malignancies [32]. If the initial CT scan was normal, further scanning was unwarranted. Patients with a diagnosis of idiopathic paresis and not paralysis may not require a CT work-up [33 ]. Among the patients diagnosed with idiopathic vocal fold paresis, 98% had normal CT studies, and the one patient whose CT scan was not normal was further evaluated with a PET-CT that was negative.
study has reported significant differences in nonlinear dynamic measures between controls and those with unilateral paralysis [38].
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Laryngeal electromyography A meta-analysis [34] of studies on the use of EMG for the diagnosis and management of paresis/paralysis patients revealed three level IV studies [7,12,35]. They were classified as level IV evidence because they were retrospective and unblinded. Another excellent review paper [6] was done on the clinical usefulness of EMG.
Acoustic measures Although they have not been reported in studies assessing patients for paresis, it might be assumed that the time-based acoustic measures of jitter and shimmer might prove useful, as they are thought to reflect asymmetries in vibration. They are valid for relatively periodic signals, and are threshold measures, meaning there is a point along a continuum that designates normal from abnormal. They are not linear, because a jitter measure of 2 is not twice as abnormal as a measure of 1. Reliability of these measures has been questioned. Another acoustic variable used in our clinic is the presence of glottal stops in the context of words ending with a vowel or /t/ and the next word beginning with a vowel sound. This can be observed during the endoscopic examination as dynamic medial–lateral movements of the false vocal folds during the task of repeated /i/ [36]. Some paresis patients, when asked to repeat /i/ syllables, cannot produce glottal stops, rather they voice continually, and no medial–lateral movement of the false vocal fold on the nerve-injured side is observed endoscopically. Listeners are able to perceptually distinguish between paresis patients and controls on this parameter [37]. This inability to produce glottal stops is present in about 60% of patients with paresis/paralysis, but is not found in normal or patients without injury to the RLN. Nonlinear dynamic measures have been put forward to assess aperiodicity in acoustic signals. They have primarily been developed to assess signals that are more aperiodic than can be analyzed using more traditional time-based measures. It remains to be seen if the subtle asymmetry of unilateral paresis patients can be captured by these measures. One
Aerodynamic measures Our clinic uses two aerodynamic measures: air flow and s/z ratio [39]. Patients with slight vocal fold asymmetry often demonstrated elevated flows, and when they were subsequently tested with EMG, they were diagnosed with paresis. Increased flow has been significantly correlated with reduced interference pattern of motor neurons (poor recruitment) [40,41], and increased patient perception of effort [42]. Since both of these can be characteristic of patients with paresis, obtaining flow signals becomes an important clinical assessment tool. If flow signals cannot be obtained, then the s/z ratio can be substituted. Ratios greater than 1.4 suggest some degree of glottal insufficiency. A ratio can demonstrate abnormality, even if the measures in the numerator and denominator are both within normal limits. However, the s/z ratio has not been correlated with patient report of increased effort or decreased recruitment. Finally, computer modeling [43] and canine studies [44 ,45 ] have been devised to explore how small differences in activation of both the RLN and SLN affect vocal fold vibration. By changing the activation of the RLN, the normal vocal fold leads during the opening phase, a larger lateral excursion is found for the paretic side, larger air flow occurs, and phonation onset pressures are affected [45 ]. Thus, phonation threshold pressures (PTPs) should be considered as a way to study the role of SLN injury in paresis patients. By changing the activation of the SLN, the side with greater tension (i.e. the normal side) leads in the opening phase, and has increased closure speed. The greater the asymmetry in activation, the more chaotic is the vibratory pattern [44 ]. &&
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CLINICAL MANAGEMENT If the time between initial evaluation and onset of symptoms is 9 months or less, the first line of clinical management can often be observation to determine if spontaneous nerve recovery will occur. Voice therapy is also an option during this time [6]. In general, if patients are not happy with the outcome following voice therapy, then the next step is to do a temporary injection medialization [6]. Injectables lasting a varying amount of time before resorption have been developed. Shorter-acting injectables include Radiesse Voice Gel and Cymetra, and are thought to last about 2–3 months. Bovine
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collagen and hyaluronic acid last a little longer, around 3–6 months. Autologous fat and Radiesse can last up to 12 months [46].
Injection medialization A newer strategy has been to introduce a trial injection before completing a temporary or permanent injection medialization [47]. Trial injections use a temporary augmentation material to determine the degree and nature of vocal quality improvement from augmentation in cases of severe vocal fold paresis when it is not clear if bulk alone will be enough to improve the voice; or allow patients to see the potential results from an augmentation procedure when other therapies have failed [47]. One study used three types of shorter-acting injectables (Cymetra, gelfoam or Radiesse Voice Gel) on 25 patients with paresis and/or atrophy. The authors used patient-subjective responses to categorize them into having a good outcome, partial improvement, or poor outcome from the trial injection. Almost all who reported a good outcome went on to have a permanent augmentation procedure, and almost none of those who reported a poor outcome went on to have a permanent augmentation. Those who went on to have a permanent augmentation procedure were satisfied with their voice outcome. A review of the current practice in injection augmentation [48] reported that for patients with paresis, half of the procedures are done in the office, and half in the operating room. Half of the procedures are unilateral injections and half bilateral. Materials used in office procedures were primarily Radiesse Voice Gel and bovine collagen. In the operating room, fat and Radiesse were also injected. A study has demonstrated significant improvements in the Voice Handicap Index-10 scores in patients with hypomobility with confirmed nerve injury 1–8 weeks following treatment with Radiesse Voice Gel [49].
