Common Diagnoses And Treatments

Otolaryngol Clin N Am 40 (2007) 1025–1061

Common Diagnoses and Treatments in Professional Voice Users Ramon A. Franco, MD*, Jennifer G. Andrus, MD Division of Laryngology, Massachusetts Eye & Ear Infirmary, Department of Otology and Laryngology, Harvard Medical School, 243 Charles Street, Boston, MA 02114, USA

Common problems among all patients with vocal difficulties seen by the laryngologist also are common among professional voice users. These include laryngopharyngeal reflux, muscle tension dysphonia, fibrovascular vocal fold lesions (eg, nodules and polyps), cysts, vocal fold scarring, and changes in vocal fold mobility. Microvascular lesions and their associated sequelae of vocal fold hemorrhage and laryngitis due to voice overuse are more common among professional voice users. Much more common among professional voice users is the negative impact that voice problems have on their ability to work, on their overall sense of well-being, and sometimes on their very sense of self. In diagnosing voice disorders in professional voice users, clinicians must possess and clearly convey an understanding of this important truism, which will facilitate trust, confidence, and the opportunity to treat the patient. This article reviews the diagnosis and treatment options for common problems among professional voice users, emphasizing the importance of gaining insight into the ‘‘whole’’ patient and of developing individualized management plans. History and physical examination The history and physical examination are addressed at length elsewhere in this issue; however, a few key points are worth mentioning here as well. First, because of the critical role that the voice plays in the livelihood of a professional voice user and the frequent association of the voice as a major component of one’s identity, changes in voice frequently create significant anxiety for these patients. This anxiety, a fear of the unknown, and a swarm of emotions commonly accompany professional voice users to * Corresponding author. E-mail address: [email protected] (R.A. Franco). 0030-6665/07/$ - see front matter Ó 2007 Elsevier Inc. All rights reserved. doi:10.1016/j.otc.2007.05.008

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the laryngologist’s office and may be barriers to the patient’s ability to clearly describe the problems he/she is having with the voice. Patient questionnaires can help to overcome this difficulty and facilitate an efficient visit. They are invaluable. The patient can be asked to fill out a history intake form in the waiting room, along with the voice-related quality of life (VRQOL) survey and a voice outcome survey. In addition to defining the effects of the voice problem on the patient’s functional capacity, the surveys are helpful for tracking the voice problem and the effect of therapy on it. Second, the history will help to establish the acuity or chronicity and severity of the problem. Along with symptoms, past medical/surgical history, allergies, and medications, particular attention should be paid to the social history, including place of residence; student or employment status; current and previous tobacco, alcohol, and drug use; exposure to second-hand smoke or chemical irritants/pollutants; and water, caffeine, carbonated beverage, chocolate, peppermint, and fatty/spicy/acidic food consumption. Changes in a patient’s routine (eg, time of day one practices, performance venue, consumption of caffeinated beverages) often yield important information. The history also gives clues as to what endoscopy may show. Clinicians are encouraged to use the history to help guide the physical examination, but are cautioned to keep an open eye for unsuspected diagnoses. Similarly, history and physical examination together will help the clinician to develop a differential diagnosis. More often than not, multiple entities contribute to one symptom complex, so the laryngologist is cautioned not to look for ‘‘the’’ single unifying diagnosis. Thinking about laryngeal pathology in terms of acute versus subacute versus chronic problems may be more useful than a traditional schema of vascular, inflammatory, traumatic, autoimmune, iatrogenic, neoplastic, or congenital problems. Nonetheless, the clinician is reminded that professional voice users are subject to the same possibilities as are other patients; therefore, neoplastic and autoimmune processes, for example, should not be overlooked. Third, many, if not most, pathologic entities in the larynx occur on a continuum and are dynamic given the demands on the professional voice user’s ‘‘instrument.’’ Ongoing, long-term (if not lifelong) voice use in any number of performance venues constantly subjects the larynx to insults, such as phonotrauma, reflux, second-hand (or first-hand) smoke, and chemical exposures, often under suboptimal conditions (poor acoustics, arid atmosphere, and concomitant physical demands, such as dancing). Any one condition is likely to wax and wane in severity depending on the patient’s general health, vocal demands, rehearsal and event schedule, performance venues, and the subsequent diet and lifestyle that ensue. Among the most important of the laryngologist’s tasks are eliciting these details, educating patients about ways to meet their professional demands while maximizing vocal hygiene, and supporting them in their efforts. Finally, laryngologists frequently see professional voice users for a second or third opinion after they have been evaluated by other otolaryngologists.

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Sometimes the patient is in denial and does not want to believe what another clinician has diagnosed or does not want to pursue the recommended treatment options. Another frequent scenario is that the patient has been told that he/she has a normal larynx and that nothing on examination can explain the symptoms. In these cases, it is especially important to elicit a detailed history and to be clear about what bothers the patient about the voice. Sometimes edema from laryngopharyngeal reflux masks a mass lesion or hyperfunction is so severe that the vocal folds are not seen easily on fiberoptic evaluation. Flexible distal-chip laryngoscopes are providing examinations superior to fiberoptic laryngoscopy and approximating rigid laryngoscopy, such that subtle findings now are being noted that may not have been seen without this technology. Of utmost importance, it is essential to listen to the patient, to acknowledge that something is wrong, even if the exact diagnosis is not obvious, to take a team approach with a voice therapist, and to ‘‘stick’’ with the patient until a diagnosis and treatment plan are formed and executed.

Voice problems in professional voices users: diagnoses and treatment options Laryngopharyngeal reflux Laryngopharyngeal reflux is the retrograde movement of gastric contents (acid and enzymes, such as pepsin) into the laryngopharynx leading to symptoms referable to the larynx, hypopharynx, and nasopharynx (Fig. 1) [1]. Typical laryngopharyngeal reflux symptoms include dysphonia, globus pharyngeus, mild dysphagia, chronic cough, excessive throat mucus, and

Fig. 1. Laryngopharyngeal reflux. Note diffuse periarytenoid and postcricoid edema, vocal fold edema, and pseudosulcus (the appearance of a ‘‘second’’ vocal fold inferior to the true vocal fold due to edema). The larynx is wet appearing; copious, thick mucus is not seen in this patient as in others.

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nonproductive chronic throat clearing [2]. In singers, voice changes, such as loss of rangedespecially in the high frequencies, voice breaks, increased vocal fatigue, anterior neck discomfort or tightness, or loss of vocal clarity may be the primary complaint and may or may not present with the aforementioned common laryngopharyngeal reflux manifestations. Symptoms may come on gradually (eg, conservatory students who are out of school for the summer but increase their vocal use over the course of a semester) or may seem to present subacutely after a sudden increase in voice use (eg, rehearsal week for a show, a speech tournament, an attorney’s long trial) or after a cold that seems to nearly resolve, but is followed by persistent cough and throat clearing. Most patients, including professional voice users, are unaware of laryngopharyngeal reflux as a symptom complex, and most have ‘‘silent reflux,’’ because only 35% of patients who have laryngopharyngeal reflux report heartburn. Laryngopharyngeal reflux is seen primarily as a problem with the upper esophageal sphincter that occurs in the upright position (as opposed to gastroesophageal reflux disease, a problem with the lower esophageal sphincter that occurs mainly in the recumbent position) [1,3]. Laryngopharyngeal reflux is believed to be most frequent during physical exertion, given the increased abdominal pressure and decreased intrathoracic pressure that occurs with bending over, Valsalva maneuver, exercise, and certainly singing, dancing, and public speaking. Chronic or severe coughdfrom an upper respiratory infection, asthma, or even having to feign a cough on staged should be considered in this group of exertions and is a ‘‘tip-off’’ to the potential presence of laryngopharyngeal reflux. Professional voice users may present with only ‘‘voice’’ problems. Therefore, once the ‘‘voice problems’’ are described adequately in the history, it is up to the laryngologist to elicit whether other common laryngopharyngeal reflux symptoms are present. Videolaryngostroboscopy (VLS) is the next key to making a clinical diagnosis of laryngopharyngeal reflux. VLS findings consistent with laryngopharyngeal reflux include postcricoid and periarytenoid edema, true vocal fold edema, a ‘‘wet’’-appearing larynx or the presence of ‘‘more’’ than the usual amount of (thick) mucus in the larynx, particularly on the true vocal folds, and pseudosulcus (Fig. 1) [4]. Together with a history consistent with reflux, these findings are sufficient to diagnose laryngopharyngeal reflux in the opinion of many investigators [1,2,5–7]; however, controversy exists as to whether physical findings alone are sufficient to diagnose laryngopharyngeal reflux, because they are prevalent in the general population (70%) [8]. Thus, many believe that further criteria for the diagnosis of laryngopharyngeal reflux should be used. The reflux finding score, an eight-item validated clinical severity scale, was introduced as a means of offering some standardization to the process of laryngopharyngeal reflux diagnosis [9]. The reflux finding score is an objective measure of the degree of laryngeal change used by a physician after endoscopic evaluation to accurately document treatment efficacy. It was found to have an

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excellent inter- and intraobserver reproducibility. When coupled with the reflux severity index, a self-administered nine-item survey (scored from 0 to 5), the investigators documented improvements in the reflux finding score and the reflux severity index with twice daily proton-pump inhibitor (PPI) therapy [10]. The 24-hour dual-sensor pH/impedance probes are considered by many to be the gold standards for diagnosing laryngopharyngeal reflux. Often, the pharyngeal probe is the key to making the diagnosis, because the esophageal probe results may be ‘‘normal.’’ The sensitivity of single-probe esophageal pH monitoring for laryngopharyngeal reflux was 62% in one study, with a positive predictive value of only 49%. Pharyngeal pH/impedance monitoring can increase the diagnostic accuracy of laryngopharyngeal reflux dramatically; however, as a diagnostic, pH-metry is expensive and not widely available. Conversely, despite superior sensitivity and specificity for acid reflux events over physical examination findings, the dual pH probe could not predict the severity of the patients’ reflux symptoms or signs in a 2002 study [11]. The investigators provided several reasons for the lack of ability of the pH probe to separate patients who did and did not have laryngopharyngeal reflux. They postulated that so little acid exposure is needed to cause laryngopharyngeal reflux that it may not register as positive during the limited 24-hour study. The 69% reproducibility of pharyngeal pH monitoring seen in another study that they cited may indicate that a 24-hour testing period is too short to accurately estimate what is going on the rest of the time [12]. The investigators also considered that there might have been another source for the irritation that was attributable to laryngopharyngeal reflux. Impedance testing may provide even better information for the diagnosis of laryngopharyngeal reflux, especially when done in combination with pH-metry. Most important in the interpretation of these tests is assessing the patterns of pH and pressure changes, whether they correspond with each other, and if they occur in the supine or upright positions. Finally, laryngopharyngeal reflux also can be diagnosed by symptomatic improvement after empiric treatment with high-dose twice-daily proton pump inhibitors. Laryngopharyngeal reflux and gastroesophageal reflux disease differ in their symptom complexes, largely because of differences in the epithelium and physiology of the larynx and esophagus. A full discussion of the topic is beyond the scope of this article; the reader is referred to additional resources to explore these differences and recent research in the area [13,14]. The mechanism of laryngopharyngeal reflux, however, is important to consider in the context of treating professional voice users with the disorder, as their understanding of the problem likely will improve its treatment. Laryngopharyngeal reflux is postulated to cause laryngeal symptoms in two ways: directly and indirectly [6]. According to the direct theory, refluxate directly irritates the laryngeal mucosa through the action of the caustic material resting on the tissues. This causes tissue edema, which is responsible for most laryngopharyngeal reflux symptoms. In the indirect theory, refluxate

