common diagnoses and treatments

Otolaryngol Clin N Am

40 (2007) 1025–1061

Common Diagnoses and Treatmentsin Professional Voice Users

Ramon A. Franco, MD*, Jennifer G. Andrus, MDDivision 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 thelaryngologist also are common among professional voice users. These in-clude laryngopharyngeal reflux, muscle tension dysphonia, fibrovascularvocal fold lesions (eg, nodules and polyps), cysts, vocal fold scarring, andchanges in vocal fold mobility. Microvascular lesions and their associatedsequelae of vocal fold hemorrhage and laryngitis due to voice overuse aremore common among professional voice users. Much more common amongprofessional voice users is the negative impact that voice problems have ontheir ability to work, on their overall sense of well-being, and sometimes ontheir very sense of self. In diagnosing voice disorders in professional voiceusers, clinicians must possess and clearly convey an understanding of thisimportant truism, which will facilitate trust, confidence, and the opportunityto treat the patient. This article reviews the diagnosis and treatment optionsfor common problems among professional voice users, emphasizing the im-portance of gaining insight into the ‘‘whole’’ patient and of developing indi-vidualized management plans.

History and physical examination

The history and physical examination are addressed at length elsewherein this issue; however, a few key points are worth mentioning here aswell. First, because of the critical role that the voice plays in the livelihoodof a professional voice user and the frequent association of the voice as a ma-jor component of one’s identity, changes in voice frequently create signifi-cant anxiety for these patients. This anxiety, a fear of the unknown, anda 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 � 2007 Elsevier Inc. All rights reserved.

doi:10.1016/j.otc.2007.05.008 oto.theclinics.com

mailto:[email protected]

1026 FRANCO & ANDRUS

the laryngologist’s office and may be barriers to the patient’s ability toclearly describe the problems he/she is having with the voice. Patient ques-tionnaires can help to overcome this difficulty and facilitate an efficient visit.They are invaluable. The patient can be asked to fill out a history intakeform in the waiting room, along with the voice-related quality of life(VRQOL) survey and a voice outcome survey. In addition to defining theeffects of the voice problem on the patient’s functional capacity, the surveysare 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 se-verity of the problem. Along with symptoms, past medical/surgical history,allergies, and medications, particular attention should be paid to the socialhistory, including place of residence; student or employment status; currentand previous tobacco, alcohol, and drug use; exposure to second-handsmoke or chemical irritants/pollutants; and water, caffeine, carbonated bev-erage, chocolate, peppermint, and fatty/spicy/acidic food consumption.Changes in a patient’s routine (eg, time of day one practices, performancevenue, consumption of caffeinated beverages) often yield important infor-mation. The history also gives clues as to what endoscopy may show. Clini-cians are encouraged to use the history to help guide the physicalexamination, but are cautioned to keep an open eye for unsuspected diagno-ses. Similarly, history and physical examination together will help the clini-cian to develop a differential diagnosis. More often than not, multipleentities contribute to one symptom complex, so the laryngologist is cau-tioned not to look for ‘‘the’’ single unifying diagnosis. Thinking about laryn-geal pathology in terms of acute versus subacute versus chronic problemsmay 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 sub-ject to the same possibilities as are other patients; therefore, neoplastic andautoimmune processes, for example, should not be overlooked.

Third, many, if not most, pathologic entities in the larynx occur on a con-tinuum and are dynamic given the demands on the professional voice user’s‘‘instrument.’’ Ongoing, long-term (if not lifelong) voice use in any numberof performance venues constantly subjects the larynx to insults, such asphonotrauma, reflux, second-hand (or first-hand) smoke, and chemical ex-posures, often under suboptimal conditions (poor acoustics, arid atmo-sphere, and concomitant physical demands, such as dancing). Any onecondition is likely to wax and wane in severity depending on the patient’sgeneral health, vocal demands, rehearsal and event schedule, performancevenues, and the subsequent diet and lifestyle that ensue. Among the mostimportant of the laryngologist’s tasks are eliciting these details, educatingpatients about ways to meet their professional demands while maximizingvocal hygiene, and supporting them in their efforts.

Finally, laryngologists frequently see professional voice users for a secondor third opinion after they have been evaluated by other otolaryngologists.

1027COMMON DIAGNOSES

Sometimes the patient is in denial and does not want to believe what anotherclinician has diagnosed or does not want to pursue the recommended treat-ment options. Another frequent scenario is that the patient has been toldthat he/she has a normal larynx and that nothing on examination canexplain the symptoms. In these cases, it is especially important to elicit adetailed history and to be clear about what bothers the patient about thevoice. Sometimes edema from laryngopharyngeal reflux masks a mass lesionor hyperfunction is so severe that the vocal folds are not seen easily onfiberoptic evaluation. Flexible distal-chip laryngoscopes are providing ex-aminations superior to fiberoptic laryngoscopy and approximating rigid lar-yngoscopy, such that subtle findings now are being noted that may not havebeen seen without this technology. Of utmost importance, it is essential tolisten to the patient, to acknowledge that something is wrong, even if the ex-act 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 areformed 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 tosymptoms referable to the larynx, hypopharynx, and nasopharynx (Fig. 1)[1]. Typical laryngopharyngeal reflux symptoms include dysphonia, globuspharyngeus, 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.


nonproductive chronic throat clearing [2]. In singers, voice changes, such asloss of rangedespecially in the high frequencies, voice breaks, increased vo-cal fatigue, anterior neck discomfort or tightness, or loss of vocal claritymay be the primary complaint and may or may not present with the afore-mentioned common laryngopharyngeal reflux manifestations. Symptomsmay come on gradually (eg, conservatory students who are out of schoolfor 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 longtrial) or after a cold that seems to nearly resolve, but is followed by persis-tent cough and throat clearing. Most patients, including professional voiceusers, are unaware of laryngopharyngeal reflux as a symptom complex, andmost have ‘‘silent reflux,’’ because only 35% of patients who have laryngo-pharyngeal reflux report heartburn.

Laryngopharyngeal reflux is seen primarily as a problem with the upperesophageal sphincter that occurs in the upright position (as opposed to gas-troesophageal reflux disease, a problem with the lower esophageal sphincterthat occurs mainly in the recumbent position) [1,3]. Laryngopharyngealreflux is believed to be most frequent during physical exertion, given theincreased abdominal pressure and decreased intrathoracic pressure thatoccurs with bending over, Valsalva maneuver, exercise, and certainly sing-ing, dancing, and public speaking. Chronic or severe coughdfrom an upperrespiratory infection, asthma, or even having to feign a cough on stagedshould be considered in this group of exertions and is a ‘‘tip-off’’ to thepotential presence of laryngopharyngeal reflux.

Professional voice users may present with only ‘‘voice’’ problems. There-fore, once the ‘‘voice problems’’ are described adequately in the history, it isup to the laryngologist to elicit whether other common laryngopharyngealreflux symptoms are present. Videolaryngostroboscopy (VLS) is the nextkey to making a clinical diagnosis of laryngopharyngeal reflux. VLS findingsconsistent with laryngopharyngeal reflux include postcricoid and periaryte-noid edema, true vocal fold edema, a ‘‘wet’’-appearing larynx or the pres-ence of ‘‘more’’ than the usual amount of (thick) mucus in the larynx,particularly on the true vocal folds, and pseudosulcus (Fig. 1) [4]. Togetherwith a history consistent with reflux, these findings are sufficient to diagnoselaryngopharyngeal reflux in the opinion of many investigators [1,2,5–7];however, controversy exists as to whether physical findings alone are suffi-cient to diagnose laryngopharyngeal reflux, because they are prevalent inthe general population (70%) [8]. Thus, many believe that further criteriafor the diagnosis of laryngopharyngeal reflux should be used. The refluxfinding score, an eight-item validated clinical severity scale, was introducedas a means of offering some standardization to the process of laryngophar-yngeal reflux diagnosis [9]. The reflux finding score is an objective measureof the degree of laryngeal change used by a physician after endoscopic eval-uation to accurately document treatment efficacy. It was found to have an


excellent inter- and intraobserver reproducibility. When coupled with thereflux severity index, a self-administered nine-item survey (scored from 0to 5), the investigators documented improvements in the reflux finding scoreand the reflux severity index with twice daily proton-pump inhibitor (PPI)therapy [10].

