2007, vol.40, issues 5, the professional voice

Otolaryngol Clin N Am

40 (2007) xi–xii

Preface

Guest Editors

Care of the professional voice is an art form that requires a thorough un-derstanding of the anatomy and physiology of normal voice production, thepathophysiology of abnormal voice production, and the vocal disability ofwhich the patient complains. The ability to assimilate each of these factorsinto a treatment plan that will improve vocal function and allow the voiceprofessional to resume vocal performance while preserving longevity ofthe voice is also important. In this issue of the Otolaryngologic Clinicsof North America, we attempt to give the practicing otolaryngologista framework for evaluating the vocal performer and interpreting findingson physical examination. The importance of obtaining a thorough under-standing of the patient’s complaints and their goals for recovery cannotbe emphasized enough. Similarly, it is extremely important to realize thatnot all ‘‘pathologic’’ findings on physical examination are necessarily path-ologic from a functional perspective for the patient. Knowing which findingsare contributing to the vocal complaint is the most essential element of pro-fessional voice care.

Voice therapy should always be an integral component of the evaluationand treatment of voice disorders, and an adequate course of voice therapyshould always be instituted before recommending surgery in all cases. Manytimes, voice therapy can limit the functional disability associated with manyvocal fold lesions, paresis, and compensatory hyperfunctional behavior,thus obviating the need for surgery. Additionally, attention should befocused on systemic medical problems, prescription medications, over-the-counter medications, and self-prescribed herbal remedies that may con-tribute to vocal difficulties.

Yolanda D. Heman-Ackah, MD Robert T. Sataloff, MD, DMA

0030-6665/07/$ - see front matter � 2007 Elsevier Inc. All rights reserved.

doi:10.1016/j.otc.2007.05.014 oto.theclinics.com

xii PREFACE

The days of ‘‘stripping’’ the vocal folds of masses for treatment or biopsyare over. This procedure will often lead to scar formation and a hoarse orunacceptable voice, especially in voice professionals who are acutely awareof subtle changes in vocal fold function. Only experienced laryngologistsshould attempt surgical procedures on vocal professionals. Even a smallamount of vocal fold scarring or stiffness can be career-ending and is an un-desirable and unacceptable outcome. Because many voice professionals donot require surgical treatment, there are several nonsurgical therapeutic op-tions that can and should be instituted prior to referring a voice professionalto a laryngologist for surgical rehabilitation.

A diagnostic paradigm is presented in this issue to serve as a frameworkfor the evaluation and treatment of this very complex group of patients.However, one must also remember that although these patients are perform-ing artists, they are patients first and are subject to the same consortium ofillnesses as others in their demographic profile. There are many systemic dis-eases that will present initially with a change in the voice that can be subtle.The voice professional is more likely to be bothered by these subtle changesthan is a nonprofessional, and will likely seek attention before the diseaseprocess begins to manifest in other bodily systems. Thus, a high index ofsuspicion and a broad knowledge base of systemic diseases that can presentas dysphonia is essential.

A comprehensive approach to voice problems is necessary in all individ-uals presenting with vocal complaints. This issue outlines the basics of anat-omy, physiology, examination, diagnostic tools, voice therapy, medicaltherapy, and surgical therapy as they pertain to the voice professional.The same principles apply in the evaluation and treatment of the nonprofes-sional voice user who is having difficulties with the voice. In the onlineversion of this issue, we present video clips of normal and abnormal strobo-scopic examinations, neurolaryngologic examinations, and laryngeal surger-ies with pre- and postoperative results.

Yolanda D. Heman-Ackah, MDRobert T. Sataloff, MD, DMA

Department of Otolaryngology–Head and Neck SurgeryDrexel University College of Medicine

1721 Pine StreetPhiladelphia, PA 19103, USA

E-mail addresses: [email protected] (Y.D. Heman-Ackah)[email protected] (R.T. Sataloff)

mailto:[email protected]



40 (2007) 909–929

Clinical Anatomy and Physiologyof the Voice

Robert T. Sataloff, MD, DMA*,Yolanda D. Heman-Ackah, MD,

Mary J. Hawkshaw, BSN, RN, CORLNDepartment of Otolaryngology–Head and Neck Surgery, Drexel University

College of Medicine, 1721 Pine Street, Philadelphia, PA 19103, USA

Anatomy

The anatomy of the voice is not limited to the region between the supra-sternal notch (top of the breast bone) and the hyoid bone. Practically allbody systems affect the voice. The larynx receives the greatest attention be-cause it is the most sensitive and expressive component of the vocal mech-anism, but anatomic interactions throughout the patient’s body must beconsidered in treating the professional voice user. It is helpful to think ofthe larynx as composed of four anatomic units: skeleton, mucosa, intrinsicmuscles, and extrinsic muscles. The glottis is the space between the vocalfolds [1]. The portions of the larynx above the vocal folds are referred toas the supraglottis. The area below the vocal folds is referred to as the sub-glottis. The vocal tract includes those portions of the aerodigestive tract in-volved in vocal production.

Larynx: skeleton

The most important parts of the laryngeal skeleton are the thyroid carti-lage, cricoid cartilage, and the two arytenoid cartilages (Fig. 1). Intrinsicmuscles of the larynx are connected to these cartilages. One of the intrinsicmuscles, the thyroarytenoid, extends on each side from the arytenoid carti-lage to the inside of the thyroid cartilage just below and behind the thyroidprominence. The medial belly of the thyroarytenoid is also known as the

This article is modified from: Sataloff RT. Professional voice: the science and art of clinical

care. 3rd edition. San Diego (CA): Plural Publishing, Inc.; 2006. p. 143–77; with permission.

* Corresponding author.

E-mail address: [email protected] (R.T. Sataloff).




910 SATALOFF et al

vocalis muscle, and it forms the body of the vocal fold. The laryngeal carti-lages are connected by soft attachments that allow changes in their relativeangles and distances, thereby permitting alterations in the shape and tensionof the tissues extended between them. The arytenoids are capable of com-plex motion. It used to be said that the arytenoids rock, glide, and rotate.More accurately, with adduction of the vocal folds the cartilages arebrought together in the midline and revolve over the cricoid, moving inferi-orly and anteriorly. It seems that people use different strategies for

Fig. 1. Cartilages of the larynx. (From SataloffRT. Professional voice: the science and art of clin-

ical care. 3rd edition. San Diego (CA): Plural Publishing, Inc.; 2006. p. 143–77; with permission.)

911CLINICAL ANATOMY AND PHYSIOLOGY OF THE VOICE

approximating the arytenoids and that such strategies may influence a per-son’s susceptibility to laryngeal trauma that can cause vocal process ulcersand laryngeal granulomas.

Larynx: mucosa

The vibratorymargin of the vocal fold is muchmore complicated than sim-ply mucosa applied to muscle or ligament. It consists of five layers (Fig. 2) [2].The thin, lubricated epithelium covering the vocal folds forms the area of con-tact between the vibrating vocal folds and acts somewhat like a capsule, help-ing to maintain vocal fold shape. The epithelium lining most of the vocal tractis pseudo-stratified, ciliated, columnar epithelium, typical respiratory epithe-lium involved in handling mucous secretions. The vibratory margin of the vo-cal fold is covered with stratified squamous epithelium, better suited towithstand the trauma of vocal fold contact. The superficial layer of the laminapropria, also known as Reinke’s space, is composed of loose fibrous compo-nents and matrix. It contains few fibroblasts. The intermediate layer of lam-ina propria consists primarily of elastic fibers and does contain fibroblasts.The deep layer of the lamina propria is composed primarily of collagenousfibers and is rich in fibroblasts. The thyroarytenoid or vocalis muscle makesup the body of the vocal fold and is one of the intrinsic laryngeal muscles. Theintermediate and deep layers of the lamina propria constitute the vocal liga-ment and lie immediately below the Reinke’s space.

Although variations along the length of the membranous vocal fold areimportant in only a few situations, the surgeon, in particular, should beaware that they exist. Particularly striking variations occur at the anteriorand posterior portion of the membranous vocal fold. Anteriorly, the inter-mediate layer of the lamina propria becomes thick, forming an oval masscalled the anterior macula flava. This structure is composed of stroma, fibro-blasts, and elastic fibers. Anteriorly, it inserts into the anterior commissuretendon, a mass of collagenous fibers that is connected to the thyroid carti-lage anteriorly, the anterior macula flava posteriorly, and the deep layerof the lamina propria laterally. As Hirano has pointed out, this arrangementallows the stiffness to change gradually from the pliable membranous vocalfold to the stiffness of the thyroid cartilage [3].

A similar gradual change in stiffness occurs posteriorly where the inter-mediate layer of the lamina propria also thickens to form the posterior mac-ula flava, another oval mass. It is structurally similar to the anterior maculaflava. The posterior macula flava attaches to the vocal process of the aryte-noid cartilage through a transitional structure that consists of chondrocytes,fibroblasts, and intermediate cells [4]. The stiffness thus progresses from themembranous vocal fold to the slightly stiffer macula flava, to the stiffer tran-sitional structure, to the elastic cartilage of the vocal process, to the hyalinecartilage of the arytenoid body. It is believed that this gradual change instiffness serves as a cushion that may protect the ends of the vocal folds

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Fig. 2. An overview of the larynx and vocal tract showing the vocal folds and the region from

which the vocal fold was sampled to obtain the cross section showing the layered structure. (Re-

printed from: Sataloff RT. The human voice. Sci Am 1992;267:108–15; with permission.)


from mechanical damage caused by contact or vibrations [4]. It may also actas a controlled damper that smoothes mechanical changes in vocal fold ad-justment. This arrangement seems particularly well suited to vibration, asare other aspects of the vocal fold architecture. For example, blood vesselsin the vibratory margin come from posterior and anterior origins and runparallel to the vibratory margin, with few vessels entering the mucosa per-pendicularly or from underlying muscle. The vibratory margin containsno glands, whose presence would likely interfere with the smoothness of vi-bratory waves. Even the elastic and collagenous fibers of the lamina propriarun approximately parallel to the vibratory margin. The more one studiesthe vocal fold, the more one appreciates the beauty of its engineering.

Functionally, the five layers have different mechanical properties andmay be thought of as somewhat like ball bearings of different sizes that al-low the smooth shearing action necessary for proper vocal fold vibration.The posterior two fifths (approximately) of the vocal folds are cartilaginous,and the anterior three fifths are membranous (from the vocal process for-ward) in adults. Under normal circumstances, most of the vibratory func-tion critical to sound quality occurs in the membranous portion.

Mechanically, the vocal fold structures act more like three layers consist-ing of the cover (epithelium and Reinke’s space), transition (intermediateand deep layers of the lamina propria), and the body (the vocalis muscles).Understanding this anatomy is important because different pathologic enti-ties occur in different layers and require different approaches to treatment.For example, fibroblasts are responsible for scar formation. Lesions that oc-cur superficially in the vocal folds (such as nodules, cysts, and most polyps)should therefore permit treatment without disturbance of the intermediateand deep layers, fibroblast proliferation, or scar formation.

In addition to the five layers discussed above, recent research has shownthat there is a complex basement membrane connecting the epithelium tothe superficial layer of the lamina propria [5]. The basement membrane isa multilayered, chemically complex structure. It gives rise to Type VII col-lagen loops that surround Type III collagen fibers in the superficial layerof the lamina propria. Knowledge of the basement membrane has alreadybeen important in changing surgical technique. Additional research is likelyto show its great importance in other matters, such as the ability to heal fol-lowing trauma, possibly the development of certain kinds of vocal fold pa-thology, and probably in histopathologic differential diagnosis.

The vocal foldsmay be thought of as the oscillators of the vocalmechanism[6]. Above the true vocal folds are tissues known as false vocal folds. Unlikethe true vocal folds, they do notmake contact during normal speaking or sing-ing. They may produce voice during certain abnormal circumstances, how-ever. This phenomenon is called ‘‘dysphonia plica ventricularis.’’ Untilrecently, the importance of the false vocal folds during normal phonationwas not appreciated. In general, they are considered to be used primarilyfor forceful laryngeal closure and they may be used excessively during

914 SATALOFF et al

pathologic conditions. Contrary to popular practice, however, surgeonsshould recognize that they cannot simply be removed without phonatory ef-fects. The physics of airflow through the larynx are complex, involving vortexshedding and sophisticated turbulence patterns that are essential to phona-tion. The false vocal folds provide a downstream resistance that is importantin this process, and they probably play a role in vocal tract resonance also.

Larynx: the intrinsic muscles

Intrinsic muscles are responsible for abduction, adduction, and tension ofthe vocal folds (Figs. 3 and 4). All but one of the muscles on each side of thelarynx are innervated by one of the two recurrent laryngeal nerves. Becausethis nerve runs a long course from the neck down into the chest and back upto the larynx (hence the name ‘‘recurrent’’), it is easily injured by trauma,neck surgery, and chest surgery. Such injuries may result in abductor andadductor paralysis of the vocal fold. The remaining muscle, the cricothyroidmuscle, is innervated by the superior laryngeal nerve on each side, which isespecially susceptible to viral and traumatic injury. The recurrent and supe-rior laryngeal nerves are branches of the 10th cranial nerve, or vagus nerve.The superior laryngeal nerve branches off the vagus high in the neck at theinferior end of the nodose ganglion. It divides into an internal and external

Fig. 3. The intrinsic muscles of the larynx. (From Sataloff RT. Professional voice: the science

and art of clinical care. 3rd edition. San Diego (CA): Plural Publishing, Inc.; 2006. p. 143–77;

with permission.)

Fig. 4. Action of the intrinsic muscles. In the bottom four figures the directional arrows suggest

muscle actions but may give a misleading impression of arytenoid motion. These drawings

should not be misinterpreted as indicating that the arytenoid cartilage rotates around a vertical

axis. The angle of the long axis of the cricoid facets does not permit some of the motion implied

in this figure. The drawing still provides a useful conceptualization of the effect of individual

intrinsic muscles, however, so long as the limitations are recognized. (From Sataloff RT. Profes-

sional voice: the science and art of clinical care. 3rd edition. San Diego (CA): Plural Publishing,

Inc.; 2006. p. 143–77; with permission.)

916 SATALOFF et al

branch. The external branch supplies the cricothyroid muscle. An extensionof this nerve may also supply motor and sensory innervation to the vocalfold. The internal branch is primarily responsible for sensation in the mu-cosa above the level of the vocal fold, but it may also be responsible forsome motor innervations of laryngeal muscles. The recurrent laryngealnerves branch off the vagus in the chest. On the left, the nerve usually loopsaround the aortic arch. On the right, it usually loops around the brachioce-phalic artery. This anatomic relationship is usually, but not always, present,and nonrecurrent recurrent nerves have been reported particularly on theright side, where they are more likely to be injured during neck surgery.There are interconnections between the superior and recurrent laryngealnerves, particularly in the region of the interarytenoid muscle.

For some purposes, including electromyography, voice therapy, and sur-gery, it is important to understand the function of individual laryngeal mus-cles in greater detail. The muscles of primary functional importance arethose innervated by the recurrent laryngeal nerve (thyroarytenoid, posteriorcricoarytenoid, lateral cricoarytenoid, and interarytenoid or arytenoideus)and the superior laryngeal nerve (cricothyroid) (see Figs. 3 and 4; Fig. 5).

The thyroarytenoid muscle adducts, lowers, shortens, and thickens thevocal fold, rounding the vocal fold edge. The cover and transition are effec-tively made more slack, whereas the body is stiffened. Adduction from

Fig. 5. The superior and recurrent laryngeal nerves branch from the vagus nerve and enter the

larynx.


vocalis contraction is active, particularly in the membranous segment of thevocal folds. It tends to lower vocal pitch. The thyroarytenoid originates an-teriorly from the posterior (interior) surface of the thyroid cartilage and in-serts into the lateral base of the arytenoid cartilage from the vocal process tothe muscular process. More specifically, the superior bundles of the muscleinsert into the lateral and inferior aspects of the vocal process and run pri-marily in a horizontal direction. The anteroinferior bundles insert into theanterolateral aspect of the arytenoid cartilage from its tip to an area lateralto the vocal process. The most medial fibers run parallel to the vocal liga-ment. There are also cranial fibers that extend into the aryepiglottic fold.Anteriorly, the vertical organization of the muscle results in a twisted con-figuration of muscle fibers when the vocal fold is adducted. The thyroaryte-noid muscle is divided into two compartments. The medial compartment isalso known as the vocalis muscle. It contains a high percentage of slowtwitch muscle fibers. The lateral compartment has predominantly fast twitchmuscle fibers. One may infer that the medial compartment (vocalis) is spe-cialized for phonation, whereas the lateral compartment (muscularis) is spe-cialized for vocal fold adduction, but these suppositions are unproven.

The lateral cricoarytenoid muscle is a small muscle that adducts, lowers,elongates, and thins the vocal fold. All layers are stiffened and the vocal foldedge takes on a more angular or sharp contour. It originates on the upperlateral border of the cricoid cartilage and inserts into the anterior lateralsurface of the muscular process of the arytenoid. The interarytenoid muscle(arytenoideus, a medium-sized intrinsic muscle) primarily adducts the carti-laginous portion of the vocal folds. It is particularly important in providingmedial compression to close the posterior glottis. It has little effect on thestiffness of the membranous portion. The interarytenoid muscle consistsof transverse and oblique fibers. The transverse fibers originate from the lat-eral margin of one arytenoid and insert into the lateral margin of the oppo-site arytenoid. The oblique fibers originate from the base of one arytenoidinto the apex of the contralateral arytenoid.

The posterior cricoarytenoid muscle abducts, elevates, elongates, andthins the vocal fold by rocking the arytenoid cartilage posterolaterally. Alllayers are stiffened, and the edge of the vocal fold is rounded. It is the secondlargest intrinsic muscle. It originates over a broad area of the posterolateralportion of the cricoid lamina and inserts on the posterior surface of the mus-cular process of the arytenoid cartilage, forming a short tendon that coversthe cranial aspect of the muscular process.

When the superior laryngeal nerves are stimulated, the cricothyroid mus-cle moves the vocal folds into the paramedian position. It also lowers,stretches, elongates, and thins the vocal fold, stiffening all layers and sharp-ening the vocal fold’s contour. It is the largest intrinsic laryngeal muscle.The cricothyroid muscle is largely responsible for longitudinal tension, animportant factor in control of pitch. Contraction tends to increase vocalpitch. The cricothyroid muscle originates from the anterior and lateral

918 SATALOFF et al

portions of the arch of the cricoid cartilage. It has two bellies. The obliquebelly inserts into the posterior half of the thyroid lamina and the anteriorportion of the inferior cornu of the thyroid cartilage. The vertical (erect)belly inserts into the inferior border of the anterior aspect of the thyroidcartilage.

Intrinsic laryngeal muscles are skeletal muscles. All skeletal muscles arecomposed primarily of three types of fibers. Type I fibers are highly resistantto fatigue, contract slowly, and use aerobic (oxidative)metabolism. They havelow glycogen levels, high levels of oxidative enzymes, and they are relativelysmaller in diameter. Type IIA fibers use principally oxidative metabolismbut contain high levels of oxidative enzymes and glycogen. They contract rap-idly but are also fatigue resistant. Type IIB fibers are the largest in diameter.They use aerobic glycolysis primarily, containing much glycogen but rela-tively few oxidative enzymes. They contract quickly, but fatigue easily.

The fiber composition of laryngeal muscles differs from that of mostlarger skeletal muscles. Elsewhere, muscle fiber diameters are fairly con-stant, ranging between 60 to 80 mm. In laryngeal muscles there is consider-ably more variability [7,8], and fiber diameters vary between 10 and 100 mm,with an average of 40 to 50 mm. Laryngeal muscles have a higher proportionof Type IIA fibers than most other muscles. The thyroarytenoid and lateralcricothyroid muscles are particularly specialized for rapid contraction. Thelaryngeal muscles in general seem to have fiber distributions and variationsthat make them particularly well suited to rapid contraction with fatigue re-sistance [9]. In addition, many laryngeal motor units have multiple neuralinnervation. There seem to be approximately 20 to 30 muscle fibers per mo-tor unit in a human cricothyroid muscle [10], suggesting that the motor unitsize of this laryngeal muscle is similar to that of extraocular and facial mus-cles [11]. In the human thyroarytenoid muscle, 70% to 80% of muscle fibershave two or more nerve endplates [12]. Some fibers have as many as fivenerve endplates. Only 50% of cricothyroid and lateral cricoarytenoid musclefibers have multiple endplates, and multiple innervation is even less commonin the posterior cricoarytenoid (5%). It is still not known whether one mus-cle fiber can be part of more than one motor unit (receive endplates fromdifferent motor neurons) [9].

Larynx: extrinsic muscles

Extrinsic laryngeal musculature maintains the position of the larynx inthe neck. This group of muscles includes primarily the strap muscles. Be-cause raising or lowering the larynx may alter the tension or angle betweenlaryngeal cartilages, thereby changing the resting lengths of the intrinsicmuscles, the extrinsic muscles are critical in maintaining a stable laryngealskeleton so that the delicate intrinsic musculature can work effectively. Inthe Western classically trained singer, the extrinsic muscles maintain the lar-ynx in a relatively constant vertical position throughout the pitch range.


Training of the intrinsic musculature results in vibratory symmetry of thevocal folds, producing regular periodicity. This phenomenon contributesto what the listener perceives as a ‘‘trained’’ sound.

The extrinsic muscles may be divided into those below the hyoid bone (in-frahyoid muscles) and those above the hyoid bone (suprahyoid muscles).

The infrahyoid muscles include the thyrohyoid, sternothyroid, sterno-hyoid, and omohyoid. The thyrohyoid originates obliquely on the thyroidlamina of the hyoid bone. Contraction brings the thyroid and hyoid bonecloser together, especially anteriorly. The sternothyroid muscle originatesfrom the first costal cartilage and posterior aspect of the manubrium ofthe sternum, and it inserts obliquely on the thyroid cartilage. Contractionof the sternothyroid muscle lowers the larynx. The sternohyoid muscle orig-inates from the clavicle and posterior surface of the manubrium of the ster-num, inserting into the lower edge of the body of the hyoid bone.Contraction of the sternohyoid muscle lowers the hyoid bone. The inferiorbelly of the omohyoid originates from the upper surface of the scapula andinserts into the intermediate tendon of the omohyoid muscle. The superiorbelly originates from the intermediate tendon and inserts into the greatercornu of the hyoid bone. The omohyoid muscle pulls down on the hyoidbone, lowering it.

The suprahyoid muscles include the digastric, mylohyoid, geniohyoid,and stylohyoid muscles. The posterior belly of the digastric muscle origi-nates from the mastoid process of the temporal bone and inserts into the in-termediate tendon, which connects to the hyoid bone. The anterior bellyoriginates from the inferior aspect of the mandible near the symphysisand inserts into the intermediate tendon. The anterior belly pulls the hyoidbone anteriorly and raises it. The mylohyoid muscle originates from the in-ner aspect of the body of the mandible (mylohyoid line) and inserts intoa midline raphe with fibers from the opposite side. It raises the hyoidbone and pulls it anteriorly. The geniohyoid muscle originates from themental spine at the mental symphysis of the mandible and inserts on the an-terior surface of the body of the hyoid bone. It raises the hyoid bone andpulls it anteriorly. The stylohyoid muscle originates from the styloid processand inserts into the body of the hyoid bone. It raises the hyoid bone andpulls it posteriorly. Coordinated interaction among the extrinsic laryngealmuscles is needed to control the vertical position of the larynx and other po-sitions, such as laryngeal tilt.

The supraglottic vocal tract

The supraglottic larynx, tongue, lips, palate, pharynx, nasal cavity (seeFig. 2), and possibly the sinuses shape the sound quality produced at thelevel of the vocal folds by acting as resonators. Minor alterations in the con-figuration of these structures may produce substantial changes in voice qual-ity. The hypernasal speech typically associated with a cleft palate or the

920 SATALOFF et al

hyponasal speech characteristic of severe adenoid hypertrophy is obvious.Mild edema from an upper respiratory tract infection, pharyngeal scarring,or muscle tension changes produce less obvious sound alterations. These areimmediately recognizable to a trained vocalist or astute critic, but they oftenelude the common listener.

The tracheobronchial tree, lungs, and thorax

The lungs supply a constant stream of air that passes between the vocalfolds and provides power for voice production. Singers often are thought ofas having ‘‘big chests.’’ Actually, the primary respiratory difference betweentrained and untrained singers is not increased total lung capacity, as is pop-ularly assumed. Rather, the trained singer learns to use a higher proportionof the air in his or her lungs, thereby decreasing his or her residual volumeand increasing respiratory efficiency [13].

The abdomen

The abdominal musculature is the so-called ‘‘support’’ of the singingvoice, although singers generally refer to their support mechanism as theirdiaphragm. The function of the diaphragm muscle in singing is complexand somewhat variable from singer to singer (or actor to actor). The dia-phragm primarily generates inspiratory force. Although the abdomen canalso perform this function in some situations [14], it is primarily an expira-tory-force generator. The diaphragm is co-activated by some performersduring singing and seems to play an important part in the fine regulationof singing [15]. Actually, the anatomy of support for phonation is compli-cated and not completely understood. The lungs and rib cage generatepassive expiratory forces under many common circumstances. Passive inspi-ratory forces also occur. Active respiratory muscles working in consort withpassive forces include the intercostal, abdominal wall, back, and diaphragmmuscles. The principle muscles of inspiration are the diaphragm, the exter-nal intercostal muscles that connect the bony ribs, and the interchondralportions of the internal intercostal muscles that connect the cartilaginousribs. Accessory muscles of inspiration include the pectoralis major; pector-alis minor; serratus anterior; subclavius; sternocleidomastoid; anterior, me-dial, and posterior scalenus; serratus posterior and superior; latissimusdorsi; and levatores costarum. During quiet respiration, expiration is largelypassive. Many of the muscles used for active expiration (forcing air out ofthe lungs) are also used in support for singing and acting. Muscles of activeexpiration either raise the intra-abdominal pressure, forcing the diaphragmupward, or lower the ribs or sternum to decrease the dimension of the tho-rax, or both. They include the internal intercostals that connect the bonyribs, stiffen the rib interspaces, and pull the ribs down; transversus thoracis,subcostal muscles, and serratus posterior inferior, all of which pull the ribsdown; and the quadratus lumborum, which depresses the lowest rib. In


addition, the latissimus dorsi, which may also act as a muscle of inspiration,is capable of compressing the lower portion of the rib cage and can act asa muscle of expiration and a muscle of inspiration. The above muscles allparticipate in active expiration (and support). The primary muscles of activeexpiration are the abdominal muscles, however. They include the externaloblique abdominus, internal oblique abdominus, rectus abdominus, andtransversus abdominus. The external oblique is a flat broad muscle locatedon the side and front of the lower chest and abdomen. On contraction, it pullsthe lower ribs down and raises the abdominal pressure by displacing abdom-inal contents inward. It is an important muscle for support of singing andacting voice tasks. It should be noted that this muscle is strengthened by ab-dominal exercises that involve the combination of rotation and contraction,and other exercises, but is not developed effectively by traditional trunk curlsit-ups. Appropriate strengthening exercises of the external oblique musclesare often inappropriately neglected in voice training. The internal oblique isa flat muscle in the side and front wall of the abdomen. It lies deep to the ex-ternal oblique. When contracted, the internal oblique drives the abdominalwall inward and lowers the lower ribs. The rectus abdominus runs parallelto the midline of the abdomen originating from the xiphoid process of thesternum and the fifth, sixth, and seventh costal cartilages. It inserts intothe pubic bone. It is encased in the fibrous abdominal aponeurosis. Contrac-tion of the rectus abdominus lowers the sternum and ribs and stabilizes theabdominal wall. The transversus abdominus is a broad muscle located underthe internal oblique on the side and front of the abdomen. Its fibers run hor-izontally around the abdomen. Contraction of the transverse abdominuscompresses the abdominal contents, elevating abdominal pressure.

The abdominal musculature receives considerable attention in vocaltraining. The purpose of abdominal support is to maintain an efficient, con-stant power source and inspiratory–expiratory mechanism. There is dis-agreement among voice teachers as to the best model for teaching supporttechnique. Some experts describe positioning the abdominal musculatureunder the rib cage; others advocate distension of the abdomen. Eithermethod may result in vocal problems if used incorrectly, but distendingthe abdomen (the inverse pressure approach) is especially dangerous, be-cause it tends to focus the singer’s muscular effort in a downward and out-ward direction, which is ineffective. The singer thus may exert considerableeffort, believing he or she is practicing good support technique, without ob-taining the desired effect. Proper abdominal muscle training is essential togood singing and speaking, and the physician must consider abdominalfunction when evaluating vocal disabilities.

The musculoskeletal system

Musculoskeletal condition and position affect the vocal mechanism andmay produce tension or impair abdominal muscle function, resulting in

922 SATALOFF et al

voice dysfunction. Stance deviation, such as from standing to supine, pro-duces obvious changes in respiratory function. Lesser changes, such as dis-tributing one’s weight over the calcaneus rather than forward over themetatarsal heads (a more athletic position), alter the configuration of theabdominal and back musculature enough to adversely influence the voice.Tensing arm and shoulder muscles promotes cervical muscle strain, whichcan adversely affect laryngeal function. Careful control of muscle tensionis fundamental to good vocal technique. In fact, some teaching methodsuse musculoskeletal conditioning as the primary focus of voice training.

The psychoneurologic system

The psychologic constitution of the singer impacts directly on the vocalmechanism. Psychologic phenomena are reflected through the autonomicnervous system, which controls mucosal secretions and other functions crit-ical to voice production. The nervous system is also important for its medi-ation of fine muscle control. This fact is worthy of emphasis, becauseminimal voice disturbances may occasionally be the first sign of serious neu-rologic disease.

