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 in-
clude 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 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 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 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, and
a swarm of emotions commonly accompany professional voice users to
* Corresponding author.
E-mail address: ramon.franco@meei.harvard.edu (R.A. Franco).
0030-6665/07/$ - see front matter Ó 2007 Elsevier Inc. All rights reserved.
doi:10.1016/j.otc.2007.05.008 oto.theclinics.com
1026 FRANCO & ANDRUS
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 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 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 se-
verity 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 bev-
erage, 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 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 physical
examination, 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, multiple
entities 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 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 sub-
ject 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 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 number
of performance venues constantly subjects the larynx to insults, such as
phonotrauma, 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 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.
COMMON DIAGNOSES 1027
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 treat-
ment 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 ex-
aminations superior to fiberoptic laryngoscopy and approximating rigid lar-
yngoscopy, 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 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 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.
nonproductive chronic throat clearing [2]. In singers, voice changes, such as

loss of rangedespecially in the high frequencies, voice breaks, increased vo-
cal fatigue, anterior neck discomfort or tightness, or loss of vocal clarity
may be the primary complaint and may or may not present with the afore-
mentioned 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 persis-
tent 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 laryngo-
pharyngeal 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 gas-
troesophageal 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 sing-
ing, 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. There-
fore, 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 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]. 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 suffi-
cient 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 laryngophar-
yngeal reflux diagnosis [9]. The reflux finding score is an objective measure
of 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 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 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/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 lar-
yngopharyngeal 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 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 the
time [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 the
diagnosis of laryngopharyngeal reflux, especially when done in combination
with pH-metry. Most important in the interpretation of these tests is assess-
ing the patterns of pH and pressure changes, whether they correspond with
each other, and if they occur in the supine or upright positions. Finally, lar-
yngopharyngeal 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 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, as
their understanding of the problem likely will improve its treatment. Lar-
yngopharyngeal reflux is postulated to cause laryngeal symptoms in two
ways: 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 for
most 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 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 eleva-
tion, and the volume of stomach contents during exertion are important
in the creation of the refluxate bolus [6]. Considering all of the possible con-
tributors 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 ad-
dresses upper and lower esophageal sphincter tone, the presence of acid in
the 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 as
alcohol, 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 belching
and 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 citrus
and pineapple), tomatoes, jams and jellies, barbecue sauces, and most salad
dressings. Spicy foods (hot mustards, curry, hot peppers/hot sauce) are sim-
ilarly irritating. Behavior modifications play a large role in the management
of 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 the
likelihood of regurgitation of contents into the esophagus and above. Pa-
tients 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 box-
spring 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-abdom-
inal 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.
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 manage-
ment of laryngopharyngeal reflux requires more aggressive and more pro-
longed 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 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 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 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 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 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 reflux
finding score can be used to assess treatment efficacy, although patient his-
tory is adequate. Professional singers are especially sensitive to subtle
changes in voice and so recognize when small changes in diet, stress, or rou-
tine exacerbate their laryngopharyngeal reflux. Once laryngopharyngeal
reflux is controlled well, some patients slowly can reintroduce a few re-
flux-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 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 side
effect profile; however, some patients, despite all best efforts, remain symp-
tomatic. 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
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, se-
vere, or refractory laryngopharyngeal reflux or complicated gastroesopha-
geal reflux disease. This awake, nonsedated procedure can be performed
in 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-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 pulmo-
nary fungal disease, if not systemic fungal disease (Fig. 2). Isolated laryngeal
disease was believed to be exceedingly rare, and suspicion of laryngeal dis-
ease nearly always prompted investigation for systemic disease and possible
immunosuppression [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 (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 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]. 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, nutri-
tional deficits, on immunosuppressive therapy, or in an immune-suppressed
state 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 ask
about associated symptoms and whether the onset of the symptoms corre-
sponded 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 er-
ythema, 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 treat-
ment 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 sys-
temic antifungal treatment if they fail to respond appropriately. Because an-
tifungal 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 malig-
nancy 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 recom-
mended to examine the esophagus and to obtain biopsies as necessary. Pa-
tients who have severe dysphonia and pain also may present with significant
honey-colored crusts in the larynx in addition to multiple white plaques over
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 in-
haled steroids at any point. Considering the broad definition of ‘‘profes-
sional voice user,’’ however, it is not difficult to imagine that this number
could 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 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 prophy-
lactic 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 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-pitched