The 24-hour dual-sensor pH/impedance probes are considered by manyto be the gold standards for diagnosing laryngopharyngeal reflux. Often,the pharyngeal probe is the key to making the diagnosis, because the esoph-ageal probe results may be ‘‘normal.’’ The sensitivity of single-probe esoph-ageal pH monitoring for laryngopharyngeal reflux was 62% in one study,with a positive predictive value of only 49%. Pharyngeal pH/impedancemonitoring can increase the diagnostic accuracy of laryngopharyngeal refluxdramatically; however, as a diagnostic, pH-metry is expensive and notwidely available. Conversely, despite superior sensitivity and specificity foracid reflux events over physical examination findings, the dual pH probecould not predict the severity of the patients’ reflux symptoms or signs ina 2002 study [11]. The investigators provided several reasons for the lackof ability of the pH probe to separate patients who did and did not have lar-yngopharyngeal reflux. They postulated that so little acid exposure is neededto cause laryngopharyngeal reflux that it may not register as positive duringthe limited 24-hour study. The 69% reproducibility of pharyngeal pH mon-itoring seen in another study that they cited may indicate that a 24-hour test-ing period is too short to accurately estimate what is going on the rest of thetime [12]. The investigators also considered that there might have been an-other source for the irritation that was attributable to laryngopharyngeal re-flux. Impedance testing may provide even better information for thediagnosis of laryngopharyngeal reflux, especially when done in combinationwith pH-metry. Most important in the interpretation of these tests is assess-ing the patterns of pH and pressure changes, whether they correspond witheach other, and if they occur in the supine or upright positions. Finally, lar-yngopharyngeal reflux also can be diagnosed by symptomatic improvementafter empiric treatment with high-dose twice-daily proton pump inhibitors.

Laryngopharyngeal reflux and gastroesophageal reflux disease differ intheir symptom complexes, largely because of differences in the epitheliumand physiology of the larynx and esophagus. A full discussion of the topicis beyond the scope of this article; the reader is referred to additional re-sources to explore these differences and recent research in the area [13,14].The mechanism of laryngopharyngeal reflux, however, is important to con-sider in the context of treating professional voice users with the disorder, astheir understanding of the problem likely will improve its treatment. Lar-yngopharyngeal reflux is postulated to cause laryngeal symptoms in twoways: directly and indirectly [6]. According to the direct theory, refluxate di-rectly irritates the laryngeal mucosa through the action of the caustic mate-rial resting on the tissues. This causes tissue edema, which is responsible formost laryngopharyngeal reflux symptoms. In the indirect theory, refluxate


does not make it onto the laryngeal tissues, but rather evokes laryngeal re-flexes by irritating other structures, such as the esophagus, that then incitea vagally mediated response (ie, chronic cough, asthma-like symptomsthrough bronchoconstriction). Regardless of the pathway, factors such asthe resting tone of the upper esophageal sphincter and lower esophagealsphincter, the duration and the amount of intra-abdominal pressure eleva-tion, and the volume of stomach contents during exertion are importantin the creation of the refluxate bolus [6]. Considering all of the possible con-tributors to laryngopharyngeal reflux guides its treatment, a multiarmedpathway directed at diet changes, lifestyle/behavior modifications, medicalintervention, and, occasionally, surgery.

The multimodality treatment for managing laryngopharyngeal reflux ad-dresses upper and lower esophageal sphincter tone, the presence of acid inthe stomach, stomach acid production, and mechanical increases in intra-abdominal pressure. Thus, diet modifications include avoidance of sub-stances that decrease upper and lower esophageal sphincter tone, such asalcohol, peppermint, fatty foods, chocolate, and caffeine. It is stressed to pa-tients that even ‘‘decaffeinated’’ products and many herbal teas contain caf-feine; reading labels to assure that goods are ‘‘caffeine-free’’ is important.Carbonated beverages, even without alcohol or caffeine, will cause belchingand lead to stomach refluxate contacting the laryngopharynx. Additionally,patients are advised to avoid acidic foods, which directly irritate the hypo-pharynx and cause inflammation. These include most fruits (especially citrusand pineapple), tomatoes, jams and jellies, barbecue sauces, and most saladdressings. Spicy foods (hot mustards, curry, hot peppers/hot sauce) are sim-ilarly irritating. Behavior modifications play a large role in the managementof laryngopharyngeal reflux. It must be stressed to patients that a little com-mon sense can go a long way in limiting the detrimental effects that laryng-opharyngeal reflux can have on the voice. Stomach distension increases thelikelihood of regurgitation of contents into the esophagus and above. Pa-tients are encouraged to eat smaller meals throughout the day, ratherthan 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 box-spring mattress on blocks inside the bed frame, or using a wedge under themattress also is recommended (especially if pH-metry and impedance testingdemonstrate significant reflux events while supine). Increased intra-abdom-inal pressure also increases the likelihood of reflux events, so patients arecounseled to avoid exercise, heavy lifting, and bending over within severalhours of eating. Professional voice users, in particular, are advised to avoidsinging/performing within 2 to 3 hours of a meal. These modifications canbe difficult for professional voice users to make, especially those who aresinging and performing evening events (concerts, shows) on the road, duringwhich days are long and a routine is hard to establish. Nonetheless, vigilantattention to diet and lifestyle changes can result in marked improvement insymptoms.


Although some patients’ laryngopharyngeal reflux is responsive to dietand behavior modifications alone, most require medication to achieve thebest result. It is well accepted among laryngologists that medical manage-ment of laryngopharyngeal reflux requires more aggressive and more pro-longed treatment than does gastroesophageal reflux disease [1]. High-dosePPI treatment is recommended for at least 6 months, with twice-daily PPIdosing because none of the delayed-release PPIs exert acid suppression formore than 16.8 hours [15,16]. Patients must know to take PPIs on an emptystomach, followed in 30 minutes by a meal. This maximizes efficacy by ac-counting for the natural physiology of the PPI mechanism of action [17].Taking PPIs on an empty stomach allows for faster transit to the smallbowel, prompt absorption, and the development of maximal plasma levels.Eating causes stomach distension and the activation of proton pumps. Theseactivated proton pumps are turned off by PPIs by the irreversible inhibitionof acid secretion that occurs when maximal plasma levels of the PPIs areachieved immediately before the meal. Some patients manifest nocturnalacid breakthrough with nocturnal cough or morning hoarseness. This is ad-dressed best with the addition of high-dose histamine-2 blockers, such as ra-nitidine, 300 mg orally, nightly before bed.

It takes a minimum of 6 to 8 weeks to achieve reduction in symptomsdand although some patients note a difference in the first few days of vigilanttherapydall should be counseled to be patient and diligent with the treat-ment plan. It takes 6 months or longer for the laryngeal findings of laryng-opharyngeal reflux to improve [1,10,18]. The reflux severity index and refluxfinding score can be used to assess treatment efficacy, although patient his-tory is adequate. Professional singers are especially sensitive to subtlechanges in voice and so recognize when small changes in diet, stress, or rou-tine exacerbate their laryngopharyngeal reflux. Once laryngopharyngealreflux is controlled well, some patients slowly can reintroduce a few re-flux-exacerbating foods or begin to wean off PPIs; however, patients shouldbe counseled to keep track of their symptoms, and laryngologists should beliberal about represcribing twice-daily PPIs at the slightest sign of return oflaryngeal signs or symptoms.

Rarely, a patient will be unresponsive or inadequately responsive to dietchanges, behavior modifications, and maximum pharmacotherapy. Somepatients have a good initial response that is maintained for some monthsbut ‘‘backslide’’ over time, despite adherence to their diet and behaviorchanges. Many of these patients develop a relative tolerance to the specificPPI that they are taking, and a change from one specific medication to an-other seems to reestablish efficacy. Sometimes, two or three changes in med-ication are necessary to obtain the best response or the least disturbing sideeffect profile; however, some patients, despite all best efforts, remain symp-tomatic. This group should be referred to a gastroenterologist and a generalsurgeon for evaluation of refractory reflux and possible fundoplication.Eliminating much of the morbidity associated with the traditional open


approach, laparoscopic fundoplication frequently is successful [19,20].Young, thin patients who have severe reflux may be particularly well servedby fundoplication.

Finally, transnasal esophagoscopy (TNE) is recommended as a screeningtool for evaluating the esophagus in patients who have long-standing, se-vere, or refractory laryngopharyngeal reflux or complicated gastroesopha-geal reflux disease. This awake, nonsedated procedure can be performedin the office with topical anesthesia alone, biopsy can be performed as nec-essary, any abnormalities identified can be documented, and gastroenterol-ogy consultation can be obtained as warranted. TNE is a high-yielddiagnostic tool that aids the laryngologist/otolaryngologist in providingcomprehensive care for one’s patients [21–23].

Fungal laryngitis

Historically, fungal laryngitis was considered an opportunistic infectionin immunocompromised hosts indicative of likely invasive local or pulmo-nary fungal disease, if not systemic fungal disease (Fig. 2). Isolated laryngealdisease was believed to be exceedingly rare, and suspicion of laryngeal dis-ease nearly always prompted investigation for systemic disease and possibleimmunosuppression [24]. In studies that diagnosed fungal laryngitis by cul-ture or biopsy, the causative organism usually was candida species (ie, Can-dida albicans) [24,25]. Other known pathogens include Blastomyces(common in the Eastern United States and Midwest), Histoplasma (endemicto the Ohio and Mississippi River Valleys), and Coccidioides (found in theSouthwestern United States and the cause of ‘‘Valley fever’’) [25,26].More recently, fungal laryngitis has been recognized as a local superficial in-fection 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 mid-

musculomembranous region of both vocal folds. Fungal laryngitis also can manifest as multiple

punctate white plaques throughout the larynx.


with risk factors that compromise mucosal barrier integrity [26–28]. Theseinclude laryngopharyngeal reflux, smoking, and the use of inhaled steroids[26–29]. Prolonged antibiotic use and radiation also have been identifiedas risk factors [26,27].