Medialization thyroplasty In our clinical experience, we have used several modalities of treatment. Over 15 years, we treated 216 patients with unilateral paresis (defined as having ratings of 1þ to 3þ on recruitment, where 4þ was normal and 0 was considered to represent paralysis) who were initially evaluated within 9 months of onset of their symptoms. Among these patients, 41% chose to be observed, 21% were injected with temporary materials, 19% had medialization thyroplasty, and 5% went for voice therapy. Another 14% equired multiple types of treatments to be 448
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satisfied with their voice outcome. In general, those whose EMG recruitment ratings were more impaired (ratings of þ1 and þ2) had more permanent and multiple treatments. Various outcome measures were made, but are not reported in this paper. Medialization thyroplasty also plays a role in patients who continue to demonstrate unilateral paresis 1 year or more after onset of symptoms. By this time, any spontaneous nerve recovery should have occurred. In our clinic, we have treated the following numbers of patients who were evaluated for at least 12 months (up to 34 years) after onset: 79 with unilateral RLN injury, 40 with unilateral RLN/SLN injuries, and one with unilateral SLN injury. Both injection medialization and medialization thyroplasty were used.
CONCLUSION To advance studies on the assessment and treatment of patients with UVF paresis, finding measures that significantly correlate with EMG results would be beneficial, especially since availability of EMG testing on a routine basis is limited. This means that those facilities that are able to obtain EMG recordings need to lead the way in investigating assessment and treatment tools for unilateral paresis patients. Comparisons of objective measures should be made between patients with unilateral vocal fold paralysis and those with UVFP. Randomized clinical trials need to be completed to provide level 1 evidence of the efficacy of various treatments. Acknowledgements None. Conflicts of interest There are no conflicts of interest.
REFERENCES AND RECOMMENDED READING Papers of particular interest, published within the annual period of review, have been highlighted as: & of special interest && of outstanding interest 1. Sulica L, Blitzer A. Vocal fold paresis: evidence and controversies. Curr Opin Otolaryngol Head Neck Surg 2007; 15:159–162. 2. Wen M-H, Cheng P-W, Liao L-J, et al. Treatment outcomes of injection laryngoplasty using cross-linked porcine collagen and hyaluronic acid. Otolaryngol Head Neck Surg 2013; 149:900–906. 3. Young VN, Smith LJ, Rosen C. Voice outcome following acute unilateral vocal fold paralysis. Ann Otol Rhinol Laryngol 2013; 122:197–204. 4. Paniello RC, Edgar JD, Kallogjeri D, Piccirillo JF. Medialization versus reinnervation for unilateral vocal fold paralysis: a multicenter randomized clinical trial. Laryngoscope 2011; 121:2172–2179. 5. Wang C-C, Chang M-H, Wang C-P, et al. Laryngeal electromyographyguided hyaluronic acid vocal fold injection for unilateral vocal fold paralysis: preliminary results. J Voice 2012; 26:506–514. 6. Sataloff RT, Praneetvatakul P, Heuer RJ, et al. Laryngeal electromyography: clinical application. J Voice 2010; 24:228–234.
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Vocal fold paresis Stager 7. Simpson CB, Cheung EJ, Jackson CJ. Vocal fold paresis: clinical and electrophysiologic features in a tertiary laryngology practice. J Voice 2007; 23:396–398. 8. Rubin AD, Sataloff RT. Vocal fold paresis and paralysis: what the thyroid surgeon should know. Surg Oncol Clin N Am 2008; 17:175–196. 9. Simpson CB, May LS, Green JK, et al. Vibratory asymmetry in mobile vocal folds: is it predictive of vocal fold paresis? Ann Ototogy Rhinol Laryngol 2011; 120:239–242. 10. Kuhn MA, Bloom G, Myssiorek D. Patient perspectives on dysphonia after & thyroidectomy for thyroid cancer. J Voice 2013; 27:111–114. This study summarizes a large scale survey of voice problems post-thyroid cancer surgery, excluding patients with pre-existing voice problems and postoperative vocal fold immobility. 11. Blitzer A, Crumley RL, Dailey SH, et al. Recommendations of the Neurolaryngology Study Group on laryngeal electromyography. Otolaryngol Head Neck Surg 2009; 140:782–793. 12. Heman-Ackah YD, Barr A. Mild vocal fold paresis: understanding clinical presentation and electromyographic findings. J Voice 2006; 20:269–281. 13. Spataro EA, Grindler DJ, Paniello RC. Etiology and time to presentation of unilateral vocal fold paralysis. Otolaryngol Head Neck Surg 2014; 151:286– 293. 14. Gregory ND, Chandran S, Lurie D, Sataloff RT. Voice disorders in the elderly. J Voice 2012; 26:254–258. 15. Echternach M, Maurer C, Mencke T, et al. Laryngeal complications after thyroidectomy. Arch Surg 2009; 144:149–153. 16. Godballe C, Madsen AR, Sørensen CH, et al. Risk factors for recurrent nerve & palsy after thyroid surgery: a national study of patients treated at Danish departments of ENT Head and Neck Surgery. Eur Arch Otorhinolaryngol 2014; 271:2267–2276. This study reports on a large-scale survey to document possible risk factors for voice problems following thyroid surgery. 17. Caroline M, Joglekar SS, Mandel SM, et al. The predictors of postoperative laryngeal nerve paresis in patients undergoing thyroid surgery: a pilot study. J Voice 2012; 26:262–266. 18. Best SR, Starmer HM, Agrawal Y, et al. Risk factors for vagal palsy following cerebellopontine angle surgery. Otolaryngol Head Neck Surg 2012; 147:364–368. 19. Xu W, Han D, Hu R, et al. Characteristics of vocal fold immobility following endotracheal intubation. Ann Otol Rhinol Laryngol 2012; l2l:689–694. 