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does not make it onto the laryngeal tissues, but rather evokes laryngeal reflexes by irritating other structures, such as the esophagus, that then incite a vagally mediated response (ie, chronic cough, asthma-like symptoms through bronchoconstriction). Regardless of the pathway, factors such as the resting tone of the upper esophageal sphincter and lower esophageal sphincter, the duration and the amount of intra-abdominal pressure elevation, and the volume of stomach contents during exertion are important in the creation of the refluxate bolus [6]. Considering all of the possible contributors to laryngopharyngeal reflux guides its treatment, a multiarmed pathway directed at diet changes, lifestyle/behavior modifications, medical intervention, and, occasionally, surgery. The multimodality treatment for managing laryngopharyngeal reflux addresses upper and lower esophageal sphincter tone, the presence of acid in the stomach, stomach acid production, and mechanical increases in intraabdominal pressure. Thus, diet modifications include avoidance of substances that decrease upper and lower esophageal sphincter tone, such as alcohol, peppermint, fatty foods, chocolate, and caffeine. It is stressed to patients that even ‘‘decaffeinated’’ products and many herbal teas contain caffeine; reading labels to assure that goods are ‘‘caffeine-free’’ is important. Carbonated beverages, even without alcohol or caffeine, will cause belching and lead to stomach refluxate contacting the laryngopharynx. Additionally, patients are advised to avoid acidic foods, which directly irritate the hypopharynx and cause inflammation. These include most fruits (especially citrus and pineapple), tomatoes, jams and jellies, barbecue sauces, and most salad dressings. Spicy foods (hot mustards, curry, hot peppers/hot sauce) are similarly irritating. Behavior modifications play a large role in the management of laryngopharyngeal reflux. It must be stressed to patients that a little common sense can go a long way in limiting the detrimental effects that laryngopharyngeal reflux can have on the voice. Stomach distension increases the likelihood of regurgitation of contents into the esophagus and above. Patients are encouraged to eat smaller meals throughout the day, rather than a few large meals, and to avoid being supine within 3 hours of eating. Raising the head of the bed by placing the frame on blocks, placing the boxspring mattress on blocks inside the bed frame, or using a wedge under the mattress also is recommended (especially if pH-metry and impedance testing demonstrate significant reflux events while supine). Increased intra-abdominal pressure also increases the likelihood of reflux events, so patients are counseled to avoid exercise, heavy lifting, and bending over within several hours of eating. Professional voice users, in particular, are advised to avoid singing/performing within 2 to 3 hours of a meal. These modifications can be difficult for professional voice users to make, especially those who are singing and performing evening events (concerts, shows) on the road, during which days are long and a routine is hard to establish. Nonetheless, vigilant attention to diet and lifestyle changes can result in marked improvement in symptoms.

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Although some patients’ laryngopharyngeal reflux is responsive to diet and behavior modifications alone, most require medication to achieve the best result. It is well accepted among laryngologists that medical management of laryngopharyngeal reflux requires more aggressive and more prolonged treatment than does gastroesophageal reflux disease [1]. High-dose PPI treatment is recommended for at least 6 months, with twice-daily PPI dosing because none of the delayed-release PPIs exert acid suppression for more than 16.8 hours [15,16]. Patients must know to take PPIs on an empty stomach, followed in 30 minutes by a meal. This maximizes efficacy by accounting for the natural physiology of the PPI mechanism of action [17]. Taking PPIs on an empty stomach allows for faster transit to the small bowel, prompt absorption, and the development of maximal plasma levels. Eating causes stomach distension and the activation of proton pumps. These activated proton pumps are turned off by PPIs by the irreversible inhibition of acid secretion that occurs when maximal plasma levels of the PPIs are achieved immediately before the meal. Some patients manifest nocturnal acid breakthrough with nocturnal cough or morning hoarseness. This is addressed best with the addition of high-dose histamine-2 blockers, such as ranitidine, 300 mg orally, nightly before bed. It takes a minimum of 6 to 8 weeks to achieve reduction in symptomsd and although some patients note a difference in the first few days of vigilant therapydall should be counseled to be patient and diligent with the treatment plan. It takes 6 months or longer for the laryngeal findings of laryngopharyngeal reflux to improve [1,10,18]. The reflux severity index and reflux finding score can be used to assess treatment efficacy, although patient history is adequate. Professional singers are especially sensitive to subtle changes in voice and so recognize when small changes in diet, stress, or routine exacerbate their laryngopharyngeal reflux. Once laryngopharyngeal reflux is controlled well, some patients slowly can reintroduce a few reflux-exacerbating foods or begin to wean off PPIs; however, patients should be counseled to keep track of their symptoms, and laryngologists should be liberal about represcribing twice-daily PPIs at the slightest sign of return of laryngeal signs or symptoms. Rarely, a patient will be unresponsive or inadequately responsive to diet changes, behavior modifications, and maximum pharmacotherapy. Some patients have a good initial response that is maintained for some months but ‘‘backslide’’ over time, despite adherence to their diet and behavior changes. Many of these patients develop a relative tolerance to the specific PPI that they are taking, and a change from one specific medication to another seems to reestablish efficacy. Sometimes, two or three changes in medication are necessary to obtain the best response or the least disturbing side effect profile; however, some patients, despite all best efforts, remain symptomatic. This group should be referred to a gastroenterologist and a general surgeon for evaluation of refractory reflux and possible fundoplication. Eliminating much of the morbidity associated with the traditional open

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approach, laparoscopic fundoplication frequently is successful [19,20]. Young, thin patients who have severe reflux may be particularly well served by fundoplication. Finally, transnasal esophagoscopy (TNE) is recommended as a screening tool for evaluating the esophagus in patients who have long-standing, severe, or refractory laryngopharyngeal reflux or complicated gastroesophageal reflux disease. This awake, nonsedated procedure can be performed in the office with topical anesthesia alone, biopsy can be performed as necessary, any abnormalities identified can be documented, and gastroenterology consultation can be obtained as warranted. TNE is a high-yield diagnostic tool that aids the laryngologist/otolaryngologist in providing comprehensive care for one’s patients [21–23]. Fungal laryngitis Historically, fungal laryngitis was considered an opportunistic infection in immunocompromised hosts indicative of likely invasive local or pulmonary fungal disease, if not systemic fungal disease (Fig. 2). Isolated laryngeal disease was believed to be exceedingly rare, and suspicion of laryngeal disease nearly always prompted investigation for systemic disease and possible immunosuppression [24]. In studies that diagnosed fungal laryngitis by culture or biopsy, the causative organism usually was candida species (ie, Candida albicans) [24,25]. Other known pathogens include Blastomyces (common in the Eastern United States and Midwest), Histoplasma (endemic to the Ohio and Mississippi River Valleys), and Coccidioides (found in the Southwestern United States and the cause of ‘‘Valley fever’’) [25,26]. More recently, fungal laryngitis has been recognized as a local superficial infection of the supraglottis or true vocal folds in immunocompetent hosts

Fig. 2. Fungal laryngitis. White fungal plaques on an erythematous base are seen in the midmusculomembranous region of both vocal folds. Fungal laryngitis also can manifest as multiple punctate white plaques throughout the larynx.

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with risk factors that compromise mucosal barrier integrity [26–28]. These include laryngopharyngeal reflux, smoking, and the use of inhaled steroids [26–29]. Prolonged antibiotic use and radiation also have been identified as risk factors [26,27]. Patients with any of the above noted risk factors, diabetes mellitus, nutritional deficits, on immunosuppressive therapy, or in an immune-suppressed state who present with dysphonia, dysphagia, odynophagia, pain, or a sensation of ‘‘burning in the throat’’ should be suspected of having fungal laryngitis [26–28]. The astute clinician who is aware of these risk factors will ask about associated symptoms and whether the onset of the symptoms corresponded to changes in risk factor profile (eg, a new inhaled steroid, a recent illness, uncontrolled blood glucose levels). Then, the clinician will look for signs on laryngoscopy that are indicative of fungal laryngitis: leukoplakia, white or gray pseudomembrane adherent to mucosa, mucosal edema and erythema, mucosal ulceration, and contact bleeding. Findings often mimic that of early oral thrush; however, the lack of white plaques, or leukoplakia, in the presence of diffuse erythema can be caused by fungal laryngitis. The laryngologist also must look for other lesions. Malignancy should be in the differential diagnosis, especially in the smoking population. Diagnosis in these patients commonly rests on clinical suspicion based on history, risk factors, laryngoscopy findings, and response to empiric treatment with oral antifungal agents [28]. Patients who fit the clinical picture of fungal laryngitis can be treated with oral fluconazole for 3 weeks (200 mg on day 1, followed by 100 mg daily on days 2 through 21) in conjunction with nystatin swish and swallow (100,000 units/mL at 10 mL three times daily for 7 to 10 days). Some clinicians treat with nystatin for 3 weeks first, followed by fluconazole if there is no response; others use only fluconazole [26,28]. Although fluconazole is known to increase liver enzymes, Stone and Anderson [28] do not routinely check liver function tests. Patients who have hepatic disease can be treated with nystatin as a first-line agent and referred to their primary care physician for evaluation of their candidacy for systemic antifungal treatment if they fail to respond appropriately. Because antifungal treatment often is concomitant with antireflux treatment, response to therapy can be multifactorial. If there is any question about the diagnosis of fungal laryngitis, should symptoms/signs not resolve, or should malignancy be a significant concern, a definitive diagnosis can be obtained with laryngeal brushings and culture or biopsy. This can be accomplished with in-office transnasal flexible laryngoscopy and biopsy through a working channel on the endoscope. Often, periodic acid-Schiff or methenamine silver stains are necessary to see fungal elements on histopathologic evaluation [26,27]. Some patients who have fungal laryngitis with severe dysphagia also may have esophageal candidiasis. If this is suspected, TNE is recommended to examine the esophagus and to obtain biopsies as necessary. Patients who have severe dysphonia and pain also may present with significant honey-colored crusts in the larynx in addition to multiple white plaques over

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erythematous bases and edema. In these patients, a bacterial superinfection can be presumed present, and oral clindamycin, 600 mg three times daily (or similar antibiotic with gram-positive and anaerobic coverage) for 3 weeks, added to the antifungal therapy. Again, this is an empiric treatment; cultures are not obtained at initial evaluation. These patients usually do not respond to antifungals alone. The literature does not reflect the number of professional voice users who have asthma or other obstructive pulmonary disease who have been on inhaled steroids at any point. Considering the broad definition of ‘‘professional voice user,’’ however, it is not difficult to imagine that this number could be significant. Therefore, laryngologists are obligated to seek this history and communicate with the prescribing physician about possible alternatives to inhaled steroids for patients who develop fungal laryngitis. It is not always possible to wean patients off inhaled steroids, in which case short holidays from steroid use may be in order, with or without low-dose prophylactic antifungal use (eg, nystatin or mycelex troches). The use of a spacer with the inhaler should be recommended [28]. Patients also must gargle with water and rinse the oral cavity/oropharynx after each inhaler use. Muscle tension dysphonia Muscle tension dysphonia is a form of voice use/misuse/abuse characterized by excessive muscular effort and usually by pressed phonation [30]. (Access Video on Supraglottic Hyperfunction in online version of this article at: http:// www.Oto.TheClinics.com.)