Patients with any of the above noted risk factors, diabetes mellitus, nutri-tional deficits, on immunosuppressive therapy, or in an immune-suppressedstate who present with dysphonia, dysphagia, odynophagia, pain, or a sensa-tion of ‘‘burning in the throat’’ should be suspected of having fungal laryn-gitis [26–28]. The astute clinician who is aware of these risk factors will askabout associated symptoms and whether the onset of the symptoms corre-sponded to changes in risk factor profile (eg, a new inhaled steroid, a recentillness, uncontrolled blood glucose levels). Then, the clinician will look forsigns on laryngoscopy that are indicative of fungal laryngitis: leukoplakia,white or gray pseudomembrane adherent to mucosa, mucosal edema and er-ythema, mucosal ulceration, and contact bleeding. Findings often mimicthat of early oral thrush; however, the lack of white plaques, or leukoplakia,in the presence of diffuse erythema can be caused by fungal laryngitis. Thelaryngologist also must look for other lesions. Malignancy should be in thedifferential diagnosis, especially in the smoking population.

Diagnosis in these patients commonly rests on clinical suspicion based onhistory, risk factors, laryngoscopy findings, and response to empiric treat-ment with oral antifungal agents [28]. Patients who fit the clinical pictureof fungal laryngitis can be treated with oral fluconazole for 3 weeks (200 mgon day 1, followed by 100 mg daily on days 2 through 21) in conjunctionwith nystatin swish and swallow (100,000 units/mL at 10 mL three timesdaily 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 andAnderson [28] do not routinely check liver function tests. Patients who havehepatic disease can be treated with nystatin as a first-line agent and referredto their primary care physician for evaluation of their candidacy for sys-temic antifungal treatment if they fail to respond appropriately. Because an-tifungal treatment often is concomitant with antireflux treatment, responseto therapy can be multifactorial. If there is any question about the diagnosisof fungal laryngitis, should symptoms/signs not resolve, or should malig-nancy be a significant concern, a definitive diagnosis can be obtained withlaryngeal brushings and culture or biopsy. This can be accomplished within-office transnasal flexible laryngoscopy and biopsy through a workingchannel on the endoscope. Often, periodic acid-Schiff or methenamine silverstains are necessary to see fungal elements on histopathologic evaluation[26,27]. Some patients who have fungal laryngitis with severe dysphagiaalso may have esophageal candidiasis. If this is suspected, TNE is recom-mended to examine the esophagus and to obtain biopsies as necessary. Pa-tients who have severe dysphonia and pain also may present with significanthoney-colored crusts in the larynx in addition to multiple white plaques over


erythematous bases and edema. In these patients, a bacterial superinfectioncan be presumed present, and oral clindamycin, 600 mg three times daily (orsimilar antibiotic with gram-positive and anaerobic coverage) for 3 weeks,added to the antifungal therapy. Again, this is an empiric treatment; culturesare not obtained at initial evaluation. These patients usually do not respondto antifungals alone.

The literature does not reflect the number of professional voice users whohave asthma or other obstructive pulmonary disease who have been on in-haled steroids at any point. Considering the broad definition of ‘‘profes-sional voice user,’’ however, it is not difficult to imagine that this numbercould be significant. Therefore, laryngologists are obligated to seek this his-tory and communicate with the prescribing physician about possible alter-natives to inhaled steroids for patients who develop fungal laryngitis. It isnot always possible to wean patients off inhaled steroids, in which case shortholidays from steroid use may be in order, with or without low-dose prophy-lactic antifungal use (eg, nystatin or mycelex troches). The use of a spacerwith the inhaler should be recommended [28]. Patients also must garglewith 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 character-ized 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-pitchedspeaking voice, poor control of the breath stream, frequent hard glottal at-tacks, obvious cervical muscle tension, and jaw and tongue tension [31,32].Muscle tension dysphonia is a form of laryngeal hyperfunction, and the twooften are considered synonymous. Other synonyms include hyperfunctionaldysphonia, muscle misuse dysphonia, hyperkinetic dysphonia, musculoskel-etal tension dysphonia, mechanical voice disorder, functional hypertensivedysphonia, laryngeal tension-fatigue syndrome, and laryngeal isometric dys-phonia [32]. All of these terms fall under an umbrella diagnosis of functionaldysphonia, classically considered an impairment of voice production in theabsence of structural change or neurogenic disease of the larynx. In the1980s and early 1990s, multiple classification schemes for muscle tensiondysphonia were proposed, with emphasis on symptom onset, voice quality,and laryngeal movement patterns [33–36]. In the last decade, an importantshift in how laryngologists think about functional dysphonia and muscletension dysphonia has occurred. Namely, it has become evident that muscletension dysphonia most likely is not a stand-alone entity, but more likely ismultifactorial 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 foldbowing in an aging patient), laryngopharyngeal reflux, vocal fold polyp, andvocal fold nodules [32,37]. More frequently, muscle tension dysphonia isthought of as a compensatory mechanism for another entity.

Another concept that is becoming clear is that although many patientswho have muscle tension dysphonia (ie, dysphonia associated with muscletension patterns on examination) actually may be compensating for organiclaryngeal pathology, many nondysphonic patients have findings consistentwith muscle tension patterns on laryngeal evaluation. Belafsky and col-leagues [37] and Sama and colleagues [38] found evidence for muscle tension(ie, glottal gap on phonation, ventricular compression, anterior–posteriorsupraglottal compression) in asymptomatic subjects. This underscores theimportance of performing a comprehensive voice evaluation of patients, in-cluding history, physical examination, VLS, and acoustic and aerodynamictesting, before diagnosing muscle tension dysphonia. Similarly, if symptomsare not consistent with muscle tension dysphonia (ie, there is no dysphonia)but muscle tension patterns are seen on examination, clinicians should thinkabout the potential for the patient to develop muscle tension dysphonia,because muscle tension patterns may signal a natural (unconscious) com-pensation for a subacute, organic process in evolution.

Given these recent developments, the treatment of muscle tension dys-phonia should change to parallel our better understanding of it. First andforemost, once muscle tension dysphonia is diagnosed based on history,physical examination, VLS, and voice evaluation, the next step is to eluci-date any and all other contributing factors. This echoes the point made pre-viously; many patients present with multiple diagnoses underlying theirsymptom complex. Once a complete understanding of the individual’s laryn-geal structure and function is attained, or at least underway (because ad-dressing reflux, for example, may reveal vocal fold masses), treatment ofmuscle tension dysphonia may begin. Voice therapy with appropriate laryn-geal manipulation is the cornerstone. In professional voice users, especiallysingers, attention to techniquedin the singing and speaking voicedis im-perative. The voice teacher and voice coach must be involved with the pa-tient, speech/voice therapist, and laryngologist. The main purpose of voicetherapy is to eliminate supraglottic compression and to retrain true vocalfold vibration. In cases where mass lesions are involved, vocal hygienewill be emphasized. If presbylarynges is underlying muscle tension dyspho-nia, injection vocal fold medialization or medialization laryngoplasty maybe considered. The same is true for patients who have muscle tension dys-phonia due to vocal fold paresis.

Vocal fold paresis

Just as muscle tension dysphonia is increasingly recognized as a compen-satory mechanism for underlying organic, and sometimes multiple, vocal


fold disorders, vocal fold paresis is receiving more attention as a commonproblem that causes dysphonia. Paralleling the paradigm shift in laryngolo-gists’ thinking about muscle tension dysphonia, more focus is being placedon ‘‘looking’’ for vocal fold paresis as a contributing factor to changes invoice and in the development of hyperfunction.

Dysphonia was universally present in 50 consecutive patients diagnosedwith vocal fold paresis by Koufman and colleagues [39] in a retrospectivereview. The next most common symptoms were effortful phonation and vo-cal fatigue (76%), diplophonia (40%), and odynophonia (12%). Similarsymptoms were described by other investigators [40,41]. Decreased projec-tion and decreased range also are symptoms of vocal fold paresis. Laryngealfindings on transnasal flexible laryngoscopy and VLS included unilateral hy-pomobility (50%), unilateral vocal fold bowing (36%), bilateral bowing(22%), bilateral hypomobility (8%), and axial rotation (8%). Muscle ten-sion patterns were nearly universally observed as anterior–posterior com-pression or false vocal fold compression. Hypomobility and bowing canbe subtle, and abduction can be affected more frequently and more notice-ably than adduction.