Physiology

The physiology of voice production is exceedingly complex and is sum-marized only briefly in this article. Greater detail may be found elsewhere[1,16–21].

Overview of phonatory physiology

Volitional voice production begins in the cerebral cortex. Complex inter-actions among centers for speech, musical expression, and artistic expressionestablish the commands for vocalization. The idea of the planned vocaliza-tion is conveyed to the precentral gyrus in the motor cortex, which transmitsanother set of instructions to motor nuclei in the brainstem and spinal cord.These areas transmit the complicated messages necessary for coordinatedactivity of the larynx, thoracic, and abdominal musculature and of the vocaltract articulators and resonators. Additional refinement of motor activity isprovided by the extrapyramidal (cerebral cortex, cerebellum, and basal gan-glion) and autonomic nervous systems. These impulses combine to producea sound that is transmitted not only to the ears of listeners but also to thoseof the speaker or singer. Auditory feedback is transmitted from the ear tothe cerebral cortex by way of the brainstem, and adjustments are made topermit the vocalist to match the sound produced with the intended sound.There is also tactile feedback from the throat and other muscles involvedin phonation that undoubtedly help in fine-tuning vocal output, althoughthe mechanism and role of tactile feedback are not fully understood. In


many trained singers, the ability to use tactile feedback effectively is culti-vated as a result of frequent interference with auditory feedback by ancillarynoise in the concert environment (eg, an orchestra or band).

The voice requires interactions among the power source (the lungs, ab-dominal and back muscles, and the vocal folds), the oscillator, and the res-onator. The power source compresses air and forces it toward the larynx.The mucosal cover of the vocal folds opens and closes when the vocal foldsare in the adducted state, permitting small bursts of air to escape betweenthem. Numerous factors affect the sound produced at the glottal level, in-cluding the pressure that builds below the vocal folds (subglottal pressure),the amount of resistance to opening the glottis (glottal impedance), volumevelocity of air flow at the glottis, and supraglottal pressure. The vocal foldsdo not vibrate like the strings on a violin. Rather, they separate and collidesomewhat like buzzing lips. The number of times they do so in any givensecond (ie, their frequency) determines the number of air puffs that escapeand, thus, the pitch of the voice. The frequency of glottal closing and open-ing is one factor in determining vocal quality. Other factors affect loudness,such as subglottal pressure, glottal resistance, and amplitude of vocal folddisplacement from the midline during each vibratory cycle. The sound cre-ated at the vocal fold level is a buzz, similar to the sound produced whenblowing between two blades of grass. This sound contains a complete setof harmonic partials and is responsible in part for the acoustic characteris-tics of the voice. Complex and sophisticated interactions in the supraglotticvocal tract may accentuate or attenuate harmonic partials, acting as a reso-nator. This portion of the vocal tract is largely responsible for the beautyand variety of the sound produced.

Interactions among the various components of the vocal tract ultimatelyare responsible for all the vocal characteristics produced. Many aspects ofthe voice still lack complete understanding and classification. Vocal rangeis reasonably well understood, and broad categories of voice classificationsare generally accepted. Other characteristics, such as vocal register, are con-troversial. Registers are expressed as quality changes within an individualvoice. From low to high, they may include vocal fry, chest voice, middlevoice, head voice, falsetto, and whistle, although not everyone agrees thatall categories exist. The term modal register, used most frequently in speechterms, refers to the voice quality generally used by healthy speakers, as op-posed to a low, gravelly vocal fry or high falsetto.

Vibrato is a rhythmic variation in frequency and intensity. Its exactsource remains uncertain, and its desirable characteristics depend on voicerange and the type of music sung. It seems most likely that the frequencymodulations are controlled primarily by intrinsic laryngeal muscles, espe-cially the cricothyroid and adductor muscles. Extrinsic laryngeal musclesand muscles of the supraglottic vocal tract may also play a role. Intensityvariations may be caused by variations in subglottal pressure, glottal adjust-ments that affect subglottal pressure, secondary effects of the frequency

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variation because of changes in the distance between the fundamental fre-quency and closest formant, or rhythmic changes in vocal tract shape thatcause fluctuations in formant frequencies. When evaluating vibrato, it ishelpful to consider the waveform of the vibrato signal, its regularity, extent,and rate. The waveform is usually fairly sinusoidal, but considerable varia-tion may occur. The regularity, or similarity, of each vibrato event to previ-ous and subsequent vibrato events is greater in trained singers than inuntrained voice users. This regularity seems to be one of the characteristicsperceived as a trained sound. Vibratory extent refers to deviation from thestandard frequency (not intensity variation) and is usually less than 0.1semitone in some styles of solo and choral singing, such as Renaissance mu-sic. For most well-trained Western operatic singing, the usual vibrato extentat comfortable loudness is 0.5 to 1 semitone for singers in most voice clas-sifications. Vibrato rate (the number of modulations per second) is generally5 to 7. Rate may also vary greatly from singer to singer, and in the samesinger. Vibrato rate can increase with increased emotional content of thematerial, and rate tends to decrease with older age (although the age atwhich this change occurs is highly variable). When variations from the cen-tral frequency become too wide, a wobble in the voice is perceived; this isgenerally referred to as tremolo. It is not generally considered a good musi-cal sound, and it is unclear whether it is produced by the same mechanismsresponsible for normal vibrato. Ongoing research should answer many ofthe remaining questions.

Respiration

Basic functions of the nose, larynx, and elemental concepts of inspirationand expiration are discussed elsewhere [1]. A brief review of selected aspectsof pulmonary function is included here to assist readers in understanding theprocesses that underlie support and in understanding pulmonary disordersand their assessment.

Starting from the mouth, the respiratory system consists of progressivelysmaller airway structures. The trachea branches at the carina into mainstembronchi, which then branch into progressively smaller bronchial passagesand terminate in alveoli. Gas exchange between the lungs and the blood-stream occurs at the alveolar level. Air moves in and out of the alveoli topermit this exchange of gases. Air is forced out of the alveoli also to createthe air stream through which phonation is produced. Ultimately, alveolarpressure is the primary power source for phonation and is responsible forthe creation of the subglottal pressure involved in phonation. Alveolar pres-sure is actually greater than subglottal pressure during phonation and expi-ration because some pressure is lost because of the airway resistancebetween the alveoli and the larynx. As the air passes from the alveoli, it en-ters first the bronchioles, which are small, collapsible airways surrounded bysmooth muscle but devoid of cartilage. From the bronchioles, air passes to


progressively larger components of the bronchial tree and eventually to thetrachea. These structures are supported by cartilage and are not fully col-lapsible, but they are compressible and respond to changes in external pres-sure during expiration and inspiration. During expiration, the pressure inthe respiratory system is greatest in the alveolus (alveolar pressure) and leastat the opening of the mouth where pressure is, theoretically, equal to atmo-spheric pressure. Theoretically, all pressure is dissipated between the alveo-lus and the mouth during expiration because of airway resistance betweenthese structures. Expiration pressure is the total of the elastic recoil com-bined with active forces created by muscular compression of the airway.The active pressure is distributed throughout all the components of the air-way, although it may exert greater effect on the alveoli and bronchioles be-cause they are fully collapsible. When the airway is opened, the air pressurein the alveoli (alveolar pressure) is equal to the atmospheric pressure in theroom. To fill the alveoli, the alveolar pressure must be decreased to less thanatmosphere pressure, creating a vacuum that sucks air into the lungs. Tobreathe out, alveolar pressure must be greater than atmospheric pressure.As discussed above, there are passive and active forces operative duringthe inspiratory–expiratory process.

To clarify the mechanisms involved, the alveoli may be thought of as tinyballoons. If a balloon is filled with air, and the filling spout is opened, theelastic properties of the balloon allow most of the air to rush out. This pro-cess is analogous to passive expiration, which relies on the elastic propertiesof the alveoli themselves. Alternatively, we may wrap our hands around theballoon and squeeze the air out. This squeezing may allow us to get the airout faster and more forcefully, and it allows us to get more of the air out ofthe balloon than is expelled through the passive process alone. This processis analogous to active expiration, which involves the abdominal, chest, andback muscles. If we partially pinch the filling spout of the balloon, air comesout more slowly because the outflow tract is partially blocked. The air alsotends to whistle as it exits the balloon. This situation is analogous to ob-structive pulmonary disease, and its commonly associated wheeze. If wetry to blow up the balloon while our hands are wrapped around it, the bal-loon is more difficult to inflate and cannot be inflated fully because it is re-stricted physically by our hands. This phenomenon is somewhat analogousto restrictive lung disease. Under these circumstances, it may also take morepressure to fill the balloon, because the filling process must overcome the re-stricting forces. Under any of these circumstances, the more we fill the alve-olar ‘‘balloon,’’ the greater the pressure, as long as the balloon is notruptured. When the pressure is greater, the increased elastic recoil resultsin more rapid and forceful air escape when the air is released. The pressureinside the balloon can be increased even above its maximal elastic recoil levelsimply by squeezing the outside of the balloon. This analogy is helpful in un-derstanding the forces involved in breathing (especially expiration) and ingenerating support for phonation.

926 SATALOFF et al

Although inspiration is extremely important, this discussion concen-trates primarily on expiration, which is linked closely to support for speechand singing. The elastic component of expiratory pressure (specifically, al-veolar pressure) depends on lung volume and the elastic forces exerted bythe chest and the lungs. The lung is never totally deflated. At rest the lungis inflated to about 40% of total lung capacity (TLC). The amount of airin the lungs at rest is the functional residual capacity (FRC). At FRC, thethorax (chest cavity) is at a volume much less than its rest (or neutral) pos-ture, which is actually closer to 75% of TLC. At FRC the thorax hasa passive tendency to expand, as happens during inspiration. Conversely,at FRC, the lung would collapse if it were not acted on by other forces.The collapsing elastic forces of the lung are balanced by the expandingelastic forces of the thorax. The lung and thorax interact closely, and theirrelative positions of contact vary constantly. This situation is facilitated bythe anatomy of their boundary zone. The inner surface of the thorax iscovered by the parietal pleura, and the lung is covered by the visceralpleura. A thin layer of pleural fluid exists between them. Hydrostaticforces hold these surfaces together while allowing them to slide freely. Un-der pathologic circumstances (eg, following surgery or radiation) these sur-faces may stick together, impairing lung function and affecting support forphonation adversely.

Thoracic and lung elastic behavior can be measured. The basic principlefor doing so involves applying pressure and noting the volume changescaused by the pressure. This change creates a pressure/volume (P/V) curve.The slope with the P/V curve for the thorax reflects its compliance (CCW)and the slope of the P/V curve for the lung represents its compliance(CL). When pressure is applied to the entire system a different P/V curveis created and its slope reflects the compliance of the entire respiratory sys-tem (CRS). Starting from FRC, if air is expelled such that the volume of thesystem is dropped below FRC, an expanding (negative pressure) force is cre-ated. The magnitude of this expanding force is increased as the volume de-creases. Conversely, during inspiration greater than FRC, collapsing(positive pressure) forces increase with increasing volume.

When one inspires, volumes increase well above FRC. Passive expiration,such as occurs during quiet breathing, occurs when one relaxes the dia-phragm. The passive elastic recoil forces air out of the alveoli, because inflat-ing them has created an alveolar pressure that is greater than atmosphericpressure (and is predictable using the P/V curve). The deeper the inspiration,the greater the difference between alveolar and atmospheric pressure, andthe elastic recoil and the expiratory air pressure are greater as a consequence.Inspiration from FRC is an active process, primarily. Thoracic muscles ele-vate the ribs and increase the diameter of the thorax. The external intercos-tal muscles are important to this process. Inspiration also involvescontraction of the diaphragm muscle, which flattens and also increases in-trathoracic volume.


Active expiration is created by forces that decrease thoracic volume. Ac-tive expiration is achieved by muscles that pull the ribs down or compressthe abdominal contents, pushing them upward and thus making the volumeof the thorax smaller. The principle muscles involved are the internal inter-costal muscles, abdominal, back, and other muscles, as reviewed earlier inthis chapter.

For projected phonations, such as singing or acting, airflow is achievedthrough active expiration. After inspiration, elastic recoil and external forcescreated by expiratory muscles determine alveolar pressure, which is substan-tially greater than atmospheric pressure. The combination of passive (elas-tic) and active (muscular) forces pushes air out against airway resistance.As the pressure decreases on the path from alveolar to atmospheric (atthe mouth) pressure, there is a point along that path at which the pressureinside the airway equals the active expiratory pressure (without the elasticrecoil component), which is called the equal pressure point (EPP). As expi-ration continues toward the mouth, pressure drops below the EPP. As air-way pressure diminishes below the EPP, the airway collapses. Thisphysiologic collapse of the airway increases airway resistance by decreasingthe diameter of the airway. The greater the active expiratory forces, thegreater the airway compression after the EPP has been passed. Expiratorypressure and airway compression are important for control of expiratoryairflow rate and are influenced by EPP.

Under normal circumstances, the EPP is reached in the cartilaginous por-tion of the airway, which does not collapse completely ordinarily, even dur-ing forceful expiration This part of the physiologic mechanism allows one tocontinue to sing while running out of air. Under pathologic circumstances,however, the location of the EPP may have shifted. Asthma is the classic ex-ample. During bronchospasm or bronchoconstriction, the diameters of thebronchioles are narrowed by smooth muscle contraction and airway resis-tance in the bronchioles is increased. As the air moves from the alveoliinto the bronchioles, airway pressure diminishes more quickly than normaland EPP may be reached closer to the alveoli and bronchioles, which col-lapse more easily and more completely. In severe circumstances, the distalairway may collapse fully, trapping air in the alveoli and causing hyperinfla-tion of the lungs. Expiratory airflow rate is lowered substantially by the in-creased resistance in the distal airway, resulting in a lower-than-normalsubglottic pressure. This phenomenon can have profoundly adverse effectson phonation.

Other lung dysfunction can also impair subglottal pressure, even if air-way resistance is normal. The classic example is emphysema, which occurscommonly in smokers. This condition results from damage to the alveoliin which the alveolar walls are destroyed and elasticity is lost. Destructionof the alveolar walls effectually causes coalescence of multiple alveoli intoone large alveolar structure, with collagen deposition and scarring in areaswhere elastic fibers were once deposited. Consequently, because elastic recoil

928 SATALOFF et al

pressures are lower and the alveolar volume is greater, alveolar pressure isdecreased compared with normal. Even if the active expiratory forces arenormal, the diminished alveolar pressure results in a lower pressure gradientbetween alveolar and atmospheric pressure over the same airway distance,shifting the location of the EPP distally toward or into collapsable airways.Even when active expiratory efforts are increased under these circumstancesthey do not help because they collapse the distal airways, trapping air in thealveoli and diminishing subglottal pressure.

Summary

This overview highlights only some of the more important components oflower respiratory physiology. Laryngologists should bear these principles inmind in understanding the importance of diagnosis and treatment of respi-ratory dysfunction in voice professionals. In patients who have ‘‘Olympicvoice demands,’’ even slight changes from optimal physiology may haveprofound consequences on phonatory function that are responsible com-monly for hyperfunctional compensatory efforts. If one treats voice hyper-function as if it were the primary problem, failing to recognize that it maybe secondary to an underlying organic or pulmonary disorder, then treat-ment will not be successful in the long term and preventable voice dysfunc-tion and vocal fold injury may ensue.

References

[1] Sataloff RT. Clinical anatomy and physiology of the voice. In: Sataloff RT, editor. Profes-

sional voice: the science and art of clinical care. 3rd edition. San Diego (CA): Plural Publish-

ing, Inc.; 2005. p. 143–78.

[2] HiranoM. Structure and vibratory pattern of the vocal folds. In: Sawashima N, Cooper FS,

editors. Dynamic aspects of the speech production. Tokyo: University of Tokyo Press; 1977.

p. 13–27.

[3] HiranoM. Surgical anatomy and physiology of the vocal folds. In: Gould WJ, Sataloff RT,

Spiegel JR, editors. Voice surgery. St. Louis (MO): Mosby-Year Book; 1993. p. 135–58.

[4] HiranoM, Yoshida T, Kurita S, et al. Anatomy and behavior of the vocal process. In: Baer

T, Sasaki C, Harris K, editors. Laryngeal function in phonation and respiration. Boston:

College-Hill Press; 1987. p. 1–13.

[5] Gray S. Basement membrane zone injury in vocal nodules. In: Gauffin J, Hammarberg B,

editors. Vocal fold physiology: acoustic, perceptual and physiologic aspects of voicemechan-

ics. San Diego (CA): Singular Publishing Group; 1991. p. 21–7.

[6] Sundberg J. The acoustics of the singing voice. Sci Am 1977;236(3):82–91.

[7] BrookeMH, EngleWK. The histographic analysis of human muscle biopsies with regard to

fibre types. 1. Adult male and female. Neurology 1969;19:221–33.

[8] Sadeh M, Kronenberg J, Gaton E. Histochemistry of human laryngeal muscles. Cell Mol

Biol 1981;27:643–8.

[9] Lindestad P. Electromyographic and laryngoscopic studies of normal and disturbed vocal

function. Stockholm: Suddinge University; 1994. 1–12.


[10] English ET, Blevins CE. Motor units of laryngeal muscles. Arch Otolaryngol 1969;89:

778–84.

[11] Faaborg-Andersen K. Electromyographic investigation of intrinsic laryngeal muscles in

humans. Acta Physiol Scand 1957;41(Suppl 140):1–149.

[12] Rossi G, Cortesina G. Morphological study of the laryngeal muscles in man: insertions and

courses of the muscle fibers, motor end-plates and proprioceptors. Acta Otolaryngol

(Stockh) 1965;59:575–92.

[13] Gould WJ, Kamura H. Static lung volumes in singers. Ann Otol Rhinol Laryngol 1973;82:

89–95.

[14] Hixon TJ, Hoffman C. Chest wall shape during singing. In: Lawrence V, editor. Transcripts

of the seventh annual symposium, care of the professional voice. New York: The Voice

Foundation; 1978;1:9–10.

[15] Sundberg J, Leanderson R, von Euler C. Activity relationship between diaphragm and

cricothyroid muscles. J Voice 1989;3(3):225–32.

[16] Letson JA, Tatchell R. Arytenoid movement. In: Sataloff RT, editor. Professional voice: the

science and art of clinical care. 3rd edition. San Diego (CA): Plural Publishing, Inc.; 2006.

p. 179–94.

[17] Baken RJ. An overview of laryngeal function for voice production. In: Sataloff RT, editor.

Professional voice: the science and art of clinical care. 3rd edition. San Diego (CA): Plural

Publishing, Inc.; 2006. p. 237–56.

[18] Scherer RC. Laryngeal function during phonation. In: Sataloff RT, editor. Professional

voice: the science and art of clinical care. 3rd edition. San Diego (CA): Plural Publishing,

Inc.; 2006. p. 257–74.

[19] Sundberg J. Vocal tract resonance. In: Sataloff RT, editor. Professional voice: the science

and art of clinical care. 3rd edition. SanDiego (CA): Plural Publishing, Inc.; 2006. p. 275–92.

[20] Bhatia R, Hawkshaw MJ, Sataloff RT. Chaos in voice research. In: Sataloff RT, editor.



[21] Baken RJ. Dynamical disorders of voice: a chaotic perspective on vocal irregularities. In:

Sataloff RT, editor. Professional voice: the science and art of clinical care. 3rd edition.

San Diego (CA): Plural Publishing, Inc.; 2006. p. 303–20.


40 (2007) 931–951

Medical History in Voice Professionals

Robert T. Sataloff, MD, DMA*, Venu Divi, MD,Yolanda D. Heman-Ackah, MD,

Mary J. Hawkshaw, BSN, RN, CORLNDepartment of Otolaryngology–Head and Neck Surgery, Drexel University College

of Medicine, 1721 Pine Street, Philadelphia, PA 19103, USA

A comprehensive history and physical examination usually reveals thecause of voice dysfunction. Effective history taking and physical examina-tion depend on a practical understanding of the anatomy and physiologyof voice production [1–3]. Because dysfunction in virtually any body systemmay affect phonation, medical inquiry must be comprehensive. The currentstandard of care for all voice patients evolved from advances inspired bymedical problems of voice professionals, such as singers and actors. Evenminor problems may be particularly symptomatic in singers and actorsbecause of the extreme demands placed on their voices. A great many otherpatients are voice professionals, however. They include teachers, salespeople, attorneys, clergy, physicians, politicians, telephone receptionists,and anyone else whose ability to earn a living is impaired in the presenceof voice dysfunction. Because good voice quality is so important in oursociety, most of our patients are voice professionals and all patients shouldbe treated as such.

The scope of inquiry and examination for most patients is similar to thatrequired for singers and actors, except that performing voice professionalshave unique needs that require additional history and examination.Questions must be added regarding performance commitments, professionalstatus and voice goals, the amount and nature of voice training, the perfor-mance environment, rehearsal practices, abusive habits during speech andsinging, and many other matters. Such supplementary information is

This article is modified from: Sataloff RT. Professional voice: the science and art of

clinical care. 3rd edition. San Diego (CA): Plural Publishing, Inc.; 2006. p. 323–38; with

permission.






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essential to proper treatment selection and patient counseling in singers andactors. Analogous factors must also be taken into account, however, forstockbrokers, factory shop foremen, elementary school teachers, home-makers with several noisy children, and many others. Physicians familiarwith the management of these challenging patients are well equipped toevaluate all patients who have voice complaints.

Patient history

Obtaining extensive historical background information is necessary forthorough evaluation of the voice patient, and the otolaryngologist whosees voice patients (especially singers) only occasionally cannot reasonablybe expected to remember all the pertinent questions. Although some laryng-ologists consider a lengthy inquisition helpful in establishing rapport, manyof us who see a substantial number of voice patients each day within a busypractice need a thorough but less time-consuming alternative. A historyquestionnaire can be extremely helpful in documenting all the necessary in-formation, helping the patient sort out and articulate his or her problemsand saving the clinician time recording information. The senior authorhas developed a questionnaire that has proved helpful [4]. The patient isasked to complete the relevant portions of the form at home before his orher office visit or in the waiting room before seeing the doctor. A similarform has been developed for voice patients who are not singers [5].

No history questionnaire is a substitute for direct, penetrating question-ing by the physician. The direction of most useful inquiry can be determinedfrom a glance at a completed questionnaire, however, obviating the need forextensive writing, which permits the physician greater eye contact with thepatient and facilitates rapid establishment of the close rapport andconfidence that are so important in treating voice patients. The physicianis also able to supplement initial impressions and historical informationfrom the questionnaire with seemingly leisurely conversation during thephysical examination. The use of the history questionnaire has addedsubstantially to the efficiency, consistent thoroughness, and ease of manag-ing these delightful, but often complex, patients. A similar set of questions isalso used by the speech-language pathologist with new patients and by manyenlightened singing teachers when assessing new students.

How old are you?

Serious vocal endeavor may start in childhood and continue throughouta lifetime. As the vocal mechanism undergoes normal maturation, the voicechanges. The optimal time to begin serious vocal training is controversial.For many years, most singing teachers advocated delay of vocal trainingand serious singing until near puberty in the female and after puberty and

933MEDICAL HISTORY IN VOICE PROFESSIONALS

voice stabilization in the male. In a child who has earnest vocal aspirationsand potential, however, starting specialized training early in childhood isreasonable. Initial instruction should teach the child to vocalize withoutstraining and to avoid all forms of voice abuse. It should not permit prema-ture indulgence in operatic bravado. Most experts agree that taxing voiceuse and singing during puberty should be minimized or avoided altogether,particularly by the male. Voice maturation (attainment of stable adult vocalquality) may occur at any age from the early teenage years to the fourth de-cade of life. The dangerous tendency for young singers to attempt to soundolder than their vocal years frequently causes vocal dysfunction.

All components of voice production are subject to normal advanced ag-ing. Abdominal and general muscular tone frequently decrease, lungs loseelasticity, the thorax loses its distensibility, the mucosa of the vocal tract at-rophies, mucous secretions change character and quantity, nerve endings arereduced in number, and psychoneurologic functions change as one advancespast the midlife. Moreover, the larynx itself loses muscle tone and bulk andmay show depletion of submucosal ground substance in the vocal folds. Thelaryngeal cartilages ossify, and the joints may become arthritic and stiff.Hormonal influence is altered. Vocal range, intensity, and quality all maybe modified. Vocal fold atrophy may be the most striking alteration. Theclinical effects of aging seem more pronounced in female singers, althoughvocal fold histologic changes may be more prominent in males. Excellentmale singers occasionally extend their careers into their 70s or beyond[6,7]. Some degree of breathiness, decreased range, decreased breathsupport, and other evidence of aging should be expected in elderly voices.Nevertheless, many of the changes we typically associate with elderly singers(wobble, flat pitch) are attributable to lack of conditioning rather than inev-itable changes of biologic aging. These aesthetically undesirable concomi-tants of aging can often be reversed.

What is your voice problem?

Careful questioning about the onset of vocal problems is needed toseparate acute from chronic dysfunction. Often an upper respiratory tractinfection sends a patient to the physician’s office, but penetrating inquiry,especially in singers and actors, may reveal a chronic vocal problem thatis the patient’s real concern. Identifying acute and chronic problems beforebeginning therapy is important so that patient and physician may haverealistic expectations and make optimal therapeutic selections.

The specific nature of the vocal complaint can provide a great deal ofinformation. Just as dizzy patients rarely walk into the physician’s officecomplaining of ‘‘rotary vertigo,’’ voice patients may be unable to articulatetheir symptoms without guidance. They may use the term ‘‘hoarseness’’ todescribe a variety of conditions that the physician must separate. Hoarse-ness is a coarse or scratchy sound that is most often associated with

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abnormalities of the leading edge of the vocal folds, such as laryngitis ormass lesions. Breathiness is a vocal quality characterized by excessive lossof air during vocalization. In some cases it is caused by improper technique.Any condition that prevents full approximation of the vocal folds can beresponsible, however. Possible causes include vocal fold paralysis, a masslesion separating the leading edges of the vocal folds, arthritis of the cricoar-ytenoid joint, arytenoid dislocation, scarring of the vibratory margin, senilevocal fold atrophy (presbyphonia), psychogenic dysphonia, malingering,and other conditions.

Fatigue of the voice is inability to continue to speak or sing for extendedperiods without change in vocal quality or control. The voice may showfatigue by becoming hoarse, losing range, changing timbre, breaking intodifferent registers, or exhibiting other uncontrolled aberrations. A well-trained singer should be able to sing for several hours without vocal fatigue.

Voice fatigue may occur through more than one mechanism. Most of thetime it is assumed to be attributable to muscle fatigue, which is often thecase in patients who have voice fatigue associated with muscle tension dys-phonia. The mechanism is most likely to be peripheral muscle fatigue causedby chemical changes or depletion in the muscle fibers. Muscle fatigue mayalso occur on a central neurologic basis. This mechanism is common in cer-tain neuropathic disorders, such as some patients who have multiple sclero-sis; may occur with myasthenia gravis, a neuromuscular junction disorder;or may be associated with paresis from various causes. The voice mayalso fatigue because of changes in the vibratory margin of the vocal fold,however. This phenomenon may be described as lamina propria fatigue.It, too, may be related to chemical or fluid changes in the lamina propriaor cellular damage associated with conditions such as phonotrauma and de-hydration. Excessive voice use, suboptimal tissue environment (eg, dehydra-tion, effects of pollution, and so on), lack of sufficient time of recoverybetween phonatory stresses, and genetic or structural tissue weaknessesthat predispose to injury or delayed recovery from trauma all may be asso-ciated with lamina propria fatigue.

Although it has not been proved, the authors suspect that fatigue mayalso be related to linear and nonlinear chaotic characteristics of the voicesignal [8]. As the voice becomes more trained, vibrations become more sym-metrical and the system becomes more linear. In many pathologic voices, thenonlinear components seem to become more prominent. If a voice is highlylinear, slight changes in the vibratory margin may have little effect on theoutput of the system. If the system is substantially nonlinear because of vo-cal fold pathology, poor tissue environment, or other causes, slight changesin the tissue (eg, slight swelling, drying, surface cell damage) may causesubstantial changes in the acoustic output of the system. A butterfly effectensues in which vocal quality changes and fatigue occur more quicklywith smaller changes in the condition than would be seen in more linearvocal systems.


Fatigue is often caused by misuse of abdominal and neck musculature,oversinging, singing too loudly, or singing too long. Vocal fatigue alsomay be a sign not only of general tiredness or vocal abuse, sometimes sec-ondary to structural lesions or glottal closure problems, but also of seriousillnesses, such as myasthenia gravis. The importance of this complaint thusshould not be understated.

Volume disturbance may manifest as inability to sing loudly or inabilityto sing softly. Each voice has its own dynamic range. Within the course oftraining, singers learn to sing louder by singing more efficiently. They alsolearn to sing softly, a more difficult task, through years of laborious practice.Actors and other trained speakers go through similar training. Most volumeproblems are secondary to intrinsic limitations of the voice or technical er-rors in voice use, although hormonal changes, aging, and neurologic diseaseare other causes. Superior laryngeal nerve paresis impairs the ability tospeak or sing loudly. This condition is a frequently unrecognized conse-quence of herpes simplex II infection (cold sores) and Lyme disease andmay also be precipitated by any viral upper respiratory tract infection.

Most highly trained singers require only about 10 to 30minutes towarmupthe voice. Prolonged warm-up time, especially in the morning, is most oftencaused by reflux laryngitis. Tickling or choking during singing is most oftena symptom of an abnormality of the vocal fold’s leading edge. The symptomof tickling or choking should contraindicate singing until the vocal folds havebeen examined. Pain while singing can indicate vocal fold lesions, laryngealjoint arthritis, infection, or gastric acid reflux irritation of the arytenoidregion. Pain is much more commonly caused by voice abuse with excessivemuscular activity in the neck rather than an acute abnormality on the leadingedge of a vocal fold, however. In the absence of other symptoms, these patientsdo not generally require immediate cessation of singing pending medicalexamination. Sudden onset of pain, usually sharp pain, while singing maybe associated with a mucosal tear or a vocal fold hemorrhage, however, andwarrants voice rest pending laryngeal examination.