Other common clinical features include an abnormally low-pitched speaking voice, poor control of the breath stream, frequent hard glottal attacks, obvious cervical muscle tension, and jaw and tongue tension [31,32]. Muscle tension dysphonia is a form of laryngeal hyperfunction, and the two often are considered synonymous. Other synonyms include hyperfunctional dysphonia, muscle misuse dysphonia, hyperkinetic dysphonia, musculoskeletal tension dysphonia, mechanical voice disorder, functional hypertensive dysphonia, laryngeal tension-fatigue syndrome, and laryngeal isometric dysphonia [32]. All of these terms fall under an umbrella diagnosis of functional dysphonia, classically considered an impairment of voice production in the absence of structural change or neurogenic disease of the larynx. In the 1980s and early 1990s, multiple classification schemes for muscle tension dysphonia were proposed, with emphasis on symptom onset, voice quality, and laryngeal movement patterns [33–36]. In the last decade, an important shift in how laryngologists think about functional dysphonia and muscle tension dysphonia has occurred. Namely, it has become evident that muscle tension dysphonia most likely is not a stand-alone entity, but more likely is multifactorial with various contributing causes [31,32,35–37]. That is to say, muscle tension dysphonia often is present on comprehensive laryngologic

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evaluation with other disorders, such as presbylarynges (bilateral vocal fold bowing in an aging patient), laryngopharyngeal reflux, vocal fold polyp, and vocal fold nodules [32,37]. More frequently, muscle tension dysphonia is thought of as a compensatory mechanism for another entity. Another concept that is becoming clear is that although many patients who have muscle tension dysphonia (ie, dysphonia associated with muscle tension patterns on examination) actually may be compensating for organic laryngeal pathology, many nondysphonic patients have findings consistent with muscle tension patterns on laryngeal evaluation. Belafsky and colleagues [37] and Sama and colleagues [38] found evidence for muscle tension (ie, glottal gap on phonation, ventricular compression, anterior–posterior supraglottal compression) in asymptomatic subjects. This underscores the importance of performing a comprehensive voice evaluation of patients, including history, physical examination, VLS, and acoustic and aerodynamic testing, before diagnosing muscle tension dysphonia. Similarly, if symptoms are not consistent with muscle tension dysphonia (ie, there is no dysphonia) but muscle tension patterns are seen on examination, clinicians should think about the potential for the patient to develop muscle tension dysphonia, because muscle tension patterns may signal a natural (unconscious) compensation for a subacute, organic process in evolution. Given these recent developments, the treatment of muscle tension dysphonia should change to parallel our better understanding of it. First and foremost, once muscle tension dysphonia is diagnosed based on history, physical examination, VLS, and voice evaluation, the next step is to elucidate any and all other contributing factors. This echoes the point made previously; many patients present with multiple diagnoses underlying their symptom complex. Once a complete understanding of the individual’s laryngeal structure and function is attained, or at least underway (because addressing reflux, for example, may reveal vocal fold masses), treatment of muscle tension dysphonia may begin. Voice therapy with appropriate laryngeal manipulation is the cornerstone. In professional voice users, especially singers, attention to techniquedin the singing and speaking voicedis imperative. The voice teacher and voice coach must be involved with the patient, speech/voice therapist, and laryngologist. The main purpose of voice therapy is to eliminate supraglottic compression and to retrain true vocal fold vibration. In cases where mass lesions are involved, vocal hygiene will be emphasized. If presbylarynges is underlying muscle tension dysphonia, injection vocal fold medialization or medialization laryngoplasty may be considered. The same is true for patients who have muscle tension dysphonia due to vocal fold paresis. Vocal fold paresis Just as muscle tension dysphonia is increasingly recognized as a compensatory mechanism for underlying organic, and sometimes multiple, vocal

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fold disorders, vocal fold paresis is receiving more attention as a common problem that causes dysphonia. Paralleling the paradigm shift in laryngologists’ thinking about muscle tension dysphonia, more focus is being placed on ‘‘looking’’ for vocal fold paresis as a contributing factor to changes in voice and in the development of hyperfunction. Dysphonia was universally present in 50 consecutive patients diagnosed with vocal fold paresis by Koufman and colleagues [39] in a retrospective review. The next most common symptoms were effortful phonation and vocal fatigue (76%), diplophonia (40%), and odynophonia (12%). Similar symptoms were described by other investigators [40,41]. Decreased projection and decreased range also are symptoms of vocal fold paresis. Laryngeal findings on transnasal flexible laryngoscopy and VLS included unilateral hypomobility (50%), unilateral vocal fold bowing (36%), bilateral bowing (22%), bilateral hypomobility (8%), and axial rotation (8%). Muscle tension patterns were nearly universally observed as anterior–posterior compression or false vocal fold compression. Hypomobility and bowing can be subtle, and abduction can be affected more frequently and more noticeably than adduction. Once vocal fold paresis is suspected based on history and examination, the clinician must decide whether laryngeal electromyography (LEMG) is indicated. This determination must be made on a case-by-case basis. Certainly, the diagnosis of vocal fold paresis rests on LEMG, because asymmetries in arytenoid movement are normal in some patients (ie, there is no decrement in the neuromuscular activity of the larynx) [39]. Differences in arytenoid movement seen on physical examination cannot be used alone to diagnose vocal fold paresis; however, the clinician is obligated to consider the physical findings as well as their impact on function. Although some patients who have LEMG-diagnosed paresis are symptomatic enough to warrant surgical therapy, many, including professional voice users, are able to function well without surgery. Conversely, even those able to function without surgical intervention may benefit from voice therapy, which can be guided by LEMG results. Before performing LEMG, it is important to evaluate with the patient whether LEMG results will influence clinical decision making. It is not surprising for a professional voice user to opt out of a diagnostic procedure if it yields a choice between surgical or nonsurgical management when the patient is ‘‘not ready’’dmentally or functionallydto consider a surgical procedure. This clinical situation is not unusual and emphasizes the importance of assessing with the patient how limiting the voice change is. If it makes sense to perform an LEMG, it should be performed at a separate visit, after which findings are reviewed briefly with the patient before complete electromyographic analysis. Review of final results is reserved for a follow-up visit, during which therapeutic options for treating the vocal fold paresis are presented, if warranted. Concomitant vocal fold pathology must be uncovered and considered in the overall management plan.

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Treatment options for vocal fold paresis include no treatment with observation for resolution or progression, voice therapy alone, and injection augmentation or medialization laryngoplasty, preceded and followed by voice therapy. Koufman and colleagues [39] performed laryngoplasty or lipoinjection in 54% of the aforementioned subjects, with significant improvement achieved in 85%. Medialization techniques are covered at length elsewhere in this issue (see the article about voice surgery). Superior laryngeal nerve (SLN) paresis deserves special mention because it may have devastating effects on singers, given the impact that it has on modulating pitch in the upper range. If loss of high range is among a singer’s complaints and hypomobility in one vocal fold is seen on examination or if symptoms do not improve on maximal laryngopharyngeal reflux therapy with singing therapy in the case of symmetric movement, LEMG is indicated to elucidate whether the SLNs are intact. If isolated SLN paresis is present without vocal fold bowing or signs that vocal fold augmentation/ medialization will be helpful, it is important to provide voice therapy to avoid development of muscle tension dysphonia, to encourage appropriate changes in repertoire, and to provide hope to the patient that the vocal fold paresis may be postviral with potential for resolution. This last point of management is critical: first, patients often are able to cope better with the idea of a temporary disability; second, if the disability is permanent, time in voice therapy and modifying repertoire will be well spent. Benign vocal fold masses: nodules, polyps, and cysts Vocal fold masses are discussed in detail elsewhere in this issue. Here, the similarities and differences in the symptoms, diagnosis, and treatment of vocal fold nodules, polyps, and cysts are presented in brief. Dysphonia is the most common presenting symptom of benign vocal fold masses. The astute clinician may develop some hypotheses as to which type of mass is present on the vocal fold based on specific voice changes, such as loss of range in the high frequencies (commonly associated with nodules) or diplophonia due to a difference in vibratory frequency of the vocal folds (often associated with a unilateral process, such as a polyp). The wise clinician is ever mindful that more than one pathologic process or more than one type of mass can be present. Obtaining a good history is important to help define the cause of the problems that the patient is having with the voice, which helps guide the development of an individualized management strategy. Vocal fold nodules are considered the most common vocal fold lesions in children and adults. They are common among professional voice users as well, especially when one includes in the definition of vocal fold nodules early fibrovascular changes (subtle irregularities of the medial vocal fold edges in the mid-musculomembranous region) that are associated with significant voice use. (Access Video on Nodules in online version of this article at: http://www.Oto.TheClinics. com.)

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Vocal fold nodules (Fig. 3) are the end result of subepithelial scar deposition, primarily changing the mass and stiffness of the vocal fold cover, with little effect on the body [42]. Vocal fold nodules frequently interfere with vocal fold closure, so hoarseness and breathiness are common symptoms. Because of the loss of vocal fold pliability that occurs as the subepithelial scar increases in size, and because of the increased size of the persistent gap as the result of premature contact with incomplete closure, there is a decrease in range and stamina with an increase in vocal fatigue. Nonetheless, the presence of nodules does not imply a change in vocal functioning in all patients. Vocal fold nodules may have been present since childhood, and many singers function exceedingly well with them. The presence of vocal fold nodules on the vocal folds is not always compromising. Vocal fold polyps, another form of subepithelial fibrosis and deposition, are histologically similar to vocal fold nodules, but differ in that they are unilateral. Vocal fold polyps also may present with hoarseness, loss of range, breathiness, and vocal fatigue. Diplophonia may occur as noted

Fig. 3. Vocal fold nodules. (A) The lesions are bilateral. (B) Premature contact is seen on VLS.

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above; dyspnea can occur if the polyp is large enough to obstruct the airway. In professional voice users, the emergence of dyspnea is unlikely; these patients probably would seek laryngologic attention before dyspnea could evolve. The one exception is a hemorrhagic polyp, which can occur suddenly and be large (Fig. 4). (Access Video on Large Obstructive Hemorrhagic Polyp in online version of this article at: http://www.Oto.TheClinics.com.)

Vocal fold cysts present primarily with hoarseness, although diplophonia also may be a problem. Vocal fold cysts are present in the superficial lamina propria and can open into the laryngeal lumen or insert onto the vocal ligament. Vocal fold cysts are categorized as epidermoid (sometimes called squamous inclusion) cysts or mucus retention cysts [42]. Epidermoid cysts are believed to arise from traumatic introduction or ingrowth of keratin into the superficial lamina propria, secondary to phonotrauma, or to be congenital. Mucus retention cysts more likely result from occlusion of mucus glands on the inferior surface of the vocal fold. (Access Video on Pre-op Subepithelial/Mucous Retention Cyst in online version of this article at: http://www.Oto.TheClinics.com.)