Once vocal fold paresis is suspected based on history and examination,the clinician must decide whether laryngeal electromyography (LEMG) isindicated. This determination must be made on a case-by-case basis. Cer-tainly, the diagnosis of vocal fold paresis rests on LEMG, because asymme-tries in arytenoid movement are normal in some patients (ie, there is nodecrement in the neuromuscular activity of the larynx) [39]. Differences inarytenoid movement seen on physical examination cannot be used aloneto diagnose vocal fold paresis; however, the clinician is obligated to considerthe physical findings as well as their impact on function. Although some pa-tients who have LEMG-diagnosed paresis are symptomatic enough to war-rant surgical therapy, many, including professional voice users, are able tofunction well without surgery. Conversely, even those able to function with-out surgical intervention may benefit from voice therapy, which can beguided by LEMG results. Before performing LEMG, it is important to eval-uate with the patient whether LEMG results will influence clinical decisionmaking. It is not surprising for a professional voice user to opt out of a di-agnostic procedure if it yields a choice between surgical or nonsurgical man-agement when the patient is ‘‘not ready’’dmentally or functionallydtoconsider a surgical procedure. This clinical situation is not unusual and em-phasizes the importance of assessing with the patient how limiting the voicechange is.

If it makes sense to perform an LEMG, it should be performed at a sep-arate visit, after which findings are reviewed briefly with the patient beforecomplete electromyographic analysis. Review of final results is reserved fora follow-up visit, during which therapeutic options for treating the vocalfold paresis are presented, if warranted. Concomitant vocal fold pathologymust be uncovered and considered in the overall management plan.


Treatment options for vocal fold paresis include no treatment with observa-tion for resolution or progression, voice therapy alone, and injection aug-mentation or medialization laryngoplasty, preceded and followed by voicetherapy. Koufman and colleagues [39] performed laryngoplasty or lipoinjec-tion in 54% of the aforementioned subjects, with significant improvementachieved in 85%. Medialization techniques are covered at length elsewherein this issue (see the article about voice surgery).

Superior laryngeal nerve (SLN) paresis deserves special mention becauseit may have devastating effects on singers, given the impact that it has onmodulating pitch in the upper range. If loss of high range is among a singer’scomplaints and hypomobility in one vocal fold is seen on examination or ifsymptoms do not improve on maximal laryngopharyngeal reflux therapywith singing therapy in the case of symmetric movement, LEMG is indi-cated to elucidate whether the SLNs are intact. If isolated SLN paresis ispresent without vocal fold bowing or signs that vocal fold augmentation/medialization will be helpful, it is important to provide voice therapy toavoid development of muscle tension dysphonia, to encourage appropriatechanges in repertoire, and to provide hope to the patient that the vocalfold paresis may be postviral with potential for resolution. This last pointof management is critical: first, patients often are able to cope better withthe 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, thesimilarities and differences in the symptoms, diagnosis, and treatment of vo-cal fold nodules, polyps, and cysts are presented in brief. Dysphonia is themost common presenting symptom of benign vocal fold masses. The astuteclinician may develop some hypotheses as to which type of mass is presenton the vocal fold based on specific voice changes, such as loss of range in thehigh frequencies (commonly associated with nodules) or diplophonia due toa difference in vibratory frequency of the vocal folds (often associated witha unilateral process, such as a polyp). The wise clinician is ever mindful thatmore than one pathologic process or more than one type of mass can bepresent. Obtaining a good history is important to help define the cause ofthe problems that the patient is having with the voice, which helps guidethe development of an individualized management strategy.

Vocal fold nodules are considered the most common vocal fold lesions inchildren and adults. They are common among professional voice users as well,especiallywhenone includes in the definition of vocal fold nodules early fibrovas-cular changes (subtle irregularities of themedial vocal fold edges in themid-mus-culomembranous region) that are associated with significant voice use.

(Access Video on Nodules in online version of this article at: http://www.Oto.TheClinics.

com.)





Vocal fold nodules (Fig. 3) are the end result of subepithelial scar depo-sition, primarily changing the mass and stiffness of the vocal fold cover, withlittle effect on the body [42]. Vocal fold nodules frequently interfere withvocal fold closure, so hoarseness and breathiness are common symptoms.Because of the loss of vocal fold pliability that occurs as the subepithelialscar increases in size, and because of the increased size of the persistentgap as the result of premature contact with incomplete closure, there is a de-crease in range and stamina with an increase in vocal fatigue. Nonetheless,the presence of nodules does not imply a change in vocal functioning in allpatients. Vocal fold nodules may have been present since childhood, andmany singers function exceedingly well with them. The presence of vocalfold 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 areunilateral. Vocal fold polyps also may present with hoarseness, loss ofrange, 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.


above; dyspnea can occur if the polyp is large enough to obstruct the airway.In professional voice users, the emergence of dyspnea is unlikely; thesepatients probably would seek laryngologic attention before dyspnea couldevolve. The one exception is a hemorrhagic polyp, which can occur suddenlyand 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 diplophoniaalso may be a problem. Vocal fold cysts are present in the superficial laminapropria and can open into the laryngeal lumen or insert onto the vocal lig-ament. Vocal fold cysts are categorized as epidermoid (sometimes calledsquamous inclusion) cysts or mucus retention cysts [42]. Epidermoid cystsare believed to arise from traumatic introduction or ingrowth of keratininto the superficial lamina propria, secondary to phonotrauma, or to be con-genital. Mucus retention cysts more likely result from occlusion of mucusglands 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 byhistory alone. VLS is the key to their diagnosis. Stroboscopy is essential toan accurate diagnosis because it allows for the assessment of vocal fold clo-sure and phase symmetry, which are not discernable in the absence of stro-boscopic light. Stroboscopy’s delineation of the mucosal wave allows thelaryngologist to assess its relationship to the mass, and, thus, whether theepithelium/basement membrane zone is involved or whether the mass liesdeeper 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.






sessile to raised to discretely nodular lesions along the medial edge of the vo-cal folds, in the midmusculomembranous region (junction of the anteriorone third and posterior two thirds of the entire vocal fold). Pronouncedvibration 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 situa-tions, persistent anterior and posterior glottic gaps; the resultant ‘‘hour-glass’’ configuration is classic. Vocal fold polyps are more frequentlyunilateral, broad-based sessile lesions that can be clear, white, or reddish,small or large, and can be pedunculated (small sessile lesions are more com-mon) [42]. Changes in vocal fold stiffness attributable to vocal fold polypsdepend on the histologic type: gelatinous polyps, with loose edematousstroma, 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 horizontaland vertical phase symmetry of the two vibrating folds; a polyp on one vocalfold can cause traumatic polypoid or fibrovascular changes in the contralat-eral fold, if not scarring. Again, incomplete closure is common. Finally, vo-cal fold cysts generally are unilateral and are distinctly subepithelial.Sometimes a discrete intracordal mass can be appreciated. Epidermoid cyststend to bulge on the superior and medial aspect of the midmusculomembra-nous region. On phonation, the epithelium often can be seen moving overthe cyst, so that it appears like an ‘‘egg in soup.’’ Mucus retention cystsoccur most frequently on the inferior aspect of the vocal fold because themedial edge is devoid of mucus glands. Edema of the contralateral fold ora contact nodule may be seen. Phase asymmetry dominates VLS, giventhe increased stiffness of the cover, and contralateral traumatic changesare common [42]. Notably, despite the excellent resolution of VLS, it canbe impossible to fully understand the nature of a vocal fold mass withoutthe higher magnification and tactile evaluation by way of palpation achiev-able during suspension microlaryngoscopy. Similarly, if therapeutic suspen-sion microlaryngoscopy is undertaken to treat a benign mass, additionalmass/vascular lesions not seen on VLS may be revealed. This possibilityshould be discussed with patients who decide to undergo surgery, so thatoccult masses discovered at that time can be addressed.

Treatment of benign vocal fold masses depends on a patient’s symptomcomplex. If laryngopharyngeal reflux is present, it should be treated first,as should muscle tension dysphonia. A course of voice therapy will addressvocal behaviors in the speaking and singing voice to which the developmentof the mass or muscle tension dysphonia may be attributed. Goals of ther-apy are to maximize vocal efficiency, thereby reducing the vibratory traumathat underlies and exacerbates the masses [43]. Although voice therapy alonecannot cure vocal fold nodules (ie, make them disappear in entirety), thesurrounding edema may reduce significantly with changes in vocal hygiene.Return to near-normal function is possible, although some professionals willcontinue to notice limitations in the voice and, thus, require surgery. Vocal


fold polyps and vocal fold cysts also should be treated with an initial courseof voice therapy to optimize vocal hygiene; however, in these cases, voicetherapy less often accomplishes significant recovery of function, and surgeryis almost always required if associated symptoms are significant. Precisephonomicrosurgical excision of the lesions, with every effort to preserve asmuch normal tissue (epithelium and superficial lamina propria) as possible,remains the surgery of choice for symptomatic benign lesions. Specifics oftechnique are addressed elsewhere in this issue. Following an immediatepostoperative course of voice rest ranging from 4 to 14 days, voice therapyis mandatory to achieve the best functional results.