Do you have any pressing voice commitments?

If a singer or professional speaker (eg, actor, politician) seeks treatmentat the end of a busy performance season and has no pressing engagements,management of the voice problem should be conservative and designed toensure long-term protection of the larynx. The physician and patient rarelyhave this luxury, however. Most often, the voice professional needs treat-ment within 1 week of an important engagement and sometimes withinless than 1 day.

Younger singers fall ill shortly before performances, not because of hypo-chondria or coincidence, but rather because of the immense physical andemotional stress of the pre-performance period. The singer is frequentlyworking harder and singing longer hours than usual. Moreover, he or she

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may be under particular pressure to learn new material and to perform wellfor a new audience. The singer may also be sleeping less than usual becauseof additional time spent rehearsing or because of the discomforts of a strangecity. Seasoned professionals make their living by performing regularly,sometimes several times a week. Consequently, any time they get sick islikely to precede a performance. Caring for voice complaints in these situa-tions requires highly skilled judgment and bold management.

Tell me about your vocal career, long-term goals, and the importanceof your voice quality and upcoming commitments

To choose a treatment program, the physician must understand theimportance of the patient’s voice and his or her long-term career plans,the importance of the upcoming vocal commitment, and the consequencesof canceling the engagement. Injudicious prescription of voice rest can bealmost as damaging to a vocal career as injudicious performance. Forexample, although a singer’s voice is usually his or her most importantcommodity, other factors distinguish the few successful artists from themultitude of less successful singers with equally good voices. These includemusicianship, reliability, and professionalism. Canceling a concert at the lastminute may seriously damage a performer’s reputation. Reliability is espe-cially critical early in a singer’s career. Moreover, an expert singer oftencan modify a performance to decrease the strain on his or her voice. Nosinger should be allowed to perform in a manner that permits serious injuryto the vocal folds, but in the frequent borderline cases the condition of thelarynx must be weighed against other factors affecting the singer as an artist.

How much voice training have you had?

Establishing how long a singer or actor has been performing seriously isimportant, especially if his or her active performance career predates the be-ginning of vocal training. Active untrained singers and actors frequently de-velop undesirable techniques that are difficult to modify. Extensive voice usewithout training or premature training with inappropriate repertoire mayunderlie persistent vocal difficulties later in life. The number of years aperformer has been training his or her voice may be a fair index of vocalproficiency. A person who has studied voice for 1 or 2 years is somewhatmore likely to have gross technical difficulties than someone who has beenstudying for 20 years. If training has been intermittent or discontinued, how-ever, technical problems are common, especially among singers. In addition,methods of technical voice use vary among voice teachers. A student whohas had many teachers in a brief period of time commonly has numeroustechnical insecurities or deficiencies that may be responsible for vocaldysfunction, especially if the singer has changed to a new teacher withinthe preceding year. The physician must be careful not to criticize the


patient’s current voice teacher in such circumstances. It often takes years ofexpert instruction to correct bad habits.

All people speak more often than they sing, yet most singers report littlespeech training. Even if a singer uses the voice flawlessly while practicingand performing, voice abuse at other times can cause damage that affectssinging.

Under what kinds of conditions do you use your voice?

The Lombard effect is the tendency to increase vocal intensity in responseto increased background noise. A well-trained singer learns to compensatefor this tendency and to avoid singing at unsafe volumes. Singers of classicalmusic usually have such training and frequently perform with only a piano,a situation in which the balance can be controlled well. Singers performingin large halls, with orchestras, or in operas early in their careers tend tooversing and strain their voices. Similar problems occur during outdoorconcerts because of the lack of auditory feedback. This phenomenon isseen even more among pop singers. Pop singers are in a uniquely difficultposition; often, despite little vocal training, they enjoy great artistic andfinancial success and endure extremely stressful demands on their timeand voices. They are required to sing in large halls or outdoor arenas notdesigned for musical performance amid smoke and other environmentalirritants and accompanied by extremely loud background music. One fre-quently neglected key to survival for these singers is the proper use of mon-itor speakers. These direct the sound of the singer’s voice toward the singeron the stage and provide auditory feedback. Determining whether the popsinger uses monitor speakers and whether they are loud enough for thesinger to hear is important.

Amateur singers are often no less serious about their music than areprofessionals, but generally they have less ability to compensate technicallyfor illness or other physical impairment. Rarely does an amateur suffera great loss from postponing a performance or permitting someone tosing in his or her place. In most cases, the amateur singer’s best interest isserved through conservative management directed at long-term maintenanceof good vocal health.

A great many of the singers who seek physicians’ advice are primarilychoral singers. They often are enthusiastic amateurs, untrained but dedi-cated to their musical recreation. They should be handled as amateur solosingers, educated specifically about the Lombard effect, and cautioned toavoid the excessive volume so common in a choral environment. Onegood way for a singer to monitor loudness is to cup a hand to his or herear, which adds about 6 dB to the singer’s perception of his or her own voiceand can be a helpful guide in noisy surroundings [9]. Young professionalsingers are often hired to augment amateur choruses. Feeling that theprofessional quartet has been hired to lead the rest of the choir, they often

938 SATALOFF et al

make the mistake of trying to accomplish that goal by singing louder thanothers in their sections. These singers should be advised to lead their sectionby singing each line as if they were soloists giving a voice lesson to the peo-ple standing next to them and as if there were a microphone in front of themrecording their choral performance for their voice teacher. This approachusually not only preserves the voice but also produces a better choral sound.

How much do you practice and exercise your voice?How, when, and where do you use your voice?

Vocal exercise is as essential to the vocalist as exercise and conditioningof other muscle systems is to the athlete. Proper vocal practice incorporatesscales and specific exercises designed to maintain and develop the vocal ap-paratus. Simply acting or singing songs and giving performances withoutroutine studious concentration on vocal technique is not adequate for thevocal performer. The physician should know whether the vocalist practicesdaily, whether he or she practices at the same time daily, and how long thepractice lasts. Actors generally practice and warm up their voices for 10 to30 minutes daily, although more time is recommended. Most serious singerspractice for at least 1 to 2 hours per day. If a singer routinely practices in thelate afternoon or evening but frequently performs in the morning (religiousservices, school classes, teaching voice, choir rehearsals, and so forth), oneshould inquire as to the warm-up procedures preceding such performancesand the cool-down procedures after voice use. Singing cold, especially earlyin the morning, may result in the use of minor muscular alterations to com-pensate for vocal insecurity produced by inadequate preparation. Suchcrutches can result in voice dysfunction. Similar problems may result frominstances of voice use other than formal singing. School teachers, telephonereceptionists, sales people, and others who speak extensively also oftenderive great benefit from 5 or 10 minutes of vocalization of scales first thingin the morning. Although singers rarely practice their scales too long, theyfrequently perform or rehearse excessively. This is especially true immedi-ately before a major concert or audition, when physicians are most likelyto see acute problems. When a singer has hoarseness and vocal fatigueand has been practicing a new role for 14 hours a day for the previous 3weeks, no simple prescription can solve the problem. A treatment regimencan usually be designed to carry the performer safely through his or hermusical obligations, however.

The physician should be aware of common habits and environments thatare often associated with abusive voice behavior and should ask about themroutinely. Screaming at sports events and at children are among the mostcommon. Extensive voice use in noisy environments also tends to be abusive.These include noisy rooms, cars, airplanes, sports facilities, and other loca-tions where background noise or acoustic design impairs auditory feedback.Dry, dusty surroundings may alter vocal fold secretions through dehydration


or contact irritation, altering voice function. Activities such as cheerleading,teaching, choral conducting, amateur singing, and frequent communicationwith hearing-impaired people are likely to be associated with voice abuse,as is extensive professional voice use without formal training. The physicianshould inquire about the patient’s routine voice use and should specificallyask about any activities that frequently lead to voice change, such as hoarse-ness or discomfort in the neck or throat. Laryngologists should ask specifi-cally about other activities that may be abusive to the vocal folds, such asweight lifting, aerobics, and the playing of some wind instruments.

Are you aware of misusing or abusing your voice during singing?

The most common technical errors involve excessive muscle tension inthe tongue, neck, and larynx; inadequate abdominal support; and excessivevolume. Inadequate preparation can be a devastating source of voice abuseand may result from limited practice, limited rehearsal of a difficult piece, orlimited vocal training for a given role. The latter error is tragically common.In some situations, voice teachers are at fault and the singer and teachermust resist the impulse to show off the voice in works that are either too dif-ficult for the singer’s level of training or simply not suited to the singer’svoice. Singers are habitually unhappy with the limitations of their voices.At some time or another, most baritones wish they were tenors and try toprove they can sing high C’s in Vesti la giubba. Singers with other vocalranges have similar fantasies. Attempts to make the voice something thatit is not, or at least that it is not yet, frequently are harmful.

Are you aware of misusing or abusing your voice during speaking?

Voice abuse or misuse should be suspected particularly in patients whocomplain of voice fatigue associated with voice use, patients whose voicesare worse at the end of a working day or week, and in any patient who ischronically hoarse. Technical errors in voice use may be the primary causeof a voice complaint, or it may develop secondarily because of a patient’seffort to compensate for voice disturbance from another cause.

Dissociation of one’s speaking and singing voices is probably the mostcommon cause of voice abuse problems in excellent singers. Too frequently,all the expert training in support, muscle control, and projection is notapplied to a singer’s speaking voice. Unfortunately, the resultant voicestrain affects the singing voice and the speaking voice. Such damage isespecially likely to occur in noisy rooms and in cars, where the backgroundnoise is louder than it seems. Backstage greetings after a lengthy perfor-mance can be particularly devastating. The singer usually is exhaustedand distracted, the environment is often dusty and dry, and generally a noisycrowd is present. Similar conditions prevail at postperformance parties,where smoking and alcohol worsen matters. These situations should be

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avoided by any singer who has vocal problems and should be controlledthrough awareness at other times.

Three particularly abusive and potentially damaging vocal activities areworthy of note. Cheerleading requires extensive screaming under the worstpossible physical and environmental circumstances. It is a highly undesirableactivity for anyone considering serious vocal endeavor. This conflict is com-mon in younger singers because the teenager who is the high school choir so-loist often is also student council president, yearbook editor, captain of thecheerleaders, and so on. Conducting, particularly choral conducting, canalso be deleterious. An enthusiastic conductor, especially of an amateurgroup, frequently sings all four parts intermittently, at volumes louder thanthe entire choir, during lengthy rehearsals. Conducting is a common avoca-tion among singers but must be done with expert technique and special pre-cautions to prevent voice injury. Hoarseness or loss of soft voice controlafter conducting a rehearsal or concert suggests voice abuse during conduct-ing. The patient should be instructed to record his or her voice throughout thevocal range singing long notes at dynamics from soft to loud to soft. Record-ings should be made before rehearsal and following rehearsal. If the voice haslost range, control, or quality during the rehearsal, voice abuse has occurred.A similar test can be used for patients who sing in choirs, teach voice, or per-form other potentially abusive vocal activities. Such problems in conductorscan generally bemanaged by additional training in conducting techniques andby voice training, including warm-up and cool-down exercises.

Teaching singing may also be hazardous to vocal health. It can be donesafely but requires skill and thought. Most teachers teach while seated at thepiano. Late in a long, hard day, this posture is not conducive to mainte-nance of optimal abdominal and back support. Usually, teachers workwith students continually positioned to the right or left of the keyboard.This positioning may require the teacher to turn his or her neck at a partic-ularly sharp angle, especially when teaching at an upright piano. Teachersalso often demonstrate vocal works in their students’ vocal ranges ratherthan their own, illustrating bad and good technique. If a singing teacheris hoarse or has neck discomfort, or his or her soft singing control deterio-rates at the end of a teaching day (assuming that the teacher warms upbefore beginning to teach voice lessons), voice abuse should be suspected.Helpful modifications include teaching with a grand piano, sitting slightlysideways on the piano bench, or alternating student position to the rightand left of the piano to facilitate better neck alignment. Retaining an accom-panist so that the teacher can stand rather than teach from sitting behinda piano, and many other helpful modifications, are possible.

Do you have pain when you talk or sing?

Odynophonia, or pain caused by phonation, can be a disturbing symp-tom. It is not uncommon, but little has been written or discussed on this


subject. A detailed review of odynophonia is beyond the scope of this pub-lication. Laryngologists should be familiar with the diagnosis and treatmentof at least a few of the most common causes [10].

What kind of physical condition are you in?

Phonation is an athletic activity that requires good conditioning andcoordinated interaction of numerous physical functions. Maladies of anypart of the body may be reflected in the voice. Failure to maintain goodabdominal muscle tone and respiratory endurance through exercise is partic-ularly harmful because deficiencies in these areas undermine the powersource of the voice. Patients generally attempt to compensate for suchweaknesses by using inappropriate muscle groups, particularly in theneck, causing vocal dysfunction. Similar problems may occur in the well-conditioned vocalist in states of fatigue. These are compounded by mucosalchanges that accompany excessively long hours of hard work. Suchproblems may be seen even in the best singers shortly before importantperformances in the height of the concert season.

A popular but untrue myth holds that great opera singers must be obese.The vivacious, gregarious personality that often distinguishes the great per-former seems to be accompanied frequently by a propensity for excess, es-pecially culinary excess. This excess is as undesirable in the vocalist as it isin most other athletic artists, and it should be prevented from the start ofone’s vocal career. Appropriate and attractive body weight has alwaysbeen valued in the pop music world and is becoming particularly importantin the opera world as this formerly theater-based art form moves to televi-sion and film media. Attempts at weight reduction in an established speakeror singer are a different matter, however. The vocal mechanism is a finelytuned, complex instrument and is exquisitely sensitive to minor changes.Substantial fluctuations in weight frequently cause deleterious alterationsof the voice, although these are usually temporary. Weight reduction pro-grams for people concerned about their voices must be monitored carefullyand designed to reduce weight in small increments over long periods. Ahistory of sudden recent weight change may be responsible for almost anyvocal complaint.

Have you noted voice or bodily weakness, tremor, fatigue, or lossof control?

Even minor neurologic disorders may be extremely disruptive to vocalfunction. Specific questions should be asked to rule out neuromuscular andneurologic diseases, such as myasthenia gravis, Parkinson disease, tremors,other movement disorders, spasmodic dysphonia, multiple sclerosis, centralnervous system neoplasm, and other serious maladies that may present withvoice complaints.

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Do you have allergy or cold symptoms?

Acute upper respiratory tract infection causes inflammation of themucosa, alters mucosal secretions, and makes the mucosa more vulnerableto injury. Coughing and throat clearing are particularly traumatic vocalactivities and may worsen or provoke hoarseness associated with a cold.Postnasal drip and allergy may produce the same response. Infectious sinus-itis is associated with discharge and diffuse mucosal inflammation, resultingin similar problems, and may actually alter the sound of a voice, especiallythe patient’s own perception of his or her voice. Futile attempts to compen-sate for disease of the supraglottic vocal tract in an effort to return the soundto normal frequently result in laryngeal strain. The expert singer or speakershould compensate by monitoring technique by tactile rather than by audi-tory feedback, or singing ‘‘by feel’’ rather than ‘‘by ear.’’

Do you have breathing problems, especially after exercise?

Voice patients usually volunteer information about upper respiratory tractinfections and postnasal drip, but the relevance of other maladies may not beobvious to them. Consequently the physician must seek out pertinent history.

Respiratory problems are especially important in voice patients. Evenmild respiratory dysfunction may adversely affect the power source of thevoice [11]. Occult asthma may be particularly troublesome [12]. A completerespiratory history should be obtained in most patients who have voice com-plaints, and pulmonary function testing is often advisable.

Have you been exposed to environmental irritants?

Anymucosal irritant can disrupt the delicate vocalmechanism. Allergies todust andmold are aggravated commonly during rehearsals and performancesin concert halls, especially older theaters and concert halls, because of numer-ous curtains, backstage trappings, and dressing room facilities that are rarelycleaned thoroughly. Nasal obstruction and erythematous conjunctivae sug-gest generalized mucosal irritation. The drying effects of cold air and dryheat may also affect mucosal secretions, leading to decreased lubrication,a scratchy voice, and tickling cough. These symptoms may be minimized bynasal breathing, which allows inspired air to be filtered, warmed, and humid-ified. Nasal breathing, whenever possible, rather than mouth breathing, isproper vocal technique. While the performer is backstage between appear-ances or during rehearsals, inhalation of dust and other irritants may becontrolled by wearing a protective mask, such as those used by carpenters,or a surgical mask that does not contain fiberglass. This practice is especiallyhelpful when sets are being constructed in the rehearsal area.

A history of recent travel suggests other sources of mucosal irritation.The air in airplanes is extremely dry, and airplanes are noisy [13]. Onemust be careful to avoid talking loudly and to maintain good hydration


and nasal breathing during air travel. Environmental changes can also bedisruptive. Las Vegas is infamous for the mucosal irritation caused by itsdry atmosphere and smoke-filled rooms. In fact, the resultant complex ofhoarseness, vocal tickle, and fatigue is referred to as ‘‘Las Vegas voice.’’A history of recent travel should also suggest jet lag and generalized fatigue,which may be potent detriments to good vocal function.

Environmental pollution is responsible for the presence of toxic substancesand conditions encountered daily. Inhalation of toxic pollutants may affectthe voice adversely by direct laryngeal injury, by causing pulmonary dysfunc-tion that results in voice maladies, or through impairments elsewhere in thevocal tract. Ingested substances, especially those that have neurolaryngologiceffects, may also adversely affect the voice. Nonchemical environmental pol-lutants, such as noise, can cause voice abnormalities also. Laryngologistsshould be familiar with the laryngologic effects of the numerous potentiallyirritating substances and conditions found in the environment. We mustalso be familiar with special pollution problems encountered by performers.Numerous materials used by artists to create sculptures, drawings, and theat-rical sets are toxic and have adverse voice effects. In addition, performers areexposed routinely to chemicals encountered through stage smoke and pyro-technic effects [14–16]. Although it is clear that some of the special effectsresult in serious laryngologic consequences, much additional study is needto clarify the nature and scope of these occupational problems.

Do you smoke, live with a smoker, or work around smoke?

The effects of smoking on voice performance were reviewed recently in theJournal of Singing [17]. Smoking of cigarettes, cigars, marijuana, and othersubstances affects the larynx, lungs, and other body systems adversely andshould be discouraged strongly in all patients, particularly voice professionals.

Do any foods seem to affect your voice?

Various foods are said to affect the voice. Traditionally, singers avoidmilk and ice cream before performances. In many people, these foodsseem to increase the amount and viscosity of mucosal secretions. Allergyand casein have been implicated, but no satisfactory explanation has beenestablished. In some cases restriction of these foods from the diet beforea voice performance may be helpful. Chocolate may have the same effectand should be viewed similarly. Chocolate also contains caffeine, whichmay aggravate reflux or cause tremor. Voice patients should be asked abouteating nuts. This question is important not only because some people expe-rience effects similar to those produced by milk products and chocolate butalso because they are extremely irritating if aspirated. The irritation pro-duced by aspiration of even a small organic foreign body may be severeand impossible to correct rapidly enough to permit performance. Highly

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spiced foods may also cause mucosal irritation. In addition, they seem to ag-gravate reflux laryngitis. Coffee and other beverages containing caffeine alsoaggravate gastric reflux and may promote dehydration or alter secretionsand necessitate frequent throat clearing in some people. Fad diets, especiallyrapid weight-reducing diets, are notorious for causing voice problems. Eat-ing a full meal before a speaking or singing engagement may interfere withabdominal support or may aggravate upright reflux of gastric juice duringabdominal muscle contraction.

Do you have morning hoarseness, bad breath, excessive phlegm, a lumpin your throat, or heartburn?

Reflux laryngitis is especially common among singers and trainedspeakers because of the high intra-abdominal pressure associated withproper support and because of lifestyle. Singers frequently perform at night.Many vocalists refrain from eating before performances because a full stom-ach can compromise effective abdominal support. They typically compen-sate by eating heartily at postperformance gatherings late at night andthen go to bed with a full stomach. Chronic irritation of arytenoid and vocalfold mucosa by reflux of gastric secretions may occasionally be associatedwith dyspepsia or pyrosis. The key features of this malady are bitter tasteand halitosis on awakening in the morning, a dry or coated mouth, oftena scratchy sore throat or a feeling of a lump in the throat, hoarseness,and the need for prolonged vocal warm-up. The physician must be alertto these symptoms and ask about them routinely; otherwise, the diagnosisis overlooked because people who have had this problem for many yearsor a lifetime do not even realize it is abnormal.

Do you have trouble with your bowels or belly?

Any condition that alters abdominal function, such as muscle spasm,constipation, or diarrhea, interferes with support and may result in a voicecomplaint. These symptoms may accompany infection, anxiety, variousgastroenterologic diseases, and other maladies.

Are you under particular stress or in therapy?

The human voice is an exquisitely sensitive messenger of emotion. Highlytrained voice professionals learn to control the effects of anxiety and otheremotional stress on their voices under ordinary circumstances. In someinstances, however, this training may break down or a performer may be in-adequately prepared to control the voice under specific stressful conditions.Pre-performance anxiety is the most common example, but insecurity, de-pression, and other emotional disturbances are also generally reflected inthe voice. Anxiety reactions are mediated in part through the autonomicnervous system and result in a dry mouth, cold clammy skin, and thick


secretions. These reactions are normal, and good vocal training coupledwith assurance that no abnormality or disease is present generallyovercomes them. Long-term, poorly compensated emotional stress andexogenous stress (from agents, producers, teachers, parents, and so forth)may cause substantial vocal dysfunction and may result in permanentlimitations of the vocal apparatus. These conditions must be diagnosedand treated expertly. Hypochondriasis is uncommon among professionalsingers, despite popular opinion to the contrary.

Recent publications have highlighted the complexity and importance ofpsychological factors associated with voice disorders [18]. It is importantfor the physician to recognize that psychological problems may not onlycause voice disorders but also delay recovery from voice disorders thatwere entirely organic in cause. Professional voice users, especially singers,have enormous psychologic investment and personality identifications asso-ciated with their voices. A condition that causes voice loss or permanent in-jury often evokes the same powerful psychologic responses seen followingthe death of a loved one. This process may be initiated even when physicalrecovery is complete if an incident, such as injury or surgery, has made thevocalist realize that voice loss is possible. Such a ‘‘brush with death’’ canhave profound emotional consequences in some patients. It is essential forthe laryngologist to be aware of these powerful factors and to managethem properly if optimal therapeutic results are to be achieved expeditiously.

Do you have problems controlling your weight? Are you excessivelytired? Are you cold when other people are warm?

Endocrine problems warrant special attention. The human voice is ex-tremely sensitive to endocrinologic changes. Many of these are reflected inalterations of fluid content of the lamina propria just beneath the laryngealmucosa, which causes alterations in the bulk and shape of the vocal foldsand result in voice change. Hypothyroidism and thyroiditis are well-recog-nized causes of such voice disorders, although the mechanisms are not fullyunderstood [19–23]. Hoarseness, vocal fatigue, muffling of the voice, loss ofrange, and a sensation of a lump in the throat may be present even with mildthyroid dysfunction. Even when thyroid function test results are within thelow normal range this diagnosis should be entertained, especially if thyroid-stimulating hormone levels are in the high normal range or are elevated.Thyrotoxicosis may result in similar voice disturbances [20].

Do you have menstrual irregularity, cyclical voice changes associatedwith menses, recent menopause, or other hormonal changes or problems?

Voice changes associated with sex hormones are encountered commonlyin clinical practice and have been investigated more thoroughly than haveother hormonal changes [24,25]. Although a correlation seems to exist

946 SATALOFF et al

between sex hormone levels and depth of male voices (higher testosteroneand lower estradiol levels in basses than in tenors), the most important hor-monal considerations in males occur during or related to puberty [24,26–28].Voice problems related to sex hormones are more common in female singersand tend to occur during menopause or several months after the cessation ofhormone replacement therapy. It is always important to ask a female patientwho complains of gradual onset of decreased range, increased instability,and vocal fatigue about her menstrual and hormonal status, particularly ifshe has performed for years without such difficulties [29–44].

Do you have jaw joint or other dental problems?

Dental disease, especially temporomandibular joint (TMJ) dysfunction, in-troduces muscle tension in the head and neck, which is transmitted to the lar-ynx directly through the muscular attachments between the mandible and thehyoid bone and indirectly as generalized increased muscle tension. Theseproblems often result in decreased range, vocal fatigue, and change in thequality or placement of a voice. Such tension often is accompanied by excesstongue muscle activity, especially pulling of the tongue posteriorly. This hy-perfunctional behavior acts through hyoid attachments to disrupt the balancebetween the intrinsic and extrinsic laryngeal musculature. TMJ problems arealso problematic for wind instrumentalists and some string players, includingviolinists. In some cases, the problemsmay actually be caused by instrumentaltechnique. The history should always include information about musical ac-tivities, including instruments other than the voice.

Do you or your blood relatives have hearing loss?

Hearing loss is often overlooked as a source of vocal problems. Auditoryfeedback is fundamental to speaking and singing. Interference with thiscontrol mechanism may result in altered vocal production, particularly ifthe person is unaware of the hearing loss. Distortion, particularly pitchdistortion (diplacusis) may also pose serious problems for the singer. Thisdistortion seems to be attributable to aesthetic difficulties in matching pitchand also to vocal strain, which accompanies pitch shifts [45].

In addition to determining whether the patient has hearing loss, inquiryshould also be made about hearing impairment occurring in familymembers, roommates, and other close associates. Speaking loudly topeople who are hard of hearing can cause substantial, chronic vocal strain.This possibility should be investigated routinely when evaluating voicepatients.

Have you suffered whiplash or other bodily injury?

Various bodily injuries outside the confines of the vocal tract may haveprofound effects on the voice. Whiplash, for example, commonly causes


changes in technique, with consequent voice fatigue, loss of range, difficultysinging softly, and other problems. These problems derive from the neckmuscle spasm, abnormal neck posturing secondary to pain, and consequenthyperfunctional voice use. Lumbar, abdominal, head, chest, supraglottic,and extremity injuries may also affect vocal technique and be responsiblefor the dysphonia that prompted the voice patient to seek medical attention.

Did you undergo any surgery before the onset of your voice problems?

A history of laryngeal surgery in a voice patient is a matter of great con-cern. It is important to establish exactly why the surgery was done, by whomit was done, whether intubation was necessary, and whether the anesthesiol-ogist reported difficulty with the intubation. It is also important to ascertainwhether voice therapy was instituted pre- or postoperatively, especially if thelesion is commonly associated with voice abuse (vocal nodules or vocalprocess granulomas). If the vocal dysfunction that sent the patient to thephysician’s office dates from the immediate postoperative period, surgicalor intubation trauma must be suspected.

Otolaryngologists frequently are asked about the effects of tonsillectomyon the voice. Singers, especially, may consult the physician after tonsillec-tomy and complain of vocal dysfunction. Certainly, removal of tonsilscan alter the voice [46,47]. Tonsillectomy changes the configuration of thesupraglottic vocal tract. In addition, scarring alters pharyngeal muscle func-tion, which is trained meticulously in the professional singer. Singers mustbe warned that they may have permanent voice changes after tonsillectomy;however, these can be minimized by dissecting in the proper plane by coldtechnique and minimal use of cautery, laser, or other thermal coagulationdevices to lessen scarring. The singer’s voice generally requires 3 to 6months to stabilize or return to normal after surgery, although it is gener-ally safe to begin limited singing within 4 to 6 weeks following surgery.Postoperative speech therapy that begins 4 weeks after surgery to stretchthe palatal musculature helps to limit the effects of palatal scarring. Aswith any procedure for which general anesthesia may be needed, the anes-thesiologist should be advised preoperatively that the patient is a profes-sional singer. Intubation and extubation should be performed with greatcare, and the use of nonirritating plastic rather than rubber or ribbed metalendotracheal tubes is preferred. Use of a laryngeal mask may be advisablefor selected procedures for mechanical reasons, but this device is often notideal for tonsillectomy and it can cause laryngeal injury, such as arytenoiddislocation.

Surgery of the neck, such as thyroidectomy, may result in permanentalterations of the vocal mechanism through scarring of the extrinsiclaryngeal musculature. The cervical (strap) muscles are important inmaintaining laryngeal position and stability of the laryngeal skeleton andthey should be retracted rather than divided whenever possible. A history

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of recurrent or superior laryngeal nerve injury may explain a hoarse,breathy, weak or easily fatigable voice.

Thoracic and abdominal surgery interfere with respiratory and abdomi-nal support. After these procedures, singing and projected speaking shouldbe prohibited until pain has subsided and healing has occurred sufficientlyto allow normal support. Abdominal exercises should be instituted beforeresumption of vocalizing. Singing and speaking without proper supportare often worse for the voice than not using the voice for performance at all.

Other surgical procedures may be important factors if they necessitateintubation or if they affect the musculoskeletal system so that the personhas to change stance or balance. For example, balancing on one foot afterleg surgery may decrease the effectiveness of the support mechanism.

What medications and other substances do you use?

A history of alcohol abuse suggests the probability of poor vocal tech-nique. Intoxication results in lack of coordination and decreased awareness,which undermine vocal discipline designed to optimize and protect thevoice. The effect of small amounts of alcohol is controversial. Althoughmany experts oppose its use because of its vasodilatory effect and conse-quent mucosal alteration, many people do not seem to be adversely affectedby small amounts of alcohol, such as a glass of wine with a meal. Somepeople have mild sensitivities to certain wines or beers. Patients who developnasal congestion and rhinorrhea after drinking beer, for example, should bemade aware that they probably have a mild allergy to that particular bever-age and should avoid it before voice commitments.