Clearly, vocal fold nodules, polyps, and cysts cannot be distinguished by history alone. VLS is the key to their diagnosis. Stroboscopy is essential to an accurate diagnosis because it allows for the assessment of vocal fold closure and phase symmetry, which are not discernable in the absence of stroboscopic light. Stroboscopy’s delineation of the mucosal wave allows the laryngologist to assess its relationship to the mass, and, thus, whether the epithelium/basement membrane zone is involved or whether the mass lies deeper to this. On VLS, vocal fold nodules most frequently are bilateral,

Fig. 4. Hemorrhagic polyp. Associated varices and resolving blood are seen in the left true vocal fold. Note concomitant bilateral pseudosulcus.

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sessile to raised to discretely nodular lesions along the medial edge of the vocal folds, in the midmusculomembranous region (junction of the anterior one third and posterior two thirds of the entire vocal fold). Pronounced vibration of the vocal folds anterior to the nodules is seen frequently [42]. In many cases, there is incomplete closure of the folds and in severe situations, persistent anterior and posterior glottic gaps; the resultant ‘‘hourglass’’ configuration is classic. Vocal fold polyps are more frequently unilateral, broad-based sessile lesions that can be clear, white, or reddish, small or large, and can be pedunculated (small sessile lesions are more common) [42]. Changes in vocal fold stiffness attributable to vocal fold polyps depend on the histologic type: gelatinous polyps, with loose edematous stroma, tend to decrease vocal fold stiffness, whereas telangiectatic polyps, with fibrin collections in the stroma, tend to increase vocal fold stiffness. Changes in the affected vocal fold often cause changes in the horizontal and vertical phase symmetry of the two vibrating folds; a polyp on one vocal fold can cause traumatic polypoid or fibrovascular changes in the contralateral fold, if not scarring. Again, incomplete closure is common. Finally, vocal fold cysts generally are unilateral and are distinctly subepithelial. Sometimes a discrete intracordal mass can be appreciated. Epidermoid cysts tend to bulge on the superior and medial aspect of the midmusculomembranous region. On phonation, the epithelium often can be seen moving over the cyst, so that it appears like an ‘‘egg in soup.’’ Mucus retention cysts occur most frequently on the inferior aspect of the vocal fold because the medial edge is devoid of mucus glands. Edema of the contralateral fold or a contact nodule may be seen. Phase asymmetry dominates VLS, given the increased stiffness of the cover, and contralateral traumatic changes are common [42]. Notably, despite the excellent resolution of VLS, it can be impossible to fully understand the nature of a vocal fold mass without the higher magnification and tactile evaluation by way of palpation achievable during suspension microlaryngoscopy. Similarly, if therapeutic suspension microlaryngoscopy is undertaken to treat a benign mass, additional mass/vascular lesions not seen on VLS may be revealed. This possibility should be discussed with patients who decide to undergo surgery, so that occult masses discovered at that time can be addressed. Treatment of benign vocal fold masses depends on a patient’s symptom complex. If laryngopharyngeal reflux is present, it should be treated first, as should muscle tension dysphonia. A course of voice therapy will address vocal behaviors in the speaking and singing voice to which the development of the mass or muscle tension dysphonia may be attributed. Goals of therapy are to maximize vocal efficiency, thereby reducing the vibratory trauma that underlies and exacerbates the masses [43]. Although voice therapy alone cannot cure vocal fold nodules (ie, make them disappear in entirety), the surrounding edema may reduce significantly with changes in vocal hygiene. Return to near-normal function is possible, although some professionals will continue to notice limitations in the voice and, thus, require surgery. Vocal

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fold polyps and vocal fold cysts also should be treated with an initial course of voice therapy to optimize vocal hygiene; however, in these cases, voice therapy less often accomplishes significant recovery of function, and surgery is almost always required if associated symptoms are significant. Precise phonomicrosurgical excision of the lesions, with every effort to preserve as much normal tissue (epithelium and superficial lamina propria) as possible, remains the surgery of choice for symptomatic benign lesions. Specifics of technique are addressed elsewhere in this issue. Following an immediate postoperative course of voice rest ranging from 4 to 14 days, voice therapy is mandatory to achieve the best functional results. The special case of rheumatoid nodules and bamboo nodes is considered here briefly (Fig. 5). First, obtaining the history of rheumatoid arthritis, or any other/additional autoimmune disease, is critical during the interview process for any complaint. If this history is obtained, the laryngologist should note all current and previous medications used to treat the disorder and the name and contact information for the patient’s rheumatologist. Second, it is important to know how well controlled the patient’s autoimmune disease is and whether he/she can correlate any changes in voice with changes in the severity of autoimmune disease. Vocal fold lesions related to rheumatoid arthritis and autoimmune disease are rare, as are their descriptions in the literature [44]; however, laryngeal involvement in rheumatoid arthritis is well documented and may be present in most patients who suffer from that disease [44–47]. The cricoarytenoid joint, which is diarthroidal, like the interphalangeal joints in the distal extremities, is involved most commonly. Laryngeal manifestations of rheumatoid arthritis in the cricoarytenoid joint include dysphonia, odynophonia, dysphagia, dyspnea, and throat pain. If nodules are present in rheumatoid arthritis or autoimmune disease, vocal roughness is a frequent complaint, as is intermittent aphonia.

Fig. 5. Rheumatoid nodules. Bilateral, horizontal-appearing intracordal masses with subtle surrounding erythema are seen.

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Clinical manifestations include hoarseness and instability in connected speech, with characteristic subepithelial nodules that appear as horizontal bars or rectangles that run perpendicular to the long axis of the vocal fold in the midmusculomembranous region. Often, these are striated in appearance and universally cause stiffness in vocal fold vibration with reduction in the magnitude of mucosal wave [44,45,48]. Rheumatoid nodules and bamboo nodes (similar lesions seen in autoimmune diseases, such as Sjo¨gren’s syndrome and systemic lupus erythematosus) are almost always bilateral; surrounding erythema is common, particularly during a flare-up of the systemic disease. Rheumatoid nodules and bamboo nodes must be treated in the context of the systemic disease. Close communication with the rheumatologist is necessary to optimize medical therapy when conservative measures fail. Surgical excision or direct injection of steroids into the rheumatoid nodules/bamboo nodes is undertaken when function demands it; however, patients must be counseled that the lesions can recur in the face of chronic disease. Perioperative reflux treatment is imperative, and an oral steroid burst is recommended preoperatively to help abate inflammation. It is not uncommon to encounter dense fibrosis around the nodules once they are exposed subepithelially by way of cordotomy, even with subepithelial injection of local anesthesia/epinephrine. Nonetheless, it is important to remove the nodule in its entirety to maximize function and minimize growth of persistent disease. Bilateral lesions can be addressed at one sitting because a superior cordotomy usually is made. Postoperative management is the same as for other benign mass lesions. Vocal fold scarring Vocal fold scar is a vexing diagnosis for patients and laryngologists. Although there is no agreement on how best to manage vocal fold scar, it is agreed that treatment outcomes are fair to good, but inconsistent at best [49–53]. This mandates continued research into the pathophysiology, histology, biology, and treatment of vocal fold scarring. A detailed discussion of these topics is beyond the scope of this article, and the reader is referred to several recent reviews [50,51,53]. Nonetheless, given the potential for permanent voice change and the impact on patients, particularly professional voice users, vocal fold scar is an area worthy of utmost attention in the clinical and research realms. Scar is derived from the Greek eschara (scab) and is defined as ‘‘fibrous tissue replacing normal tissues destroyed by injury or disease’’ [54]. Causes of vocal fold scar are diverse and include inflammatory, neoplastic, traumatic, and iatrogenic entities [49]. Although the incidence and epidemiology of vocal fold scar are not well documented in the general population or professional voice users, one can imagine that inflammatory and iatrogenic causes are the most common among professional voice users. In addition to vocal misuse and abuse (which predispose to fibrovascular change and

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mass lesions, themselves associated with scar), laryngopharyngeal reflux, bacterial laryngotracheitis, and prior aggressive endolaryngeal surgery are associated with vocal fold scar [49,53,55]. Sulcus vocalis is a specific entity often considered under the ‘‘umbrella’’ of vocal fold scar, because it, too, consists of fibrous tissue replacing normal tissue in the vocal fold. Sulcus vocalis is discussed further in this section. In the vocal fold, the ‘‘normal tissue’’ destroyed by scar in varying degree and thickness is the delicate multilayered structure composed of epithelium, superficial lamina propria, intermediate lamina propria, deep lamina propria, and muscle. This fibrous insult compromises vocal fold pliability, the exact property that allows production and modulation of voice, by causing contraction of the vocal fold cover and effecting loss of vocal fold volume [53]. The result is an increase in vocal fold stiffness and subsequent decrease in vibratory capacity [49]. (Access Video on Left Vocal Fold Scar in online version of this article at: http://www.Oto. TheClinics.com.)

Effects on voice depend on the location of vocal fold scar relative to the vocal fold’s medial edge and midmusculomembranous region, the depth of scar, the presence of other lesions/pathologic entities, and the patient’s innate or trained compensatory mechanisms of producing voice. Patients may develop a strained, harsh, or breathy voice, diplophonia, or hoarseness [49]. In addition to change in voice, common complaints include vocal fatigue, loss of range, and loss of stamina. These complaints also apply to sulcus vocalis. Sulcus vocalis is a linear invagination of epithelium along the medial edge of the vocal fold into or beyond the superficial layer of the lamina propria. Sulcus vocalis can extend into the intermediate or deep layer of the lamina propria or to the vocalis muscle. Depth of migration generally correlates with symptom severity, as well as the prognosis for successful treatment. Ford and colleagues [56] developed a classification scheme for sulcus deformities, which is helpful in thinking about their effect on the mucosal wave. Types I and II sulcus vocalis are longitudinal depressions in the epithelium, generally extending the length of the musculomembranous vocal fold (from vocal process to anterior commissure), and they differ only in depth of penetration. Type I sulcus vocalis extends into the superficial lamina propria only, but does not reach the vocal ligament (intermediate and deep layers of the lamina propria, the transition layer); type II sulcus vocalis extends to or beyond the vocal ligament, causing loss of superficial lamina propria. Type III sulcus vocalis is a deep, focal indentation of epithelium on the medial surface of the vocal fold that does not extend its entire length, but often resembles a ‘‘pit’’ or pocket (Figs. 6 and 7). In our experience, keratotic debris frequently accumulates in type III sulcus vocalis, such that initial evaluation in the clinic may raise the question of an intracordal cyst because they are shallow, cause minimal loss of superficial lamina propria, and generally result in only mild change of the mucosal wave. Type I sulcus

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Fig. 6. Vocal fold sulcus. (A) Longitudinal scar is seen along the superomedial edge of the right true vocal fold. (B) On suspension microlaryngoscopy, palpation with a right-angle hook revealed this to be a ‘‘pocket’’ sulcus, or type III sulcus. It was removed successfully with phonomicrosurgical techniques.