The special case of rheumatoid nodules and bamboo nodes is consideredhere briefly (Fig. 5). First, obtaining the history of rheumatoid arthritis, orany other/additional autoimmune disease, is critical during the interviewprocess for any complaint. If this history is obtained, the laryngologistshould note all current and previous medications used to treat the disorderand the name and contact information for the patient’s rheumatologist. Sec-ond, it is important to know how well controlled the patient’s autoimmunedisease is and whether he/she can correlate any changes in voice withchanges in the severity of autoimmune disease. Vocal fold lesions relatedto rheumatoid arthritis and autoimmune disease are rare, as are their de-scriptions in the literature [44]; however, laryngeal involvement in rheuma-toid arthritis is well documented and may be present in most patients whosuffer from that disease [44–47]. The cricoarytenoid joint, which is diarthroi-dal, like the interphalangeal joints in the distal extremities, is involved mostcommonly. Laryngeal manifestations of rheumatoid arthritis in the cricoar-ytenoid joint include dysphonia, odynophonia, dysphagia, dyspnea, andthroat pain. If nodules are present in rheumatoid arthritis or autoimmunedisease, vocal roughness is a frequent complaint, as is intermittent aphonia.

Fig. 5. Rheumatoid nodules. Bilateral, horizontal-appearing intracordal masses with subtle sur-

rounding erythema are seen.


Clinical manifestations include hoarseness and instability in connectedspeech, with characteristic subepithelial nodules that appear as horizontalbars or rectangles that run perpendicular to the long axis of the vocal foldin the midmusculomembranous region. Often, these are striated in appear-ance and universally cause stiffness in vocal fold vibration with reduction inthe magnitude of mucosal wave [44,45,48]. Rheumatoid nodules and bam-boo nodes (similar lesions seen in autoimmune diseases, such as Sjogren’ssyndrome and systemic lupus erythematosus) are almost always bilateral;surrounding erythema is common, particularly during a flare-up of thesystemic disease. Rheumatoid nodules and bamboo nodes must be treatedin the context of the systemic disease. Close communication with the rheu-matologist is necessary to optimize medical therapy when conservativemeasures fail. Surgical excision or direct injection of steroids into the rheu-matoid nodules/bamboo nodes is undertaken when function demands it;however, patients must be counseled that the lesions can recur in the faceof chronic disease. Perioperative reflux treatment is imperative, and anoral steroid burst is recommended preoperatively to help abate inflamma-tion. It is not uncommon to encounter dense fibrosis around the nodulesonce they are exposed subepithelially by way of cordotomy, even with sub-epithelial injection of local anesthesia/epinephrine. Nonetheless, it is impor-tant to remove the nodule in its entirety to maximize function and minimizegrowth of persistent disease. Bilateral lesions can be addressed at one sittingbecause a superior cordotomy usually is made. Postoperative management isthe 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, itis agreed that treatment outcomes are fair to good, but inconsistent atbest [49–53]. This mandates continued research into the pathophysiology,histology, biology, and treatment of vocal fold scarring. A detailed discus-sion of these topics is beyond the scope of this article, and the reader isreferred to several recent reviews [50,51,53]. Nonetheless, given the potentialfor permanent voice change and the impact on patients, particularly profes-sional voice users, vocal fold scar is an area worthy of utmost attention inthe clinical and research realms.

Scar is derived from the Greek eschara (scab) and is defined as ‘‘fibroustissue replacing normal tissues destroyed by injury or disease’’ [54]. Causesof vocal fold scar are diverse and include inflammatory, neoplastic, trau-matic, and iatrogenic entities [49]. Although the incidence and epidemiologyof vocal fold scar are not well documented in the general population or pro-fessional voice users, one can imagine that inflammatory and iatrogeniccauses are the most common among professional voice users. In additionto vocal misuse and abuse (which predispose to fibrovascular change and


mass lesions, themselves associated with scar), laryngopharyngeal reflux,bacterial laryngotracheitis, and prior aggressive endolaryngeal surgery areassociated with vocal fold scar [49,53,55]. Sulcus vocalis is a specific entityoften considered under the ‘‘umbrella’’ of vocal fold scar, because it, too,consists of fibrous tissue replacing normal tissue in the vocal fold. Sulcusvocalis is discussed further in this section.

In the vocal fold, the ‘‘normal tissue’’ destroyed by scar in varying degreeand thickness is the delicate multilayered structure composed of epithelium,superficial lamina propria, intermediate lamina propria, deep lamina prop-ria, and muscle. This fibrous insult compromises vocal fold pliability, theexact property that allows production and modulation of voice, by causingcontraction of the vocal fold cover and effecting loss of vocal fold volume[53]. The result is an increase in vocal fold stiffness and subsequent decreasein 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 thevocal fold’s medial edge and midmusculomembranous region, the depth ofscar, the presence of other lesions/pathologic entities, and the patient’s innateor trained compensatory mechanisms of producing voice. Patients may de-velop a strained, harsh, or breathy voice, diplophonia, or hoarseness [49]. Inaddition to change in voice, common complaints include vocal fatigue, lossof range, and loss of stamina. These complaints also apply to sulcus vocalis.

Sulcus vocalis is a linear invagination of epithelium along the medial edgeof 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 laminapropria or to the vocalis muscle. Depth of migration generally correlateswith symptom severity, as well as the prognosis for successful treatment.Ford and colleagues [56] developed a classification scheme for sulcus defor-mities, 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 (fromvocal process to anterior commissure), and they differ only in depth of pen-etration. Type I sulcus vocalis extends into the superficial lamina propriaonly, but does not reach the vocal ligament (intermediate and deep layersof the lamina propria, the transition layer); type II sulcus vocalis extendsto or beyond the vocal ligament, causing loss of superficial lamina propria.Type III sulcus vocalis is a deep, focal indentation of epithelium on themedial surface of the vocal fold that does not extend its entire length, butoften resembles a ‘‘pit’’ or pocket (Figs. 6 and 7). In our experience, kera-totic debris frequently accumulates in type III sulcus vocalis, such that ini-tial evaluation in the clinic may raise the question of an intracordal cystbecause they are shallow, cause minimal loss of superficial lamina propria,and generally result in only mild change of the mucosal wave. Type I sulcus





vocalis has been termed ‘‘physiologic sulcus.’’ Types II and III sulcus vocalisare considered pathologic; type II also is referred to as ‘‘sulcus vergeture.’’

The key to diagnosing vocal fold scar or sulcus vocalis is a thoroughhistory (including specific vocal complaints and surgical history) andphysical examination, the most important aspect of which is VLS. VLSfeatures include asymmetric amplitude of vibration, the scarred side hav-ing reduced or absent amplitude of vibration and loss of mucosal wave(which may be focal or diffuse); incomplete glottic closure requiringhigh pressure to sustain phonation given significant stiffness; and nonvi-brating segment in the affected vocal fold that prevents mucosal wavepropagation [49].

Ventricular hyperfunction may or may not be seen, but usually appearsas the glottal gap increases in size. A complete voice evaluation with aero-dynamic and acoustic batteries is imperative once vocal fold sulcus/sulcus

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 pho-

nomicrosurgical techniques.


vocalis has been identified so that effects of therapy, whether medical orsurgical, can be assessed and followed.

Most important, the best approach to treating vocal fold scar is prevent-ing it. Encouraging good vocal hygiene and technique in professional voiceusers of all ages is important to accomplish this goal. Nonetheless, with con-tinued use over time, some degree of scarring seems inevitable. As in thetreatment of benign vocal fold masses, voice therapy is the first line of treat-ment for scarring to maximize vocal efficiency and to stretch the scar tissueto improve its pliability. In operative cases, voice therapy helps to maximizevocal hygiene and technique preoperatively in preparation for postoperativetherapy [49,53]. Patients have the best chance of improvement, with or with-out 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 appro-priate procedure. These were outlined nicely by Dailey and Ford [53] andinclude discussions of endoscopic versus open approaches; potential useof autologous implants requiring separate harvest site; whether a short- orlong-term solution is desirable; approaches appropriate for mild versussevere cases; approaches that are direct versus indirect; and approachesthat address glottal gap, loss of pliability, or both. A full discussion ofeach procedure’s technical aspects, advantages, and disadvantages is beyondthe scope of this article; readers are referred to other sources, including thearticle on voice surgery in this issue [49,53,56–59]. Briefly, correction of theglottal insufficiency associated with scarring can be addressed with vocalfold augmentation or medialization techniques. These do not address theloss of pliability and do not address the scar/sulcus directly. Such proce-dures include injection of alloplastic substances into vocal folds or paraglot-tic space (collagen, micronized dermis, hyaluronic acid, hydroxyl apatite);

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.


autologous fat or fascia also can be used. Medialization thyroplasty withGore-Tex or silastic blocks also will close a glottal gap. Direct approachesto sulcus deformities that aim to address the loss of pliability include endo-scopic procedures, such as cold instrument undermining of the sulcus byway of a longitudinal epithelial cordotomy, scar release, and flap redraping;cold instrument excision of the scar, similar to the redraping procedure butwith removal of scar tissue to its depth; laser undermining with redraping;and slicing technique that involves full-thickness releasing cuts in the flapmedial and perpendicular to its longitudinal axis [56,60]. These techniquesdo not always address glottal insufficiency. Finally, other procedures that at-tempt to address lack of pliability and glottal insufficiency include those thatadd an implant to scar release or excision. These also are endoscopic proce-dures 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 hasbeen performed by large numbers of surgeons or on large numbers of pa-tients. The development of multiple techniques to address sulcus reflectsour poor understanding of it and parallels the lack of consensus on howbest to address it. Continued research in this area is imperative to improvingpatient care.