Patients frequently acquire antihistamines to help control postnasal dripor other symptoms. The drying effect of antihistamines may result indecreased vocal fold lubrication, increased throat clearing, and irritability,leading to frequent coughing. Antihistamines may be helpful to some voicepatients but they must be used with caution and are best taken at bedtime tominimize daytime side effects.

When a voice patient seeking the attention of a physician is alreadytaking antibiotics, it is important to find out the dose and the prescribingphysician, if any, and whether the patient frequently treats himself orherself with inadequate courses of antibiotics often supplied by colleagues.Singers, actors, and other speakers sometimes have a sore throat shortlybefore important vocal presentations and start themselves on inappropriateantibiotic therapy, which they generally discontinue after theirperformance.

Diuretics are also popular among some performers. They are oftenprescribed by gynecologists at the vocalist’s request to help deplete excesswater in the premenstrual period. They are not effective in the larynx inthis scenario, because they cannot diurese the protein-bound water in thelaryngeal ground substance. Unsupervised use of these drugs may cause


dehydration and consequent mucosal dryness, placing the singer at risk forvocal fold tear and mucosal lesions.

Hormone use, especially the use of oral contraceptives, must be men-tioned specifically during the physician’s inquiry. Women frequently donot mention them routinely when asked whether they are taking anymedications. Vitamins and herbal supplements are also frequently notmentioned. Most vitamin therapies seem to have little effect on the voice.High-dose vitamin C (5 to 6 g/d), which some people use to prevent upperrespiratory tract infections, seems to act as a mild diuretic and may lead todehydration and xerophonia [48]. Herbal remedies should be used by singerswith caution, because the side-effect profile of most herbal remedies is un-known and many can cause mucosal drying.

Cocaine use is common, especially among pop musicians. This drug canbe extremely irritating to the nasal mucosa, causes marked vasoconstriction,and may alter the sensorium, resulting in decreased voice control anda tendency toward vocal abuse.

Many pain medications, including aspirin and nonsteroidal anti-inflam-matory medications, psychotropic medications, and many others, may be re-sponsible for a voice complaint. So far, no adverse vocal effects have beenreported with selective cyclooxygenase-2 inhibiting (COX-2) anti-inflamma-tory medications, such as Celecoxib (Celebrex, Pfizer Inc., New York) andvaldecoxib (Bextra, Pharmacia Corp., New York). The effects of othernew medications, such as sildenafil citrate (Viagra, Pfizer Inc.) and medica-tions used to induce abortion remain unstudied and unknown but it seemsplausible that these types of medications may affect voice function, at leasttemporarily. Laryngologists must be familiar with the laryngologic effects ofthe many substances ingested medically and recreationally.

References

[1] SataloffRT. Professional singers: the science and art of clinical care. Am JOtolaryngol 1981;

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[2] Sataloff RT. The human voice. Sci Am 1992;267:108–15.

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[6] AckermanR, PfanW.Gerontology studies on the susceptibility to voice disorders in profes-

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[7] vonLedenH.Speechandhearingproblems in the geriatric patient. JAmGeriatr Soc 1977;25:422–6.

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[11] Spiegel JR, Cohn JR, SataloffRT, et al. Respiratory function in singers: medical assessment,

diagnoses, treatments. J Voice 1988;2:40–50.

[12] Cohn JR, Sataloff RT, Spiegel JR, et al. Airway reactivity-induced asthma in singers

(ARIAS). J Voice 1991;5:332–7.

[13] Feder RJ. The professional voice and airline flight. Otolaryngol Head Neck Surg 1984;92:

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[15] Opperman DA. Pyrotechnics in the entertainment industry: an overview. In: Sataloff RT,

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(CA): Plural Publishing, Inc.; 2006. p. 737–50.

[16] Rossol M. Pyrotechnics: health effects. In: Sataloff RT, editor. Professional voice: the


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hypothyroidism. Ear Nose Throat J 1997;56:10–21.

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ations de la voix au cours des thyrotoxioses. Ann Endocrinol (Paris) 1977;38:171–2.

[21] Michelsson K, Sirvio P. Cry analysis in congenital hypothyroidism. Folia Phoniatr (Basel)

1976;28:40–7.

[22] Ritter FN. The effect of hypothyroidism on the larynx of the rat. Ann Otol Rhinol Laryngol

1964;67:404–16.

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Philadelphia: Saunders; 1973. p. 727–34.

[24] MeuserW, Nieschlag E. Sex hormones and depth of voice in the male [German]. DtschMed

Wochenschr 1977;102:261–4.

[25] Schiff M. The influence of estrogens on connective tissue. In: Asboe-Hansen G, editor.

Hormones and connective tissue. Coopenhagen (Denmark): Munksgaard Press; 1967.

p. 282–341.

[26] Brodnitz F. The age of the castrato voice. J Speech Hear Disord 1975;40:291–5.

[27] Brodnitz F. Hormones and the human voice. Bull N Y Acad Med 1971;47:183–91.

[28] Sataloff RT, Linville SE. The effects of age on the voice. In: Sataloff RT, editor. Professional


Inc.; 2006. p. 497–512.

[29] von Gelder L. Psychosomatic aspects of endocrine disorders of the voice. J CommunDisord

1974;7:257–62.

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[31] Wendler J. The influence of menstruation on the voice of the female singer. Folia Phoniatr

(Basel) 1972;24:259–77.

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the seventh annual symposium. Care of the professional voice. New York: The Voice Foun-

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[33] Dordain M. Etude Statistique de l’influence des contraceptifs hormonaux sur la voix. Folia

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[34] Pahn J, Goretzlehner G. Voice changes following the use of oral contraceptives. Zentralbl

Gynakol 1978;100:341–6.

[35] Schiff M. ‘‘The pill’’ in otolaryngology. Trans Am Acad Ophthalmol Otolaryngol 1968;72:

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[36] von Deuster CV. Irreversible vocal changes in pregnancy. HNO 1977;25:430–2.

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schaft auf die augsgebildete Gesangsstimme? Folia Phoniatr (Basel) 1968;21:199–210.

[38] Arndt HJ. Stimmstorungen nach Behandlung mit Androgenen und anabolen Hormonen.

Munch Med Wochenschr 1974;116:1715–20.

[39] Bourdial J. Les troubles de la voix provoques par la therapeutique hormonale androgene.

Ann Otolaryngol Chir Cervicofac 1970;87:725–34.

[40] Damste PH. Virilization of the voice due to anabolic steroids. Ned Tijdschr Geneeskd 1963;

107:891–2.

[41] Damste PH.Voice changes in adult women caused by virilizing agents. J SpeechHearDisord

1967;32:126–32.

[42] Saez S, Francoise S. Recepteurs d’androgenes: mise en evidence dans la fraction cytosolique

de muqueuse normale et d’epitheliomas phryngolarynges humains. C R Acad Sci Hebd

Seances Acad Sci D 1975;280:935–8.

[43] Vuorenkoski V, Lenko HL, Tjernlund P, et al. Fundamental voice frequency during normal

and abnormal growth, and after androgen treatment. Arch Dis Child 1978;53:201–9.

[44] Imre V. Hormonell bedingte Stimmstorungen. Folia Phoniatr (Basel) 1968;20:394–404.

[45] Sundberg J, PrameE, Iwarsson J. Replicability and accuracy of pitch patterns in professional

singers. In: Davis PJ, Fletcher NH, editors. Vocal fold physiology: controlling chaos and

complexity. San Diego (CA): Singular Publishing Group Inc; 1996. p. 291–306.

[46] Rubin JS, SataloffRT,KorovinGS.Diagnosis and treatment of voice disorders. 3rd edition.

San Diego, (CA): Plural Publishing, Inc.; 2006. p. 334.

[47] Wallner LJ, Hill BJ, WaldropW, et al. Voice changes following adenotonsillectomy. Laryn-

goscope 1968;78:1410–8.

[48] Lawrence VL. Medical care for professional voice (panel). In: Lawrence VL, editor. Tran-

scripts from the annual symposium. Care of the professional voice. New York: The Voice

Foundation; 1978 [3]. p. 17–18.


40 (2007) 953–969

Physical Examination of VoiceProfessionals

Robert T. Sataloff, MD, DMA*,Mary J. Hawkshaw, BSN, RN, CORLN,

Venu Divi, MD,Yolanda D. Heman-Ackah, MD

Department of Otolaryngology–Head and Neck Surgery, Drexel University College

of Medicine, 1721 Pine Street, Philadelphia, PA 19103-6771, USA

Physical examination

A detailed history frequently reveals the cause of a voice problem evenbefore a physical examination is performed. A comprehensive physical ex-amination, often including objective assessment of voice function, also is es-sential, however [1–3]. Physical examination must include a thorough ear,nose, and throat evaluation and assessment of the patient’s general physicalcondition. A patient who is extremely obese or seems fatigued, agitated,emotionally stressed, or otherwise generally ill has increased potential forvoice dysfunction. This dysfunction could be attributable to any numberof factors: altered abdominal support, loss of fine motor control of laryngealmuscles, decreased bulk of the submucosal vocal fold ground substance,change in the character of mucosal secretions, or other similar mechanisms.Any physical condition that impairs the normal function of the abdominalmusculature is suspect as cause for dysphonia. Some conditions, such aspregnancy, are obvious; however, a sprained ankle or broken leg that re-quires the singer to balance in an unaccustomed posture may distract himor her from maintaining good abdominal support and thereby result in voicedysfunction. A tremorous neurologic disorder, endocrine disturbances suchas thyroid dysfunction or menopause, the aging process, and other systemic


clinical care. 3rd edition. San Diego (CA): Plural Publishing, Inc.; 2006. p. 343–53; with per-

mission.






954 SATALOFF et al

conditions also may alter the voice. The physician must remember that mal-adies of almost any body system may result in voice dysfunction, and thedoctor must remain alert for conditions outside of the head and neck. Ifthe patient uses his or her voice professionally for singing, acting, or othervocally demanding professions, physical examination should also include as-sessment of the patient during typical professional vocal tasks. For example,a singer should be asked to sing. Evaluation techniques for assessing the per-formance mechanism are described in greater detail elsewhere [4–10].

Complete ear, nose, and throat examination

Examination of the ears must include assessment of hearing acuity. Evena slight hearing loss may result in voice strain as a singer tries to balance hisor her vocal intensity with that of associate performers. Similar effects areencountered among speakers, but they are less prominent in the early stagesof hearing loss. This observation is especially true of hearing losses acquiredafter vocal training has been completed. The effect is most pronounced withsensorineural hearing loss. Diplacusis, distortion of pitch perception, makesvocal strain even worse. With conductive hearing loss, singers tend to singmore softly than appropriate rather than too loudly, and this is less harmful.

During an ear, nose, and throat examination, the conjunctivae andsclerae should be observed routinely for erythema that suggests allergy orirritation, for pallor that suggests anemia, and for other abnormalities,such as jaundice. These observations may reveal the problem reflected inthe vocal tract even before the larynx is visualized. Hearing loss in a spouseor family member may be problematic also if the voice professional strainsvocally to communicate.

The nose should be assessed for patency of the nasal airway, character ofthe nasal mucosa, and nature of secretions, if any. A patient who is unableto breathe through the nose because of anatomic obstruction is forced tobreathe unfiltered, unhumidified air through the mouth. Pale gray allergicmucosa or swollen infected mucosa in the nose suggests abnormal mucosaelsewhere in the respiratory tract.

Examination of the oral cavity should include careful attention to thetonsils and lymphoid tissue in the posterior pharyngeal wall and to the mu-cosa. Diffuse lymphoid hypertrophy associated with a complaint of scratchyvoice and irritative cough may indicate infection. The amount and viscosityof mucosal and salivary secretions also should be noted. Xerostomia is par-ticularly important. The presence of scalloping of the lateral aspects of thetongue should be noted. This finding is caused commonly by tongue thrustand may be associated with inappropriate tongue tension and muscle ten-sion dysphonia. Dental examination should focus not only on oral hygienebut also on the presence of wear facets suggestive of bruxism. Bruxism isa clue to excessive tension and may be associated with dysfunction of thetemporomandibular joints, which should also be assessed routinely.

955PHYSICAL EXAMINATION OF VOICE PROFESSIONALS

Thinning of the enamel of the central incisors in a normal or underweightpatient may be a clue to bulimia. It may also result from excessive ingestionof lemons, which some singers eat to help thin their secretions.

The neck should be examined for masses, restriction of movement, excessmuscle tension or spasm, and scars from prior neck surgery or trauma. La-ryngeal vertical mobility is also important. For example, tilting of the larynxproduced by partial fixation of cervical muscles cut during previous surgerymay produce voice dysfunction, as may fixation of the trachea to overlyingneck skin. Particular attention should be paid to the thyroid gland. Enlarge-ment of the gland may signal subclinical hypothyroidism or thyroiditis, bothof which can affect the vocal folds, their vibratory function, and the integrityof the laryngeal nerves, in some cases contributing to paresis and paralysisof the superior or recurrent laryngeal nerves. Examination of posterior neckmuscles and range of motion should not be neglected. Neck muscle spasm,decreased range of motion, and cervical spine abnormalities can contributeto increased neck tension and hyperfunctional voice behaviors. The cranialnerves should also be examined. Diminished fifth nerve sensation, dimin-ished gag reflex, palatal deviation, or other mild cranial nerve deficits mayindicate cranial polyneuropathy. Postviral, infectious neuropathies may in-volve the superior laryngeal nerve and cause weakness of the vocal fold mus-cle secondary to decreased neural input, fatigability, and loss of range andprojection in the voice. The recurrent laryngeal nerve is also affected insome cases. More serious neurologic disease may also be associated withsuch symptoms and signs.

Laryngeal examination

Examination of the larynx begins when the singer or other voice patiententers the physician’s office. The range, ease, volume, and quality of thespeaking voice should be noted. If the examination is not being conductedin the patient’s native language, the physician should be sure to listen toa sample of the patient’s mother tongue also. Voice use is often different un-der the strain or habits of foreign language use. Rating scales used to de-scribe the quality of the speaking voice may be helpful [11,12]. Theclassification proposed by the Japanese Society of Logopedics and Phoniat-rics is one of the most widely used. It is known commonly as the GRBASVoice Rating Scale [13].

Physicians are not usually experts in voice classification. Physicians shouldat least be able to discriminate substantial differences in range and timbre,however, such as between bass and tenor, or alto and soprano. Althoughthe correlation between speaking and singing voices is not perfect, a speakerwho has a low, comfortable bass voice who reports that he is a tenor maybe misclassified and singing inappropriate roles with consequent voice strain.This judgment should be deferred to an expert, but the observation shouldlead the physician to make the appropriate referral. Excessive volume or

956 SATALOFF et al

obvious strain during speaking clearly indicates that voice abuse is presentand may be contributing to the patient’s singing complaint. The speakingvoice can be evaluated more consistently and accurately using standardizedreading passages [14], and such assessments are performed routinely byspeech-language pathologists, phoniatricians, and sometimes bylaryngologists.

Any patient who has a voice complaint should be examined by indirectlaryngoscopy, at least. It is not possible to judge voice range, quality, orother vocal attributes by inspection of the vocal folds. The presence or ab-sence of nodules, mass lesions, contact ulcers, hemorrhage, erythema, paral-ysis, arytenoid erythema (reflux), and other anatomic abnormalities must beestablished, however. Erythema and edema of the laryngeal surface of theepiglottis is seen often in association with muscle tension dysphonia andwith frequent coughing or clearing of the throat. It is caused by directtrauma from the arytenoids during these maneuvers. The mirror or a laryn-geal telescope often provides a better view of the posterior portion of the en-dolarynx than is obtained with flexible endoscopy. Stroboscopicexamination adds substantially to diagnostic abilities (Fig. 1). Another oc-casionally helpful adjunct is the operating microscope. Magnification allowsvisualization of small mucosal disruptions and hemorrhages that may be sig-nificant but overlooked otherwise. This technique also allows photographyof the larynx with a microscope camera. Magnification may also be achievedthrough magnifying laryngeal mirrors or by wearing loupes. Loupes usuallyprovide a clearer image than do most of the magnifying mirrors available.

A laryngeal telescope may be combined with a stroboscope to provide ex-cellent visualization of the vocal folds and related structures. The authorsusually use a 70� laryngeal telescope, although 90� telescopes are requiredfor some patients. The combination of a telescope and stroboscope providesoptimal magnification and optical quality for assessment of vocal fold

Fig. 1. Photograph of normal larynx showing the true vocal folds (V), false vocal folds (F), ar-

ytenoids (A), and epiglottis (E). (From Sataloff RT. Professional voice: the science and art of

clinical care. 3rd edition. San Diego [CA]: Plural Publishing, Inc.; 2006. p. 343–53; with

permission.)


vibration. It is generally performed with the tongue in a fixed position, how-ever, and the nature of the examination does not permit assessment of thelarynx during normal phonatory gestures.

Flexible fiberoptic laryngoscopy can be performed as an office procedureand allows inspection of the vocal folds in patients whose vocal folds are dif-ficult to visualize indirectly. In addition, it permits observation of the vocalmechanism in a more natural posture than does indirect laryngoscopy, per-mitting sophisticated dynamic voice assessment. In the hands of an experi-enced endoscopist, this method may provide a great deal of informationabout speaking and singing techniques. The combination of a fiberoptic laryn-goscope with a laryngeal stroboscope may be especially useful. This systempermits magnification, photography, and detailed inspection of vocal foldmotion. Sophisticated systems that permit flexible or rigid fiberoptic strobo-videolaryngoscopy are currently available commercially. They are invaluableassets for routine clinical use. The video system also provides a permanent re-cord, permitting reassessment, comparison over time, and easy consultation.A refinement not currently available commercially is stereoscopic fiberopticlaryngoscopy, accomplished by placing a laryngoscope through each nostril,fastening the two together in the pharynx, and observing the larynx throughthe eyepieces [15]. This method allows visualization of laryngeal motion inthree dimensions. It is used primarily in a research setting, however.

Rigid endoscopy under general anesthesia may be reserved for the rarepatient whose vocal folds cannot be assessed adequately by other meansor for patients who need surgical procedures to remove or biopsy laryngeallesions. In many cases this may be done with local anesthesia, avoiding theneed for intubation and the traumatic coughing and vomiting that may oc-cur even after general anesthesia administered by mask. Coughing after gen-eral anesthesia may be minimized by using topical anesthesia in the larynxand trachea. Topical anesthetics may act as severe mucosal irritants ina small number of patients, however. They may also predispose the patientto aspiration in the postoperative period. If a patient has had difficulty witha topical anesthetic administered in the office it should not be used in theoperating room. When used in general anesthesia cases, topical anestheticsshould usually be applied at the end of the procedure. If inflammation oc-curs, it will not interfere with performance of microsurgery. Postoperativeduration of anesthesia is also optimized. The authors have had the least dif-ficulty with 4% Xylocaine.

Objective tests

Reliable, valid, objective analysis of the voice is extremely important and isan essential part of a comprehensive physical examination [2]. It is as valuableto the laryngologist as audiometry is to the otologist [16,17]. Familiarity withsome of the measures and technological advances currently available is help-ful. This information is covered in greater detail elsewhere [5].

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Strobovideolaryngoscopy

Integrity of the vibratory margin of the vocal fold is essential for the com-plex motion required to produce good vocal quality. Under continuouslight, the vocal folds vibrate approximately 256 times per second while pho-nating at middle C. Naturally, the human eye cannot discern the necessarydetails during such rapid motion. The vibratory margin may be assessedthrough high-speed photography, strobovideolaryngoscopy, high-speedvideo, videokymography, electroglottography (EGG), or photoglottogra-phy. Strobovideolaryngoscopy provides the necessary clinical informationin a practical fashion. Stroboscopic light allows routine slow-motion evalu-ation of the mucosal cover layer of the leading edge of the vocal fold. Thisstate-of-the-art physical examination permits detection of vibratory asym-metries, structural abnormalities, small masses, submucosal scars, and otherconditions that are invisible under ordinary light [18,19]. Documentation ofthe procedure by coupling stroboscopic light with the video camera allowslater reevaluation by the laryngologist or other health care providers.

Stroboscopy does not provide a true slow-motion image, as obtainedthrough high-speed photography. The stroboscope actually illuminates dif-ferent points on consecutive vocal fold waves, each of which is retained onthe retina for 0.2 seconds. The stroboscopically lighted portions of the suc-cessive waves are fused visually; thus the examiner is actually evaluatingsimulated cycles of phonation. The slow-motion effect is created by havingthe stroboscopic light desynchronized with the frequency of vocal fold vi-bration by approximately 2 Hz. When vocal fold vibration and the strobo-scope are synchronized exactly, the vocal folds appear to stand still ratherthan move in slow motion. In most instances, this approximation of slowmotion provides all the clinical information necessary [5,19]. We use a mod-ification of the standardized method of subjective assessment of strobovi-deolaryngoscopic images, as proposed by Hirano and colleagues [20,21].Characteristics evaluated include the fundamental frequency, the symmetryof movements, periodicity, glottic closure, the amplitude of vibration, themucosal wave, the presence of nonvibrating portions of the vocal fold,and other unusual findings. With practice, perceptual judgments of strobo-scopic images provide a great deal of information. It is easy for the inexpe-rienced observer to draw unwarranted conclusions because of normalvariations in vibration, however. Vibrations depend on fundamental fre-quency, intensity, and vocal register. For example, failure of glottic closureoccurs normally in falsetto phonation. Consequently, it is important to notethese characteristics and to examine each voice under various conditions.

Other techniques to examine vocal fold vibration

Other techniques to examine vocal fold vibration include ultrahigh-speedphotography, EGG, photoelectroglottography and ultrasound glottogra-phy, and most recently videokymography and high-speed video (digital or


analog) [22]. Ultrahigh-speed photography provides images that are in trueslow motion, rather than simulated. High-speed video offers similar advan-tages without most of the disadvantages of high-speed motion pictures. Vid-eokymography offers high-speed imaging of a single line along the vocalfold. EGG uses two electrodes placed on the skin of the neck above the thy-roid laminae. It traces the opening and closing of the glottis and can be com-pared with stroboscopic images [23]. EGG allows objective determination ofthe presence or absence of glottal vibrations and easy determination of thefundamental period of vibration and is reproducible. It reflects the glottalcondition more accurately during its closed phase. Photo electroglottogra-phy and ultrasound glottography are less useful clinically [13].

Measures of phonatory ability

Objective measures of phonatory ability are easy to use, readily availableto the laryngologist, helpful in treatment of professional vocalists who havespecific voice disorders, and are useful in assessing the results of surgicaltherapies. Maximum phonation time is measured with a stopwatch. The pa-tient is instructed to sustain the vowel /a/ for as long as possible after deepinspiration, vocalizing at a comfortable frequency and intensity. The fre-quency and intensity may be determined and controlled by an inexpensivefrequency analyzer and sound level meter. The test is repeated three timesand the greatest value is recorded. Normal values have been determined[13]. Frequency range of phonation is recorded in semitones and documentsthe vocal range from the lowest note in the modal register (excluding vocalfry) to the highest falsetto note. This range is the physiologic frequencyrange of phonation and disregards quality. The musical frequency rangeof phonation measures lowest to highest notes of musically acceptable qual-ity. Tests for maximum phonation time, frequency ranges, and many of theother parameters discussed later (including spectrographic analysis) may bepreserved on a tape recorder or digitized and stored for analysis at a conve-nient future time and used for pre- and posttreatment comparisons. Record-ings should be made in a standardized, consistent fashion.

Frequency limits of vocal register also may be measured. The registers are(from low to high) vocal fry, chest, mid, head, and falsetto. Classification ofregisters is controversial, however, and many other classifications are used.Although the classification listed above is common among musicians, atpresent most voice scientists prefer to classify registers as pulse, modal,and loft. Overlap of frequency among registers occurs routinely.

Testing the speaking fundamental frequency often reveals excessively lowpitch, an abnormality associated with chronic voice abuse and developmentof vocal nodules. This parameter may be followed objectively throughouta course of voice therapy. Intensity range of phonation (IRP) has proveda less useful measure than frequency range. It varies with fundamental fre-quency (which should be recorded) and is greatest in the middle frequency

960 SATALOFF et al

range. It is measured in sound pressure level (SPL) in reference to 0.0002 mi-crobar. For normal adults who are not professional vocalists, measuring ata single fundamental frequency, IRP averages 54.8 dB for males and 51 dBfor females [24]. Alterations of intensity are common in voice disorders, al-though IRP is not the most sensitive test to detect them. Information fromthese tests may be combined in a fundamental frequency-intensity profile[13], also called a phonetogram.

Glottal efficiency (ratio of the acoustic power at the level of the glottis tosubglottal power) provides useful information but is not clinically practicalbecause measuring acoustic power at the level of the glottis is difficult. Sub-glottic power is the product of subglottal pressure and airflow rate. Thesecan be determined clinically. Various alternative measures of glottic effi-ciency have been proposed, including the ratio of radiated acoustic powerto subglottal power [25], airflow intensity profile [26], and ratio of theroot mean square value of the AC component to the mean volume velocity(DC component) [27]. Although glottal efficiency is of great interest, none ofthese tests is particularly helpful under routine clinical circumstances.

Aerodynamic measures

Traditional pulmonary function testing provides the most readily acces-sible measure of respiratory function. The most common parameters mea-sured include: (1) tidal volume, the volume of air that enters the lungsduring inspiration and leaves during expiration in normal breathing; (2)functional residual capacity, the volume of air remaining in the lungs atthe end of inspiration during normal breathing, which can be divided intoexpiratory reserve volume (maximal additional volume that can be exhaled)and residual volume (the volume of air remaining in the lungs at the end ofmaximal exhalation); (3) inspiratory capacity, the maximal volume of airthat can be inhaled starting at the functional residual capacity; (4) totallung capacity, the volume of air in the lungs following maximal inspiration;(5) vital capacity, the maximal volume of air that can be exhaled from thelungs following maximal inspiration; (6) forced vital capacity, the rate ofair flow with rapid, forceful expiration from total lung capacity to residualvolume; (7) FEV1, the forced expiratory volume in 1 second; (8) FEV3, theforced expiratory volume in 3 seconds; (9) maximal mid-expiratory flow, themean rate of air flow over the middle half of the forced vital capacity (be-tween 25% and 75% of the forced vital capacity).

For singers and professional speakers who have an abnormality caused byvoice abuse, abnormal pulmonary function tests may confirm deficiencies inaerobic conditioning or reveal previously unrecognized asthma [28]. Flowglottography with computer inverse filtering is also a practical and valuablediagnostic tool for assessing flow at the vocal fold level, evaluating the voicesource, and imaging the results of the balance between adductory forces andsubglottal pressure [17,29]. It also has therapeutic value as a biofeedback tool.


The spirometer, readily available for pulmonary function testing, can alsobe used for measuring airflow during phonation.

Air volume is measured by the use of a mask fitted tightly over the face orby phonating into a mouthpiece while wearing a nose clamp. Measurementsmay be made using a spirometer, pneumotachograph, or hot-wire anemom-eter. The normal values for mean flow rate under habitual phonation, withchanges in intensity or register, and under various pathologic circumstances,were determined in the 1970s [13]. Normal values are available for adultsand children. Mean flow rate also can be measured and is a clinically usefulparameter to follow during treatment of vocal nodules, recurrent laryngealnerve paralysis, spasmodic dysphonia, and other conditions.

Glottal resistance cannot be measured directly, but it may be calculatedfrom the mean flow rate and mean subglottal pressure. Normal glottal resis-tance is 20 to 100 dyne s/cm5 at low and medium pitches and 150 dyne s/cm5

at high pitches [25]. The normal values for subglottal pressure under varioushealthy and pathologic voice conditions have also been determined by nu-merous investigators [13]. The phonation quotient is the vital capacity di-vided by the maximum phonation time. It has been shown to correlateclosely with maximum flow rate [30] and is a more convenient measure. Nor-mative data determined by various authors have been published [13]. Thephonation quotient provides an objective measure of the effects of treatmentand is particularly useful in cases of recurrent laryngeal nerve paralysis andmass lesions of the vocal folds, including nodules.

Acoustic analysis

Acoustic analysis equipment can determine frequency, intensity, har-monic spectrum, cycle-to-cycle perturbations in frequency (jitter), cycle-to-cycle perturbations in amplitude (shimmer), harmonics/noise ratios, breath-iness index, cepstral peak prominence, and many other parameters. TheDSP Sona-Graph Sound Analyzer Model 5500 (Kay Elemetrics, LincolnPark, New Jersey) is an integrated voice analysis system. It is equippedfor sound spectrography capabilities. Spectrography provides a visual re-cord of the voice. The acoustic signal is depicted using time (x axis), fre-quency (y axis) and intensity (z axis) shading of light versus dark. Usingthe band pass filters, generalizations about quality, pitch, and loudnesscan be made. These observations are used in formulating the voice therapytreatment plan. Formant structure and strength can be determined using thenarrow-band filters, of which various configurations are possible. In clinicalsettings in which singers and other professional voice users are evaluatedand treated routinely, this feature is extremely valuable. A sophisticatedvoice analysis program (an optional program) may be combined with theSona-Graph and is an especially valuable addition to the clinical laboratory.The voice analysis program (Computer Speech Lab, Kay Elemetrics, Lin-coln Park, New Jersey) measures speaking fundamental frequency,

962 SATALOFF et al

frequency perturbation (jitter), amplitude perturbation (shimmer), har-monics/noise ratio, and provides many other values. An electroglottographmay be used in conjunction with the Sona-Graph to provide some of thesevoicing parameters. Examining the EGG waveform alone is possible withthis setup, but its clinical usefulness has not yet been established. An impor-tant feature of the Sona-Graph is the long-term average spectrum (LTAS)capability that permits analysis of longer voice samples (30–90 seconds).The LTAS analyzes only voiced speech segments and may be useful inscreening for hoarse or breathy voices. In addition, computer interface ca-pabilities (also an optional program) have solved many data storage andfile maintenance problems.