vocalis has been termed ‘‘physiologic sulcus.’’ Types II and III sulcus vocalis are considered pathologic; type II also is referred to as ‘‘sulcus vergeture.’’ The key to diagnosing vocal fold scar or sulcus vocalis is a thorough history (including specific vocal complaints and surgical history) and physical examination, the most important aspect of which is VLS. VLS features include asymmetric amplitude of vibration, the scarred side having reduced or absent amplitude of vibration and loss of mucosal wave (which may be focal or diffuse); incomplete glottic closure requiring high pressure to sustain phonation given significant stiffness; and nonvibrating segment in the affected vocal fold that prevents mucosal wave propagation [49]. Ventricular hyperfunction may or may not be seen, but usually appears as the glottal gap increases in size. A complete voice evaluation with aerodynamic and acoustic batteries is imperative once vocal fold sulcus/sulcus

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Fig. 7. Bilateral sulcus vocalis with significant loss of superficial lamina propria, vocal fold bowing, and lateral cricoarytenoid hyperfunction. Significant muscle tension dysphonia also is seen on phonation.

vocalis has been identified so that effects of therapy, whether medical or surgical, can be assessed and followed. Most important, the best approach to treating vocal fold scar is preventing it. Encouraging good vocal hygiene and technique in professional voice users of all ages is important to accomplish this goal. Nonetheless, with continued use over time, some degree of scarring seems inevitable. As in the treatment of benign vocal fold masses, voice therapy is the first line of treatment for scarring to maximize vocal efficiency and to stretch the scar tissue to improve its pliability. In operative cases, voice therapy helps to maximize vocal hygiene and technique preoperatively in preparation for postoperative therapy [49,53]. Patients have the best chance of improvement, with or without therapy, if other exacerbating factors (eg, laryngopharyngeal reflux, smoking, voice abuse) are treated/prevented. If a procedure is considered, multiple questions should be addressed with the patient to choose the appropriate procedure. These were outlined nicely by Dailey and Ford [53] and include discussions of endoscopic versus open approaches; potential use of autologous implants requiring separate harvest site; whether a short- or long-term solution is desirable; approaches appropriate for mild versus severe cases; approaches that are direct versus indirect; and approaches that address glottal gap, loss of pliability, or both. A full discussion of each procedure’s technical aspects, advantages, and disadvantages is beyond the scope of this article; readers are referred to other sources, including the article on voice surgery in this issue [49,53,56–59]. Briefly, correction of the glottal insufficiency associated with scarring can be addressed with vocal fold augmentation or medialization techniques. These do not address the loss of pliability and do not address the scar/sulcus directly. Such procedures include injection of alloplastic substances into vocal folds or paraglottic space (collagen, micronized dermis, hyaluronic acid, hydroxyl apatite);

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autologous fat or fascia also can be used. Medialization thyroplasty with Gore-Tex or silastic blocks also will close a glottal gap. Direct approaches to sulcus deformities that aim to address the loss of pliability include endoscopic procedures, such as cold instrument undermining of the sulcus by way of a longitudinal epithelial cordotomy, scar release, and flap redraping; cold instrument excision of the scar, similar to the redraping procedure but with removal of scar tissue to its depth; laser undermining with redraping; and slicing technique that involves full-thickness releasing cuts in the flap medial and perpendicular to its longitudinal axis [56,60]. These techniques do not always address glottal insufficiency. Finally, other procedures that attempt to address lack of pliability and glottal insufficiency include those that add an implant to scar release or excision. These also are endoscopic procedures and include implantation of fat, fascia, or acellular dermis (AlloDerm) in the superficial lamina propria. The reader is advised that none of the aforementioned procedures has been performed by large numbers of surgeons or on large numbers of patients. The development of multiple techniques to address sulcus reflects our poor understanding of it and parallels the lack of consensus on how best to address it. Continued research in this area is imperative to improving patient care. Varices Prominent or enlarged vessels within the vocal folds’ superficial lamina propria are variably termed microvascular lesions, varices, varicosities, ectasias, capillary ectasias, papillary ectasias, or spider telangiectasias [61–67]. Typically, the applied term reflects the size and shape of the concerned vessel, but the nomenclature is not standardized. The best way of classifying these vessels may be to adhere simply to Stedman’s [54] definitions. Varix is derived from the Latin varix (dilated vein) and refers to a dilated vein or an enlarged and tortuous vein, artery, or lymphatic vessel. Ectasia is derived from the Greek ectasis (a stretching) and refers to dilation of a tubular structure. Because the definition of varix includes ectasias, it seems simplest and appropriate to apply the former to all enlarged vessels of the vocal folds; diagnosis and management strategies are the same for all of them. Vocal fold varices are found most frequently on the superior surface of the vocal fold (Fig. 8) [61,62,67]. Their next most common location is the medial surface, with a superior/medial location ratio of approximately 3:1 in one study, which also noted that more than half of the superior varices occurred at the lateral extent of the mucosal wave [67]. The exact reason for this is not known. The possibility of maximal shearing forces occurring at the superolateral limit of the mucosal wave has been proposed, but is not proven [67]. Because they are dilations of normal vasculature, most vocal fold varices run in an anterior–posterior direction, paralleling the vector of the vocal fold; however, this is not always the case, and vocal fold varices,

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Fig. 8. Vocal fold varices. Prominent varices (with ectasias) are seen bilaterally. This patient also has a left vocal fold paresis.

or dilations within them, may occur at oblique angles or even perpendicular to the direction of the vocal fold. The true incidence of vocal fold varices is not known. It is agreed, however, that they are not common, are seen most frequently in professional voice users, and are more common in women [61–64,66]. These trends were largely accepted, but anecdotal observations, until Postma and colleagues’ [66] first systematic evaluation of the treatment of vocal fold varices in 1998. In this retrospective review of all patients with benign laryngeal disorders and dysphonia evaluated between 1992 and 1995 at the Vanderbilt Voice Center, only 25 of 800 patients (3.1%) had isolated vocal fold varices (patients who had hemorrhagic polyps, nodules, cysts, granulomas, and large arteriovenous malformations with or without vocal fold varices were excluded). Of these 25 patients, 22 (88%) were professional voice users, including 13 professional singers; 19 (76%) were women. The incidence of vocal fold varices was higher among all women (4.5%) than among all men (1.6%), and similarly higher among female professional voice users (14%) than among male professional voice users (5.0%). This increased prevalence in professional voice users, reported by other investigators as well, influences the number of patients who have vocal fold varices seen by the laryngologist. It is important to consider, however, that the incidence in the population at large could be much higher and that most people who have vocal fold varices are asymptomatic or are not bothered by them because of the negligible effects on the voice. The higher incidence of vocal fold varices in women indicates at least a female predisposition to them, if not a hormonal role in varix formation. Again, although this has been proposed by many investigators, the influence of hormones on vocal fold varices has not been studied well [63,65,66,68,69]. Although Postma and colleagues [66] did not include the number of patients who presented with vocal fold varices in conjunction with another

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benign lesion, this clinical finding is frequent among professional voice users. In Hochman and colleagues’ [67] review of 42 patients who were treated for ectasias and varices, 39 patients (93%) had additional lesions (eg, polyps, nodules). Again, most patients were female (81%), and most were professional/semiprofessional voice users or students (93%). Similarly, all of the 12 patients who had microvascular lesions treated with KTP (potassium-titanyl-phosphate) laser by Hirano and colleagues [70] had associated lesions requiring surgical treatment. In our experience, it is not unusual to find vocal fold varices with other benign lesions of the vocal folds in professional voice users. Still, it is not known whether vocal fold varices cause other benign lesions (eg, nodules or polyps) to develop, whether the presence of a mass lesion on the vocal folds predisposes them to developing vocal fold varices, or both. It has been hypothesized that the enlargement of vocal fold blood vessels with significant vocal use or abuse will increase vocal fold mass and stiffness, changing vocal fold vibratory patterns, possibly inducing vocal fold edema and subsequent mass lesion development [62]. Certainly, varices and mass lesions share the common pathway of significant vocal use, as in the case of professional voice users, as well as vocal overuse or misuse in other patients. It is difficult to know the most common symptom caused by vocal fold varices given their relative low-documented incidence and their coexistence with other lesions. The most common complaint among patients in Postma and colleagues’ [66] review was hoarseness (72%), followed by decreased vocal range (16%) and vocal fatigue (12%). Often, these symptoms are intermittent, varying with voice use, and are widely accepted as common by other clinicians as well. We have had the same experience; however, we also see a number of young conservatory singers in the laryngology clinic for baseline evaluations at the recommendation of their voice teachers. These students have been singing through childhood and high school, often competitively. Anecdotally, most of them have signs of laryngopharyngeal reflux, and many have varices; however, most are asymptomatic. Sataloff and colleagues [64] also observed asymptomatic patients who had vocal fold varices. The treatment of vocal fold varices in professional voice users is the same as that for other patients with these lesions; however, as is the case with treating any lesion in the vocal professional, the recommendation and timing of treatment must be individualized to account for their potential impact on career goals and professional obligations. Also, the varices may need to be treated in conjunction with other lesions. An asymptomatic isolated varix does not require active treatment, but it should be followed with regular VLS. Patients need to be educated about the possibility of vocal fold hemorrhage, because of the fragility of these lesions, and counseled that if any acute significant voice change occurs, especially related to voice use or upper respiratory tract infection, strict voice rest should be observed and immediate laryngologic evaluation obtained. Symptomatic vocal fold varices should be treated in a staged fashion, depending on the frequency and

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severity of symptoms and on the evolution of the lesion (ie, change in their size or number). Medical treatment almost always includes aggressive treatment of laryngopharyngeal reflux, because it is nearly ubiquitous among professional voice users. Decreasing reflux-associated vocal fold edema should reduce the resultant increase in vocal fold mass, which likely predisposes the patient to develop or exacerbate varices as increased effort is made to produce voice. Decreasing reflux-associated mucus may decrease throat clearing and its resultant trauma. A three-armed antireflux protocol, including diet changes, behavior modification, and PPIs, is imperative. Maintaining adequate hydration also is important. Some investigators also institute mucolytic therapy as necessary [66]. The second major step in medical therapy is to obtain a comprehensive voice evaluation, including an acoustic and aerodynamic test battery and flexible and rigid video endoscopy with and without stroboscopy. This will be used to tailor individualized voice therapy to optimize vocal technique and minimize vocal trauma in the speaking and singing voice. Baseline voice evaluation and voice therapy also are critical to obtain should surgical intervention be required later. The most widely accepted indication for surgical treatment of vocal fold varices is recurrent vocal fold hemorrhage in patients who have an identifiable varix in the vocal fold sustaining this injury and who have a resultant irreversible unacceptable change in the voice [61–63,65–67,69,70]. As with surgery for most benign laryngeal disease, patients must be counseled of the risk involved in the surgery, which can be voice and career saving, but nonetheless is elective. Other indications for surgery were outlined nicely by Postma and colleagues, [66] however, some laryngologists may think of these as relative indications for surgery. These indications include enlargement of the varix, development of a mass in conjunction with a varix or hemorrhage, or unacceptable dysphonia secondary to persistent vibratory abnormality seen on serial VLS after maximal medical and voice therapy. One successful approach prioritizes the patient’s self-assessment of vocal function and commitment to good vocal hygiene and technique. If vocal hygiene and technique are sufficiently good and consistent, but vocal function is inadequate, other lesions have been treated or excluded, and medical therapy has failed, surgery should be offered to the patient. If all of these criteria are met, but there are other mass lesions that require treatment, these should be treated operatively at the same time as treating the vocal fold varices. Most important, as emphasized by other investigators, consent must be obtained to treat/excise any mass lesions newly discovered on suspension microlaryngoscopy that by size, position, or character could be affecting the voice [67,70]. The decision to treat bilateral vocal fold lesions in one or two stages is made intraoperatively and depends on the lesions’ locations relative to each other and to the medial edge of the midmusculomembranous region. A two-stage approach is selected if there is considerable risk for postoperative apposition of the operative sites and,