Varices

Prominent or enlarged vessels within the vocal folds’ superficial laminapropria are variably termed microvascular lesions, varices, varicosities, ecta-sias, capillary ectasias, papillary ectasias, or spider telangiectasias [61–67].Typically, the applied term reflects the size and shape of the concerned ves-sel, but the nomenclature is not standardized. The best way of classifyingthese vessels may be to adhere simply to Stedman’s [54] definitions. Varixis derived from the Latin varix (dilated vein) and refers to a dilated veinor an enlarged and tortuous vein, artery, or lymphatic vessel. Ectasia is de-rived from the Greek ectasis (a stretching) and refers to dilation of a tubularstructure. Because the definition of varix includes ectasias, it seems simplestand appropriate to apply the former to all enlarged vessels of the vocalfolds; diagnosis and management strategies are the same for all of them.

Vocal fold varices are found most frequently on the superior surface ofthe vocal fold (Fig. 8) [61,62,67]. Their next most common location is themedial surface, with a superior/medial location ratio of approximately 3:1in one study, which also noted that more than half of the superior varicesoccurred at the lateral extent of the mucosal wave [67]. The exact reasonfor this is not known. The possibility of maximal shearing forces occurringat the superolateral limit of the mucosal wave has been proposed, but is notproven [67]. Because they are dilations of normal vasculature, most vocalfold varices run in an anterior–posterior direction, paralleling the vectorof the vocal fold; however, this is not always the case, and vocal fold varices,


or dilations within them, may occur at oblique angles or even perpendicularto the direction of the vocal fold.

The true incidence of vocal fold varices is not known. It is agreed, how-ever, that they are not common, are seen most frequently in professionalvoice users, and are more common in women [61–64,66]. These trendswere largely accepted, but anecdotal observations, until Postma and col-leagues’ [66] first systematic evaluation of the treatment of vocal fold varicesin 1998. In this retrospective review of all patients with benign laryngeal dis-orders and dysphonia evaluated between 1992 and 1995 at the VanderbiltVoice Center, only 25 of 800 patients (3.1%) had isolated vocal fold varices(patients who had hemorrhagic polyps, nodules, cysts, granulomas, andlarge arteriovenous malformations with or without vocal fold varices wereexcluded). Of these 25 patients, 22 (88%) were professional voice users,including 13 professional singers; 19 (76%) were women. The incidence ofvocal fold varices was higher among all women (4.5%) than among allmen (1.6%), and similarly higher among female professional voice users(14%) than among male professional voice users (5.0%). This increasedprevalence in professional voice users, reported by other investigators aswell, influences the number of patients who have vocal fold varices seenby the laryngologist. It is important to consider, however, that the incidencein the population at large could be much higher and that most people whohave vocal fold varices are asymptomatic or are not bothered by thembecause of the negligible effects on the voice. The higher incidence of vocalfold varices in women indicates at least a female predisposition to them, ifnot a hormonal role in varix formation. Again, although this has been pro-posed by many investigators, the influence of hormones on vocal fold vari-ces has not been studied well [63,65,66,68,69].

Although Postma and colleagues [66] did not include the number ofpatients who presented with vocal fold varices in conjunction with another

Fig. 8. Vocal fold varices. Prominent varices (with ectasias) are seen bilaterally. This patient

also has a left vocal fold paresis.


benign lesion, this clinical finding is frequent among professional voiceusers. In Hochman and colleagues’ [67] review of 42 patients who weretreated for ectasias and varices, 39 patients (93%) had additional lesions(eg, polyps, nodules). Again, most patients were female (81%), and mostwere 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 asso-ciated lesions requiring surgical treatment. In our experience, it is notunusual to find vocal fold varices with other benign lesions of the vocal foldsin professional voice users. Still, it is not known whether vocal fold varicescause other benign lesions (eg, nodules or polyps) to develop, whether thepresence of a mass lesion on the vocal folds predisposes them to developingvocal fold varices, or both. It has been hypothesized that the enlargement ofvocal fold blood vessels with significant vocal use or abuse will increasevocal fold mass and stiffness, changing vocal fold vibratory patterns, possi-bly inducing vocal fold edema and subsequent mass lesion development [62].Certainly, varices and mass lesions share the common pathway of significantvocal use, as in the case of professional voice users, as well as vocal overuseor misuse in other patients.

It is difficult to know the most common symptom caused by vocal foldvarices given their relative low-documented incidence and their coexistencewith other lesions. The most common complaint among patients in Postmaand colleagues’ [66] review was hoarseness (72%), followed by decreasedvocal range (16%) and vocal fatigue (12%). Often, these symptoms are inter-mittent, varying with voice use, and are widely accepted as common by otherclinicians as well. We have had the same experience; however, we also seea number of young conservatory singers in the laryngology clinic for baselineevaluations at the recommendation of their voice teachers. These studentshave been singing through childhood and high school, often competitively.Anecdotally, most of them have signs of laryngopharyngeal reflux, andmany 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 sameas that for other patients with these lesions; however, as is the case withtreating any lesion in the vocal professional, the recommendation andtiming of treatment must be individualized to account for their potentialimpact on career goals and professional obligations. Also, the varices mayneed to be treated in conjunction with other lesions. An asymptomaticisolated varix does not require active treatment, but it should be followedwith regular VLS. Patients need to be educated about the possibility of vocalfold hemorrhage, because of the fragility of these lesions, and counseled thatif any acute significant voice change occurs, especially related to voice use orupper respiratory tract infection, strict voice rest should be observed andimmediate laryngologic evaluation obtained. Symptomatic vocal fold vari-ces should be treated in a staged fashion, depending on the frequency and


severity of symptoms and on the evolution of the lesion (ie, change in theirsize or number). Medical treatment almost always includes aggressivetreatment of laryngopharyngeal reflux, because it is nearly ubiquitousamong professional voice users. Decreasing reflux-associated vocal foldedema should reduce the resultant increase in vocal fold mass, which likelypredisposes the patient to develop or exacerbate varices as increased effort ismade to produce voice. Decreasing reflux-associated mucus may decreasethroat 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 investigatorsalso institute mucolytic therapy as necessary [66]. The second major stepin medical therapy is to obtain a comprehensive voice evaluation, includingan acoustic and aerodynamic test battery and flexible and rigid videoendoscopy with and without stroboscopy. This will be used to tailor individ-ualized voice therapy to optimize vocal technique and minimize vocaltrauma in the speaking and singing voice. Baseline voice evaluation andvoice therapy also are critical to obtain should surgical intervention berequired later.

The most widely accepted indication for surgical treatment of vocal foldvarices is recurrent vocal fold hemorrhage in patients who have an identifi-able varix in the vocal fold sustaining this injury and who have a resultantirreversible unacceptable change in the voice [61–63,65–67,69,70]. As withsurgery for most benign laryngeal disease, patients must be counseled ofthe risk involved in the surgery, which can be voice and career saving, butnonetheless is elective. Other indications for surgery were outlined nicelyby Postma and colleagues, [66] however, some laryngologists may think ofthese as relative indications for surgery. These indications include enlarge-ment of the varix, development of a mass in conjunction with a varix orhemorrhage, or unacceptable dysphonia secondary to persistent vibratoryabnormality seen on serial VLS after maximal medical and voice therapy.One successful approach prioritizes the patient’s self-assessment of vocalfunction and commitment to good vocal hygiene and technique. If vocalhygiene and technique are sufficiently good and consistent, but vocal func-tion is inadequate, other lesions have been treated or excluded, and medicaltherapy has failed, surgery should be offered to the patient. If all of thesecriteria are met, but there are other mass lesions that require treatment,these should be treated operatively at the same time as treating the vocalfold varices. Most important, as emphasized by other investigators, consentmust be obtained to treat/excise any mass lesions newly discovered onsuspension microlaryngoscopy that by size, position, or character couldbe affecting the voice [67,70]. The decision to treat bilateral vocal foldlesions in one or two stages is made intraoperatively and depends on thelesions’ locations relative to each other and to the medial edge of the mid-musculomembranous region. A two-stage approach is selected if there isconsiderable risk for postoperative apposition of the operative sites and,


thus, risk for web formation, or if extensive work in the superficial laminapropria may compromise function after bilateral surgery.