In analyzing acoustic signals, the microphone may be placed at the levelof the mouth or positioned in or over the trachea, although intratracheal re-cordings are used for research purposes only. The position should be stan-dardized in each office or laboratory [31]. Various techniques are beingdeveloped to improve the usefulness of acoustic analysis. Because of theenormous amount of information carried in the acoustic signal, further re-finements in objective acoustic analysis should prove particularly valuable tothe clinician.

Laryngeal electromyography

Electromyography (EMG) requires an electrode system, an amplifier, anoscilloscope, a loudspeaker, and a recording system [32]. Needle electrodesare placed transcutaneously into laryngeal muscles. EMG can be extremelyvaluable in confirming cases of vocal fold paresis, in differentiating paralysisfrom arytenoid dislocation, distinguishing recurrent laryngeal nerve paralysisfrom combined recurrent and superior nerve paralysis, diagnosing othermoresubtle neurolaryngologic pathology, and documenting functional voice disor-ders andmalingering. It is also recommended for needle localization when us-ing botulinum toxin to treat spasmodic dysphonia and other conditions.

Psychoacoustic evaluation

Because the human ear and brain are the most sensitive and complex an-alyzers of sound currently available, many researchers have tried to stan-dardize and quantify psychoacoustic evaluation. Unfortunately, evendefinitions of basic terms, such as hoarseness and breathiness, are still con-troversial. Psychoacoustic evaluation protocols and interpretations are notstandardized. Consequently, although subjective psychoacoustic analysisof voice is of great value to the individual skilled clinician, it remains gener-ally unsatisfactory for comparing research among laboratories or for report-ing clinical results.

The GRBAS scale helps standardize perceptual analysis for clinical pur-poses. It rates the vocal characteristics of grade, roughness, breathiness,


asthenia, and strain on a scale from 0 to 3. Modification of the GRBASscale using a continual line, with one end being most normal and the othermost abnormal, has been shown to produce reliable ratings that show goodintrarater and interrater reliability [33]. Grade 0 is normal, 1 is slightly ab-normal, 2 is moderately abnormal, and 3 is extremely abnormal [13]. Graderefers to the overall degree of voice abnormality. Roughness refers to whatmany describe as raspiness, the auditory impression of an irregularly peri-odic voice signal. Breathiness refers to the auditory perception of air leakageor escape mixed into the voice signal. Asthenia is the perception of vocalweakness or lack of power. Strain refers to the auditory perception of hyper-function. For example, a patient’s voice might be graded as G2, R2, B1, A1,S2, or on a continual scale from 1 to 100 as G-68, R-61, B-37, A-28, S-72.

Outcomes assessment

Measuring the impact of a voice disorder on the function of an individualin his or her normal activities of daily living has always been challenging.Recent advances have begun to address this problem, however. Validatedinstruments, such as the Voice Handicap Index (VHI) and the Voice RelatedQuality of Life (VRQOL) [34] are currently in clinical use, and are likely tobe used widely in future years [35]. Current trends and future directions inmeasuring voice treatment outcomes are discussed elsewhere [36].

Voice impairment and disability

Quantifying voice impairment and assigning a disability rating (percent-age of whole person) remain controversial. This subject is still not addressedcomprehensively even in the most recent editions (2001, 5th edition) of theAmerican Medical Association’s Guidelines for the Evaluation of Impairmentand Disability (The Guides). The Guides still do not take into account theperson’s profession when calculating disability. Alternative approacheshave been proposed, and advances in this complex arena are anticipatedover the next few years. This subject is discussed elsewhere [37].

Evaluation of the singing voice

The physician must be careful not to exceed the limits of his or her exper-tise, especially in caring for singers. If voice abuse or technical error is sus-pected, or if a difficult judgment must be reached on whether to allow a sicksinger to perform, a brief observation of the patient’s singing may provideinvaluable information. This observation is accomplished best by askingthe singer to stand and sing scales either in the examining room or ina soundproof audiology booth. Similar maneuvers may be used for

964 SATALOFF et al

professional speakers, including actors (who can vocalize and recite lines),clergy and politicians (who can deliver sermons and speeches), and virtuallyall other voice patients. The singer’s stance should be balanced, with theweight slightly forward. The knees should be bent slightly and the shoulders,torso, and neck should be relaxed. The singer should inhale through thenose whenever possible allowing filtration, warming, and humidificationof inspired air. In general, the chest should be expanded, but most of the ac-tive breathing is abdominal. The chest should not rise substantially witheach inspiration, and the supraclavicular musculature should not be in-volved obviously in inspiration. Shoulders and neck muscles should notbe tensed even with deep inspiration. Abdominal musculature should becontracted shortly before the initiation of the tone. This contraction maybe evaluated visually or by palpation (Fig. 2). Muscles of the neck andface should be relaxed. Economy is a basic principle of all art forms. Wastedenergy and motion and muscle tension are incorrect and usually deleterious.

The singer should be instructed to sing a scale (a five-note scale is usuallysufficient) on the vowel /a/, beginning on any comfortable note. Technical er-rors are usually most obvious as contraction of muscles in the neck and chin,retraction of the lower lip, retraction of the tongue, or tightening of the mus-cles of mastication. The singer’s mouth should be open widely but comfort-ably. When singing /a/, the singer’s tongue should rest in a neutral positionwith the tip of the tongue lying against the back of the singer’s mandibular in-cisors. If the tongue pulls back or demonstrates obvious muscular activity asthe singer performs the scales, improper voice use can be confirmed by positiveevidence (Fig. 3). The position of the larynx should not vary substantially withpitch changes. Rising of the larynx with ascending pitch is evidence of techni-cal dysfunction. This examination also gives the physician an opportunity toobserve any dramatic differences between the qualities and ranges of the pa-tient’s speaking voice and the singing voice. A physical examination summaryform has proven helpful in organization and documentation [3].

Remembering the admonition not to exceed his or her expertise, the phy-sician who examines many singers can often glean valuable informationfrom a brief attempt to modify an obvious technical error. For example, de-ciding whether to allow a singer who has mild or moderate laryngitis to per-form is often difficult. On the one hand, an expert singer has technical skillsthat allow him or her to compensate safely. On the other hand, if a singerdoes not sing with correct technique and does not have the discipline tomodify volume, technique, and repertoire as necessary, the risk for vocal in-jury may be increased substantially even by mild inflammation of the vocalfolds. In borderline circumstances, observation of the singer’s techniquemay greatly help the physician in making a judgment.

If the singer’s technique seems flawless, the physician may feel somewhatmore secure in allowing the singer to proceed with performance commit-ments. More commonly, even good singers demonstrate technical errorswhen experiencing voice difficulties. In a vain effort to compensate for


dysfunction at the vocal fold level, singers often modify their technique inthe neck and supraglottic vocal tract. In the good singer, this usually meansgoing from good technique to bad technique. The most common error in-volves pulling back the tongue and tightening the cervical muscles. Al-though this increased muscular activity gives the singer the illusion ofmaking the voice more secure, this technical maladjustment undermines vo-cal efficiency and increases vocal strain. The physician may ask the singer tohold the top note of a five-note scale; while the note is being held, the singermay simply be told, ‘‘Relax your tongue.’’ At the same time the physicianpoints to the singer’s abdominal musculature. Most good singers immedi-ately correct to good technique. If they do, and if upcoming performancesare particularly important, the singer may be able to perform with a re-minder that meticulous technique is essential. The singer should be advisedto ‘‘sing by feel rather than by ear,’’ to consult his or her voice teacher, andto conserve the voice except when it is absolutely necessary to use it. Ifa singer is unable to correct from bad technique to good technique

Fig. 2. Bimanual palpation of the support mechanism. The singer should expand posteriorly

and anteriorly with inspiration. Muscles should tighten before onset of the sung tone. (From

Sataloff RT. Professional voice: the science and art of clinical care. 3rd edition. San Diego

[CA]: Plural Publishing, Inc.; 2006. p. 343–53; with permission.)

966 SATALOFF et al

promptly, especially if he or she uses excessive muscle tension in the neckand ineffective abdominal support, it is generally safer not to performwith even a mild vocal fold abnormality. With increased experience andtraining, the laryngologist may make other observations that aid in provid-ing appropriate treatment recommendations for a patient who is a singer.Once these skills have been mastered for the care of singers, applyingthem to other patients is relatively easy if the laryngologist takes the timeto understand the demands of the individual’s professional, avocational,and recreational vocal activities.

If treatment is to be instituted, making at least a tape recording of the voiceis advisable in most cases and essential before any surgical intervention. Theauthor routinely uses strobovideolaryngoscopy for diagnosis and documenta-tion in virtually all cases along withmany of the objective measures discussed.Pretreatment testing is extremely helpful clinically and medicolegally.

Additional examinations

A general physical examination should be performed whenever thepatient’s systemic health is questionable. Debilitating conditions, such as

Fig. 3. Proper relaxed position of the anterior (A) and posterior (B) portions of the tongue.

Common improper use of the tongue pulled back from the teeth (C) and raised posteriorly

(D). (From Sataloff RT. Professional voice: the science and art of clinical care. 3rd edition.

San Diego [CA]: Plural Publishing, Inc.; 2006. p. 343–53; with permission.)


mononucleosis, may be noticed first by the singer as vocal fatigue. A neuro-logic assessment may be particularly revealing. The physician must be care-ful not to overlook dysarthrias and dysphonias, which are characteristic ofmovement disorders and of serious neurologic disease. Dysarthria is a defectin rhythm, enunciation, and articulation that usually results from neuro-muscular impairment or weakness, such as may occur after a stroke. Itmay be seen with oral deformities or illness also. Dysphonia is an abnormal-ity of vocalization usually caused by problems at the laryngeal level.

Physicians should be familiar with the six types of dysarthria, their symp-toms, and their importance [38,39]. Flaccid dysarthria occurs in lower motorneuron or primary muscle disorders, such as myasthenia gravis and tumorsor strokes involving the brainstem nuclei. Spastic dysarthria occurs in uppermotor neuron disorders (pseudobulbar palsy), such as multiple strokes andcerebral palsy. Ataxic dysarthria is seen with cerebellar disease, alcohol in-toxication, and multiple sclerosis. Hypokinetic dysarthria accompanies Par-kinson disease. Hyperkinetic dysarthria may be spasmodic, as in the Gillesde la Tourette disease, or dystonic, as in chorea and cerebral palsy. Mixeddysarthria occurs in amyotrophic lateral sclerosis (Lou Gehrig disease).The preceding classification actually combines dysphonic and dysarthriccharacteristics but is useful clinically. The value of a comprehensive neuro-laryngologic evaluation [40] cannot be overstated. More specific details ofvoice changes associated with neurologic dysfunction and their localizingvalue are available elsewhere [41–43].

It is extremely valuable for the laryngologist to assemble an arts-medicineteam that includes not only a speech-language pathologist, singing voicespecialist, acting voice specialist, and voice scientist, but also medicalcolleagues in other disciplines. Collaboration with an expert neurologist,pulmonologist, endocrinologist, psychologist, psychiatrist, internist, phys-iatrist, and others with special knowledge of, and interest in, voice disordersis invaluable in caring for patients who have voice disorders. Such interdis-ciplinary teams have not only changed the standard of care in voice evalu-ation and treatment but also are largely responsible for the rapid andproductive growth of voice as a subspecialty.

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40 (2007) 971–989

Neurolaryngologic Evaluationof the Performer

Adam D. Rubin, MDa,b,*aLakeshore Professional Voice Center, Lakeshore Ear, Nose and Throat Center,

21000 E. Twelve Mile Road, Suite 111, Saint Clair Shores, MI 48081, USAbDepartment of Otolaryngology-Head and Neck Surgery, University of Michigan Medical

Center, 1904 Taubman Center, 1500 E. Medical Center Drive, Ann Arbor,

MI 48109-0312, USA

Innervation of voice and speech

The neuroanatomy of voice and speech is complex. An intricate neuralnetwork is responsible for ensuring that the larynx performs its mainfunctions: providing and protecting the airway, producing cough and Val-salva, and producing voice. The complexity is greater considering all ofthe other muscles of support and articulation that need to be coordinatedduring voice and speech production. Human beings have more voluntarycontrol over the laryngeal and articulating muscles than other animalspecies. Although more primitive visceromotor pathways are involved,particularly with more cathartic vocal functions, human voice productionis marked by greater cortical control [1]. As with other voluntary motorsystems, the neuromuscular pathway of voice and speech production in-volves upper and lower motor neurons, the basal ganglia and cerebellum,neuromuscular junctions, and the target muscle.

Central innervation

Uppermotor neurons relay signals from the cortex to lowermotor neuronsin the brainstem and spinal cord to initiate voluntary movement [2]. Numer-ous cortical areas contribute to vocalization. Some areas are excitatory,whereas others are inhibitory. Cortical input affecting vocal fold movementis bilateral, which is why a unilateral cortical injury seldom results in a com-plete vocal fold paralysis. There is hemispheric specialization with speech

* Corresponding author. Lakeshore ENT, Lakeshore Professional Voice Center, 21000 E.

Twelve Mile Road, Suite 111, Saint Clair Shores, MI 48081.

E-mail address: [email protected]




972 RUBIN

production, however, with the left primarymotor cortex playing amore dom-inant role [3,4]. The right motor cortex likely plays an important role in theprosody, or melody, of speech [5].

The cell bodies of the laryngeal nerves lie within the nucleus ambiguus inthe medulla. In addition to upper motor neuron input, these lower motorneurons receive input from other brainstem nuclei, including the nucleustractus solitarius and nucleus parabrachialis. This complex network of inter-connections integrates afferent input and modifies reflexes. Other synapsesoccur from neurons in the periaqueductal gray matter, the final pathwayof the visceromotor system, and are likely involved in the cathartic functionsof voice, such as during crying or screaming [1,4]. The lower motor neuron isthe final common pathway to the target muscle [1].

Extrapyramidal system

Upper and lower motor neurons are part of the pyramidal system andcontrol voluntary movement. The basal ganglia and cerebellum are partof the extrapyramidal system. The extrapyramidal system is important incontrolling gross motor function. It inhibits erratic movements and helpsmaintain muscle tone. The basal ganglia inhibit the rapid firing of motorneurons (the ‘‘release phenomenon’’). They receive input from most corticalareas and send output to areas of the frontal cortex involved with planningmovement. The cerebellum improves accuracy of movement by comparingcentral motor commands with sensory input from the periphery [2]. It islikely involved in vocal self-monitoring and fine-tune adjustments in pitchand airflow [1]. Neurodegenerative processes involving the extrapyramidalsystem may result in abnormal movement, such as tremor, dystonia, dysdia-dokinesia, as well as, abnormal muscle tone [2].

Peripheral innervation

The motor nerves (cranial and spinal) synapse at the motor endplate ofthe target muscle. This synapse is called the neuromuscular junction. Theneurotransmitter acetylcholine is released from the nerve terminal andtriggers an action potential, which results in muscle contraction.

The intrinsic muscles of the larynx are supplied by the recurrent (RLN)and superior (SLN) laryngeal nerves. The nerve fibers travel within the va-gus nerve through the jugular foramen of the skull base. The RLN branchesfrom the vagus within the superior mediastinum and loops around the aorticarch on the left and subclavian artery on the right. It travels back superiorlywithin or just lateral to the tracheoesophageal groove until it enters thelarynx posterior to the cricothyroid joint. The SLN branches off the vagusnerve just inferior to the nodose ganglion. The nodose ganglion containsthe sensory cell bodies of the SLN. The SLN travels inferiorly along theside of the pharynx, medial to the carotid artery, and splits into twobranches at about the level of the hyoid bone. The internal division of the

973NEUROLARYNGOLOGIC EVALUATION OF THE PERFORMER

SLN penetrates the thyrohyoid membrane with the superior laryngeal arteryand supplies sensory innervation to the larynx. The external division of theSLN provides motor innervation to the cricothyroid (CT) muscle.

The RLN innervates all of the intrinsic muscles of the larynx except the cri-cothyroid. These include the thyroarytenoid (TA), posterior cricoarytenoid(PCA), lateral cricoarytenoid (LCA), and interarytenoid (IA) muscles. Mus-cle innervation is unilateral except for the IA muscle, which receivescontributions from both RLNs [6]. The TA and LCA muscles are vocal foldadductors. Unilateral denervation of these muscles results in an inability toclose the glottis, with resulting breathy voice and possible aspiration [7].

The PCA is the main vocal fold abductor. Paralysis of this muscle resultsin an inability to abduct during inspiration. When both PCA muscles aredenervated, airway obstruction may occur. Denervation of the PCA maycause the arytenoid cartilage to subluxate anteromedially in unilateral vocalfold paralysis. The denervated PCA no longer counters the anterior pull onthe arytenoid cartilage by the vocal ligament [6,7].

The SLN branches from the vagus nerve just inferior to the nodose gan-glion, which contains the sensory cell bodies of the SLN. The SLN branchesinto an internal and external division. The internal division of the SLNpenetrates the thyrohyoid membrane with the superior laryngeal arteryand supplies sensory innervation to the larynx. The external division ofthe SLN provides motor innervation to the cricothyroid (CT) muscle. Un-opposed CT muscle contraction lengthens the vocal fold, increasing tensionand thus the fundamental frequency of the voice [7].

Although the intrinsic laryngeal muscles are classically described asabductors and adductors, their functions are more complex. Antagonisticmuscles contract simultaneously during normal vocal function. For example,unopposed TA contraction results in shortening of the vocal fold. It actssynergistically with the CT muscle to affect vocal fold tension [8]. CT musclefunction may also depend on the position of the vocal fold at the time ofcontraction. It may be active with some voice production regardless of pitchvariation. Different patterns of intrinsic muscle activation are seen dependingon the purpose of motion. For example, different muscles may be activated ordeactivated during adduction or abduction depending on whether the motionoccurs during cough, respiration, or voice production. TheCTmuscle is activeduring abduction with sniff, but not respiration [1,8].

Manifestations of neurologic disease

Neurologic disorders may affect voice and speech production in severalways. Central injury may affect initiation, coordination, and quality of voiceand speech. Direct effects on the larynx can affect glottic closure patternsand efficiency along with laryngeal muscle tone. Denervation of musclesinvolved in the support mechanism of the voice, such as the diaphragm orchest wall musculature, affects voice strength and quality. Dysfunction of

974 RUBIN

oropharyngeal musculature may affect resonance. A palatal paralysis resultsin a more hypernasal voice. Impairment of cranial nerve V, VII, or XII func-tion can affect articulation. Findings on general neurologic and laryngealexamination depend on which nerves are involved and where the disorderaffects the neuromuscular pathway (Table 1).

Motor neuron diseases

Motor neuron diseases may result from degeneration of upper motorneurons, lower motor neurons, or both. When both upper and lower motorneurons are involved, the diagnosis of amyotrophic lateral sclerosis (ALS)or Lou Gherig’s Disease is made [9]. ALS is fatal, usually from respiratoryfailure, but the clinical course is variable. Other examples of upper motorneuron disease processes include progressive lateral sclerosis and pseudobul-bar palsy. Primary lateral sclerosis typically involves destruction of uppermotor neurons only. The diagnosis is typically made after 4 years ofpredominantly upper motor neuron involvement [10]. Pseudobulbar palsyresults from interruption of bilateral corticospinal tract axons from otherdisease processes, such as stroke, multiple sclerosis, or tumor, as opposedto destruction of the neuronal cell body itself [11]. Patients who have pseu-dobulbar palsy often have inappropriate emotional outbursts. A pseudobul-bar palsy affect is often seen in patients who have ALS [12].

Lower motor neuron diseases include ALS, progressive bulbar palsy, andspinal muscle atrophy. Progressive bulbar palsy is essentially ALS affectingonly the cranial nerves. Progressive spinal atrophy includes several autoso-mal-recessive disorders that involve degeneration of the anterior horn cellsof the spinal cord. Although some forms present in adulthood, many presentin younger patients [9].

Table 1

Laryngeal and general findings of neurologic disease

Site of lesion General findings Laryngeal/speech findings

Upper motor neuron Spasticity, hyperreflexia,

rigidity, positive Babinski

sign, myoclonus

Spastic vocal fold paralysis/

paresis, spastic dysarthria,

laryngeal myoclonus

Lower motor neuron Weakness, flaccidity,

fasciculations

Flaccid vocal fold paralysis/

paresis, glottic insufficiency,

hypernasal speech, flaccid

dysarthria

Extrapyramidal Tremor (pill-rolling in

Parkinson’s disease),

dystonia, dyskinesia,

dysdiadochokinesia

Vocal fold bowing, mid-fold

insufficiency, tremor,

laryngeal dystonia,

dysdiadochokinesia

Peripheral nerve Weakness, atrophy, sensory

deficits

Hypomobility, immobility,

?atrophy (tone depends on

degree of reinnervation)

Myopathy Weakness, flaccidity Hypomobility, flaccidity


Physical findings differ between upper and lower motor neuron processes.Upper motor neuron findings include spasticity of musculature and hyper-reflexia. Spasticity of laryngeal musculature often results in a strained voicethat might be misconstrued as spasmodic dysphonia. Patients may sufferfrom intermittent laryngospasm. Spasticity of oral musculature results instrained, effortful dysarthria. Myoclonus may occur. Extremity involvementmay be noted. A positive Babinski reflex is a classic finding of upper motorneuron disease [9,11].

Lower motor neuron processes result in flaccid paralysis, muscle atrophy,and fasciculations. Patients may develop weak, breathy voices, bowing ofthe vocal folds, and poor cough. Palatal involvement may lead to nasalregurgitation and hypernasal speech. Pharyngeal musculature involvementleads to oropharyngeal dysphagia. Tongue and facial muscle involvementleads to slurred speech and oral dysphagia. With poor oral motor function,pharyngeal squeeze, and glottic incompetence, these patients are often atsignificant risk for aspiration [9,11,13,14].

Cerebrovascular accident

Cerebrovascular accidents may present with upper and lower motor neu-ron findings depending on the size and location of the stroke. Strokes mayresult from ischemia (secondary to thrombosis or hypotension) or hemor-rhage. Unilateral cortical strokes are unlikely to result in complete vocalfold paralysis because of bilateral cerebral innervation of the laryngealnerves. Brainstem stroke may cause vocal fold paralysis if disruption ofthe nucleus ambiguus or corticobulbar fibers synapsing with the nucleusambiguus occurs. Isolated vocal fold paralysis secondary to stroke is rare.Wallenberg syndrome or lateral medullary syndrome results from occlusionof the posterior inferior cerebellar artery. It may result in some combinationof vocal fold paresis or paralysis, decrease in ipsilateral facial pain and tem-perature, decrease in contralateral body pain and temperature, dysphagia,dysarthria, vertigo, Horner syndrome, ataxia, and hiccoughs [15]. Strokepatients often are debilitated, which also contributes to poor voice quality.Abnormal body positioning and strength contribute to vocal problems. Inaddition, these patients often have significant dysphagia and are at highrisk for aspiration pneumonia.

Extrapyramidal diseases

Diseases of the extrapyramidal system include Parkinson’s disease, spas-modic dysphonia, and laryngeal tremor. Parkinson’s disease is a movementdisorder resulting from degeneration of dopamine-secreting cells within thesubstantia nigra of the brainstem. This process results in loss of the neuralpathways through the basal ganglia that are involved in control of move-ment. Classic findings include tremor, rigidity, bradykinesia, and posturalinstability.

976 RUBIN

(Access Video on Parkinsonian Cogwheeling in online version of this article at: http://

www.oto.theclinics.com/.)

More than 70% of patients who have Parkinson’s disease have voice andspeech manifestations. Patients who have Parkinson’s disease often havesoft, breathy, monotonal voices. Laryngeal tremor is common. Patients of-ten perceive their voice as normal. Affect is often flat (‘‘masked’’). In addi-tion, patients who have Parkinson’s disease may have significant dysarthriaand dysphagia. Characteristic laryngeal signs include vocal fold bowing,glottic insufficiency, and slow vibration. The glottic insufficiency and poorbreath support attributable to debilitation and chest wall rigidity result ina soft, breathy voice quality [5,11,16–18].

Vocal fold paralysis should raise suspicion of a Parkinson plus syndrome,such as progressive supranuclear palsy, Shy-Drager syndrome, andmultisystematrophy. These disease processes are usually more rapidly progressing and lessresponsive to medication. In addition, patients who have multisystem atrophyare at risk for bilateral vocal fold paralysis and airway obstruction [11,18,19].

Spasmodic dysphonia

Spasmodic dysphonia (SD) is a focal dystonia the larynx. As with otherdystonias, it is characterized by involuntary muscle contractions or spasms.These spasms are task-specific. Adductory spasmodic dysphonia (AdSD)accounts for 80% of the cases of SD, with abductory (AbSD) and mixeddysphonias occurring less frequently. Patients who have AdSD have a char-acteristic strained/pressed quality to their voices.

(Access Video on Adductor Spasms in online version of this article at: http://www.oto.

theclinics.com/.)

They suffer voice breaks with voiced consonants. Patients who haveAbSD have spasms of the PCA muscle with voiceless consonants, resultingin intermittent breathiness [5,20].

(Access Video on Mixed adductor/abductor Spasms in online version of this article at:

http://www.oto.theclinics.com/.)

The pathophysiology of SD is uncertain. It may be attributable to dys-function of the laryngeal feedback systems resulting in disinhibition oflaryngeal muscle action [5,21]. Laryngeal tremor may be present in additionto the dystonia. The combination of tremor and dystonia is referred to asdystonic tremor. These entities can be difficult to distinguish at times [22].Spasmodic dysphonia might also be difficult to distinguish from muscletension dysphonia or other functional dysphonias.

Laryngeal tremor

Vocal tremor presents as nearly regular oscillations of the laryngeal andpharyngeal musculature.

http://dx.doi.org/10.1016/j.otc.2007.05.005

http://www.oto.theclinics.com/








(Access Video on Laryngeal Tremor in online version of this article at: http://www.oto.

theclinics.com/.)

The voice is unstable with frequent breaks. Tremor may be seen asa manifestation of several neurologic diseases, including Parkinson’s,ALS, and cerebellar diseases [23]. Usually other neurologic signs and symp-toms are present when a more severe neurologic disease is present. Tremormay also be seen with and is often difficult to distinguish from spasmodicdysphonia [22]. When laryngeal tremor is present, a thorough neurologicevaluation is required, with assessment of cranial nerve, extremity, and cer-ebellar function and gait.

When no other signs or symptoms are present, vocal tremor is usuallya manifestation of essential tremor, one of the most common causes of voicetremor. It may be the only manifestation, but typically the extremities areinvolved also. The voice is affected in approximately 20% of cases of essentialtremor [24]. In addition to the intrinsic laryngeal muscles, the extrinsic laryn-gealmuscles, pharyngealmuscles, andmuscles of respirationmay be involved.The pathophysiology of tremor is incompletely understood.Electromyographstudies have demonstrated that various laryngeal muscles may oscillate at dif-ferent frequencies, suggesting multiple foci of central stimulus, or peripheralcontribution to the oscillatory pattern by a reflex arc. In addition, there maybe different degrees of severity amongst each of the laryngeal muscles [25].

Myoclonus

Segmental myoclonus may occur within the pharynx and larynx. Typi-cally, involuntary, arrhythmic, jerk-like movements are seen. Usually it isbilateral, although it may occur unilaterally. Palatopharyngeal myoclonusmay produce slow, regular voice arrests that may be missed in runningspeech. It may also be triggered by speech and result in more rapid, dramaticvoice arrests [26]. Myoclonus is believed most commonly to arise fromdysfunction or lesions within the dentate, red, and inferior olivary nuclei.Unlike tremor, it typically does not involve opposing muscle groups.Myoclonus may be seen in neurodegenerative diseases [4,5,15,26,27].

Neuromuscular junction

Myasthenia gravis is an autoimmune disease characterized by muscleweakness exacerbated by repetitive use and improved with rest. Antibodiesare produced to the postsynaptic acetylcholine receptor at the neuromuscu-lar junction. Although ocular involvement is most common, laryngeal my-asthenia may present independently or in conjunction with other muscles[4,11,28].

Laryngeal finding are best appreciated with fiberoptic laryngeal examina-tions. Vocal fold fatigability with repetitive phonatory tasks is characteris-tic. Fluctuating movement asymmetry may be observed (one side appears




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to move more briskly and then appears more sluggish in comparison withthe contralateral side) [5,11,28]. Patients may also suffer from dysphagiaand dysarthria.

Peripheral nerve

Peripheral nerve injury, specifically to the vagus nerve or the recurrent orsuperior laryngeal nerve branches, typically presents with absent or sluggishvocal fold movement. Proximal vagal injuries may also present with palataland pharyngeal paralysis. Clinically, unilateral RLN paralysis typicallypresents as a breathy voice. Diplophonia and aspiration may occur [7].

Classically, paralysis of the SLN results in loss of a patient’s upper reg-ister [29,30]. Normally, the CT muscle contracts briskly in falsetto or modalphonation to increase tension in the vocal fold [31]. The inability to increasevocal tension results in poor vocal performance, especially at higher pitches[29,30]. The clinical manifestations specific to SLN paralysis are likely moretroublesome for singers and professional speakers [5,7]. Moreover, theinternal division of the SLN carries afferent fibers from the larynx to thecentral nervous system. This afferent input likely plays a role in vocalcontrol and modulation [8].