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thus, risk for web formation, or if extensive work in the superficial lamina propria may compromise function after bilateral surgery. Techniques for surgical treatment of vocal fold varices have evolved over time, paralleling the development of direct laryngoscopy, laser technology, and microsurgical instrumentation. Baker [61] described ‘‘picking’’ off the prominent vessel without ‘‘biting’’ into the vocal fold by way of direct laryngoscopy. Cold instruments were used to remove vocal fold varices up until the development of the CO2 laser, after which it was used on lowpower settings and with defocused spot sizes and short single pulses to ablate vocal fold varices [62,63,67,69]; however, with concern for thermal damage to the vocal fold, the CO2 laser fell out of favor, and microsurgical technique has been used more routinely [67,69,70]. This technique involves making several epithelial cordotomies directly overlying the varix, meticulously dissecting it away from the surrounding superficial lamina propria, then excising it with scissors or microforceps, applying epinephrine-soaked pledgets to achieve hemostasis, and allowing the cordotomies to heal primarily [67]. More recently, angiolytic lasers have been used to treat vocal fold varices, primarily in conjunction with other lesions (ie, polyps, nodules) [70,71]. The senior author routinely uses the 585-nm pulsed-dye laser (Photogenica SV, Cynosure, Littleton, Massachusetts) at 500 to 700 millijoules (mJ), to treat vocal fold varices and ‘‘normal’’-appearing vocal fold vessels that seem to ‘‘feed’’ a lesion when performing surgery for mass lesions [72,73]. The pulsed angiolytic lasers are safe and provide precise ablation of vocal fold vessels. Further basic science and clinical research with longterm patient follow-up is required to define the best role for the pulseddye laser (PDL) and KTP lasers in the treatment of vocal fold varices and other laryngeal processes. There are more data in the literature to support PDL use than to support the KTP laser [71–74]. Retrospective evaluations of both lasers are ongoing, and prospective studies are in order. Vocal fold hemorrhage Vocal fold hemorrhage is a laryngologic emergency that warrants immediate strict voice rest for 7 to 14 days and VLS to document the effects on the mucosal wave (Fig. 9). Most frequently, patients note a sudden significant change in the voice with increased voice use or vocal abuse (singing or public speaking for prolonged or intense periods, yelling) or in association with upper respiratory tract irritation and inflammation (coughing, sneezing) [61,63,65,68,69,75–79]. Rarely, subtle chronic change in the voice may be the presenting symptom of vocal fold hemorrhage [65,69,77]. Vocal fold hemorrhage usually occurs in one vocal fold, although bilateral vocal fold hemorrhage has been reported [63,65]. The demographics of vocal fold hemorrhage parallel those of vocal fold varices: vocal fold hemorrhage is more common in professional voice users and in women. A strong correlation between hormonal imbalance and vocal fold hemorrhage, especially

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Fig. 9. Vocal fold hemorrhage sequelae. Fibrotic vocal folds after multiple recurrent bilateral vocal fold hemorrhages.

recurrent vocal fold hemorrhage, also has been noted by multiple investigators [63,67–69]. In addition to vocal fold hemorrhage occurring in perimenstrual women (just before or during menstruation), women in hormone supplement withdrawal, pregnant women, or women having undergone gynecologic surgery [63,65], other risk factors for vocal fold hemorrhage in patients who have vocal fold varices have been identified, including consumption of aspirin and aspirin products, use of nonsteroidal anti-inflammatory drugs, coumadin therapy, and upper respiratory tract infections [61–63,65,66,76]. Laryngeal trauma, whether external or internal/iatrogenic, is another cause of vocal fold hemorrhage that is rare and not specific to professional voice users, but something of which they should be aware so that they take proper safety measures (wearing seatbelts in motor vehicles and well-fitted harnesses as warranted in their work). As with vocal fold varices, it is possible that the apparent higher incidence of vocal fold hemorrhage in professional voice users compared with the general population is simply a reflection of the makeup of most laryngology practices and the sensitivity of professional voice users to changes in voice. The incidence of vocal fold hemorrhage in the population at large may be much higher, but underdiagnosed. Most professional voice users who experience sudden decrement in the voice self-impose voice rest and seek laryngologic evaluation. Voice rest is believed to minimize the potential for further bleeding into the affected vocal fold as well as the potential for trauma to the opposite vocal fold during phonation. If seen in the immediate hours after hemorrhage, the vocal fold may be bulging with blood/hematoma; after several days, it usually flattens, but remains red; with time, blood is metabolized, and the color changes from red to yellow because of hemosiderin staining and eventually back to white. At any time after vocal fold hemorrhage, before complete resolution, VLS reveals vocal fold stiffness and decreases in the amplitude and

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magnitude of the mucosal wave [65,68,69]. Most investigators recommend 7 days of strict voice rest and cessation of anticoagulants, if medically safe. If applicable, resumption of hormone (eg, estrogen) therapy may be recommended in conjunction with an endocrinologist or gynecologist. Close followup and repeat VLS with assessment of vocal fold stiffness and mucosal wave are imperative. Sometimes, longer periods of voice rest are necessary. Most commonly, the hemorrhage is a brief event, and a bulging vocal fold begins to flatten out within a few days. Rarely, this is not the case, and a significant hematoma persists. In this instance, it is necessary to evacuate the hematoma by way of suspension microlaryngoscopy in the operating room. A small superiorly based cordotomy is made, and careful suction evacuation of the hematoma is performed [65,69]. Voice rest for an additional 7 to 10 days is instituted postoperatively. All patients who have vocal fold hemorrhage, regardless of the need for operative treatment, require follow-up voice evaluation and voice therapy. If a vocal fold varix is identified in the hemorrhagic vocal fold, this is followed closely and patients counseled on the potential for recurrent hemorrhage and the possibility of resection of the varix (see above). Standing the test of time: aging and the professional voice user Perhaps among the highest concerns of professional voice users are the effects of age on the voice and their potential impact on career longevity. For many professional voice users, ‘‘age-related’’ voice changes may be due to scarring or fibrovascular changes from long-term use/overuse/misuse of the voice. The resultant increase in pitch and harshness of the voice, with decreased vocal efficiency from vocal fold stiffness, are not specific to age and can occur in young patients. More common complaints among aging professional voice users include a wobbly quality to the voice, lack of clarity, singing flat, and an inability to sing softly [80]; however, more frequently these changes are due to deficits in overall conditioning rather than irreversible aging changes in the larynx. Therefore, it is important for the laryngologist to be able to differentiate between physiologic age-related changes in the larynx and functional changes in the voice that may occur for reasons including, but not limited to, senescent global deconditioning. Hirano and colleagues elicited gender-specific histologic changes in the vocal folds [81,82]. The vocalis muscle atrophies in men and women. In men, the intermediate layer of the lamina propria also atrophies, but the deep layer thickens as a result of increased collagen deposition. In women, the epithelium and superficial and intermediate layers of the lamina propria thicken with age. The superficial lamina propria also becomes more edematous. Age-related changes in the supraglottis also ensue in men and women and include atrophy of seromucous glands in the respiratory epithelium’s submucosa (more pronounced for the mucous versus serous glands), associated fatty infiltration, and fragmentation of false vocal fold connective

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tissue. The most prominent clinical correlate to these changes is scalloping of the medial edge of the vocal fold (or ‘‘vocal fold bowing’’), seen on laryngoscopy, the hallmark of presbylarynges. Lateral cricoarytenoid hyperfunction also may be seen with prominence of the vocal processes on quiet respiration and phonation onset, creating a posterior chink and lack of glottal closure. Additional laryngeal changes that occur with age include ossification of the laryngeal cartilages and diffuse loss of muscle tone and bulk; the joints may become arthritic and stiff [83]. Effects of these changes on voice can be extracted (ie, decreased range, flexibility, efficiency, and stamina), but are not well described. The deconditioning that can accompany natural aging (although neither universal nor predictable among patients of the same age or gender) affects all components of voice production, not just the vocal folds [83]. These include the abdominal muscles and diaphragm with decreased tone and strength; the lungs and thorax with decreased elasticity and distensibility, respectively; the peripheral nervous system with a decrease in the number of nerve endings; and the central nervous system with cortical atrophy and sometimes dementia. Any localized or systemic illnesses that affect any part of the vocal tract will have an attendant effect on voice production and quality. Professional voice users, singing teachers and voice coaches, speech language pathologists, laryngologists, gynecologists, and a myriad of other women’s health care providers are aware of the wide variety of voice changes that can accompany menopause. Although it is accepted that the larynx is sensitive to endocrinologic changes, and, in fact, developmentally driven by changes in sex-hormone levels during childhood, puberty, menopause, and senescence, basic science and clinical research in the area is sparse [84–90]. More importantly, objective findings in studies that attempt to evaluate the role of estrogen in menopause-related voice change and to delineate changes in measurable vocal parameters are not reliably reproducible and do not always correlate with clinical experience [85,91]. Much of the literature centers on subjective patient surveys. Together, these issues make the study of voice in climacteric medicine a wide-open frontier. Despite the lack of a large body of evidence to relate menopause directly to specific changes in the vocal folds and in the voice, several repeating themes, as well as several intriguing studies, can be found in the literature. Voice changes that are described frequently as occurring during and after menopause include new-onset hoarseness and sometimes cracking, decreased intensity, increased fatigue, and deepening of the voice [84,90–93]. This may be due to the decrease in ovarian estrogen and relative increase in ovarian androgen found during menopause. Given its close relationship to pitch, fundamental frequency (F0) has been studied in the context of menopause: some investigators found a reduction in F0, whereas others demonstrated that changes in F0 were not statistically significant [91,92,94–96]. Based on the temporal relationship seen clinically between changes in voice