20. Mayes RW, Jackson-Menaldi C, DeJonckere PH, et al. Laryngeal electroglottography as a predictor of laryngeal electromyography. J Voice 2008; 22:756–759. 21. Carroll TJ, Gartner-Schmidt J, Statham MM, Rosen CA. Vocal process granuloma and glottal insufficiency: an overlooked etiology? Laryngoscope 2010; 120:114–120. 22. Halum SL, Miller P, Early K. Laryngeal granulomas associated with superior laryngeal nerve paresis. J Voice 2010; 24:490–493. 23. Rafii B, Taliercio S, Achlatis S, et al. Incidence of underlying laryngeal && pathology in patients initially diagnosed with laryngopharyngeal reflux. Laryngoscope 2014; 124:1420–1424. This study illustrates the complex interactions of vocal fold disorders. 24. Bach KK, Belafsky PC, Wasylik K, et al. Validity and reliability of the glottal function index. Arch Otolaryngol Head Neck Surg 2005; 131:961–964. 25. Rubin AD, Praneetvatakul V, Heman-Ackah Y, et al. Repetitive phonatory tasks for identifying vocal fold paresis. J Voice 2005; 19:679–686. 26. Mortensen M, Woo P. High-speed imaging used to detect vocal fold paresis: a case report. Ann Otol Rhinol Laryngol 2008; 117:684–687. 27. Krenmayr A, Wollner T, Supper N, Zorowka P. Visualizing phase relations of the vocal folds by means of high-speed videoendoscopy. J Voice 2012; 26:471– 479. 28. Carroll TL, Wu Y-HE, McRay M, Gherson S. Frame by frame analysis of glottic insufficiency using laryngovideostroboscopy. J Voice 2012; 26:220–225. 29. Pei Y-C, Fang T-J, Li H-Y, Wong AMK. Cricothyroid muscle dysfunction && impairs vocal fold vibration in unilateral vocal fold paralysis. Laryngoscope 2014; 124:201–206. This study demonstrates an interesting quantitative measure of glottal gap.
30. Sufyan AS, Kincaid JC, Wannemuehler TJ, Halum SL. The interarytenoid spatial relationship: accuracy and interrater reliability for determining sidedness in cases of unilateral adductor paresis. J Voice 2013; 27:90–94. 31. Wong K-P, Lang BH-H, Ng S-H, et al. A prospective, assessor-blind evalua& tion of surgeon-performed transcutaneous laryngeal ultrasonography in vocal cord examination before and after thyroidectomy. Surgery 2013; 154:1158– 1165. This study suggests a possible new tool to select patients who need direct laryngoscopy before and after thyroidectomy. 32. Tsikoudas A, Paleri V, El-Badawey MR, Zammit-Maempel I. Recommendations on follow-up strategies for idiopathic vocal fold paralysis: evidencebased review. J Laryngol Otol 2012; 126:570–573. 33. Badia PI, Hillel AT, Shah MD, et al. Computed tomography has low yield in the && evaluation of idiopathic unilateral true vocal foldparesis. Laryngoscope 2013; 123:204–207. This is an important study with ramifications for bringing down cost of evaluating patients with idiopathic unilateral vocal fold paresis. 34. Meyer TK, Hillel AD. Is laryngeal electromyography useful in the diagnosis and management of vocal fold paresis/paralysis? Laryngoscope 2011; 121:234– 235. 35. Statham MM, Rosen CA, Smith LJ, Munin MC. Electromyographic laryngeal synkinesis alters prognosis in vocal fold paralysis. Laryngoscope 2010; 120:285–290. 36. Stager SV, Bielamowicz SA, Regnell JR, et al. Supraglottic activity: evidence of laryngeal articulation vs. vocal misuse. J Speech Lang Hearing Res 2000; 43:229–238. 37. Leydon C, Bielamowicz SA, Stager SV. Perceptual ratings of vocal characteristics and voicing features in untreated patients with unilateral vocal fold paralysis. J Commun Disord 2005; 38:163–185. 38. Yan N, Wang L, Ng ML. Acoustical analysis of voices produced by Cantonese patients of unilateral vocal fold paralysis. 2013 IEEE International Conference on Signal Processing, Communications and Computing, ICSPCC 2013; 6664001. 39. Stager SV. Objective evaluation of patients with vocal fold paralysis and paresis. Paper presented at International Federation of Oto-Rhino-Laryngological Societies in Seoul, South Korea. 2013. 40. Bielamowicz SA, Stager SV. Diagnosis of unilateral recurrent laryngeal nerve paralysis: laryngeal electromyography, subjective rating scales, acoustic and aerodynamic measures. Laryngoscope 2006; 116:359–364. 41. Sanuki T, Yumoto E, Nishimoto K, Minoda R. Laryngeal muscle activity in unilateral vocal fold paralysis patients using electromyography and coronal reconstructed images. Otolaryngol Head Neck Surg 2014; 150: 625–630. 42. Stager SV, Bielamowicz SA. Perceived vocal fatigue and effort in relation to laryngeal functional measures in paresis patients. Laryngoscope 2014; 124:1631–1637. 43. Zhang Z, Luu TH. Asymmetric vibration in a two-layer vocal fold model with left-right stiffness asymmetry: experiment and simulation. J Acoust Soc Am 2012; 132:1626–1635. 44. Chhetri DK, Neubauer J, Bergeron JL, et al. Effects of asymmetric superior && laryngeal nerve stimulation on glottic posture, acoustics, vibration. Laryngoscope 2013; 123:3110–3116. The procedure for studying asymmetry was well thought out. 45. Chhetri DK, Neubauer J, Sofer E. Influence of asymmetric recurrent laryngeal && nerve stimulation on vibration, acoustics, and aerodynamics. Laryngoscope 2014. [Epub ahead of print] The procedure for studying asymmetry was well thought out. 46. Mallur PS, Rosen CA. Vocal fold injection: review of indications, techniques, and materials for augmentation. Clin Exp Otorhinolaryngol 2010; 3:177–182. 47. Carroll TL, Rosen CA. Trial vocal fold injection. J Voice 2010; 24:494–498. 48. Sulica L, Rosen CA, Postma GN, et al. Current practice in injection augmentation of the vocal folds: Indications, treatment, principles, techniques, and complications. Laryngoscope 2010; 120:319–325. 49. Mallur PS, Morrison MP, Postma GN, et al. Safety and efficacy of carboxymethylcellulose in the treatment of glottic insufficiency. Laryngoscope 2012; 122:322–326.