More subtle paresis of the SLN or RLN may cause numerous voicecomplaints, including vocal fatigue, hoarseness, impairment of volume,loss of upper range, loss of projection, and breathiness. Vocal fatigue maybe caused by the additional effort required to raise vocal pitch and project,and by hyperfunctional compensatory gestures. Patients who have eitherRLN or SLN paresis often develop a compensatory, hyperfunctionalMTD to generate a ‘‘stronger’’ voice [32].

Other symptoms may occur with injury to the vagus or the laryngealnerve branches. Hypoesthesia of the supraglottic larynx suggests injury tothe internal division of the superior laryngeal nerve and may cause intermit-tent choking symptoms. Hypoesthesia in addition to pharyngeal dysfunc-tion can place the patient at significant risk for aspiration [33,34].Neuralgia or paresthesia of the laryngeal nerves may also manifest as orcontribute to chronic cough, globus, or laryngeal pain syndromes [35,36].

Dysphagia often occurs with vocal fold paralysis and paresis. Patientsmay aspirate, particularly if there is significant pharyngeal involvement. In-jury to the SLN may result in dysphagia by several mechanisms. Injury tothe internal division results in loss of afferent input to the swallowing centerin the brainstem. In addition, recent evidence has suggested that the externaldivision of the SLN may supply innervation to the cricopharyngeus. Dener-vation may result in cricopharyngeal dysfunction and subsequent dysphagia[37].

Laryngeal findings usually depend on which nerves are involved and theseverity of injury. A vocal fold paralysis results in absent motion on theaffected side. Vocal fold paresis may be more subtle. Vocal fold lag, or


sluggishness, is the most common sign. This lag may only become apparentwith repetitive tasks that cause the patient to fatigue. Asymmetry in motionshould raise suspicion of a paresis, but does not always indicate whichnerves in particular are involved [38–40]. Supraglottic hyperfunction is oftenpresent in patients who have paresis and may make the examination moredifficult to interpret. Efforts to try to relax or ‘‘unload’’ the hyperfunctionmay help in determining which muscles are affected. Asymmetry may bepresent in patients who have muscle tension dysphonia without paresis.

Vocal fold tone is variable after injury to the recurrent laryngeal nerveand depends on the degree of reinnervation. Reinnervation prevents muscleatrophy. Spontaneous reinnervation may occur after nerve transection. Thesource of the reinnervation is not known, but may include regeneratingfibers from the transected RLN, the SLN, cervical autonomic nerves, andnerve branches innervating pharyngeal constrictors [41].

Should reinnervation occur after nerve transection, it is usually notdetectable for about 4 months [41,42]. The clinical course after 4 monthsis determined by the degree of reinnervation and synkinesis. Althoughreinnervation after a complete RLN transection prevents muscle wasting,typically it does not restore useful movement to the vocal fold because ofsynkinesis. Synkinesis results from nonselective reinnervation of adductorand abductor muscles. As a result, muscles that perform opposing functionscontract simultaneously, resulting in immobility or hypomobility of thevocal fold. The clinical picture depends on the proportion of adductorand abductor fibers reinnervated and the ability of the contralateral vocalfold to compensate by crossing the midline of the glottis [6,7].

Myopathy

Myopathies may be inherited or result from metabolic or inflammatoryprocesses [43]. Isolated laryngeal myopathy is rarely reported, althoughchronic steroid inhaler use has been insinuated as a cause [44]. Laryngealfindings include loss of muscle tone and hypomobility. These findings aresimilar to those that may be seen with motor neuropathy. Some have sug-gested that myopathy is underdiagnosed as a laryngeal disorder, becausewe tend to think more about nerve injuries when we see weak, flaccid vocalfolds [44].

Neurolaryngologic evaluation

A thorough neurologic evaluation should be routine for any patientpresenting with voice complaints. A thorough history should be performed,including presenting symptoms, rapidity of onset, progressive nature, andinciting or precipitating factors, such as a URI or neck surgery. Specificsabout the patient’s voice complaints should be elicited. For example, doesthe patient complain of raspiness, breathiness, loss of range, vocal

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instability, air hunger, or fatigability? Given the close interrelationship ofvoice, swallowing, and airway function, questions should address these is-sues also. Laryngospasm, although often caused by reflux, may also occurwith neurologic disease [45]. Patients should be asked about dysphagia,choking, cough, and airway obstruction. A complete neurologic review ofsystems and family history should be obtained.

The general appearance of the patient can give clues as to underlyingneurologic disease. Abnormal posturing, muscle tone, gait, and extremityor head tremor should be noted. Listening to voice and speech patterns iscritical. Dysarthria, or poor articulation, is an ominous sign of a central pro-cess. Abnormalities in voice quality should be noted, including voice breaks,spasms, spastic quality, breathiness, tremor, and pitch range. Attentionshould be paid to speech prosody.

Specific voice tasks may help distinguish pathology. For example,counting from 80 to 89 and 60 to 69 are good tasks for assessing for spas-modic dysphonia. Patients who have adductor SD have spasms inter-mittently during the voiced consonants of the 80 to 89 tasks, whereasabductory SD presents as breathy breaks during voiceless consonants ofthe 60 to 69 tasks. Mixed SD has intermittent spasms during both, whereasfunctional disorders are usually pressed through the entirety of each of thevocal tasks.

(Access Videos on Adductor Spasms, Mixed Adductor/Abductor Spasms, Supraglottic

Hyperfunction in online version of this article at: http://www.oto.theclinics.com/.)

These tasks should be attempted when no endoscopy is being performed,because distractions, such as endoscopy, often can suppress the spasms.Moreover, patients should be asked to sing and speak in a high-pitched‘‘Minnie Mouse’’ voice, which may help distinguish SD from functional dis-orders. Patients who have SD tend to have fewer spasms with caricaturevoicing and singing tasks [5,40].

A thorough head and neck examination should be obtained with partic-ular attention to cranial nerve function. Flaccidity of oral motor muscula-ture is a sign of lower motor neuron disease. Spasm of facial musculaturemay indicate upper motor neuron disease, a focal dystonia or other extrapy-ramidal process. A detached or flat affect manifested as limited facial expres-sion may also suggest an extrapyramidal process, such as Parkinson’sdisease [5,8,16,17].

Oral motor function should be assessed closely. The tongue should beinspected for atrophy, strength, ‘‘bag of worm’’ fasciculations, and symme-try in motion. Symmetry in palatal elevation and gag reflex should betested. Unilateral palatal paralysis suggests a high vagal lesion, whereasasymmetry in gag may suggest a glossopharyngeal nerve paresis. Palatalmyoclonus may be observed. Systemic neurologic examination should beperformed when there is suspicion of a more diffuse neurodegenerativeprocess.





Endoscopic visualization of the larynx is a critical part of the evaluationof any patient who has a voice complaint. A dynamic voice assessment isbest performed with a flexible rhinolaryngoscope to allow the patient tobe in as physiologic positioning as possible to evaluate the movements ofthe larynx and vocal tract during unaltered vocal posturing. Rigid videostro-boscopy is essential to look for vibratory abnormalities and to assessdiscrepancies in vocal process height. Protrusion of the tongue during rigidvideostroboscopy creates a nonphysiologic position for vocalization andtherefore is less useful at assessing for fine movement abnormalities of thelarynx than is the flexible rhinolaryngoscope.

The patient should be asked to perform various vocal tasks (Table 2) toobserve the movement of the vocal folds [8,38–40,46].

(Access Video on Normal Neurolaryngeal Examination in online version of this article at:

http://www.Oto.TheClinics.com.)

One should inspect for asymmetry in motion, hyperfunction, tremor,spasms, dysdiadochokinesia, and other irregular motions. Vocal fold pa-resis may be subtle. Rapid repetitive phonatory tasks are useful for elic-iting subtle vocal fold lag, which can be a sign of vocal fold paresis[7,38–40]. Repeated maneuvers alternating a sniff with the sound /i/ areparticularly helpful in unmasking mild PCA paresis. Repeated rapid pho-nation on /i/ with a complete stop between each phonation during thetask /i/-/hi/-/i/-/hi/-/i/-/hi/ frequently causes increased vocal fold lag,because the pathologic side fatigues more rapidly than the normal side.Having the patient repeat /pa/-/ta/-/ka/-/pa/-/ta/ka/-pa/ta/ka isanalogous to rapid alternating maneuvers performed in a general neuro-logic examination. It is useful for identifying dysdiadochokinesia, rigidity,and cogwheeling.

Table 2

Dynamic voice evaluation

Vocal task Findings

Count 1–10 in comfortable pitch range Symmetry, hyperfunction, aberrant motion

Count 1–10 in high pitch range Symmetry, hyperfunction, aberrant motion

Whistle ‘‘Yankee Doodle’’ Symmetry

Glissando Symmetry in longitudinal tension, rotation of

posterior larynx, vocal process levels

5 rapid sniffs Symmetry in PCA (abductor) function

Sniff-/i/-sniff-/i/-. Symmetry, fatigability, abductor and adductor

function

i/-/hi/-/i/-/hi/-/i/-/hi/. Symmetry, fatigability, adductor function

/pa/-/ta/-/ka/-/pa/-/ta/ka/-pa/ta/ka Dysdiadochokinesia, rigidity, cogwheeling

Singing, performing sample Manifestations and compensatory technique in

professional voice

Sustained /i/ under stroboscopic light Vocal process height, amplitude of wave, muscle

tonicity, presence of mass lesions


http://www.Oto.TheClinics.com

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(Access Video on Dysdiadokinesia and Parkinsonian Cogwheeling in online version of

this article at: http://www.oto.theclinics.com/.)

Vocal fold lag is sometimes easier to see during whistling, which may helpdistinguish lag resulting from a true paresis from asymmetry created fromsupraglottic muscle tension. The open laryngeal posture during whistlingprovides particularly good visibility of rapid vocal fold motions for easierassessment of asymmetries in vocal fold mobility [7].

A glissando maneuver, asking the patient to slide slowly from his or herlowest to highest note and then slide back down is invaluable for assessingSLN function. If a superior laryngeal nerve is injured, longitudinal tensiondoes not increase as effectively on the abnormal side, disparities in vocal foldlength are apparent at higher pitches, and the vocal folds may actually‘‘scissor’’ slightly, with the normal fold being higher. This height discrep-ancy is easier to observe with rigid videostroboscopy. The classic findingof rotation of the posterior larynx to the side of SLN injury is likely to occuronly with complete and isolated unilateral SLN paralysis [7,47].

The patient should also be asked to use the voice as he or she would in thework environment. Singers should be asked to demonstrate their vocalrange, whereas professional speakers or teachers should give a sample oftheir day-to-day vocal demands. This gives more insight to the patient’scapability of performing in the workplace and reveals how much he orshe is compensating to meet these vocal demands.

Other studies

Laryngeal electromyography

Laryngeal electromyography (LEMG) evaluates the integrity of thenerves and muscles of the larynx. Although its usefulness remains unprovenby evidence-based data, it remains the most objective means of evaluatingneuromuscular function of the larynx. In addition to identifying RLN orSLN paresis, it is useful for evaluating lower and upper motor neurondisorders, neuromuscular junction disorders, prognosis for recovery of vocalfold paralysis, differentiation of paralysis and arytenoid fixation, differenti-ation of malingering and psychogenic dysphonia, basal ganglia disorders,laryngeal dystonias and tremors, and myopathic disorders. Edrophoniumchloride may be administered to test for myasthenia. Repetitive nervestimulation and single-fiber EMG may also be useful [7,18]. For many ofthe neurodegenerative processes, EMG of other muscle groups (eg, tongue)may be helpful in establishing the diagnosis.

LEMG is useful for localization of specific muscles for injection of Botoxin the treatment of spasmodic dysphonia [43,48–54]. Diagnostic LEMGmaybe useful in helping to confirm the presence of dystonia and in identifyingwhich muscles are most involved [39]. Some have suggested its usefulness




for identifying muscles most affected by laryngeal tremor to target Botoxtherapy [25].

LEMG can confirm or refute clinical suspicions obtained from the phys-ical examination. Asymmetric vocal fold motion seen on flexible examina-tion may suggest the presence of a mild vocal fold paresis [38–40]. Even ifa paresis is present, however, the examiner might predict the nerve or sideinvolved incorrectly. A recent study by Rubin and colleagues [38] demon-strated that 25% of the time a unilateral mild paresis was suspected inpatients who had mobile vocal folds on endoscopic examination, laryngealEMG disagreed with the side of paresis predicted. In addition, in some casesin which the laryngeal examination was believed to be normal, LEMGdemonstrated bilateral paresis. The failure to predict paresis on examinationin these cases was likely because movement was fairly symmetrical becauseboth sides were affected [38]. Heman-Ackah and Barr found that LEMGagreed with the nerve predicted to be involved in only 64% of cases [39].In both of these studies, however, LEMG confirmed the presence of neurop-athy in more than 85% of suspected cases. LEMG is also useful in determin-ing site of lesion. Koufman and colleagues [51] reported on 50 patientswho had vocal fold paresis. They found 40% had both RLN and SLNinvolvement, whereas 60% had involvement of either the RLN or SLN.

LEMG can be helpful for management of patients who have movementabnormalities on examination. Voice therapy routines can be created tofocus on strengthening muscles specifically affected by the paresis. Forexample, for isolated SLN injury, exercises such as a glissando in thirdsor fifths can be performed to strengthen the cricothyroid muscles, takingcare to avoid compensatory hyperfunction in other muscles. Moreover,the information obtained can give clinical insight for surgical planning.For example, a patient who seems on examination to have a unilateralparesis may benefit from bilateral thyroplasty if a bilateral paresis is notedon LEMG. Also, one might choose to medialize a patient with injection lar-yngoplasty at the time of mass excision should the patient have significantparesis. By revealing an underlying neurologic problem, the LEMG maybring insight and comfort to a patient who eventually requires a surgicalprocedure for glottic insufficiency and to the voice team that has beenunable to remedy the problem with behavioral intervention alone [7,38].

Imaging studies

In a patient who has RLN injury, a CT scan with contrast from the skullbase through the mediastinum is essential. If the paralysis involves recurrentand superior laryngeal nerves or if there are other neurologic findings, intra-cranial studies should be considered as well. Because of the seriousness ofmissing intracranial lesions, many physicians obtain MRI with and withoutgadolinium of the brain and the path of the 10th cranial nerve in all cases.This practice certainly is not unreasonable. MRI of the brain may be useful

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if motor neuron disease or other central nervous system processes aresuspected.

Serology

Serologic testing may be appropriate in some cases. For example, ifmyasthenia is suspected one should order antiacetylcholine receptor, anti-striatal muscle, and anti– muscle-specific tyrosine kinase (MuSK) anti-bodies. Anti-MuSK antibodies are found in 40% of seronegative patientswho have myasthenia gravis. In these patients, weakness typically affectsneck and respiratory muscles [55]. Myasthenia symptoms may be isolatedto the larynx, but serologic tests are often negative.

Although the usefulness of serologic testing in patients who have vocalfold paralysis is controversial, certain tests may be useful, particularlywhen the history is suggestive. Some serologic tests to consider include:thyroid function tests, thyroid antibodies, autoimmune labs (eg, anti-nuclearantibodies, rheumatoid factor, erythrocyte sedimentation rate), tests fortertiary syphilis and Lyme disease, fasting blood glucose, cholesterol, andtriglycerides.

Flexible endoscopic evaluation of swallowing with sensory testing

Flexible endoscopic evaluation of swallowing with sensory testing(FEESST) is a useful tool for patients who have dysphagia in identifyingthe presence of laryngeal sensory deficits, evaluating aspiration risk, plan-ning swallowing therapy, and providing strategies to enable patients to eatthe least restrictive diet possible. Flexible endoscopic evaluation of swallow-ing (FEES) and modified barium swallow (MBS) are useful tools for evalu-ating swallowing physiology. Sensory testing, however, provides additionalinformation concerning sensory deficits that can contribute to dysphagiaand aspiration risk. Air pulses are delivered by way of a port in a flexiblelaryngoscope (or sheath over a flexible laryngoscope) to mucosa innervatedby the internal division of the superior laryngeal nerve. Sensory capacity ismeasured by thresholds required to elicit the laryngeal adductor reflex[33,34]. A randomized prospective study failed to demonstrate any signifi-cant difference in outcomes of dysphagia patients managed with FEESSTor MBS. In stroke patients managed by FEESST, however, the incidenceof aspiration pneumonia was significantly lower than in those managed byMBS [56].

Voice laboratory

Computerized voice analysis can help distinguish between some neuro-logic processes and is a useful tool for analyzing effectiveness of treatment[22]. In addition, a recent study in our voice laboratory demonstrated that


electroglottography (EGG) can help in the evaluation of suspected paresisto determine if LEMG is warranted in patients who have asymmetric butmobile vocal folds. More than 90% of patients who had a normal EGGwaveform despite asymmetry in vocal fold motion had a normal LEMG.A normal EGG waveform thus had a negative predictive value of greaterthan 90%, suggesting LEMG would be low yield in such patients [57].

Considerations for the performer who has neurolaryngologic issues

The performer likely is more sensitive to vocal changes than others whoselivelihood is not so dependent on their voices. As a result, the performerwho has early underlying neurologic disease may present to the laryngolo-gist before presenting to the neurologist. The laryngologist therefore hasto be aware of the vocal manifestations of neurologic disease. Unfortu-nately, other manifestations of the disease may become of higher priorityfor the patient’s well-being, but vocal problems are still likely to weighheavily on the performer’s mind and quality of life.

Performers who have vocal fold paralysis may need urgent interventionto help them return to work. Early voice therapy is important to avoidthe development of hyperfunctional compensatory habits that could bedifficult to break if nerve function returns. In some cases, voice therapycan provide enough improvement in the voice that surgery can be avoided.Injection laryngoplasty is an excellent option when it is unclear if nervefunction will return. Extra care must be taken to avoid superficial injectioninto Reinke space, which impedes mucosal wave and delays vocal optimiza-tion. Laryngeal framework surgery is appropriate after 1 year from time ofinjury or if nerve recovery is not expected (eg, after nerve transection).Expectations should be tempered depending on the vocal demands ofeach individual patient.

The best treatment of vocal fold paralysis is prevention. Performers con-templating thyroid or cervical spine surgery in cases without absolute indi-cations need to be clear about the risk for voice change after surgery (even ifthe nerve is not transected). For instance, the soprano who has a thyroidnodule of borderline size and indeterminate fine needle aspiration (FNA)might want to follow the nodule clinically before proceeding to hemithyroi-dectomy. Obviously, one should not risk missing a malignancy, but all thepotential risks need to be weighed and presented to the patient so that heor she can make the best informed decision possible.

Treatment of the performerwhohas a subtle vocal fold paresis ismore com-plex, particularly if the performer is able to obtain glottic closure. Voice com-plaints are oftenmultifactorial andnonspecific. It is often difficult to be certainthat even if a paresis is present, it is the cause of the problem. Perhaps the pa-resis has been there for years and another insult (eg, reflux) has caused the pa-tient to become symptomatic. The same is true for a small mass on the vocalfold of a performer. Performers seldom have baseline examinations (when

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they are not having problems) for comparison. If one excises a mass beforetreating all other potential contributing factors, one risks making the voiceworse. The same is true when approaching a suspected paresis.

History is helpful, but still not always completely enlightening. Forinstance, voice change after thyroid or neck surgery without any evidenceof mucosal or vibratory abnormality is likely caused by nerve injury. Thesame could be said for symptoms starting after an upper respiratoryinfection [32]. Unfortunately, evaluation often reveals other pathology,such as edema or a mass. Conservative management, particularly in subtlecases, is always wise. Voice therapy and treatment of all possible contribut-ing factors, (eg, reflux, allergies) should always be attempted before consid-ering surgical intervention. Some performers want earlier intervention andmore immediate effects, however, to meet their obligations.

The future

Current treatment options for vocal fold paresis, paralysis, and otherneurologic disorders are suboptimal. We still are unable to restoremovement to the paralyzed vocal fold. Ideal treatment of many neurodegen-erative disorders needs to address neuronal preservation and regeneration.Techniques such as stem cell implantation and gene therapy are promising[58–60]. The issue of synkinesis offers additional challenges for restoringuseful vocal fold motion after paralysis. Innovative techniques have beensuggested, but most have not been proven effective in clinical practice[61]. Laryngeal pacing holds some promise [62–64].

Summary

A thorough neurolaryngologic evaluation is important for the assessmentof any patient who has voice complaints. Voice changes may be the initialpresentation of neurologic disease. The otolaryngologist must be familiarwith laryngeal neuroanatomy and laryngologic manifestations of neurologicdisorders. Collaboration with a neurologist is essential when systemic orcentral neuromuscular disease is suspected. The otolaryngologist can playan important role in the care of patients who have voice, swallowing, andairway issues resulting from neurodegenerative disease.

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40 (2007) 991–1001

Strobovideolaryngoscopyand Laboratory Voice Evaluation

Scott M. Kaszuba, MD, C. Gaelyn Garrett, MD*Department of Otolaryngology, Vanderbilt Voice Center, Vanderbilt University,

7302 Medical Center East, South Tower, 1215 21st Avenue South, Nashville,

TN 37232-8783, USA

Although some laryngeal abnormalities affect the true vocal folds inknown manners, not all patients who have the same vocal pathology exhibitthe same subjective complaint, clinical finding, or physiologic impairment.There is no single best method of laryngeal examination for all voice pa-tients. One notable limitation of simple indirect laryngoscopy is that the ex-amination does not yield a recordable and reproducible image of the larynxand vocal tract. More importantly, the unaided human eye is unable to vi-sualize the vibratory patterns of the true vocal folds during phonation. Thisinadequacy may lead to inappropriate management decisions. Strobovideo-laryngoscopy and laboratory vocal testing are most valuable to the voicespecialist in this clinical scenario [1,2].

Recognition of the advantages and disadvantages of current diagnostictechniques allows for optimal appreciation and instrumentation selectionfor supplemental diagnostic laryngeal testing. Although it is agreed thatthere is no one gold standard algorithm for the diagnostic process of a pa-tient who has a voice disorder, most practitioners would agree that someadditional laboratory testing is indicated in most patients. This articlediscusses current diagnostic techniques available for physiologic vibratorytesting and anatomic and functional assessment of the vocal tract.

Strobovideolaryngoscopy

True vocal fold vibration is a complicated physiologic function, the ob-servation of which far outreaches the visual capabilities of the human eyewith a normal light source. The human adducted vocal folds cyclically


E-mail address: [email protected] (C.G. Garrett).




992 KASZUBA & GARRETT

open and close between 60 to 1500 times per second, depending on the pho-natory pitch. Stroboscopic light visually makes the vocal fold vibrations ap-pear to slow down so that the impression of vocal fold vibrations can beobserved and processed. Stroboscopy capitalizes on the inherent optic prop-erties of our visual organ and exploits the limitations of observation of theunaided eye. According to Talbot’s law, the human eye can perceive nomore than five distinct images per second. Each image therefore lingerson the retina for approximately 0.2 seconds after exposure. Stroboscopicflashes make the vocal folds appear to slow down by advancing the lightpulse through successive glottal cycles in percentage increments. Individualstill images are recorded at selected points from sequential vibratory cyclesand the human eye automatically fills in the missing pieces by fusing the im-ages into what it sees as motion. This apparent motion is attributable toa phenomenon called persistence of vision. Additional instrumentationadded to the stroboscopic light can facilitate the recording and documenta-tion of the perceived vocal fold vibratory properties [2–4]. Strobovideolar-yngoscopy as a whole allows the physician to observe important vocalfold activities, which allows appropriate diagnostic decision making.

A brief historical overview allows full appreciation of the evolution of stro-bovideolaryngoscopy. Indirect laryngoscopy was first described, but not yetpopularized, by Bozzini in 1806 when he constructed an angled speculumwith a mirror insert that was meant to examine various body cavities, includ-ing the human larynx. It was not until 1854 that indirect laryngoscopy gainedwider acceptance when Manuel Garcia, a Spanish-born voice teacher who hada limited gag reflex, first visualized his larynx with a small dental mirror usingsunlight as a light source. In 1895, Oertel followed suit and was credited withcreating the first laryngostroboscope. His device consisted of a variable-speedperforated disc that was interspersed between a light source and the practi-tioner’s head mirror [5,6]. Since that time, strobovideolaryngoscopy hasevolved into finely controlled, high-intensity light sources with fiberoptic endo-scopes or distal camera scopes coupled with analog or digital recordingdevices.

Strobovideolaryngoscopy in current clinical practice relies on a combi-nation of several instruments: a stroboscopic light source, an endoscope,a microphone, a video camera, a recording device, and a video monitor.Stroboscopy is best performed in conjunction with video recording and ar-chiving for complete clinical review and documentation. The examinationmay be performed by transnasal flexible laryngoscopy with distal chip tech-nology or perorally with a rigid angled telescope. Video cameras are nowavailable in single-chip and three-chip versions. A single-chip camera usesa single array of light-sensing elements known as charge couple devices(CCDs). Three-chip cameras use a dichroic prism, which divides the incom-ing images into the three primary colors and offers more accurate color andhigher resolution. Analog or digital recording technologies are then used forimage capture, documentation, and reproduction [3,7].

993STROBOVIDEOLARYNGOSCOPY AND LABORATORY EVALUATION

The illusion of apparent slow motion of the vibrating vocal folds duringstrobovideolaryngoscopy evolves from the collection of several sequentialstill images of the folds at selected time intervals during repeated glottal cy-cles at a given vibratory frequency. This illusion is called the stroboscopicglottal cycle and can be of any desirable duration. In addition, the strobo-scopic flashes can be emitted either at the same frequency as phonation,known as synchronization, or at a slight variation of the frequency, knownas asynchronization. This feature of stroboscopy is producible through tech-nological communication between the microphone and the strobe lightsource. By synchronizing the stroboscopic flashes to the fundamental fre-quency of the vibrating vocal folds, a perceptual stopped image or standstillof the vocal folds is produced. An asynchronized mode is generated by cal-ibrating the stroboscopic flashes at a consistent frequency slightly differentthan the produced phonatory fundamental frequency. This variation allowssuccessive light impulses to strike at different phases of the vibratory cycleand produce a video image of one apparent cycle of vibration actually ob-tained from different portions of several cycles. Another option, which al-lows the examiner to manipulate the apparent glottal cycle by operationof a rocking foot pedal, furthers the stop-action capability of the strobovideo-laryngoscopy system. This feature is particularly useful when the exact loca-tion of the vocal fold lesion is being determined in relation to movement ofthe upper and lower lips during an approximation phase of the cycle [2,3,7].

The strobovideolaryngoscopic examination is most clinically useful to thepractitioner when a standard protocol is used for the acquisition of the dataand its interpretation. Phonatory tasks during the examination should beperformed at low, normal, and high pitches and in the range of the speakingor singing problem area, if known. Once recorded, a standardized approachto the interpretation of the examination allows consistency in diagnosingand comparing laryngeal pathology. Once the initial examination is com-pleted and recorded, additional repeat testing at predetermined time inter-vals allows for evaluation of response to treatment. Although there isarguably no one gold standard for the interpretation of a strobovideolar-yngoscopic examination, several aspects of the examination are often rated.The specific features of the vibratory pattern of the true vocal folds oftenaddressed include symmetry, periodicity, mucosal wave ratings, amplitudeof vibration, shape and contour of the glottal margin, and glottic closure.Particular attention is also given to any adynamic segments and the presenceor absence of vertical phase difference [2,6,7]. Vocal fold symmetry remainsintact in the absence of abnormalities along the glottal margin. Periodicityrefers to the regularity of the vibratory cycles with the idea that normal vo-cal folds should vibrate in mirror image to each other and vibrate the samewith successive cycles. Aperiodic vibrations may prohibit the synchroniza-tion of the strobe light. The mucosal wave is generally described as the trav-eling wave across the vocal fold superior surface from medial to lateral.Abnormalities of the mucosal cover, including the epithelial layer or


superficial lamina propria, are the most common causes of mucosal wave re-duction. The mucosal wave should be differentiated from the vertical phasedifference, which is created normally by the presence of an upper lip andlower lip at the medial vibratory vertical closing surface. Amplitude of vi-bration is a relative feature of the mucosal wave judged by the trained ob-server as reduced, normal, or excessive. Normal variations in amplitudeoccur with changes in vocal intensity. Glottal closure is described as com-plete; incomplete with anterior, mid, or posterior glottal chinks; and hour-glass, usually secondary to mid-vocal fold lesions.

From a clinical standpoint, strobovideolaryngoscopy has proved to bea valuable tool for the diagnosis of laryngeal pathology given the detailedphysical examination it provides of the vocal tract and the vibratory marginof the vocal fold. Stroboscopic features of nodules, for example, often in-clude symmetric but reduced amplitude of vibration, maintenance of period-icity, intact mucosal waves, and hourglass closure. Vocal fold polyps, whichare frequently unilateral, have asymmetric vibration and variable periodicitydepending on the size and shape of the polyp. Mucosal wave can be absentbecause of mass effect with large polyps or intact with broader-based polyps.The wave is generally intact on the contralateral side. Glottic closure is un-derstandably asymmetric. Cysts within the vocal fold lamina propria canhave the greatest adverse effect of the nonneoplastic lesions on the vibratorycharacteristics. Mucosal wave is frequently absent and aperiodic if present.A change in diagnosis and altered assessment of vocal pathology based onthe strobovideolaryngoscopic findings can occur in 10% to 30% of cases[4,8]. Furthermore, abnormal findings have been reported in up to 58% ofhealthy, asymptomatic professional singers stressing the importance ofscreening examinations for certain populations of patients [9].