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and menopause, as well as menstruation, pregnancy, gynecologic surgery, and hormonal treatment of gynecologic diseases (eg, endometriosis, fibrocystic breast disease, and premenstrual/menstrual dysfunction), the larynx is considered by many to be a secondary sex organ [84,90,97]. Estrogenbinding sites have been found in normal larynges, laryngeal papilloma, and laryngeal carcinoma [90,98–100]. Abitbol and colleagues [97] demonstrated that vaginal and laryngeal epithelial smears are similar at various times during the ovarian cycle. Many clinicians and performers also have noted coincidental improvements in voice when menopausal women are treated with hormone replacement therapy for other reasons (genital atrophy, decreased libido, osteoporosis, prevention of cardiovascular and Alzheimer’s disease, hot flashes, psychoemotional changes, insomnia). Hormone replacement therapy is not considered a primary treatment for menopause-associated dysphonia, but it has been used by some clinicians to forestall it [85,101]. Based on this, Lindholm and colleagues [85] compared the changes in measured voice values and subjective voice/laryngeal symptoms in postmenopausal women who did not undergo hormonal therapy with those using estrogen alone or an estrogen-progestin combination. Among the 42 subjects, estrogen replacement seemed to protect against detrimental changes in fundamental frequency and voice quality more than the estrogen-progestin combination; women with no hormone replacement suffered the largest negative impacts. Caruso and colleagues [90] investigated the effects of estrogen replacement on laryngeal cytology in postmenopausal women. They found that laryngeal and vaginal epithelial smears in women on estrogen replacement therapy had similar minimal cytologic changes compared with those of women without estrogen therapy in whom both smears showed aspects of atrophydystrophy. This work supports the idea that hormone replacement therapy may improve voice in postmenopausal women. Laryngologists should consider this when caring for perimenopausal professional voice users and discuss the possibilities of hormone replacement therapy with gynecologist colleagues on a case-by-case basis. Most important, however, is that professional voice users entering or beyond menopause be under the care of an experienced voice team that can address perimenopausal voice changes appropriately. As with all voice complaints, ‘‘my voice is getting old’’ must be investigated thoroughly. A diagnosis of presbylarynges cannot be made without a complete laryngeal and neurologic evaluation for other underlying etiologies. This point was demonstrated well by Woo and colleagues [102] in a retrospective review of 151 dysphonic patients who were older than 60 years: only 6 had dysphonia due to physiologic aging alone. The remaining 145 patients were dysphonic secondary to specific disease processes, many of them related to age, but nonetheless pathologic. These included central neurologic disorders affecting laryngeal function (eg, stroke, Parkinson’s disease, essential tremor, Alzheimer’s disease), benign vocal fold lesions (eg, Reinke’s edema, benign and dysplastic epithelial lesions), inflammatory disorders

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(eg, laryngitis sicca, medication effect), laryngeal neoplasia, and laryngeal paralysis. Despite the best voice training, professional voice users are not immune to the development of disease in the middle and older years. Thus, the laryngologist is obligated to keep a broad differential diagnosis in mind while treating this select group of aging patients. Most presbyphonic patients will benefit from voice therapy [80]. Specific vocal fold pathology can be treated surgically as indicated. Voice overuse One of the most common problems in professional voice users, especially singers and actors, is laryngitis associated with voice overuse. This is to be distinguished from infectious laryngitis, also common in this population during peak performance times, which are associated with long hours, lack of sleep, and often, poor nutrition. Reflux laryngitis also may be an underlying problem; however, overuse in and of itself can cause dysphonia in the singing and the speaking voice, odynophonia, loss of range, loss of clarity, and early vocal fatigue. This is seen frequently in performers who are on the road and in the middle or toward the end of a rigorous concert schedule (eg, four to seven performances in a week for 6 to 16 consecutive weeks). Pop, rock, country, and musical theater singers who sing in large open venues with variable acoustics seem, anecdotally, to be at particular risk for the effects of voice overuse. Many performers believe that they have infinite use of their vocal folds and do not realize that they are athletes who need to rest and recover after an event. Frequent high-energy performance can result in vocal fold edema that requires more ‘‘pushing’’ over time to get the same results; this results in a vicsous cycle phonotrauma. Any number of findings may be present on laryngoscopy. Vocal fold edema, assumed to be subacute, overlying chronic fibrovascular changes, and sulcus deformities are common. Varices and resolving hemorrhage may be seen. The best treatment of this condition is relative voice rest. Sometimes, complete voice rest for a few days may be appropriate. A frank discussion with the performer about short- and long-term goals and obligations is important to developing a management strategy. If a performance is imminent, the patient has to decide how important it isdfinancially, professionally, and emotionally. The laryngologist also has to weigh in on how dangerous further voice use is to the patient’s long-term vocal health. Doctor’s orders for voice rest can be a welcome relief to a performer. Conversely, the laryngologist may encounter significant resistance to this recommendation. If this is the casedand especially if a performance is of paramount importanced a short course of high-dose oral steroids (burst and taper) can be prescribed. One practical approach is to prescribe methylprednisolone at a high first dose with rapid taper. For example, this can be methylprednisolone, 16 mg, days 1 through 3, with a rapid taper over 3 to 4 days (eg, 12 mg, days 4 and

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5; 8 mg, day 6; 4 mg, day 7). Patients are cautioned to mark during rehearsals or not sing at all and to use the voice minimally otherwise. Sometimes performers have to tell their audiences that they cannot sing in full voice. Finally, all patients must be counseled that the risk for vocal fold hemorrhage and tear is higher when on steroid therapy. If any sudden decrement in voice occurs, they are instructed to observe immediate full voice rest and to seek laryngologic evaluation as soon as possible. The patient is reevaluated once voice rest has been prescribed for overuse and the larynx has had time to recover. Symptoms and findings on VLS are tracked. Resumption of normal practice and performance schedules needs to be undertaken with serious caution and an appreciation for the fragility of the larynx, and it can take place once the larynx has shown signs of improvement (decreased edema, erythema, size of varices). Performers are encouraged to improve vocal hygiene, maintain excellent hydration, and observe regular periods of voice rest throughout the day. Most are able to accomplish this while meeting their professional demands. The addition of voice therapy is an important vehicle for teaching and reinforcing these strategies and is an important management option for voice overuse. Special considerations in caring for the professional voice user Emphasis was placed on the importance of obtaining a complete history as well as understanding the professional voice user’s priorities to establish trust and to facilitate comprehensive patient care. Similarly, it is important to approach this care with a team model, including voice therapists (sometimes singing and speech therapists), the singing teacher/voice coach, and other physicians who care for the patient. Many patients are otherwise healthy and do not see other clinicians, in which case the laryngologist frequently plays a primary care role, tending to questions of health maintenance and serving as a referral base as necessary. This is particularly true for young patients, many of whom live away from home as students or as traveling performers. Obtaining complete social histories and taking time to educate patients about the importance of hydration, rest, and tobacco, marijuana, alcohol, and other drug avoidance are critical to comprehensive care. Young patients also benefit from discussions regarding short- and long-term professional goals so that they begin to develop a realistic perspective on the impact that their voice use has on its integrity. Because many professional voice users have multiple physicians who care for them and several may be on multiple medications, communication with other physicians is critical to coordinated care. Summary Multiple diagnoses may be present simultaneously in the professional voice user. Each needs to be considered in the context of the other,

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such that treatment of one problem does not ignore the influence of others on its resolution. The presence of a benign vocal fold lesion in a professional voice user does not mandate treatment if it is not compromising function. Surgical treatment of asymptomatic benign vocal fold lesions in professional voice users with the goal of preventing a problem must be approached with caution, because any trauma to the vocal fold cover by intubation or surgical instrumentation, including lasers, can change the voice. Although incidence and prevalence of inflammatory processes in the larynx are not well documented, they seem common in professional voice users; include laryngopharyngeal reflux (common), laryngitis from voice overuse (common), and fungal laryngitis (uncommon in general, but being recognized more frequently in patients on inhaled steroids); and warrant aggressive treatment to restore the voice. Muscle tension dysphonia is a frequent compensatory mechanism for other processes that should be sought out if muscle tension dysphonia is identified. Vocal fold paresis can cause glottal insufficiency and subsequent breathiness. It is diagnosed best by LEMG and can be treated in a stepwise fashion with voice therapy and augmentation. Vocal fold scar is associated with long-term voice use or frequent phonotrauma, resulting in stiff vocal folds, increase in fundamental frequency, and roughness. Treatment is controversial. Vocal fold varices are seen more frequently in professional voice users than in nonprofessional voice users and are more frequent in women than in men. They generally do not require treatment unless recurrent hemorrhage occurs. Voice changes as related to age, menopause, and voice overuse are of particular relevance to professional voice users. Understanding these areas of laryngology is important to the continuity of care provided to these patients by the laryngologist. References [1] Koufman JA, Aviv JE, Casiano RR, et al. Laryngopharyngeal reflux: position statement of the Committee on Speech, Voice, and Swallowing Disorders of the American Academy of Otolaryngology-Head and Neck Surgery. Otolaryngol Head Neck Surg 2002;127:32–5. [2] Koufman JA. The otolaryngologic manifestations of gastroesophageal reflux disease (GERD): a clinical investigation of 225 patients using ambulatory 24-hour pH monitoring and an experimental investigation of the role of acid and pepsin in the development of laryngeal injury. Laryngoscope 1991;101:1–78. [3] Sivarao DV, Goyal RK. Functional anatomy and physiology of the upper esophageal sphincter. Am J Med 2000;108(Suppl-4a):27S–37S. [4] Hickson C, Simpson CB, Falcon R. Laryngeal pseudosulcus as a predictor of laryngopharyngeal reflux. Laryngoscope 2001;111:1742–5. [5] Koufman JA. Laryngopharyngeal reflux 2002: a new paradigm of airway disease. Ear Nose Throat J 2002;81:2–6.