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Vocal fold paresis: etiology, clinical diagnosis and clinical management Sheila V. Stager
Purpose of review Recent papers on incidence of unilateral paresis in general and for specific causes; techniques to assist clinical diagnosis; computer and animal modeling leading to new assessment tools; and studies on the effectiveness of clinical management. Recent findings There is much interest in being able to assess unilateral paresis in patients both pre and post-thyroidectomy. Because the gold standard for defining the presence of paresis is by laryngeal electromyography, which is not routinely available, much interest has been placed in finding other measures that correlate with electromyographic findings, including use of ultrasound imaging and high-speed videoendoscopy. Paresis is also being seen as an underlying factor in other voice disorders, such as reflux and presence of granulomas. Animal modeling is providing insights into the mechanisms that will help our understanding of vocal fold asymmetry. The development of trial injections to determine if more permanent interventions will provide good outcomes is an important step in good patient care. Summary Randomized clinical trials need to be completed to provide level 1 evidence for the efficacy of treatments. Centers that have access to laryngeal electromyography need to lead the way in developing assessment tools and treatment trials for patients with paresis. Keywords animal models, asymmetry, injection medialization, paresis, translaryngeal airflow
INTRODUCTION The standard definition of unilateral vocal fold paralysis is immobility of the arytenoid cartilage on the recurrent laryngeal nerve (RLN)-injured side [1–5]. In our clinic, in a subset of patients with unilateral nerve injury confirmed by laryngeal electromyography (EMG) with an onset of 9 months or less who sought treatment between 1999 and 2009, only 15% (13/88) demonstrated no mobility of the arytenoid cartilage. The assumption, then, is that the remainder of the patients with EMG-confirmed unilateral nerve injury will be diagnosed with paresis. Unilateral vocal fold paresis (UVFP), then, is defined in terms of results from EMG assessment, rather than endoscopic assessment. A decrease in motor unit recruitment due to fewer normal motor units and reduced volitional activity (as evidenced by a reduced interference pattern of motor neurons during modal voice or high-pitched voice) and/or evidence of fibrillations or insertional fibrillations and/or nascent or spontaneous activity suggest paresis, if present, in recordings from either the www.co-otolaryngology.com
thyroarytenoid and/or cricothyroid muscles [6]. Paresis patients also demonstrate a constellation of signs or symptoms, although not all are present in every patient [6]. These include: reports of vocal fatigue; changes in pitch range, especially the higher pitches; lack of projection; subtle vocal fold asymmetry (lag) of mucosal wave; incomplete glottal closure; and impaired mobility of the arytenoid cartilage [7–9, 10 ,11]. This review will discuss research papers written from 2011 to the present in the areas of cause and incidence, clinical assessment and clinical management, specifically for UVFP. &
Voice Treatment Center, Medical Faculty Associates, Division of Otolaryngology, Department of Surgery, The George Washington University Medical Center, Washington, District of Columbia, USA Correspondence to Sheila V. Stager, PhD, CCC-SLP, Voice Treatment Center, Medical Faculty, Associates, 2021K Street NW, Suite 206, Washington, DC 20006, USA. Tel: +1 202 741 3265; fax: +1 202 741 3218; e-mail: sstager@mfa,gwu.edu Curr Opin Otolaryngol Head Neck Surg 2014, 22:444–449 DOI:10.1097/MOO.0000000000000112 Volume 22 Number 6 December 2014
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Vocal fold paresis Stager
KEY POINTS The gold standard for diagnosing unilateral paresis is either RLN or SLN injury as assessed by laryngeal electromyography.
Iatrogenic Incidence data for iatrogenic cause are primarily from studies following thyroid surgery. In one study, the incidence of RLN injury resulting in vocal fold weakness following thyroidectomy was 6.6% in 320 patients [15]. In a Danish study [16 ], after a median of 7 months after surgery, 142 of the 6859 individuals (2%) were found to have unilateral ‘permanent’ palsy (permanent palsy defined as any partial or complete immobility). Of these 142 patients, 76 (54%) were from surgeries with benign histology. Another study reported that 17/26 individuals with EMG data before and after surgery were found to have unilateral or bilateral paresis prior to thyroidectomy surgery, but only seven reported any vocal symptoms. Following surgery, only five reported voice complaints [17]. Incidence data have also been reported for surgical resection of cerebellopontine angle tumors. Among 181 patients, 10% were found to have unilateral palsy (defined as unilateral vocal fold motion impairment) [18]. &
The glottal function index may prove to be a valuable subjective rating scale for demonstrating improvement following treatment. Aerodynamic measure of translaryngeal mid-vowel flow provides useful information to diagnosis and evaluating treatment effects. Patients with idiopathic unilateral paresis may not require a CT work-up, whereas those with idiopathic unilateral paralysis should be followed up with a CT work-up. Trial injections are a good way to determine if more permanent augmentation will improve voice outcomes.