speaking 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 two
often are considered synonymous. Other synonyms include hyperfunctional
dysphonia, muscle misuse dysphonia, hyperkinetic dysphonia, musculoskel-
etal tension dysphonia, mechanical voice disorder, functional hypertensive
dysphonia, laryngeal tension-fatigue syndrome, and laryngeal isometric dys-
phonia [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
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 col-
leagues [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, in-
cluding 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) 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 and
foremost, 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 their
symptom 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 of
muscle tension dysphonia may begin. Voice therapy with appropriate laryn-
geal manipulation is the cornerstone. In professional voice users, especially
singers, 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 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 dyspho-
nia, injection vocal fold medialization or medialization laryngoplasty may
be 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 common

problem that causes dysphonia. Paralleling the paradigm shift in laryngolo-
gists’ 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 vo-
cal fatigue (76%), diplophonia (40%), and odynophonia (12%). Similar
symptoms were described by other investigators [40,41]. Decreased projec-
tion and decreased range also are symptoms of vocal fold paresis. Laryngeal
findings 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 can
be 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) is
indicated. 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 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 pa-
tients who have LEMG-diagnosed paresis are symptomatic enough to war-
rant surgical therapy, many, including professional voice users, are able to
function well without surgery. Conversely, even those able to function with-
out surgical intervention may benefit from voice therapy, which can be
guided by LEMG results. Before performing LEMG, it is important to eval-
uate 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 di-
agnostic procedure if it yields a choice between surgical or nonsurgical man-
agement when the patient is ‘‘not ready’’dmentally or functionallydto
consider a surgical procedure. This clinical situation is not unusual and em-
phasizes 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 sep-
arate 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.
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 voice
therapy. Koufman and colleagues [39] performed laryngoplasty or lipoinjec-
tion 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 indi-
cated 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 vo-
cal 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 fibrovas-
cular changes (subtle irregularities of the medial vocal fold edges in the mid-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, 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 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 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.
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 lig-
ament. 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 con-
genital. 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 clo-
sure and phase symmetry, which are not discernable in the absence of stro-
boscopic 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.
sessile to raised to discretely nodular lesions along the medial edge of the vo-
cal 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 situa-
tions, persistent anterior and posterior glottic gaps; the resultant ‘‘hour-
glass’’ 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 com-
mon) [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 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 cysts
tend to bulge on the superior and medial aspect of the midmusculomembra-
nous 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 achiev-
able during suspension microlaryngoscopy. Similarly, if therapeutic suspen-
sion 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 ther-
apy 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
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. Sec-
ond, 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 de-
scriptions in the literature [44]; however, laryngeal involvement in rheuma-
toid arthritis is well documented and may be present in most patients who
suffer from that disease [44–47]. The cricoarytenoid joint, which is diarthroi-
dal, like the interphalangeal joints in the distal extremities, is involved most
commonly. Laryngeal manifestations of rheumatoid arthritis in the cricoar-
ytenoid 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 sur-
rounding erythema are seen.
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 appear-
ance and universally cause stiffness in vocal fold vibration with reduction in
the magnitude of mucosal wave [44,45,48]. Rheumatoid nodules and bam-
boo nodes (similar lesions seen in autoimmune diseases, such as Sjögren’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 rheu-
matologist is necessary to optimize medical therapy when conservative
measures 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 face
of chronic disease. Perioperative reflux treatment is imperative, and an
oral steroid burst is recommended preoperatively to help abate inflamma-
tion. It is not uncommon to encounter dense fibrosis around the nodules
once 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 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 discus-
sion 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 profes-
sional 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, trau-
matic, and iatrogenic entities [49]. Although the incidence and epidemiology
of vocal fold scar are not well documented in the general population or pro-
fessional 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
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 prop-
ria, 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 de-
velop 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 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 (from
vocal process to anterior commissure), and they differ only in depth of pen-
etration. 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, 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 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
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 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 hav-
ing 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 nonvi-
brating 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 aero-
dynamic and acoustic batteries is imperative once vocal fold sulcus/sulcus
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 prevent-
ing it. Encouraging good vocal hygiene and technique in professional voice
users of all ages is important to accomplish this goal. Nonetheless, with con-
tinued 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 treat-
ment 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 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] 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 proce-
dures include injection of alloplastic substances into vocal folds or paraglot-
tic space (collagen, micronized dermis, hyaluronic acid, hydroxyl apatite);
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 endo-
scopic 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 at-
tempt to address lack of pliability and glottal insufficiency include those that
add 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 has
been performed by large numbers of surgeons or on large numbers of pa-
tients. 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, 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 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 de-
rived 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,
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, how-
ever, 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 col-
leagues’ [66] first systematic evaluation of the treatment of vocal fold varices
in 1998. In this retrospective review of all patients with benign laryngeal dis-
orders 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 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 of
patients who presented with vocal fold varices in conjunction with another
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 asso-
ciated 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, possi-
bly 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 inter-
mittent, 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 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 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 individ-
ualized 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 identifi-
able 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 enlarge-
ment 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 func-
tion 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 mid-
musculomembranous region. A two-stage approach is selected if there is
considerable risk for postoperative apposition of the operative sites and,
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 low-
power 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, meticu-
lously 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 pri-
marily [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 (Pho-
togenica 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 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 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 imme-
diate 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 signifi-
cant change in the voice with increased voice use or vocal abuse (singing
or 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 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 corre-
lation between hormonal imbalance and vocal fold hemorrhage, especially
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 investiga-
tors [63,67–69]. In addition to vocal fold hemorrhage occurring in peri-
menstrual women (just before or during menstruation), women in
hormone 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, including
consumption 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 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 hem-
orrhage in professional voice users compared with the general population is
simply 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, 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 flat-
tens, 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
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 recommen-
ded in conjunction with an endocrinologist or gynecologist. Close follow-
up 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 sig-
nificant hematoma persists. In this instance, it is necessary to evacuate the he-
matoma 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 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 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 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 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 edema-
tous. 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), associ-
ated fatty infiltration, and fragmentation of false vocal fold connective
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 lar-
yngoscopy, the hallmark of presbylarynges. Lateral cricoarytenoid hyper-
function 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 sta-
mina), 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 in-
clude the abdominal muscles and diaphragm with decreased tone and
strength; the lungs and thorax with decreased elasticity and distensibility, re-
spectively; 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 lan-
guage 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, meno-
pause, 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 reproduc-
ible 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, 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 increase
in ovarian androgen found during menopause. Given its close relationship
to 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 larynx
is 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 various
times 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, 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 with-
out estrogen therapy in whom both smears showed aspects of atrophy-
dystrophy. This work supports the idea that hormone replacement therapy
may improve voice in postmenopausal women. Laryngologists should con-
sider 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 investi-
gated thoroughly. A diagnosis of presbylarynges cannot be made without
a 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 them
related to age, but nonetheless pathologic. These included central neurologic
disorders affecting laryngeal function (eg, stroke, Parkinson’s disease, essen-
tial tremor, Alzheimer’s disease), benign vocal fold lesions (eg, Reinke’s
edema, benign and dysplastic epithelial lesions), inflammatory disorders
(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 lar-
yngologist 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 un-
derlying problem; however, overuse in and of itself can cause dysphonia in
the 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 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 in-
finite 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 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 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 laryng-
ologist 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
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 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 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 laryngo-
logic 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 im-
provement (decreased edema, erythema, size of varices). Performers are en-
couraged 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 (some-
times 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 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 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 per-
spective 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,
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. Surgi-
cal 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 lar-
ynx 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 breath-
iness. 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 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 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 par-
ticular relevance to professional voice users. Understanding these areas
of laryngology is important to the continuity of care provided to these
patients by the laryngologist.
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Common Diagnoses and Treatments