Techniques for surgical treatment of vocal fold varices have evolved overtime, paralleling the development of direct laryngoscopy, laser technology,and microsurgical instrumentation. Baker [61] described ‘‘picking’’ off theprominent vessel without ‘‘biting’’ into the vocal fold by way of directlaryngoscopy. Cold instruments were used to remove vocal fold varices upuntil the development of the CO2 laser, after which it was used on low-power settings and with defocused spot sizes and short single pulses toablate vocal fold varices [62,63,67,69]; however, with concern for thermaldamage to the vocal fold, the CO2 laser fell out of favor, and microsurgicaltechnique has been used more routinely [67,69,70]. This technique involvesmaking several epithelial cordotomies directly overlying the varix, meticu-lously dissecting it away from the surrounding superficial lamina propria,then excising it with scissors or microforceps, applying epinephrine-soakedpledgets to achieve hemostasis, and allowing the cordotomies to heal pri-marily [67]. More recently, angiolytic lasers have been used to treat vocalfold varices, primarily in conjunction with other lesions (ie, polyps, nodules)[70,71]. The senior author routinely uses the 585-nm pulsed-dye laser (Pho-togenica SV, Cynosure, Littleton, Massachusetts) at 500 to 700 millijoules(mJ), to treat vocal fold varices and ‘‘normal’’-appearing vocal fold vesselsthat seem to ‘‘feed’’ a lesion when performing surgery for mass lesions[72,73]. The pulsed angiolytic lasers are safe and provide precise ablationof vocal fold vessels. Further basic science and clinical research with long-term patient follow-up is required to define the best role for the pulsed-dye laser (PDL) and KTP lasers in the treatment of vocal fold varices andother laryngeal processes. There are more data in the literature to supportPDL use than to support the KTP laser [71–74]. Retrospective evaluationsof both lasers are ongoing, and prospective studies are in order.

Vocal fold hemorrhage

Vocal fold hemorrhage is a laryngologic emergency that warrants imme-diate strict voice rest for 7 to 14 days and VLS to document the effects onthe mucosal wave (Fig. 9). Most frequently, patients note a sudden signifi-cant change in the voice with increased voice use or vocal abuse (singingor public speaking for prolonged or intense periods, yelling) or in associa-tion with upper respiratory tract irritation and inflammation (coughing,sneezing) [61,63,65,68,69,75–79]. Rarely, subtle chronic change in the voicemay be the presenting symptom of vocal fold hemorrhage [65,69,77]. Vocalfold hemorrhage usually occurs in one vocal fold, although bilateralvocal fold hemorrhage has been reported [63,65]. The demographics of vocalfold hemorrhage parallel those of vocal fold varices: vocal fold hemorrhageis more common in professional voice users and in women. A strong corre-lation between hormonal imbalance and vocal fold hemorrhage, especially

recurrent vocal fold hemorrhage, also has been noted by multiple investiga-tors [63,67–69]. In addition to vocal fold hemorrhage occurring in peri-menstrual women (just before or during menstruation), women inhormone supplement withdrawal, pregnant women, or women having un-dergone gynecologic surgery [63,65], other risk factors for vocal fold hemor-rhage in patients who have vocal fold varices have been identified, includingconsumption of aspirin and aspirin products, use of nonsteroidal anti-in-flammatory 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 toprofessional voice users, but something of which they should be aware sothat they take proper safety measures (wearing seatbelts in motor vehiclesand well-fitted harnesses as warranted in their work). As with vocal foldvarices, it is possible that the apparent higher incidence of vocal fold hem-orrhage in professional voice users compared with the general population issimply a reflection of the makeup of most laryngology practices and the sen-sitivity of professional voice users to changes in voice. The incidence of vo-cal fold hemorrhage in the population at large may be much higher, butunderdiagnosed.

Most professional voice users who experience sudden decrement in thevoice self-impose voice rest and seek laryngologic evaluation. Voice rest isbelieved to minimize the potential for further bleeding into the affected vocalfold as well as the potential for trauma to the opposite vocal fold duringphonation. If seen in the immediate hours after hemorrhage, the vocalfold may be bulging with blood/hematoma; after several days, it usually flat-tens, but remains red; with time, blood is metabolized, and the color changesfrom red to yellow because of hemosiderin staining and eventually back towhite. At any time after vocal fold hemorrhage, before complete resolution,VLS reveals vocal fold stiffness and decreases in the amplitude and

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

vocal fold hemorrhages.



magnitude of the mucosal wave [65,68,69]. Most investigators recommend 7days of strict voice rest and cessation of anticoagulants, if medically safe. Ifapplicable, resumption of hormone (eg, estrogen) therapy may be recommen-ded in conjunction with an endocrinologist or gynecologist. Close follow-up and repeat VLS with assessment of vocal fold stiffness and mucosalwave are imperative. Sometimes, longer periods of voice rest are necessary.Most commonly, the hemorrhage is a brief event, and a bulging vocal foldbegins to flatten out within a few days. Rarely, this is not the case, and a sig-nificant hematoma persists. In this instance, it is necessary to evacuate the he-matoma by way of suspension microlaryngoscopy in the operating room. Asmall superiorly based cordotomy is made, and careful suction evacuation ofthe hematoma is performed [65,69]. Voice rest for an additional 7 to 10 daysis instituted postoperatively.

All patients who have vocal fold hemorrhage, regardless of the need foroperative treatment, require follow-up voice evaluation and voice therapy.If a vocal fold varix is identified in the hemorrhagic vocal fold, this is fol-lowed closely and patients counseled on the potential for recurrent hemor-rhage 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 theeffects of age on the voice and their potential impact on career longevity.For many professional voice users, ‘‘age-related’’ voice changes may bedue to scarring or fibrovascular changes from long-term use/overuse/misuseof the voice. The resultant increase in pitch and harshness of the voice, withdecreased vocal efficiency from vocal fold stiffness, are not specific to ageand can occur in young patients. More common complaints among agingprofessional voice users include a wobbly quality to the voice, lack of clarity,singing flat, and an inability to sing softly [80]; however, more frequentlythese changes are due to deficits in overall conditioning rather than irrevers-ible aging changes in the larynx. Therefore, it is important for the laryngol-ogist to be able to differentiate between physiologic age-related changes inthe larynx and functional changes in the voice that may occur for reasonsincluding, but not limited to, senescent global deconditioning.

Hirano and colleagues elicited gender-specific histologic changes in thevocal folds [81,82]. The vocalis muscle atrophies in men and women. Inmen, the intermediate layer of the lamina propria also atrophies, but thedeep layer thickens as a result of increased collagen deposition. In women,the epithelium and superficial and intermediate layers of the lamina propriathicken with age. The superficial lamina propria also becomes more edema-tous. Age-related changes in the supraglottis also ensue in men and womenand include atrophy of seromucous glands in the respiratory epithelium’ssubmucosa (more pronounced for the mucous versus serous glands), associ-ated fatty infiltration, and fragmentation of false vocal fold connective


tissue. The most prominent clinical correlate to these changes is scallopingof the medial edge of the vocal fold (or ‘‘vocal fold bowing’’), seen on lar-yngoscopy, the hallmark of presbylarynges. Lateral cricoarytenoid hyper-function also may be seen with prominence of the vocal processes onquiet respiration and phonation onset, creating a posterior chink and lackof glottal closure. Additional laryngeal changes that occur with age includeossification of the laryngeal cartilages and diffuse loss of muscle tone andbulk; the joints may become arthritic and stiff [83]. Effects of these changeson voice can be extracted (ie, decreased range, flexibility, efficiency, and sta-mina), but are not well described.

The deconditioning that can accompany natural aging (although neitheruniversal nor predictable among patients of the same age or gender) affectsall components of voice production, not just the vocal folds [83]. These in-clude the abdominal muscles and diaphragm with decreased tone andstrength; the lungs and thorax with decreased elasticity and distensibility, re-spectively; the peripheral nervous system with a decrease in the number ofnerve endings; and the central nervous system with cortical atrophy andsometimes dementia. Any localized or systemic illnesses that affect anypart of the vocal tract will have an attendant effect on voice productionand quality.

Professional voice users, singing teachers and voice coaches, speech lan-guage pathologists, laryngologists, gynecologists, and a myriad of otherwomen’s health care providers are aware of the wide variety of voicechanges that can accompany menopause. Although it is accepted that thelarynx is sensitive to endocrinologic changes, and, in fact, developmentallydriven by changes in sex-hormone levels during childhood, puberty, meno-pause, and senescence, basic science and clinical research in the area issparse [84–90]. More importantly, objective findings in studies that attemptto evaluate the role of estrogen in menopause-related voice change and todelineate changes in measurable vocal parameters are not reliably reproduc-ible and do not always correlate with clinical experience [85,91]. Much of theliterature centers on subjective patient surveys. Together, these issues makethe study of voice in climacteric medicine a wide-open frontier.