ETIOLOGY Incidence
Intubation
A review of 739 patients over 4 years from a tertiary care practice produced 195 who were thought to have paralysis or paresis [7]. Six were found to have paresis due to RLN damage, one due to superior laryngeal nerve (SLN) damage and two had evidence of combined RLN/SLN nerve damage. No information on the etiology of these cases was provided. An early study reported 31% of the 22 patients with iatrogenic etiology, 23% with viral, 18% with idiopathic, 14% with trauma and another 14% with accompanying muscle tension dysphonia [12]. In our clinic, over a 15-year period, using the criterion of decreased recruitment [6,7] in patients whose onset of symptoms was 9 months or less from the time of initial evaluation, 238 patients were found to have unilateral RLN paresis, 121 had combined unilateral RLN/SLN paresis and eight had unilateral SLN paresis. As far as etiologies were concerned, for those with RLN paresis, 36% were iatrogenic, 32% idiopathic, 13% intubation, 11% malignant and 8% viral. For those with combined RLN/SLN paresis, 44% were iatrogenic, 40% idiopathic, 11% viral, 4% intubation and 2% malignant. For those with SLN paresis, 63% were iatrogenic, 25% idiopathic and 12% viral. To compare, the following percentages have been reported for etiologies of unilateral paralysis: surgical (iatrogenic), 55.6%; malignancy, 17.8%; idiopathic, 13.2%; intubation, 6.2% and central, 1.9% [13]. In a study specifically of elderly patients (65–89 years), the incidence of paresis was found to be 72% (126/175), based on EMG assessment [14].
Normal or limited arytenoid movement and impaired vocal fold movement were documented in 11% (7/60) individuals following arytenoid dislocation due to endotracheal intubation. EMG studies revealed unilateral nerve injury in these individuals [19].
Association of paresis with other disorders Patients with paresis frequently complain of vocal fatigue. It has been thought that part of that percept of fatigue may be due to using vocally hyperfunctional behaviors, as they try to compensate for deficits resulting from nerve injury [6,20]. Granulomas have been also associated with vocal hyperfunction. One study demonstrated 53% of patients with granuloma may have had underlying glottal insufficiency, and one possible cause of that glottal insufficiency was decreased mobility of the arytenoid [21]. An earlier study also reported granulomas on the contralateral vocal process in three patients with unilateral SLN injury [22]. Paresis has been associated with not only development of granuloma but also with reflux disease. A third of the patients with an original diagnosis of reflux disease that proved recalcitrant to proton pump inhibitor therapy were subsequently found to have paresis [23 ]. Two studies have listed other voice disorders that co-occurred in patients with unilateral or bilateral paresis involving injury to RLN and/or SLN [6,12].
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CLINICAL ASSESSMENT Assessment of paresis currently is based on patient report, followed by endoscopic examination, followed by EMG assessment for confirmation of nerve injury. Very few objective measures have been used. Finding sensitive-enough measures may be difficult, given the subtlety of the symptoms and the other voice disorders that can co-occur with paresis. The following section offers some suggestions.
Self-rating scales The diagnosis of paresis is suspected when patients report vocal fatigue, an inability to project, and loss of their higher register. For example, in a survey of frequency of voice symptoms in thyroid cancer patients following surgery, the largest percentages of complaints were inability to get loud (52.5%), inability to sing (54%), and pain while speaking (29.2%) [10 ]. The glottal function index is a 4-question 6-point Likert self-rating scale of severity of patient symptoms, specifically vocal effort, vocal fatigue, throat pain after talking, and voice cracking or sounding different [24]. It has been validated with the degree of glottal insufficiency [24]. Changes in patients’ responses to this index may provide a mechanism to track perceived change following treatment. &
Endoscopy and high-speed videoendoscopy Endoscopic findings from patients with paresis can include the following: asymmetry between left and right vocal fold mucosal waves (also known as lag or ‘chasing wave’); incomplete glottal closure; and impaired mobility of the arytenoid cartilage. However, there are several issues that preclude using endoscopic examination as the gold standard for diagnosis. Because of the subtlety of the asymmetry, several studies have focused on ways to accentuate it during the endoscopic examination. Repetitive phonatory tasks have been used for patients with SLN paresis [25]. These tasks are meant to ‘fatigue’ the system, thereby making asymmetry more obvious. While these tasks did improve the ability to assess mild asymmetry, looking at the whole endoscopic examination was most helpful in identifying the injured side. Asking the patient to whistle has also been used to make the asymmetry more pronounced [8]. Asymmetry has also been studied using high-speed videoendoscopy. In a case study, analyzing the cycle by cycle vocal fold vibration using high-speed videoendoscopy brought out asymmetry not visible during the traditional endoscopic and stroboscopic techniques [26]. Another study also 446
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used a technique called Fourier image to quantify phase relations between parts of the vocal folds from high-speed videoendoscopy recordings. Asymmetries were found in normophonic speakers, suggesting that this methodology may be sensitive to the subtle asymmetries of unilateral paresis patients [27]. A second endoscopic finding – incomplete glottal closure – has been studied using a frame-byframe determination of percentage of closure duration. The number of frames in which the vocal folds are closing or are closed is calculated, and this is divided by the total number of frames in a vibratory cycle [28]. Patients with paresis had a shorter percentage of closure duration (34% compared to 50% in normal). Another study had looked at the size of the glottal gap to compare RLN and SLN injury. Glottal gap was larger in those with SLN injury during the closed phase and smaller during the open phase, which was interpreted to mean that there were poorer vibration dynamics during vibration with SLN injury [29 ]. Several studies have demonstrated lack of agreement between raters asked to determine the side of the nerve injury, especially if both arytenoids demonstrate full extent of movement, closure is good, and hyperfunctional compensatory behaviors are present [9,30]. The interarytenoid spatial relationship was developed to see if improvements could be made in residents’ abilities to determine the correct side of paresis, the side demonstrating EMG abnormality recorded from the lateral cricoarytenoid (LCA) muscle [30]. The spatial relationship between the cuneiform and corniculate cartilages is different on the nerve-injured side compared to the normal side. With training on visualizing these differences, residents were able to improve their accuracy [30]. &&
Ultrasound Colleagues in Asia have been examining the usefulness of pre and postoperative ultrasound recordings in determining which patients have paresis following thyroidectomy. One study claims good sensitivity and specificity of ultrasound in determining those who may have unilateral paresis following surgery when compared with laryngoscopic images [31 ]. &
Computed tomography and other imaging This was one area in which the diagnosis of paresis or paralysis was important. A review article summarizing results from five studies suggested that computed tomography (CT) testing should be completed following a diagnosis of idiopathic paralysis (not paresis), as an average of 81% were found to Volume 22 Number 6 December 2014
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Vocal fold paresis Stager
have malignancies [32]. If the initial CT scan was normal, further scanning was unwarranted. Patients with a diagnosis of idiopathic paresis and not paralysis may not require a CT work-up [33 ]. Among the patients diagnosed with idiopathic vocal fold paresis, 98% had normal CT studies, and the one patient whose CT scan was not normal was further evaluated with a PET-CT that was negative.