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[6] Franco RA Jr. Laryngopharyngeal reflux. Allergy Asthma Proc 2006;27:21–5. [7] Koufman J, Sataloff RT, Toohill R. Laryngopharyngeal reflux: consensus conference report. J Voice 1996;10:215–6. [8] Hicks DM, Ours TM, Abelson TI, et al. The prevalence of hypopharynx findings associated with gastroesophageal reflux in normal volunteers. J Voice 2002;16:564–79. [9] Belafsky PC, Postma GN, Koufman JA. The validity and reliability of the reflux finding score (RFS). Laryngoscope 2001;111:1313–7. [10] Belafsky PC, Postma GN, Koufman JA. Laryngopharyngeal reflux symptoms improve before changes in physical findings. Laryngoscope 2001;111:979–81. [11] Noordzij JP, Khidr A, Desper E, et al. Correlation of pH probe-measured laryngopharyngeal reflux with symptoms and signs of reflux laryngitis. Laryngoscope 2002;112:2192–5. [12] Ulualp SO, Toohill RJ, Arnsdorfer R, et al. Revelations about 24-hour ambulatory pharyngeal pH monitoring. Gastroenterology 1998;114:G1290. [13] Axford SE, Sharp N, Ross PE, et al. Cell biology of laryngeal epithelial defenses in health and disease: preliminary studies. Ann Otol Rhinol Laryngol 2001;110:1099–108. [14] Altman KW, Waltonen JD, Hammer ND, et al. Proton pump (Hþ/Kþ-ATPase) expression in human laryngeal seromucinous glands. Otolaryngol Head Neck Surg 2005;133: 718–24. [15] Chiverton SG, Howden CW, Burget DW, et al. Omeprazole (20 mg) daily given in the morning or evening: a comparison of effects on gastric acidity, and plasma gastrin and omeprazole concentration. Aliment Pharmacol Ther 1992;6:103–11. [16] Kahrilas PJ, Falk GW, Johnson DA, et al. Esomeprazole improves healing and symptom resolution as compared with omeprazole in reflux oesophagitis patients: a randomized controlled trial. The Esomeprazole Study investigators. Aliment Pharmacol Ther 2000;14: 1249–58. [17] Vanderhoff BT, Rundsarah MT. Proton pump inhibitors: an update. Available at: http:// www.aafp.org/afp/20020715/273.html. Accessed December 12, 2006. [18] Aviv JE, Liu H, Parides M, et al. Laryngopharyngeal sensory deficits in patients with laryngopharyngeal reflux and dysphagia. Ann Otol Rhinol Laryngol 2000;109:1000–6. [19] Koufman JA, Wright SC. Laryngopharyngeal reflux and voice disorders. In: Rubin JS, Sataloff RT, Korovin GW, editors. Diagnosis and treatment of voice disorders. 3rd edition. San Diego (CA): Plural Publishing, Inc.; 2006. p. 419–30. [20] Westcott CJ, Hopkins MB, Bach K, et al. Fundoplication for laryngopharyngeal reflux disease. J Am Coll Surg 2004;199:23–30. [21] Belafsky PC, Postma GN, Daniel E, et al. Transnasal esophagoscopy. Otolaryngol Head Neck Surg 2001;125:588–9. [22] Postma GN, Bach KK, Belafsky PC, et al. The role of transnasal esophagoscopy in head and neck oncology. Laryngoscope 2002;112:2242–3. [23] Andrus JG, Dolan RW, Anderson TD. Transnasal esophagoscopy: a high-yield diagnostic tool. Laryngoscope 2005;115:993–6. [24] Pabuccuoglu U, Tuncer C, Sengiz S. Histopathology of candidal hyperplastic lesions of the larynx. Pathol Res Pract 2002;198:675–8. [25] Vrabec DP. Fungal infections of the larynx. Otolaryngol Clin North Am 1993;26: 1091–114. [26] Forrest LA, Weed H. Candida laryngitis appearing as leukoplakia and GERD. J Voice 1998;12:91–5. [27] Mehanna HM, Kuo T, Chaplin J, et al. Fungal laryngitis in immunocompetent patients. J Laryngol Otol 2004;118:379–81. [28] Stone RS, Anderson TD. The changing diagnosis, management and demographics of fungal laryngitis. Presented at the American Laryngological Society Annual Meeting. Boca Raton, Florida; May 14, 2005. [29] Hanania NA, Chapman KR, Kesten S. Adverse effects of inhaled corticosteroids. Am J Med 1995;98:196–208.

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[56] Ford CN, Inagi K, Khidr A, et al. Sulcus vocalis: a rational analytical approach to diagnosis and management. Ann Otol Rhinol Laryngol 1996;105:189–200. [57] Rosen CA. Vocal fold scar: evaluation and treatment. Otolaryngol Clin North Am 2000;33: 1081–6. [58] Ford CN. Advances and refinements in phonosurgery. Laryngoscope 1999;109:1891–900. [59] Mortensen M, Woo P. Office steroid injections of the larynx. Laryngoscope 2006;116: 1735–9. [60] Pontes P, Behlau M. Treatment of sulcus vocalis: auditory perceptual and acoustical analysis of the slicing mucosa surgical technique. J Voice 1993;7:365–76. [61] BAKER DC Jr. Laryngeal problems in singers. Laryngoscope 1962;72:902–8. [62] Feder RJ. Varix of the vocal cord in a professional voice user. Otolaryngol Head Neck Surg 1983;91:435–6. [63] Lin PT, Stern JC, Gould WJ. The risk factors and management of vocal cord hemorrhages: an experience with 44 cases. J Voice 1991;5:74–7. [64] Sataloff RT, Speigel JR, Hawkshaw M, et al. Vocal fold varicosities. Ear Nose Throat J 1993;72:194. [65] Spiegel JR, Sataloff RT, Hawkshaw M, et al. Vocal fold hemorrhage. Ear Nose Throat J 1996;75:784–9. [66] Postma GN, Courey MS, Ossoff RH. Microvascular lesions of the true vocal fold. Ann Otol Rhinol Laryngol 1998;107:472–6. [67] Hochman I, Sataloff RT, Hillman RE, et al. Ectasias and varices of the vocal fold: clearing the striking zone. Ann Otol Rhinol Laryngol 1999;108:10–6. [68] Abitbol J. Vocal cord hemorrhages in voice professionals. J Voice 1988;2:261–6. [69] Sataloff RT, Hawkshaw MJ. Vocal fold hemorrhage. In: Sataloff RT, editor. Professional voice: the science and art of clinical care. 3rd edition. San Diego (CA): Plural Publishing, Inc.; 2005. p. 1291–307. [70] Hirano S, Yamashita M, Kitamura M, et al. Photocoagulation of microvascular and hemorrhagic lesions of the vocal fold with the KTP laser. Ann Otol Rhinol Laryngol 2006;115:253–9. [71] Zeitels SM, Akst LM, Bums JA, et al. Pulsed angiolytic laser treatment of ectasias and varices in singers. Ann Otol Rhinol Laryngol 2006;115:571–80. [72] Franco RA Jr, Zeitels SM, Farinelli WA, et al. 585-nm pulsed dye laser treatment of glottal papillomatosis. Ann Otol Rhinol Laryngol 2002;111:486–92. [73] Franco RA Jr, Zeitels SM, Farinelli WA, et al. 585-nm pulsed dye laser treatment of glottal dysplasia. Ann Otol Rhinol Laryngol 2003;112:751–8. [74] Zeitels SM, Franco RA Jr, Dailey SH, et al. Office-based treatment of glottal dysplasia and papillomatosis with the 585-nm pulsed dye laser and local anesthesia. Ann Otol Rhinol Laryngol 2004;113:265–76. [75] Bastian RW, et al. Benign vocal fold mucosal disorders. In: Lustig LR, Gillespie MB, Messner A, editors. Cummings otolaryngology head & neck surgery. 4th edition. Philadelphia: Elsevier; 2006. p. 2160–1. [76] Neely JL, Rosen C. Vocal fold hemorrhage associated with coumadin therapy in an opera singer. J Voice 2000;14:272–7. [77] Sataloff RT, Hawkshaw M, Rosen DC, et al. Acute vocal fold hemorrhage with minimal dysphonia. Ear Nose Throat J 1996;75:583. [78] Sataloff RT, Hawkshaw M, Spiegel JR. Varicosities, hemorrhages and vocal fold masses. Ear Nose Throat J 1998;77:808. [79] Sataloff RT, Spiegel JR, Heuer RJ. Consequences of vocal cord hemorrhage. Ear Nose Throat J 1993;72:252. [80] Sataloff RT, Hawkshaw MJ. Common medical diagnoses and treatments in patients with voice disorders. In: Rubin JS, Sataloff RT, Korovin GS, editors. Diagnosis and treatment of voice disorders. 3rd edition. San Diego (CA): Plural Publishing, Inc; 2006. p. 331–47. [81] Hirano M, Kurita S, Sakaguchi S. Ageing of the vibratory tissue of human vocal folds. Acta Otolaryngol 1989;107:428–33.

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[82] Sasaki CT, Kim Y, Hundal J. Anatomy of the human larynx. In: Rubin JS, Sataloff RT, Korovin GS, editors. Diagnosis and treatment of voice disorders. 3rd edition. San Diego: Plural Publishing, Inc.; 2006. p. 31–45. [83] Sataloff RT, Hawkshaw MJ, Anticaglia J. Patient history. In: Rubin JS, Sataloff RT, Korovin GS, editors. Diagnosis and treatment of voice disorders. 3rd edition. San Diego (CA): Plural Publishing; 2006. p. 151–77. [84] Anderson TD, Anderson DD, Sataloff RT. Endocrine dysfunction. In: Sataloff DM, editor. Professional voice: the science and art of clinical care, vol. II. 3rd edition. San Diego (CA): Plural Publishing, Inc.; 2005. p. 537–49. [85] Lindholm P, Vilkman E, Raudaskoski T, et al. The effect of postmenopause and postmenopausal HRT on measured voice values and vocal symptoms. Maturitas 1997;28:47–53. [86] Newman SR, Butler J, Hammond EH, et al. Preliminary report on hormone receptors in the human vocal fold. J Voice 2000;14:72–81. [87] Abitbol J, Abitbol P, Abitbol B. Sex hormones and the female voice. J Voice 1999;13: 424–46. [88] Hollien H. ‘Old voices’: what do we really know about them? J Voice 1987;1:2–17. [89] Boulet MJ, Oddens BJ. Female voice changes around and after the menopause–an initial investigation. Maturitas 1996;23:15–21. [90] Caruso S, Roccasalva L, Sapienza G, et al. Laryngeal cytological aspects in women with surgically induced menopause who were treated with transdermal estrogen replacement therapy. Fertil Steril 2000;74:1073–9. [91] Mendes-Laureano J, Sa MF, Ferriani RA, et al. Comparison of fundamental voice frequency between menopausal women and women at menacme. Maturitas 2006;55: 195–9. [92] Abitbol J, Abitbol B. The voice and menopause: the twilight of the divas. Contracept Fertil Sex 1998;26:649–55. [93] Kilic MA, Ogut F, Dursun G, et al. The effects of vowels on voice perturbation measures. J Voice 2004;18:318–24. [94] Stoicheff ML. Speaking fundamental frequency characteristics of nonsmoking female adults. J Speech Hear Res 1981;24:437–41. [95] Meurer EM, Wender MC, von Eye Corleta H, et al. Female suprasegmental speech parameters in reproductive age and postmenopause. Maturitas 2004;48:71–7. [96] Meurer EM, Wender MC, von Eye Corleta H, et al. Phono-articulatory variations of women in reproductive age and postmenopausal. J Voice 2004;18:369–74. [97] Abitbol J, deBrux J, Millot G, et al. Does a hormonal vocal cord cycle exist in women? Study of vocal premenstrual syndrome in voice performers by videostroboscopy-glottography and cytology on 38 women. J Voice 1989;2:157–62. [98] Fergusson BJ, Hudson WR, McCarty KS. Sex steroid receptor distribution in the human larynx and laryngeal carcinoma. Arch Dermatol 1987;113:1311–5. [99] Essman EJ, Abramson A. Estrogen binding sites on membranes from human laryngeal papilloma. Int J Cancer 1984;33:33–6. [100] Virolainen E, Tuohimaa P, Aitasalo K, et al. Steroid hormone receptors in laryngeal carcinoma. Otolaryngol Head Neck Surg 1986;94:512–7. [101] Sataloff DM, Linville SE. The effects of aging on the voice. In: Sataloff RT, editor. Professional voice: the science and art of clinical care, vol. II. 3rd edition. San Diego (CA): Plural Publishing, Inc.; 2005. p. 497–511. [102] Woo P, Casper J, Colton R, et al. Dysphonia in the aging: physiology versus disease. Laryngoscope 1992;102:139–44.