Strobovideolaryngoscopy is not a test to be done in the absence of otherclinical data. It is only a valuable complement to a thorough vocal historyand physical examination. The technique inherently suffers from the limita-tion of being a composite recording made from several glottal cycles, in con-trast to high-speed photography or high-speed digital video, which recordsan entire vibratory cycle and provides detailed cycle-to-cycle variations.Even with this limitation, strobovideolaryngoscopy remains an invaluabletool in the diagnostic armamentarium of the voice specialist.

Glottography

Glottography is a general technique that monitors the vibration of thevocal folds by the transmission of a probe signal from one side of the larynxto the other. The probe signal itself can be directed in either a vertical planeor horizontal plane. Current probing signals most commonly used in glot-tography include electrical current flow, light transmission, and ultrasonicwaves. The time variation of the glottis combined with laryngeal tissues


that are in constant partial stages of contact during phonation modulatesthe probe’s properties. This modulation is then detected and recorded sup-plying immediate objective data in the form of graphic displays that can beclinically interpreted. Glottography thus makes possible the physical mea-surement of acoustic parameters, such as pitch, jitter (frequency perturba-tions), shimmer (amplitude perturbations), or other perturbations. It alsoprovides a possible objective method that can be used to evaluate and detectvocal fold pathology. Overall, glottography provides some clinical dataabout vocal fold vibration. This technique fails to determine the vibrationcapacity of an individual vocal fold or diagnose individual laryngeal lesionswithout an additional visual examination [10,11].

Electroglottography

Electroglottography (EGG) is a technique based on the principle that hu-man tissue can conduct an electrical current with laryngeal tissues beinga moderately good conductor of electricity. It is performed by placing twoelectrodes above the thyroid laminae on the external neck and measuringthe impedance between them with a high-frequency, low-current signal.Ohm’s law states that a current must flow through a system if its resistanceis to be measured. Based on this law, when the vocal folds are touchinga greater current flows through them compared with when they are open.The electroglottographic signal represents the contact area between thetwo vocal folds and can be used to determine when the vocal folds are closedand how fast they are closing [10–13]. This characteristic contrasts with pho-toglottography (PGG), which gives information about the separation of thevocal folds and little information about the nature of vocal fold contact.

Various manufacturers provide instrumentation that produces, records,and displays the electroglottographic signal. Several authors over the pasttwo decades have commented on the shape of the EGGwaveform as it relatesto the underlying physiology of vocal fold vibration. Interpretation of EGGwaveforms remains controversial, however, especially as it relates to analyzingvocal fold pathology. When used in conjunction with other laboratory tech-niques, the interpretation of the EGG display becomes more reliable. For ex-ample, synchronized strobovideolaryngoscopy and EGG have been shown tobe an effective tool for verifying information from the EGG waveform withstroboscopic images [12,14]. Also, recent research is moving toward standard-ization of normal EGG measurements with the goal of allowing this test toserve as a reference for the diagnosis and follow-up of dysphonic patients [15].

There are limitations of EGG.Themost obvious one for the voice specialistis that it cannot be used with all dysphonic subjects. Patients who have a uni-lateral vocal fold paralysis have a considerably diminished or absent signalbecause of lack of good contact of the vocal folds. Obese or thick necksmay impede proper placement of the electrodes or hinder the electrical currentresulting in a poor EGG tracing. Finally, severe hoarseness may render


laryngeal tissue irritable and passing an electrical current through this envi-ronment may produce an undesirable physiologic response [10,13].

Photoglottography

Photoglottography is a technique that estimates glottal area during pho-nation. The principle of PGG is based on the concept that the glottis mayact like a shutter through which light can pass in proportion to the degreeof opening of the vocal folds. Light is usually directed transnasally fromabove the glottis and is detected by an optoelectronic device over the skinof the trachea immediately beneath the vocal folds. The external photosen-sor then converts the light intensity absorbed into electric voltage, which canbe recorded and converted into a graphic display. The direction of the lightpath during the study has no impact on the ability to record the PGG signal;therefore the light source may be placed above or below the glottis or on theexternal neck with the photosensor in the opposite complementary position.Typically, for the best functional examination with the additional advantageof simultaneous laryngeal observation, a transnasal flexible laryngoscope isused as the light source with the photosensor placed externally on the neck.

PGG gives some clinical data during the open phase of phonation withtwo common measurements routinely obtained. The speed quotient mea-sures the symmetry of the opening and closing parts of the open phase,and the open quotient is the time of the open phase of the vocal folds di-vided by the total period of vibration. Some problems may exist with thevalidity of the quantitative information obtained from this technique. Theseare most often believed to be attributable to several extrinsic factors, includ-ing inability to standardize the amount of light projected on the larynx,changes in light-transmission characteristics of the glottis because of its ver-tical movement during phonation, and volume changes of the hypopharynxand supraglottis during different vowel productions. Overall, the PGGwaveform is considered complementary to the EGG signal [10,11,13].

Ultrasound glottography

Ultrasound glottography (UGG) is a technique in which ultrasonic wavesare constantly applied across the laryngeal area of the neck during phonation.The border between the vocal fold surface and the glottal air is determined bythe difference in acoustic impedance between two media (air and soft tissue).Like all ultrasound studies, it is based on the frequency shift produced whena continuous ultrasonic beam is reflected back from or transmitted througha tissuemedium. InUGG, a narrow-beam ultrasound transducer is placed ex-ternally on one side of the neck near the larynx with a receiver on the otherside. The ultrasonic signal is aimed at the air tissue interface of the glottis.


Air is an extremely poor ultrasound transmissionmedium and therefore whenthe glottis is open the ultrasonic beam is not transmitted across it to the re-ceiver on the opposite side of the neck. This continuous wave glottographythen displays an open–closed pattern that corresponds to the open and closedphases of phonation. Unfortunately, the space resolution of ultrasound glot-tograms is not very high and therefore few reports are available regardingvoice function. Nonetheless, it remains a noninvasive means of laryngealmonitoring and combined with newer technological advances may holdpromise for future clinical voice research [10,11,13].

Videokymography

Videokymography is a laboratory technique that was developed asa means of using television technology to visualize real-time vibratory acti-vities of a small area of the glottis. This visualization is accomplished by us-ing a line scan camera that is capable of limiting its entire field of view andscanning of the endoscopic image to a rapid repetition of a single line. Eachnew scan of the same line is stacked on top of the others from superior toinferior so that a screen image is built up with time represented in thevertical direction. The line scan camera therefore records a small area ofthe vocal fold in a real-time fashion while it vibrates and allows for subtleaperiodic irregularities or phase asymmetries to be observed and doc-umented. A major shortcoming of this technique is that any movementof either the larynx or endoscope during signal acquisition changes the locusbeing observed. Also, the line image produced is not a complete image of thelarynx. Some training is also required for interpretation of the examinationresults. Although still regarded as mainly an experimental technique forlaboratory voice testing, new generation digital videokymographic systemsare currently being developed in hopes of becoming an important tool forroutine clinical laryngeal examination [10,16,17].

High-speed photography and digital imaging

High-speed photography and digital imaging are laboratory techniquesthat were developed to overcome the limitations of strobovideolaryngoscopy.As previously discussed, stroboscopy is a technique that produces a virtualslow-motion image of the larynx from the summation of images obtainedfrom several glottal cycles. The clinical use of this technique is based on vocaltract pathology being periodic and stable at a given phonatory frequency.Dysphonic patients suffering from aperiodic phonatory disorders may notcompletely benefit from the examination, therefore. High-speed photographyand digital imaging overcome these limitations by providing real-time imagesof successive glottal cycles of the larynx during phonation.


High-speed photography requires several expensive pieces of equipmentthat require technical expertise for proper operation. The main piece ofequipment is a camera capable of taking pictures at a rate of 3000 to4000 frames per second. The recorded events are then viewed back and an-alyzed in ultraslow motion. The technique itself requires that dysphonic pa-tients be able to position themselves over a laryngeal mirror during thecamera recording, which is not always tolerated well. This technical diffi-culty combined with increased cost and time expenditure necessary to com-plete the examination have limited its clinical use. Nonetheless, high-speedphotography using a laryngeal mirror has provided valuable informationabout vocal function when used in a clinical setting.

High-speed digital imaging has seen recent activity over the last severalyears with the development of new camera image sensor systems with in-creased image resolution combined with improved computer processingspeed and storage capacity. The technique uses standard rigid endoscopesto record full images of the superior surface of the larynx at sampling ratesfrom 1000 to 8000 frames per second. The recorded images are typically inblack and white and can be played back in ultraslow motion for clinicalanalysis. The current cost of the equipment has still limited its use as a rou-tine clinical examination conducted by the voice specialist.

Limited availability of this equipment in the clinical setting has resulted infew studies being performed regarding the application of this modality in di-recting patient care. From a research standpoint, high-speed digital imaginghas been used to identify characteristics of normal and abnormal vocal foldvibration. Digitization of the images enables accurate quantification of vocalfold vibrating parameters not possible with strobovideolaryngoscopy. High-speed digital imaging has also been used to examine the basic physiology ofdifferent singing styles, in the assessment of vocal tremor, and in the differen-tiation of spasmodic dysphonia from muscle tension dysphonia. Some re-searchers have combined the technique with a laser calibration tool forestimated measurements of glottal parameters, including scarring and otherelastic properties of the vocal folds [18,19]. Further development of this tech-nology may lead to a better understanding of vocal fold elasticity measure-ments and possibly direct the development of new laryngeal injectionmaterials. More widespread clinical use of high-speed digital imaging in thefuture is expected as the cost of the instrumentation decreases.

Acoustic voice measurements

Phonatory tasks for normal and dysphonic patients may be obtained forobjective voice analysis. Speech samples obtained typically consist of sus-tained vowel phonation, reading, and conversational speech. Measured pa-rameters can include fundamental frequency, maximum phonation time,vocal intensity, harmonics-to-noise ratio, jitter, and shimmer. These objec-tive measurements have been used in numerous clinical settings to compare


pretreatment to posttreatment phonatory characteristics after a specific sur-gical or nonsurgical intervention has been performed by the voice specialist.

Several commercially available pitch meters/analyzers are available to thevoice specialist, including the VisiPitch (Kay Elemetrics Corporation) in-strument. This equipment is most useful for obtaining fundamental frequencyand vocal intensity and can provide othermeasures of speech parameters also.In addition, numerous computer programs, some used in conjunction withstrobovideolaryngoscopy, also exist. Computerized Speech Lab (CSL, KayElemetrics Corporation, Lincoln Park,New Jersey), CSpeech, andDr. SpeechScience (Tiger Electronics, Seattle, Washington) run on PC-compatible com-puters. MacSpeech Lab is available for the Macintosh computer. These pro-grams provide a multidimensional voice analysis of the above-mentionedparameters and are relatively simple to use. Research suggests that althoughthese systems are not necessarily comparable in absolute figures, their judg-ment against normative data is typically similar. Ambulatory monitoring ofthe dysphonic patient in the form of miniature accelerometers placed on theanterior neck has also been reported andmay show future promise in the clin-ical assessment and management of voice disorders [13,20,21].

Speech spectrograms represent ameasure of the vibratory characteristics ofthe vocal folds and the vocal tract. They are useful for analyzing and display-ing changes in the spectral characteristics of vocal fold sound. Care must betaken to use the same vowel while comparing spectrograms of a patient toeliminate the vocal tract as a variable and therefore allow independent analy-sis of the vocal folds. The most useful measure from a speech spectrogram isthe harmonics-to-noise ratio (signal-to-noise ratio). It represents a ratio of theenergy in the harmonics of the vocal signal against the noise energy in the sig-nal. Dysphonic voices exhibit a greater noise signal and therefore the ratio isdecreased when compared with normative data. The computer software pro-grams previously mentioned produce good-quality speech spectrograms. Ad-ditional instrumentation may obtained by the voice specialist to producehigher-quality spectrograms at a greater expense [13].

Perturbationmeasures rely on the inherent ability to determine an accuratefundamental frequency and are usually measured using sustained vowel frag-ments.Dysphonic voice samples are often onlymarginally periodic at best andare often difficult to obtain. Furthermore, most dysphonias are multifactorialin nature and often times show variability at different points in a patient’s vo-cal range. Connected speechmay overcome some of these obstacles and there-fore be a more appropriate stimulus for the dysphonic patient because it ismore representative of functional vocal productions over a broader vocalrange. An inherent difficulty with the analysis of connected speech by typicalperturbation methods as previously mentioned is that these measures areinfluenced by intonation and other modulation effects. Long-term averagespeech spectrum (eg, spectral tilt) and derivations of the spectrum such ascepstral peak prominence overcome these difficulties. These measures donot rely on determination of fundamental frequency and are not confounded


by variables such as recording technique and recording volume. Several au-thors have noted that measures of the cepstrum, a Fourier transformationof the spectrum of the signal, better correlate with perceptual measures ofoverall dysphonia compared with more traditional measures of periodicityor perturbation [22]. Special software is needed to complete these measuresand currently is not available in any commercial software program [23,24].

Vocal quality-of-life measures

The degree to which a dysphonia impacts a patient’s day-to-day activities isoften difficult to measure. Factors such as the severity of the voice disorderand the vocal needs of the patient are central to the determination of howthe dysphonia alters his or her physical, social, and emotional well-being.Two well-known instruments that quantify the psychosocial consequencesof voice disorders are the Voice-Related Quality of Life Measure and theVoice Handicap Index. Both instruments have been shown to be valid andreliable as a vocal quality-of-life measure [25,26]. They allow for subjectiveperceptual analysis of a given clinical intervention by the voice specialistand are a low burden in a population of patients who have a diverse groupof voice disorders [27]. One drawback of all outcome instruments fordysphonia is the large number of questions that need to be answered to receivea complete score. Recently, the development and validation of the VoiceHandicap Index-10 has been introduced as one instrument that may decreasethis burden [28]. Overall, outcome instruments for vocal quality of life areimportant indices of patient functional capacity that enhance the voicespecialist’s ability to successfully treat patients who have voice disorders.

Summary

Laboratory and strobovideolaryngoscopy voice evaluation are importantparts of the clinical work-up of the dysphonic patient. When selected appro-priately with appreciation of their limitations, the techniques discussedafford the voice specialist the opportunity to make informed diagnosticdecisions and improve the overall quality of care delivered.

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40 (2007) 1003–1023

Laryngeal Electromyography

Yolanda D. Heman-Ackah, MDa,*,Steven Mandel, MDb, Ramon Manon-Espaillat, MDb,Mona M. Abaza, MDc, Robert T. Sataloff, MD, DMAa

aDepartment of Otolaryngology–Head and Neck Surgery, Drexel University College

of Medicine, 1721 Pine Street, Philadelphia, PA 19103, USAbDepartment of Neurology, Thomas Jefferson University, Jefferson Medical College,

Philadelphia, PA, USAcDepartment of Otolaryngology, University of Colorado School of Medicine,

Denver, CO, USA

Laryngeal electromyogragphy (LEMG) is an invaluable adjunct to lar-yngologic assessment, diagnosis, and treatment of voice disorders. It iseasy to perform, well-tolerated, and presents minimal risks to patients. Itis useful in the evaluation of numerous laryngeal disorders, allowing clini-cians to differentiate among upper motor neuron, lower motor neuron, pe-ripheral nerve, neuromuscular junction, myopathic, and mechanicaldisorders. It is also useful in establishing prognosis in laryngeal nerve palsiesand for guidance during the injection of botulinum toxin in the treatment ofspasmodic dysphonia. Judgements regarding when to use LEMG, selectionof muscles to be studied, and the choice of EMG techniques depend upona comprehensive history and physical examination. LEMG requires expertinterpretation, taking the clinical scenario into account. A skilled electro-myographer is an immeasurable asset to the voice care team.

Basic neurophysiology

The interior of a muscle or nerve cell is electrically negative with respectto its exterior [1–3]. This electrical potential difference is called the restingmembrane potential. In muscles it is on the order of 90 millivolts; for lower

This article is modified from: Sataloff RT, Mandel S, Heman-Ackah Y, et al. Laryngeal

electromyography. 2nd edition. San Diego (CA): Plural Publishing, Inc.; 2006. p. 47–101;

with permission.


E-mail address: [email protected] (Y.D. Heman-Ackah).




1004 HEMAN-ACKAH et al

motor neurons it is about 70 millivolts. The resting membrane potentialreflects the ionic gradient of the cell membrane. The intracellular and inter-stitial fluids are in osmotic and electrical equilibrium with each other; how-ever, the distribution of the ions between the two compartments is unequal.The intracellular compartment has a high concentration of potassium andthe extracellular compartment has a high concentration of sodium and chlo-ride, a gradient that is maintained by active transport over the cellmembrane.

With the application of an appropriate stimulus, nerves and muscles gen-erate action potentials. The action potential is a fast and transient reversalof the membrane potential caused by a temporary change in membrane per-meability. The action potential is generated by depolarization of the cellmembrane to the membrane threshold potential. This action potential ispropagated along the fiber without decrement [4,5].

The motor unit consists of a single lower motor neuron and the musclefibers that it innervates. It, therefore, includes the cell body of the lowermotor neuron in the spinal cord, its axon with its terminal arborization,the neuromuscular junctions, and all the muscle fibers innervated bythem. Every muscle unit has an innervation ratio, which is a measure ofthe total number of muscle fibers in the muscle to the total number of motoraxons innervating that muscle. The innervation ratio in small muscles, suchas the laryngeal muscles, external rectus oculi, and tensor tympani muscles,is approximately 25:1. The innervation ratio of the medial head of the gas-trocnemius muscle, a large muscle, is approximately 1700:1. Muscles thatperform fine motor movements typically require low innervation ratios.Muscles with high innervation ratios are typically involved in more grossmotor movements. The individual muscle fibers belonging to a given motorunit are scattered diffusely in the muscles, without grouping [6].

There are two types of muscle fibers based on histochemical characteris-tics. Type 1 fibers are rich in mitochondrial oxidative enzymes but poor inmyofibrillar adenosine triphosphatase (ATPase), whereas Type 2 fibers arerich in myofibrillar ATPase and low in mitochondrial oxidative enzymes.The muscle fibers of an individual motor unit are all of the same histochem-ical type. The lower motor neuron has trophic influence on the muscle fiberso that a muscle fiber may change its histochemical characteristics when re-innervated by motor neuron from a different motor unit type. Type 1 musclefibers are best suited for producing sustained, low-intensity muscle contrac-tions; Type 2 fibers are best suited for short bursts of high intensity musclecontractions [7]. In the spinal cord, smaller motor neurons innervate Type 1fibers and large motor neurons innervate Type 2 fibers. Smaller motor neu-rons are typically activated at low muscle tension; therefore, they are thefirst ones to be observed during the electromyographic (EMG) evaluation.Large motor neurons are recruited during high muscle tension and are there-fore seen during maximal muscle contraction. Small motor neurons fire ata lower rate, typically less than 20 Hz; large motor neurons are capable of

1005LARYNGEAL ELECTROMYOGRAPHY

firing at rates as high as 100 Hz. With aging, there is a significant loss ofmotor neurons in the anterior horn cells, which causes an increase in theinnervation ratio of the surviving units [8].

The electrodiagnostic apparatus

Bioelectrical potentials from the muscles or nerves being examined aredetected by an active recording electrode connected to a differential ampli-fier with a typical common mode rejection ratio of 100,000:1 and a highinput impedance of at least 100,000. The frequencies of muscle action poten-tials range between 2 Hz and 10,000 Hz and the frequency band of the EMGmachine is typically set at 10 Hz to 10,000 Hz. The reference electrode is alsoconnected to the amplifier. The signal of interest is measured as the potentialdifference between the active and reference electrodes. The patient must begrounded to reduce the risk for electrical injury and 60 Hz interference. Theelectrodiagnostic signal is displayed on a cathode ray oscilloscope in realtime and can be heard through a loudspeaker. The amplified signal canthen be monitored visually and acoustically. The signal can be stored perma-nently on magnetic tape, a computer disk, or paper. In addition to the qual-itative analysis used most commonly, quantitative EMG assessment is alsopossible. In modern systems, the amplifier signal is also connected to ananalog-to-digital converter, a microprocessor, and a video monitor for a dig-ital display of the signal. This connection permits rapid mathematic manip-ulation of the raw data. In addition, there is an electrical stimulatorincorporated into the system that is connected to the microprocessor andthe oscilloscope so that it can trigger the recording system when stimulationis provided. The ability of an amplifier to reject common mode signals isindicated by its common mode rejection ratio (CMRR). The higher the ra-tio, the greater the ability of the amplifier to reject common mode potentials.In clinical EMG, amplifiers with a CMRR of 10,000 are preferred, whichmeans that unequal potential differences between the two inputs of theamplifier is amplified 10,000 times more than potentials equal to both inputs[9,10].

In most EMG laboratories, sophisticated, multichannel systems are used.There are several excellent systems available commercially. They have manyadvantages, including permitting simultaneous, multichannel recording, butEMG systems are fairly expensive. For otolaryngologists who plan to uselaryngeal EMG for needle guidance when injecting botulinum toxin or foroccasional diagnostic purposes, less expensive, conveniently portablesystems are now available, such as the device manufactured by Xomed(Jacksonville, Florida). In its basic form, this EMG unit provides only au-ditory information and single-channel recording; but it can be connectedto a computer to provide a visual display. Such compact devices are alsovaluable for bedside, in-patient testing of patients who have laryngealtrauma in whom differentiation between arytenoid injury and vocal fold


paralysis is necessary. They are especially convenient during evenings andweekends, when formal EMG laboratory facilities may not be available.Another cost-effective option for otolaryngologists is the use of the brain-stem-evoked response (ABR) audiometer found in many offices. MostABR units can be used (sometimes with minor modifications) for single-channel EMG recordings. Although such devices can be used for specificclinical indications when formal EMG cannot be performed, they shouldbe used in addition to, not in place of, a sophisticated, multichannelEMG system for diagnostic testing.

Electrodes

The flow of current in biologic tissues occurs as a result of the movementof ions. In electronic systems, it is caused by the movement of electrons. Theconversion of ionic activity into electron movements occurs at the electrode–tissue interface, using electrodes that conduct electricity well, these may in-clude surface or needle electrodes.

Surface electrodes are placed on the skin or mucosa and do not penetratethe surface. Although they are noninvasive, they are the least selective elec-trode type. Surface electrodes are used in the study of nerve conductionvelocity and neuromuscular transmission. The potential that is recorded rep-resents the sum of all individual potentials produced by the nerve or musclefibers that are activated. These electrodes are not suitable for recording de-tails of electrical events associated with individual motor units.

There are several types of needle electrodes: monopolar, bipolar, concen-tric, hooked wire, and single-fiber (Figs. 1 and 2). The concentric needleelectrode consists of a hollow steel needle; a silver, steel, or platinum wireruns through the needle, which is insulated fully except at the tip. Thepotential difference between the outer shaft of the needle, which serves asa local reference electrode, and the tip of the wire is measured by connectingit to one side of the differential amplifier. Because the electrode cannula actsas a shield, the electrode has directional recording characteristics that arecontrolled by the angle and position of the bevel. Simple rotation of the elec-trode may alter significantly which individual motor units are recorded.

The monopolar needle electrode is a solid stainless steel needle that is insu-lated except at its tip. The recording area from this electrode is circular. Poten-tials therefore tend to be larger and longer and have more phases than thoserecorded with concentric needle electrodes, primarily because more muscle fi-bers are within the zone of detection and there is less cancellation because ofpotentials being recorded from the cannula of the electrode. The referenceelectrode is at a remote location on the body and may be a surface electrode.

The bipolar electrode is a hollow needle containing two platinum wires,each of which is insulated except at its tip. The outer shaft is groundedand the two internal wires are each connected to one side of the differentialamplifier so that the potential difference between the two wires is measured.


The recording range of the bipolar electrode is restricted to the area betweenthe two wires within the shaft, which makes it unsatisfactory for many rou-tine clinical purposes. The potentials are shorter and lower in voltage thanthose recorded with concentric needle electrodes [11].

With single-fiber EMG, a fine wire that is capable of recording a singlemuscle fiber action potential is embedded at the tip of a needle shaft thatacts as the reference electrode. A hooked wire electrode is completely insu-lated except at the tip, which is hooked. A needle is used to insert the elec-trode. When the needle is withdrawn, the hook on the end of the wire acts asa barb, stabilizing the position of the electrode in the muscle. Obviously,these electrodes cannot be repositioned once they have been placed, butthey bend easily and can thus be withdrawn without difficulty. Hookedwire electrodes are extremely well tolerated and can be left in place forlong periods of time (hours, or even days).

Technical considerations

The authors use percutaneous monopolar needle electrodes routinely.The patient is placed in the supine position, with the neck extended. Because

Fig. 1. Needle electrodes. (A) Concentric electrode with the active electrode embedded in the

bevel of the needle. The needle shaft serves as the reference. (B) Monopolar electrode with

the active electrode occupying the needle tip. The reference electrode may be a surface electrode

placed on the skin or a needle electrode placed elsewhere. (C) Bipolar electrode with two plat-

inum wires and a grounded outer shaft. (D) Single-fiber electrode. The reference is the cut end of

a wire embedded in a hole in the side of the shaft. (E) Two hooked-wire electrodes inside an

insertion needle. (From Sataloff RT, Mandel S, Heman-Ackah Y, et al. Laryngeal electromyog-

raphy. 2nd edition. San Diego [CA]: Plural Publishing, Inc.; 2006. p. 54; with permission.)


the procedure is generally not very painful, and because local anesthesiamay alter results (especially in the cricothyroid muscle), local anesthesia isnot used. A surface electrode is used as the ground electrode, and a reference(also surface) is placed on the cheek. For diagnostic purposes, routinely wetest cricothyroid, thyroarytenoid, and posterior cricoarytenoid muscles. Insome cases, additional muscles are tested also. If there are questions re-garding hysteria, malingering, or synkinesis, simultaneous recordings of ab-ductors and adductors are obtained. In cases of laryngeal dystonia, electricalrecordings may be coordinated with acoustic data. Blitzer and colleaguesobserved that the normal delay between the onset of the electrical signaland the onset of the acoustic signal (0–200 milliseconds) can be increasedto a delay of 500 milliseconds to 1 second in patients who have spasmodicdysphonia [12,13].

After cleaning the skin with alcohol, the needle electrode is inserted intothe muscle belly. The cricothyroid (CT) notch is the anatomic reference forneedle insertion. To locate the CT notch, the patient’s neck is extended andthe cricoid cartilage is identified. Immediately above the cricoid cartilage isa small depression, which is the CT notch (also known as the CT space) andthe CT membrane region. The CT notch may be difficult to find in obese pa-tients or those who have had a tracheotomy. The CT muscles are evaluatedby inserting the needle approximately 0.5 cm from the midline and angledlaterally 30� to 45� (Fig. 3). The needle first passes through the sternohyoidmuscle. The CT muscle is approximately 1 cm deep. To validate the positionof the electrode, the patient is asked to phonate /i/ at a low pitch and thenasked to raise the pitch. If the electrode is in a normal CT muscle, the EMGactivity increases sharply.

To evaluate the thyroarytenoid (TA) muscle, the needle is inserted ap-proximately 0.5 cm from the midline of the CT notch and is angled

Fig. 2. Zones of detection for concentric (A), monopolar (B), bipolar (C), and single-fiber (D)

needle electrodes. (From Sataloff RT, Mandel S, Heman-Ackah Y, et al. Laryngeal electromy-

ography. 2nd edition. San Diego [CA]: Plural Publishing, Inc.; 2006. p. 55; with permission.)

Fig. 3. Position of insertion of electrodes into the laryngeal muscles for electromyography.

Muscles illustrated include the cricothyroid (A), lateral and posterior cricoarytenoid muscles

(B), and the interarytenoid and thyroarytenoid (vocalis) muscles (vocalis is labeled ‘‘vocal

fold’’ in this figure) (C). Also shown are the positions of insertion into five major laryngeal mus-

cles (D, E). It is possible in some patients to place a needle in the PCA by passing through the

interarytenoid muscle and the cricoid cartilage (usually a few millimeters to the left or right of

the midline posteriorly). (From Sataloff RT, Mandel S, Heman-Ackah Y, et al. Laryngeal elec-

tromyography. 2nd edition. San Diego [CA]: Plural Publishing, Inc.; 2006. p. 76; with

permission.)



superiorly and laterally 30� to 45�. The TA muscle is encountered approxi-mately 1 to 2 cm beneath the skin. Triggering of a cough with the insertionof the electrode generally indicates that the needle has penetrated the airwayand is causing irritation of the mucosa. In that case, the needle should bewithdrawn and reinserted. The position of the needle is validated by askingthe patient to say and sustain the vowel sound /i/. During this maneuver,there is a sharp and sustained increase in EMG activity. If the needle is inthe lateral cricoarytenoid muscle there is an increase and rapid drop-off inEMG activity.

The posterior cricoarytenoid muscle (PCA) can be accessed by rotatingthe larynx and passing the electrode posterior to the thyroid lamina, by fol-lowing the line along the superior border of the cricoid cartilage, or by pass-ing a needle through the cricothyroid membrane, airway, and cricoidcartilage posteriorly. The latter technique is successful usually only innon-ossified larynges, such as those of young women. The PCA lies lowerin the neck than many physicians realize; inserting the electrode too highis a common reason for difficulty in locating the PCA. Position is confirmedthrough detection of increased EMG activity during sniffing, and with muchless EMG activity during swallowing and phonating the sound /i/. Thyroar-ytenoid, posterior cricoarytenoid, lateral cricoarytenoid, and interarytenoidelectrodes can also be positioned indirectly under flexible fiberoptic guid-ance or directly in the operating room [14,15].

Safety considerations

Current may leak from the electrodiagnostic system because of capacitycoupling. This current leakage may lead to death or injury in a patient bycausing ventricular fibrillation. To minimize the risk for this complication,every patient must be grounded. Also, the current leakage from the instru-ment should not exceed 10 mA [16].