study has reported significant differences in nonlinear dynamic measures between controls and those with unilateral paralysis [38].
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Laryngeal electromyography A meta-analysis [34] of studies on the use of EMG for the diagnosis and management of paresis/paralysis patients revealed three level IV studies [7,12,35]. They were classified as level IV evidence because they were retrospective and unblinded. Another excellent review paper [6] was done on the clinical usefulness of EMG.
Acoustic measures Although they have not been reported in studies assessing patients for paresis, it might be assumed that the time-based acoustic measures of jitter and shimmer might prove useful, as they are thought to reflect asymmetries in vibration. They are valid for relatively periodic signals, and are threshold measures, meaning there is a point along a continuum that designates normal from abnormal. They are not linear, because a jitter measure of 2 is not twice as abnormal as a measure of 1. Reliability of these measures has been questioned. Another acoustic variable used in our clinic is the presence of glottal stops in the context of words ending with a vowel or /t/ and the next word beginning with a vowel sound. This can be observed during the endoscopic examination as dynamic medial–lateral movements of the false vocal folds during the task of repeated /i/ [36]. Some paresis patients, when asked to repeat /i/ syllables, cannot produce glottal stops, rather they voice continually, and no medial–lateral movement of the false vocal fold on the nerve-injured side is observed endoscopically. Listeners are able to perceptually distinguish between paresis patients and controls on this parameter [37]. This inability to produce glottal stops is present in about 60% of patients with paresis/paralysis, but is not found in normal or patients without injury to the RLN. Nonlinear dynamic measures have been put forward to assess aperiodicity in acoustic signals. They have primarily been developed to assess signals that are more aperiodic than can be analyzed using more traditional time-based measures. It remains to be seen if the subtle asymmetry of unilateral paresis patients can be captured by these measures. One
Aerodynamic measures Our clinic uses two aerodynamic measures: air flow and s/z ratio [39]. Patients with slight vocal fold asymmetry often demonstrated elevated flows, and when they were subsequently tested with EMG, they were diagnosed with paresis. Increased flow has been significantly correlated with reduced interference pattern of motor neurons (poor recruitment) [40,41], and increased patient perception of effort [42]. Since both of these can be characteristic of patients with paresis, obtaining flow signals becomes an important clinical assessment tool. If flow signals cannot be obtained, then the s/z ratio can be substituted. Ratios greater than 1.4 suggest some degree of glottal insufficiency. A ratio can demonstrate abnormality, even if the measures in the numerator and denominator are both within normal limits. However, the s/z ratio has not been correlated with patient report of increased effort or decreased recruitment. Finally, computer modeling [43] and canine studies [44 ,45 ] have been devised to explore how small differences in activation of both the RLN and SLN affect vocal fold vibration. By changing the activation of the RLN, the normal vocal fold leads during the opening phase, a larger lateral excursion is found for the paretic side, larger air flow occurs, and phonation onset pressures are affected [45 ]. Thus, phonation threshold pressures (PTPs) should be considered as a way to study the role of SLN injury in paresis patients. By changing the activation of the SLN, the side with greater tension (i.e. the normal side) leads in the opening phase, and has increased closure speed. The greater the asymmetry in activation, the more chaotic is the vibratory pattern [44 ]. &&
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CLINICAL MANAGEMENT If the time between initial evaluation and onset of symptoms is 9 months or less, the first line of clinical management can often be observation to determine if spontaneous nerve recovery will occur. Voice therapy is also an option during this time [6]. In general, if patients are not happy with the outcome following voice therapy, then the next step is to do a temporary injection medialization [6]. Injectables lasting a varying amount of time before resorption have been developed. Shorter-acting injectables include Radiesse Voice Gel and Cymetra, and are thought to last about 2–3 months. Bovine
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collagen and hyaluronic acid last a little longer, around 3–6 months. Autologous fat and Radiesse can last up to 12 months [46].
Injection medialization A newer strategy has been to introduce a trial injection before completing a temporary or permanent injection medialization [47]. Trial injections use a temporary augmentation material to determine the degree and nature of vocal quality improvement from augmentation in cases of severe vocal fold paresis when it is not clear if bulk alone will be enough to improve the voice; or allow patients to see the potential results from an augmentation procedure when other therapies have failed [47]. One study used three types of shorter-acting injectables (Cymetra, gelfoam or Radiesse Voice Gel) on 25 patients with paresis and/or atrophy. The authors used patient-subjective responses to categorize them into having a good outcome, partial improvement, or poor outcome from the trial injection. Almost all who reported a good outcome went on to have a permanent augmentation procedure, and almost none of those who reported a poor outcome went on to have a permanent augmentation. Those who went on to have a permanent augmentation procedure were satisfied with their voice outcome. A review of the current practice in injection augmentation [48] reported that for patients with paresis, half of the procedures are done in the office, and half in the operating room. Half of the procedures are unilateral injections and half bilateral. Materials used in office procedures were primarily Radiesse Voice Gel and bovine collagen. In the operating room, fat and Radiesse were also injected. A study has demonstrated significant improvements in the Voice Handicap Index-10 scores in patients with hypomobility with confirmed nerve injury 1–8 weeks following treatment with Radiesse Voice Gel [49].