Despite the lack of a large body of evidence to relate menopause directlyto specific changes in the vocal folds and in the voice, several repeatingthemes, as well as several intriguing studies, can be found in the literature.Voice changes that are described frequently as occurring during and aftermenopause include new-onset hoarseness and sometimes cracking, de-creased intensity, increased fatigue, and deepening of the voice [84,90–93].This may be due to the decrease in ovarian estrogen and relative increasein ovarian androgen found during menopause. Given its close relationshipto pitch, fundamental frequency (F0) has been studied in the context of men-opause: some investigators found a reduction in F0, whereas others demon-strated that changes in F0 were not statistically significant [91,92,94–96].Based on the temporal relationship seen clinically between changes in voice


and menopause, as well as menstruation, pregnancy, gynecologic surgery,and hormonal treatment of gynecologic diseases (eg, endometriosis, fibro-cystic breast disease, and premenstrual/menstrual dysfunction), the larynxis considered by many to be a secondary sex organ [84,90,97]. Estrogen-binding sites have been found in normal larynges, laryngeal papilloma,and laryngeal carcinoma [90,98–100]. Abitbol and colleagues [97] demon-strated that vaginal and laryngeal epithelial smears are similar at varioustimes during the ovarian cycle.

Many clinicians and performers also have noted coincidental improve-ments in voice when menopausal women are treated with hormone replace-ment therapy for other reasons (genital atrophy, decreased libido,osteoporosis, prevention of cardiovascular and Alzheimer’s disease, hotflashes, psychoemotional changes, insomnia). Hormone replacement therapyis 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 voicevalues and subjective voice/laryngeal symptoms in postmenopausal womenwho did not undergo hormonal therapy with those using estrogen alone oran estrogen-progestin combination. Among the 42 subjects, estrogenreplacement seemed to protect against detrimental changes in fundamentalfrequency 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 replacementon laryngeal cytology in postmenopausal women. They found that laryngealand vaginal epithelial smears in women on estrogen replacement therapyhad similar minimal cytologic changes compared with those of women with-out estrogen therapy in whom both smears showed aspects of atrophy-dystrophy. This work supports the idea that hormone replacement therapymay improve voice in postmenopausal women. Laryngologists should con-sider this when caring for perimenopausal professional voice users and discussthe possibilities of hormone replacement therapy with gynecologist colleagueson a case-by-case basis. Most important, however, is that professional voiceusers entering or beyondmenopause be under the care of an experienced voiceteam that can address perimenopausal voice changes appropriately.

As with all voice complaints, ‘‘my voice is getting old’’ must be investi-gated thoroughly. A diagnosis of presbylarynges cannot be made withouta complete laryngeal and neurologic evaluation for other underlying etiolo-gies. This point was demonstrated well by Woo and colleagues [102] in a ret-rospective review of 151 dysphonic patients who were older than 60 years:only 6 had dysphonia due to physiologic aging alone. The remaining 145 pa-tients were dysphonic secondary to specific disease processes, many of themrelated to age, but nonetheless pathologic. These included central neurologicdisorders affecting laryngeal function (eg, stroke, Parkinson’s disease, essen-tial tremor, Alzheimer’s disease), benign vocal fold lesions (eg, Reinke’sedema, benign and dysplastic epithelial lesions), inflammatory disorders


(eg, laryngitis sicca, medication effect), laryngeal neoplasia, and laryngealparalysis.

Despite the best voice training, professional voice users are not immuneto the development of disease in the middle and older years. Thus, the lar-yngologist is obligated to keep a broad differential diagnosis in mind whiletreating this select group of aging patients. Most presbyphonic patients willbenefit from voice therapy [80]. Specific vocal fold pathology can be treatedsurgically as indicated.

Voice overuse

One of the most common problems in professional voice users, especiallysingers and actors, is laryngitis associated with voice overuse. This is to bedistinguished from infectious laryngitis, also common in this populationduring peak performance times, which are associated with long hours,lack of sleep, and often, poor nutrition. Reflux laryngitis also may be an un-derlying problem; however, overuse in and of itself can cause dysphonia inthe singing and the speaking voice, odynophonia, loss of range, loss of clar-ity, and early vocal fatigue. This is seen frequently in performers who are onthe 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 openvenues with variable acoustics seem, anecdotally, to be at particular riskfor the effects of voice overuse. Many performers believe that they have in-finite use of their vocal folds and do not realize that they are athletes whoneed to rest and recover after an event. Frequent high-energy performancecan result in vocal fold edema that requires more ‘‘pushing’’ over time to getthe same results; this results in a vicsous cycle phonotrauma. Any number offindings may be present on laryngoscopy. Vocal fold edema, assumed to besubacute, overlying chronic fibrovascular changes, and sulcus deformitiesare 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 discussionwith the performer about short- and long-term goals and obligations is im-portant 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 dangerousfurther voice use is to the patient’s long-term vocal health. Doctor’s ordersfor voice rest can be a welcome relief to a performer. Conversely, the laryng-ologist may encounter significant resistance to this recommendation. If thisis the casedand especially if a performance is of paramount importanceda short course of high-dose oral steroids (burst and taper) can be prescribed.One practical approach is to prescribe methylprednisolone at a high firstdose 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


5; 8 mg, day 6; 4 mg, day 7). Patients are cautioned to mark during rehearsalsor not sing at all and to use the voice minimally otherwise. Sometimes per-formers 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 tearis higher when on steroid therapy. If any sudden decrement in voice occurs,they are instructed to observe immediate full voice rest and to seek laryngo-logic evaluation as soon as possible.

The patient is reevaluated once voice rest has been prescribed for overuseand the larynx has had time to recover. Symptoms and findings on VLS aretracked. Resumption of normal practice and performance schedules needsto be undertaken with serious caution and an appreciation for the fragilityof the larynx, and it can take place once the larynx has shown signs of im-provement (decreased edema, erythema, size of varices). Performers are en-couraged to improve vocal hygiene, maintain excellent hydration, andobserve regular periods of voice rest throughout the day. Most are able toaccomplish this while meeting their professional demands. The addition ofvoice therapy is an important vehicle for teaching and reinforcing thesestrategies 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 historyas well as understanding the professional voice user’s priorities to establishtrust and to facilitate comprehensive patient care. Similarly, it is importantto approach this care with a team model, including voice therapists (some-times singing and speech therapists), the singing teacher/voice coach, andother physicians who care for the patient. Many patients are otherwisehealthy and do not see other clinicians, in which case the laryngologist fre-quently plays a primary care role, tending to questions of health mainte-nance and serving as a referral base as necessary. This is particularly truefor young patients, many of whom live away from home as students or astraveling performers. Obtaining complete social histories and taking timeto educate patients about the importance of hydration, rest, and tobacco,marijuana, alcohol, and other drug avoidance are critical to comprehensivecare. Young patients also benefit from discussions regarding short- andlong-term professional goals so that they begin to develop a realistic per-spective on the impact that their voice use has on its integrity. Becausemany professional voice users have multiple physicians who care for themand several may be on multiple medications, communication with otherphysicians is critical to coordinated care.

Summary

Multiple diagnoses may be present simultaneously in the professionalvoice user. Each needs to be considered in the context of the other,


such that treatment of one problem does not ignore the influence ofothers on its resolution.

The presence of a benign vocal fold lesion in a professional voice userdoes not mandate treatment if it is not compromising function. Surgi-cal treatment of asymptomatic benign vocal fold lesions in professionalvoice users with the goal of preventing a problem must be approachedwith caution, because any trauma to the vocal fold cover by intubationor surgical instrumentation, including lasers, can change the voice.

Although incidence and prevalence of inflammatory processes in the lar-ynx are not well documented, they seem common in professional voiceusers; include laryngopharyngeal reflux (common), laryngitis fromvoice 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 forother processes that should be sought out if muscle tension dysphoniais identified.

Vocal fold paresis can cause glottal insufficiency and subsequent breath-iness. It is diagnosed best by LEMG and can be treated in a stepwisefashion with voice therapy and augmentation.

Vocal fold scar is associated with long-term voice use or frequent phono-trauma, resulting in stiff vocal folds, increase in fundamental fre-quency, and roughness. Treatment is controversial.

Vocal fold varices are seen more frequently in professional voice usersthan in nonprofessional voice users and are more frequent in womenthan in men. They generally do not require treatment unless recurrenthemorrhage occurs.

Voice changes as related to age, menopause, and voice overuse are of par-ticular relevance to professional voice users. Understanding these areasof laryngology is important to the continuity of care provided to thesepatients by the laryngologist.

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