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Common Diagnoses and Treatments

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Otolaryngol Clin N Am

Common Diagnoses and Treatments

History and physical examination

the laryngologist’s oﬃce and may be barriers to the patient’s ability to

Voice problems in professional voices users: diagnoses and treatment

nonproductive chronic throat clearing [2]. In singers, voice changes, such as

excellent inter- and intraobserver reproducibility. When coupled with the

Although some patients’ laryngopharyngeal reﬂux is responsive to diet

approach, laparoscopic fundoplication frequently is successful [19,20].

erythematous bases and edema. In these patients, a bacterial superinfection

Muscle tension dysphonia

Other common clinical features include an abnormally low-pitched

evaluation with other disorders, such as presbylarynges (bilateral vocal fold

Vocal fold paresis

fold disorders, vocal fold paresis is receiving more attention as a common

Benign vocal fold masses: nodules, polyps, and cysts

Vocal fold cysts present primarily with hoarseness, although diplophonia

Clearly, vocal fold nodules, polyps, and cysts cannot be distinguished by

Clinical manifestations include hoarseness and instability in connected

Vocal fold scarring

mass lesions, themselves associated with scar), laryngopharyngeal reﬂux,

vocalis has been identiﬁed so that eﬀects of therapy, whether medical or

autologous fat or fascia also can be used. Medialization thyroplasty with

or dilations within them, may occur at oblique angles or even perpendicular

benign lesion, this clinical ﬁnding is frequent among professional voice

Vocal fold hemorrhage

magnitude of the mucosal wave [65,68,69]. Most investigators recommend 7

tissue. The most prominent clinical correlate to these changes is scalloping

and menopause, as well as menstruation, pregnancy, gynecologic surgery,

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

Special considerations in caring for the professional voice user

[6] Franco RA Jr. Laryngopharyngeal reﬂux. Allergy Asthma Proc 2006;27:21–5.

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