Medialization thyroplasty In our clinical experience, we have used several modalities of treatment. Over 15 years, we treated 216 patients with unilateral paresis (defined as having ratings of 1þ to 3þ on recruitment, where 4þ was normal and 0 was considered to represent paralysis) who were initially evaluated within 9 months of onset of their symptoms. Among these patients, 41% chose to be observed, 21% were injected with temporary materials, 19% had medialization thyroplasty, and 5% went for voice therapy. Another 14% equired multiple types of treatments to be 448
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satisfied with their voice outcome. In general, those whose EMG recruitment ratings were more impaired (ratings of þ1 and þ2) had more permanent and multiple treatments. Various outcome measures were made, but are not reported in this paper. Medialization thyroplasty also plays a role in patients who continue to demonstrate unilateral paresis 1 year or more after onset of symptoms. By this time, any spontaneous nerve recovery should have occurred. In our clinic, we have treated the following numbers of patients who were evaluated for at least 12 months (up to 34 years) after onset: 79 with unilateral RLN injury, 40 with unilateral RLN/SLN injuries, and one with unilateral SLN injury. Both injection medialization and medialization thyroplasty were used.
CONCLUSION To advance studies on the assessment and treatment of patients with UVF paresis, finding measures that significantly correlate with EMG results would be beneficial, especially since availability of EMG testing on a routine basis is limited. This means that those facilities that are able to obtain EMG recordings need to lead the way in investigating assessment and treatment tools for unilateral paresis patients. Comparisons of objective measures should be made between patients with unilateral vocal fold paralysis and those with UVFP. Randomized clinical trials need to be completed to provide level 1 evidence of the efficacy of various treatments. Acknowledgements None. Conflicts of interest There are no conflicts of interest.
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Vocal fold paresis Stager 7. Simpson CB, Cheung EJ, Jackson CJ. Vocal fold paresis: clinical and electrophysiologic features in a tertiary laryngology practice. J Voice 2007; 23:396–398. 8. Rubin AD, Sataloff RT. Vocal fold paresis and paralysis: what the thyroid surgeon should know. Surg Oncol Clin N Am 2008; 17:175–196. 9. Simpson CB, May LS, Green JK, et al. Vibratory asymmetry in mobile vocal folds: is it predictive of vocal fold paresis? Ann Ototogy Rhinol Laryngol 2011; 120:239–242. 10. Kuhn MA, Bloom G, Myssiorek D. Patient perspectives on dysphonia after & thyroidectomy for thyroid cancer. J Voice 2013; 27:111–114. This study summarizes a large scale survey of voice problems post-thyroid cancer surgery, excluding patients with pre-existing voice problems and postoperative vocal fold immobility. 11. Blitzer A, Crumley RL, Dailey SH, et al. Recommendations of the Neurolaryngology Study Group on laryngeal electromyography. Otolaryngol Head Neck Surg 2009; 140:782–793. 12. Heman-Ackah YD, Barr A. Mild vocal fold paresis: understanding clinical presentation and electromyographic findings. J Voice 2006; 20:269–281. 13. Spataro EA, Grindler DJ, Paniello RC. Etiology and time to presentation of unilateral vocal fold paralysis. Otolaryngol Head Neck Surg 2014; 151:286– 293. 14. Gregory ND, Chandran S, Lurie D, Sataloff RT. Voice disorders in the elderly. J Voice 2012; 26:254–258. 15. Echternach M, Maurer C, Mencke T, et al. Laryngeal complications after thyroidectomy. Arch Surg 2009; 144:149–153. 16. Godballe C, Madsen AR, Sørensen CH, et al. Risk factors for recurrent nerve & palsy after thyroid surgery: a national study of patients treated at Danish departments of ENT Head and Neck Surgery. Eur Arch Otorhinolaryngol 2014; 271:2267–2276. This study reports on a large-scale survey to document possible risk factors for voice problems following thyroid surgery. 17. Caroline M, Joglekar SS, Mandel SM, et al. The predictors of postoperative laryngeal nerve paresis in patients undergoing thyroid surgery: a pilot study. J Voice 2012; 26:262–266. 18. Best SR, Starmer HM, Agrawal Y, et al. Risk factors for vagal palsy following cerebellopontine angle surgery. Otolaryngol Head Neck Surg 2012; 147:364–368. 19. Xu W, Han D, Hu R, et al. Characteristics of vocal fold immobility following endotracheal intubation. Ann Otol Rhinol Laryngol 2012; l2l:689–694. 20. Mayes RW, Jackson-Menaldi C, DeJonckere PH, et al. Laryngeal electroglottography as a predictor of laryngeal electromyography. J Voice 2008; 22:756–759. 21. Carroll TJ, Gartner-Schmidt J, Statham MM, Rosen CA. Vocal process granuloma and glottal insufficiency: an overlooked etiology? Laryngoscope 2010; 120:114–120. 22. Halum SL, Miller P, Early K. Laryngeal granulomas associated with superior laryngeal nerve paresis. J Voice 2010; 24:490–493. 23. Rafii B, Taliercio S, Achlatis S, et al. Incidence of underlying laryngeal && pathology in patients initially diagnosed with laryngopharyngeal reflux. Laryngoscope 2014; 124:1420–1424. This study illustrates the complex interactions of vocal fold disorders. 24. Bach KK, Belafsky PC, Wasylik K, et al. Validity and reliability of the glottal function index. Arch Otolaryngol Head Neck Surg 2005; 131:961–964. 25. Rubin AD, Praneetvatakul V, Heman-Ackah Y, et al. Repetitive phonatory tasks for identifying vocal fold paresis. J Voice 2005; 19:679–686. 26. Mortensen M, Woo P. High-speed imaging used to detect vocal fold paresis: a case report. Ann Otol Rhinol Laryngol 2008; 117:684–687. 27. Krenmayr A, Wollner T, Supper N, Zorowka P. Visualizing phase relations of the vocal folds by means of high-speed videoendoscopy. J Voice 2012; 26:471– 479. 28. Carroll TL, Wu Y-HE, McRay M, Gherson S. Frame by frame analysis of glottic insufficiency using laryngovideostroboscopy. J Voice 2012; 26:220–225. 29. Pei Y-C, Fang T-J, Li H-Y, Wong AMK. Cricothyroid muscle dysfunction && impairs vocal fold vibration in unilateral vocal fold paralysis. Laryngoscope 2014; 124:201–206. This study demonstrates an interesting quantitative measure of glottal gap.
30. Sufyan AS, Kincaid JC, Wannemuehler TJ, Halum SL. The interarytenoid spatial relationship: accuracy and interrater reliability for determining sidedness in cases of unilateral adductor paresis. J Voice 2013; 27:90–94. 31. Wong K-P, Lang BH-H, Ng S-H, et al. A prospective, assessor-blind evalua& tion of surgeon-performed transcutaneous laryngeal ultrasonography in vocal cord examination before and after thyroidectomy. Surgery 2013; 154:1158– 1165. This study suggests a possible new tool to select patients who need direct laryngoscopy before and after thyroidectomy. 32. Tsikoudas A, Paleri V, El-Badawey MR, Zammit-Maempel I. Recommendations on follow-up strategies for idiopathic vocal fold paralysis: evidencebased review. J Laryngol Otol 2012; 126:570–573. 33. Badia PI, Hillel AT, Shah MD, et al. Computed tomography has low yield in the && evaluation of idiopathic unilateral true vocal foldparesis. Laryngoscope 2013; 123:204–207. This is an important study with ramifications for bringing down cost of evaluating patients with idiopathic unilateral vocal fold paresis. 34. Meyer TK, Hillel AD. Is laryngeal electromyography useful in the diagnosis and management of vocal fold paresis/paralysis? Laryngoscope 2011; 121:234– 235. 35. Statham MM, Rosen CA, Smith LJ, Munin MC. Electromyographic laryngeal synkinesis alters prognosis in vocal fold paralysis. Laryngoscope 2010; 120:285–290. 36. Stager SV, Bielamowicz SA, Regnell JR, et al. Supraglottic activity: evidence of laryngeal articulation vs. vocal misuse. J Speech Lang Hearing Res 2000; 43:229–238. 37. Leydon C, Bielamowicz SA, Stager SV. Perceptual ratings of vocal characteristics and voicing features in untreated patients with unilateral vocal fold paralysis. J Commun Disord 2005; 38:163–185. 38. Yan N, Wang L, Ng ML. Acoustical analysis of voices produced by Cantonese patients of unilateral vocal fold paralysis. 2013 IEEE International Conference on Signal Processing, Communications and Computing, ICSPCC 2013; 6664001. 39. Stager SV. Objective evaluation of patients with vocal fold paralysis and paresis. Paper presented at International Federation of Oto-Rhino-Laryngological Societies in Seoul, South Korea. 2013. 40. Bielamowicz SA, Stager SV. Diagnosis of unilateral recurrent laryngeal nerve paralysis: laryngeal electromyography, subjective rating scales, acoustic and aerodynamic measures. Laryngoscope 2006; 116:359–364. 41. Sanuki T, Yumoto E, Nishimoto K, Minoda R. Laryngeal muscle activity in unilateral vocal fold paralysis patients using electromyography and coronal reconstructed images. Otolaryngol Head Neck Surg 2014; 150: 625–630. 42. Stager SV, Bielamowicz SA. Perceived vocal fatigue and effort in relation to laryngeal functional measures in paresis patients. Laryngoscope 2014; 124:1631–1637. 43. Zhang Z, Luu TH. Asymmetric vibration in a two-layer vocal fold model with left-right stiffness asymmetry: experiment and simulation. J Acoust Soc Am 2012; 132:1626–1635. 44. Chhetri DK, Neubauer J, Bergeron JL, et al. Effects of asymmetric superior && laryngeal nerve stimulation on glottic posture, acoustics, vibration. Laryngoscope 2013; 123:3110–3116. The procedure for studying asymmetry was well thought out. 45. Chhetri DK, Neubauer J, Sofer E. Influence of asymmetric recurrent laryngeal && nerve stimulation on vibration, acoustics, and aerodynamics. Laryngoscope 2014. [Epub ahead of print] The procedure for studying asymmetry was well thought out. 46. Mallur PS, Rosen CA. Vocal fold injection: review of indications, techniques, and materials for augmentation. Clin Exp Otorhinolaryngol 2010; 3:177–182. 47. Carroll TL, Rosen CA. Trial vocal fold injection. J Voice 2010; 24:494–498. 48. Sulica L, Rosen CA, Postma GN, et al. Current practice in injection augmentation of the vocal folds: Indications, treatment, principles, techniques, and complications. Laryngoscope 2010; 120:319–325. 49. Mallur PS, Morrison MP, Postma GN, et al. Safety and efficacy of carboxymethylcellulose in the treatment of glottic insufficiency. Laryngoscope 2012; 122:322–326.
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