Basic components of electromyography examination

The EMG examination is performed and evaluated in four parts: (1) dur-ing insertion, (2) at rest, (3) during minimal voluntary contraction, and (4)during maximal voluntary contraction.

Insertional activity

Insertional activity is the burst of electrical signal that is produced as theneedle is introduced into the muscle. This activity should last no more thanseveral hundred milliseconds. This burst of electrical activity results fromthe needle itself having some electrical energy that, when placed near themuscle membrane, causes a relative change in the surrounding electricalenergy.


If the electrical charges surrounding the muscle membrane are unstable,such as occurs during early nerve and muscle injuries, the insertional activityis prolonged. With late nerve and muscle injuries, healing sometimes resultsin replacement of normal muscle with scar tissue or fat, which insulates theremaining muscle fibers and causes a decrease in the insertional activity.

Spontaneous activity

Spontaneous activity refers to the presence of electrical activity in a rest-ing muscle. Under normal conditions there should be no spontaneous elec-trical activity at rest. Electrical activity arises from neural impulses thatsignal the muscle to contract. Spontaneous electrical activity occurs in a se-verely denervated muscle with unstable electrical charges. The presence ofspontaneous activity implies that the muscle is degenerating or that thenerve has been injured and the process that caused the injury is ongoing.This finding is true in muscles throughout the body, including those in thelarynx [17,18]. Spontaneous activity usually begins 2 to 3 weeks after dener-vation has occurred, because of the length of time it takes for enough de-generation to occur to cause an absence of electrical impulses from thenerve to the muscle. This degree of denervation occurs only with severenerve injury, and the presence of spontaneous activity indicates a poorprognosis for recovery. Once regeneration begins, the muscle begins to re-ceive electrical impulses from the regenerating nerve and the spontaneousactivity ceases.

Waveform morphology

Waveformmorphology refers to the shape, amplitude, and duration of themotor unit potentials, which are the electrical signals captured by EMG. Thenormal laryngeal motor unit potential is biphasic; that is, it has an upwardpositive spike and a downward negative spike (Fig. 4). It also has an ampli-tude of 200 to 500 microvolts and a duration of about 5 to 6 milliseconds.The amplitude of the motor unit potential reflects the number and thestrength of the muscle fibers innervated by one nerve ending. The durationof the motor unit potential reflects the velocity of the neural input, whichis influenced by insulation of the nerve. Nerves that are insulated well andhave an intact and functioning sheath are able to transmit electrical impulsesfaster than those that are not, because electrical impulses are then transmit-ted from one node of Ranvier to another. The shape of the motor unit poten-tial reflects changes in the electrical activity of the muscle membrane. Undernormal circumstances, this is biphasic. The waveform morphology of themotor unit potential provides information regarding likelihood of recovery.

After injury, the nerve undergoes a process of denervation followed byregeneration. The length of time that denervation and regeneration occurcan vary from one situation to another and can last for periods of weeksto months each. It is unknown what determines the degree of denervation


or regeneration in any given nerve. During denervation, there is no neuralinput into the muscle and thus no abnormal waveforms are produced. Ab-normal motor unit potential morphologies are produced during the periodof regeneration.

During the early phases of regeneration, tiny nerves begin to course backinto the muscles that have atrophied during the period of denervation.Early in regrowth, the insulation of the nerve is decreased. The combina-tion of tiny, minimally insulated nerves and weak muscle fibers producesmotor unit potentials that have small amplitudes, long durations, and poly-phasic shapes on laryngeal EMG (LEMG). These waveforms are some-times referred to as nascent units; they imply the presence of a recentnerve injury.

As the regeneration progresses, the nerves become healthier and betterinsulated through regrowth of their sheaths, and the muscle fibers becomestronger and gain more mass. Not all of the nerve fibers regenerate. Thoseneurons that regenerate branch more than before the injury to innervate asmany muscle fibers that lack innervation as possible. The motor unit poten-tials that are produced as a result of this ongoing regeneration have greateramplitudes than normal (because of the greater number of muscle fibers inthe motor unit), are polyphasic (because of changes in the muscle membranepotentials), and have a prolonged duration (because of changes in the mye-lin sheath and nerve conduction velocity). These motor unit potentials areusually described as being polyphasic or as giant polyphasic potentials; theirpresence implies an old nerve injury.

If the nerve is uninjured and the muscle is damaged, the morphology ofthe motor unit potential is different. The nerve is intact and functioning well,so the duration of the motor unit potential is normal. The electrical charges

Fig. 4. Normal motor unit (arrow) recorded from the cricothyroid muscle. (From Sataloff RT,

Mandel S, Heman-Ackah Y, et al. Laryngeal electromyography. 2nd edition. San Diego [CA]:

Plural Publishing, Inc.; 2006. p. 79; with permission.)


in the muscle membrane are abnormal, resulting in a polyphasic shape. Theamplitude, which reflects the decreased muscle mass and force of contrac-tion, is decreased.

Recruitment

Recruitment refers to the serial activation of motor units during increasedvoluntary muscle contraction. Normally, as the intensity of the muscle con-traction increases, the motor units have increased activity and new motorunits are recruited to maintain the strength of the contraction. This processis seen on LEMG as an increase in the number and density of motor unitpotentials (Fig. 5). This density of motor unit potentials is the recruitment.Recruitment thus reflects the degree of innervation, which is a reflection ofthe number of active nerve fibers within a given muscle.

Common abnormal electromyography findings

Increased insertional activity occurs when the burst of electrical potentialproduced by insertion or movement of the needle electrode in the musclelasts more than several hundred milliseconds. This finding is an indicationof muscle membrane instability and occurs in myopathic and neurogenicprocesses. Insertional activity also can be reduced, indicating loss of musclefiber and replacement of it by fibrotic tissue or lipoid degeneration. Thisprocess is observed in end-stage myopathic and some neuropathic processes.

At rest, different kinds of abnormal spontaneous activity can be ob-served. Fibrillation potentials (Fig. 6) are spontaneous, single-fiber muscleaction potentials with a typical amplitude of several hundred microvoltsand duration of less than 2 milliseconds, firing regularly at 1 to 50 Hz.They can occur spontaneously or with movement of the needle. They typi-cally have a biphasic or triphasic appearance with an initial positive deflec-tion. This abnormality is seen more commonly when denervation hasoccurred. Rarely, it can be seen in myopathic processes also. A positivesharp wave is characterized by a large positive deflection of several hundredmicrovolts lasting less than 2 milliseconds, followed by a negative deflectionof 10 to 30 milliseconds and regular firing at 1 to 50 Hz. Fibrillation poten-tials and positive sharp waves usually occur together and produce character-istic noises on the loudspeaker that some describe as sounding like machinegun firing, thus allowing one to identify these potentials even without look-ing at the oscilloscope screen. It takes approximately 2 to 3 weeks after de-nervation occurs to observe fibrillation potentials or positive sharp waves.After a nerve injury, the presence of fibrillations and positive sharp wavesindicates denervation and axonal loss.

Complex repetitive discharges (Fig. 7) occur when a group of muscle fi-bers discharges repetitively in near synchrony through ephaptic activation.These discharges typically have an abrupt onset and cessation and a bizarreconfiguration. The discharge rate is anywhere between 5 and 100 Hz, with


Fig. 5. (A) Maximal contraction,normal recruitmentpattern. (B)Maximal contraction;motorunit

recruitment decreased approximately 30%. (C) Maximal contraction; motor unit recruitment de-

creased approximately 50%. (From SataloffRT,Mandel S, Heman-AckahY, et al. Laryngeal elec-

tromyography.2ndedition.SanDiego [CA]:PluralPublishing, Inc.; 2006. p. 81–2;withpermission.)


an amplitude of 100 mV to 1 mV. This abnormality indicates chronicity, andit can be observed in neuropathic and myopathic processes.

Myotonic potentials (Fig. 8) are repetitive discharges at rates of 20 to150 Hz and amplitudes of 20 mV to 1 mV, with the appearance of fibrilla-tion potentials or positive sharp waves. The amplitude and the frequencyof the potentials wax and wane, which causes a characteristic ‘‘divebomber’’ sound in the loudspeaker of the EMG machine. These potentialsoccur spontaneously with insertion of the needle, with percussion of themuscle, or with voluntary contractions. They indicate muscle membraneinstability and are observed most commonly in disorders of clinical

Fig. 7. Low-amplitude complex repetitive discharges (arrows) recorded from the right thy-

roarytenoid muscle in a patient who has recurrent laryngeal neuropathy. (From Sataloff RT,



Fig. 6. Fibrillation potentials (solid arrow) and positive sharp wave (open arrow) recorded from

the right thyroarytenoid muscle in a patient who has recurrent laryngeal neuropathy. (From

Sataloff RT, Mandel S, Heman-Ackah Y, et al. Laryngeal electromyography. 2nd edition.

San Diego [CA]: Plural Publishing, Inc.; 2006. p. 60; with permission.)


myotonia, such as myotonic dystrophy. Rarely, they can be observed inchronic neurogenic and myopathic processes, such as fibromyalgia withoutclinical myotonia.

Lower motor neuropathy

During minimal voluntary muscle contraction, the morphology of themotor unit potential is evaluated. Abnormalities are characterized bychanges in the duration, amplitude, and number of phases (Fig. 9). In a neu-ropathic process, the motor unit potential typically has a prolonged dura-tion and increased number (more than four) of phases (Fig. 10). Duringearly reinnervation, the amplitude is decreased and, when reinnervation iscompleted, the amplitude is increased.

With maximal muscle contraction, the interference pattern and recruit-ment are evaluated. When a nerve impulse arrives at a motor end plate, mus-cle fibers depolarize and contract. Because there are numerous fibers in anymuscle motor unit, and their distances from the neuromuscular junctionvary, not all muscle fibers in a motor unit contract simultaneously [19,20].In reality, numerous motor units are involved during muscle contraction.As the contraction increases, motor units fire more frequently and, progres-sively, additional motor units are activated. Consequently, recorded motorunits overlap, creating an interference pattern. Potentials that can be iden-tified visually and audibly during weak contraction overlap during strongercontraction; therefore, some fading can result in a recruitment pattern inwhich some of the spikes appear to be lost. By looking at, or listening to,the EMG signal, a skilled electromyographer can determine the conditionof the muscle. For example, under normal circumstances, the interferencepattern described above is present. In complete paralysis, initially there iselectrical silence; however, positive sharp waves or fibrillation potentialsgenerally appear within a few weeks. Reinnervation is characterized bylarger motor units with polyphasic, high-amplitude, and long-durationresponses. There is usually loss of motor units following paralysis, whichresults in decreased recruitment (a less dense interference pattern). In

Fig. 8. Myotonic potentials. (From Sataloff RT, Mandel S, Heman-Ackah Y, et al. Laryngeal

electromyography. 2nd edition. San Diego [CA]: Plural Publishing, Inc.; 2006. p. 62; with

permission.)


neuropathic processes, there is decreased recruitment, with a few motorunits firing at high frequency and a decreased interference pattern (Fig. 11).

Myopathy

In a myopathic process, there is rapid and early recruitment with a lowvoltage, and a full interference pattern in the context of a weak muscle con-traction. The duration of the motor unit potential is short, with an increasednumber of phases and decreased amplitude.

Upper motor neuropathy

In upper motor neuron disorders, the insertional activity is normal. Theamplitude and duration of the motor unit potential are normal, and there

Fig. 9. Differences in the appearance of the motor unit potential in diseases. (From Sataloff RT,




are no excessive polyphasic motor units. Recruitment is decreased. Thefiring rate of the motor unit is slow. Most upper motor neuron diseases dem-onstrate hyperactive reflexes with increased tone and no muscle atrophy.There is a paucity of studies in the literature evaluating laryngeal functionwith EMG in patients who have upper motor neuron disorders.

Basal ganglia disorders

The insertional activity is normal in basal ganglia disorders. Abnormalspontaneous activity is absent. At rest there may be excessive motor unit

Fig. 11. Incomplete interference pattern showing decreased recruitment with rapid discharge

rate recorded from the right thyroarytenoid muscle in a patient who has recurrent laryngeal

neuropathy. (From Sataloff RT, Mandel S, Heman-Ackah Y, et al. Laryngeal electromyogra-

phy. 2nd edition. San Diego [CA]: Plural Publishing, Inc.; 2006. p. 64; with permission.)

Fig. 10. Polyphasic (solid arrow) and normal (open arrow) motor units recorded from the left

cricothyroid muscle. (From Sataloff RT, Mandel S, Heman-Ackah Y, et al. Laryngeal electro-

myography. 2nd edition. San Diego [CA]: Plural Publishing, Inc.; 2006. p. 63; with permission.)


potentials, indicating failure of complete relaxation of the muscle. Theremay also be poor coordination between agonistic and antagonistic mus-cles, or inappropriate activation. In addition, rhythmic and periodic dis-charges of motor unit potentials can be observed in patients who havevoice tremor [21]. Stuttering may also be associated with tremor-likeEMG activity [22].

Laryngeal dystonia (spasmodic dysphonia)

In laryngeal dystonia, there are intermittent sudden increases in muscleactivity coinciding with momentary voice rest [13,23,24]. The EMG canbe helpful in differentiating adductor versus abductor or mixed dystonias[25]. Rodriguez and colleagues [26] found abnormal activity in 81.3% ofpatients who have spasmodic dysphonia but found no EMG abnormalitypredictive of severity. LEMG is used routinely to guide botulinum injectionin patients who have laryngeal dystonia [27,28]. As noted above, an abnor-mal delay between the onset of electrical and acoustic activity can help con-firm a diagnosis of dystonia. EMG may also help identify the musclesaffected most by the dystonia, thereby guiding therapeutic intervention.

Laryngeal myasthenia

In myasthenia gravis (MG), the insertional activity is normal. There is noabnormal spontaneous activity. With minimal muscle contraction, the motorunit potential exhibits variation in amplitude and duration, reflecting inter-mittent failure of conduction across the neuromuscular junction. The recruit-ment and interference patterns are normal. Repetitive nerve stimulationstudies are usually abnormal and reveal a lack of increased recruitmentwith each repetitive stimulation.Myasthenia gravis can be a cause of intermit-tent and fluctuating hoarseness and voice fatigue. Laryngeal manifestationsmay be the first and only sign of systemic myasthenia gravis [29]. LaryngealMGmay occur with systemicMGor as a focal disorder similar to ocularMG.

Repetitive stimulation and Tensilon testing

If there is evidence of fluctuating nerve weakness on laryngeal examina-tion, repetitive stimulation studies and Tensilon testing may be performed.Repetitive stimulation involves presenting the nerve with a series of electricalshocks and recording the neuromuscular response by EMG. Because of itseasy, subcutaneous access, the nerve stimulated is often the spinal accessorynerve at its insertion into the trapezius muscle. Repetitive stimulation pro-vides information regarding the integrity of the neuromuscular junction.With a normal neuromuscular system, recruitment remains normal duringrepetitive stimulation. If the stimulation causes a progressively decreasing re-cruitment response, then an abnormality in the neuromuscular junction is


suspected. A decrease in the recruitment response implies that motor unitsthat were previously recruited are unable to be actively and continuallyrecruited during repetitive stimulation. That they were able to be recruitedinitially and give normal waveform morphology implies that the nerve fi-bers themselves are intact and that the muscles are able to respond toan impulse signal. The inability of the motor units to keep up with the re-petitive stimulation implies that there is an abnormality in the transfer ofinformation across the neuromuscular junction that is only apparent whenthe system is stressed. If the laryngeal evaluation is abnormal, or if thereare other abnormalities noted during the LEMG, then Tensilon (edropho-nium chloride, Hoffman-LaRoche, Inc., Nutley, New Jersey) testing maybe performed. Repetitive stimulation testing is contraindicated in patientswho have pacemakers.

Tensilon is an anticholinesterase that inhibits acetylcholinesterase at theneuromuscular junction, resulting in increased exposure of the muscle recep-tors to acetylcholine during neural stimulation. In normal muscles, this haslittle effect on muscle activity. In muscles with decreased numbers of avail-able receptors for acetylcholine (as occurs with myasthenia), in those withincreased activity of acetylcholinesterase, or in those with decreased releaseof acetylcholine from the nerve ending, the presence of Tensilon results inincreased muscle contraction from the prolonged exposure to acetylcholine.When LEMG is repeated following administration of Tensilon, the recruit-ment patterns revert to a more normal pattern with voluntary contractionand with repetitive stimulation. Voice quality may also improve with reso-lution of breathiness, softness, and fatigue. This positive response to Tensi-lon further isolates the problem to the neuromuscular junction.

Tensilon testing involves the intravenous injection of edrophonium chlo-ride into a vein and repeating the LEMG. A syringe containing 10 mg of Ten-silon is used for intravenous injection. Initially, 2 mg is injected over 15 to 30seconds. If there is no reaction after 45 seconds, the remaining 8 mg is in-jected. If a cholinergic reaction occurs after injection of 2 mg, the test is dis-continued and 0.4 to 0.5 mg of atropine sulfate is administered intravenously.Typical signs of a cholinergic reaction include skeletal muscle fasciculations,increased muscle weakness, and muscarinic side effects. In patients who havehad such reactions, the test may be repeated 30 minutes after administrationof atropine sulfate. In patients who have inaccessible veins, Tensilon may begiven as an intramuscular injection. Tensilon testing can also be performed inchildren, with doses adjusted according to the child’s weight.

Tensilon testing is contraindicated in patients who have urinary or intes-tinal obstructions, or in those who have known hypersensitivity to anticho-linesterase agents. The effects of Tensilon last an average of 10 minutes.Occasionally, severe cholinergic reactions occur. Caution must be exercised,particularly in patients who have bronchial asthma or cardiac arrhythmias.The transient bradycardia that sometimes occurs following Tensilon injec-tion can be relieved by atropine sulfate, but isolated incidents of cardiac


and respiratory arrest have occurred following administration of Tensilon.A syringe containing 1 mg of atropine sulfate should be available at all timesfor emergency rescue. Tensilon also contains sodium sulfite. Allergic reac-tions to sulfites can occur and are more common in patients who haveasthma than in others. The safety of Tensilon for use during pregnancy orlactation has not been established. Use of Tensilon in pregnant womenand nursing mothers is relatively contraindicated.

Summary

LEMG is easy to perform and well tolerated in the office setting withminimal risks. It is useful in the evaluation of numerous laryngeal disorders,allowing clinicians to differentiate among upper motor neuron, lower motorneuron, peripheral nerve, neuromuscular junction, myopathic, and mechan-ical disorders. It is also useful in establishing prognosis in laryngeal nervepalsies and for guidance during the injection of botulinum toxin in spas-modic dysphonia. Our experience and that of others are similar to that ofKoufman and colleagues, who reported 415 LEMG studies, 83% of whichrevealed a neuropathic process [30–32]. They reported unexpected findingsin 26% and LEMG altered clinical management in 40% of cases, highlight-ing the importance of this simple, quick procedure in the practice of laryn-gology. We concur and believe that collaboration between the laryngologistand a skilled laryngeal electromyographer is an invaluable and essentialasset to the voice care team. There is a striking paucity of evidence-basedresearch to confirm or refute scientifically and incontrovertibly the valueof LEMG for most of the purposes for which we use and recommend it,however [33]. Additional prospective, controlled LEMG research shouldbe encouraged and supported, and should be used to formulate formal prac-tice guidelines for clinical use of LEMG.

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40 (2007) 1025–1061

Common Diagnoses and Treatmentsin Professional Voice Users

Ramon A. Franco, MD*, Jennifer G. Andrus, MDDivision of Laryngology, Massachusetts Eye & Ear Infirmary,

Department of Otology and Laryngology, Harvard Medical School,

243 Charles Street, Boston, MA 02114, USA

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

History and physical examination

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


E-mail address: [email protected] (R.A. Franco).




1026 FRANCO & ANDRUS

the laryngologist’s office and may be barriers to the patient’s ability toclearly describe the problems he/she is having with the voice. Patient ques-tionnaires can help to overcome this difficulty and facilitate an efficient visit.They are invaluable. The patient can be asked to fill out a history intakeform in the waiting room, along with the voice-related quality of life(VRQOL) survey and a voice outcome survey. In addition to defining theeffects of the voice problem on the patient’s functional capacity, the surveysare helpful for tracking the voice problem and the effect of therapy on it.

Second, the history will help to establish the acuity or chronicity and se-verity of the problem. Along with symptoms, past medical/surgical history,allergies, and medications, particular attention should be paid to the socialhistory, including place of residence; student or employment status; currentand previous tobacco, alcohol, and drug use; exposure to second-handsmoke or chemical irritants/pollutants; and water, caffeine, carbonated bev-erage, chocolate, peppermint, and fatty/spicy/acidic food consumption.Changes in a patient’s routine (eg, time of day one practices, performancevenue, consumption of caffeinated beverages) often yield important infor-mation. The history also gives clues as to what endoscopy may show. Clini-cians are encouraged to use the history to help guide the physicalexamination, but are cautioned to keep an open eye for unsuspected diagno-ses. Similarly, history and physical examination together will help the clini-cian to develop a differential diagnosis. More often than not, multipleentities contribute to one symptom complex, so the laryngologist is cau-tioned not to look for ‘‘the’’ single unifying diagnosis. Thinking about laryn-geal pathology in terms of acute versus subacute versus chronic problemsmay be more useful than a traditional schema of vascular, inflammatory,traumatic, autoimmune, iatrogenic, neoplastic, or congenital problems.Nonetheless, the clinician is reminded that professional voice users are sub-ject to the same possibilities as are other patients; therefore, neoplastic andautoimmune processes, for example, should not be overlooked.

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

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

1027COMMON DIAGNOSES

Sometimes the patient is in denial and does not want to believe what anotherclinician has diagnosed or does not want to pursue the recommended treat-ment options. Another frequent scenario is that the patient has been toldthat he/she has a normal larynx and that nothing on examination canexplain the symptoms. In these cases, it is especially important to elicit adetailed history and to be clear about what bothers the patient about thevoice. Sometimes edema from laryngopharyngeal reflux masks a mass lesionor hyperfunction is so severe that the vocal folds are not seen easily onfiberoptic evaluation. Flexible distal-chip laryngoscopes are providing ex-aminations superior to fiberoptic laryngoscopy and approximating rigid lar-yngoscopy, such that subtle findings now are being noted that may not havebeen seen without this technology. Of utmost importance, it is essential tolisten to the patient, to acknowledge that something is wrong, even if the ex-act diagnosis is not obvious, to take a team approach with a voice therapist,and to ‘‘stick’’ with the patient until a diagnosis and treatment plan areformed and executed.

Voice problems in professional voices users: diagnoses and treatment

options

Laryngopharyngeal reflux

Laryngopharyngeal reflux is the retrograde movement of gastric contents(acid and enzymes, such as pepsin) into the laryngopharynx leading tosymptoms referable to the larynx, hypopharynx, and nasopharynx (Fig. 1)[1]. Typical laryngopharyngeal reflux symptoms include dysphonia, globuspharyngeus, mild dysphagia, chronic cough, excessive throat mucus, and

Fig. 1. Laryngopharyngeal reflux. Note diffuse periarytenoid and postcricoid edema, vocal fold

edema, and pseudosulcus (the appearance of a ‘‘second’’ vocal fold inferior to the true vocal

fold due to edema). The larynx is wet appearing; copious, thick mucus is not seen in this patient

as in others.


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

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

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


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

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

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


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

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


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

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

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


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

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

Fungal laryngitis

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

Fig. 2. Fungal laryngitis. White fungal plaques on an erythematous base are seen in the mid-

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

punctate white plaques throughout the larynx.


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

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

Diagnosis in these patients commonly rests on clinical suspicion based onhistory, risk factors, laryngoscopy findings, and response to empiric treat-ment with oral antifungal agents [28]. Patients who fit the clinical pictureof fungal laryngitis can be treated with oral fluconazole for 3 weeks (200 mgon day 1, followed by 100 mg daily on days 2 through 21) in conjunctionwith nystatin swish and swallow (100,000 units/mL at 10 mL three timesdaily for 7 to 10 days). Some clinicians treat with nystatin for 3 weeks first,followed by fluconazole if there is no response; others use only fluconazole[26,28]. Although fluconazole is known to increase liver enzymes, Stone andAnderson [28] do not routinely check liver function tests. Patients who havehepatic disease can be treated with nystatin as a first-line agent and referredto their primary care physician for evaluation of their candidacy for sys-temic antifungal treatment if they fail to respond appropriately. Because an-tifungal treatment often is concomitant with antireflux treatment, responseto therapy can be multifactorial. If there is any question about the diagnosisof fungal laryngitis, should symptoms/signs not resolve, or should malig-nancy be a significant concern, a definitive diagnosis can be obtained withlaryngeal brushings and culture or biopsy. This can be accomplished within-office transnasal flexible laryngoscopy and biopsy through a workingchannel on the endoscope. Often, periodic acid-Schiff or methenamine silverstains are necessary to see fungal elements on histopathologic evaluation[26,27]. Some patients who have fungal laryngitis with severe dysphagiaalso may have esophageal candidiasis. If this is suspected, TNE is recom-mended to examine the esophagus and to obtain biopsies as necessary. Pa-tients who have severe dysphonia and pain also may present with significanthoney-colored crusts in the larynx in addition to multiple white plaques over


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

The literature does not reflect the number of professional voice users whohave asthma or other obstructive pulmonary disease who have been on in-haled steroids at any point. Considering the broad definition of ‘‘profes-sional voice user,’’ however, it is not difficult to imagine that this numbercould be significant. Therefore, laryngologists are obligated to seek this his-tory and communicate with the prescribing physician about possible alter-natives to inhaled steroids for patients who develop fungal laryngitis. It isnot always possible to wean patients off inhaled steroids, in which case shortholidays from steroid use may be in order, with or without low-dose prophy-lactic antifungal use (eg, nystatin or mycelex troches). The use of a spacerwith the inhaler should be recommended [28]. Patients also must garglewith water and rinse the oral cavity/oropharynx after each inhaler use.

Muscle tension dysphonia

Muscle tension dysphonia is a form of voice use/misuse/abuse character-ized by excessive muscular effort and usually by pressed phonation [30].

(Access Video on Supraglottic Hyperfunction in online version of this article at: http://

www.Oto.TheClinics.com.)

Other common clinical features include an abnormally low-pitchedspeaking voice, poor control of the breath stream, frequent hard glottal at-tacks, obvious cervical muscle tension, and jaw and tongue tension [31,32].Muscle tension dysphonia is a form of laryngeal hyperfunction, and the twooften are considered synonymous. Other synonyms include hyperfunctionaldysphonia, muscle misuse dysphonia, hyperkinetic dysphonia, musculoskel-etal tension dysphonia, mechanical voice disorder, functional hypertensivedysphonia, laryngeal tension-fatigue syndrome, and laryngeal isometric dys-phonia [32]. All of these terms fall under an umbrella diagnosis of functionaldysphonia, classically considered an impairment of voice production in theabsence of structural change or neurogenic disease of the larynx. In the1980s and early 1990s, multiple classification schemes for muscle tensiondysphonia were proposed, with emphasis on symptom onset, voice quality,and laryngeal movement patterns [33–36]. In the last decade, an importantshift in how laryngologists think about functional dysphonia and muscletension dysphonia has occurred. Namely, it has become evident that muscletension dysphonia most likely is not a stand-alone entity, but more likely ismultifactorial with various contributing causes [31,32,35–37]. That is to say,muscle tension dysphonia often is present on comprehensive laryngologic





evaluation with other disorders, such as presbylarynges (bilateral vocal foldbowing in an aging patient), laryngopharyngeal reflux, vocal fold polyp, andvocal fold nodules [32,37]. More frequently, muscle tension dysphonia isthought of as a compensatory mechanism for another entity.

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

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

Vocal fold paresis

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


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

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

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

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


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

Superior laryngeal nerve (SLN) paresis deserves special mention becauseit may have devastating effects on singers, given the impact that it has onmodulating pitch in the upper range. If loss of high range is among a singer’scomplaints and hypomobility in one vocal fold is seen on examination or ifsymptoms do not improve on maximal laryngopharyngeal reflux therapywith singing therapy in the case of symmetric movement, LEMG is indi-cated to elucidate whether the SLNs are intact. If isolated SLN paresis ispresent without vocal fold bowing or signs that vocal fold augmentation/medialization will be helpful, it is important to provide voice therapy toavoid development of muscle tension dysphonia, to encourage appropriatechanges in repertoire, and to provide hope to the patient that the vocalfold paresis may be postviral with potential for resolution. This last pointof management is critical: first, patients often are able to cope better withthe idea of a temporary disability; second, if the disability is permanent,time in voice therapy and modifying repertoire will be well spent.

Benign vocal fold masses: nodules, polyps, and cysts

Vocal fold masses are discussed in detail elsewhere in this issue. Here, thesimilarities and differences in the symptoms, diagnosis, and treatment of vo-cal fold nodules, polyps, and cysts are presented in brief. Dysphonia is themost common presenting symptom of benign vocal fold masses. The astuteclinician may develop some hypotheses as to which type of mass is presenton the vocal fold based on specific voice changes, such as loss of range in thehigh frequencies (commonly associated with nodules) or diplophonia due toa difference in vibratory frequency of the vocal folds (often associated witha unilateral process, such as a polyp). The wise clinician is ever mindful thatmore than one pathologic process or more than one type of mass can bepresent. Obtaining a good history is important to help define the cause ofthe problems that the patient is having with the voice, which helps guidethe development of an individualized management strategy.

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

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

com.)





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

Vocal fold polyps, another form of subepithelial fibrosis and deposition,are histologically similar to vocal fold nodules, but differ in that they areunilateral. Vocal fold polyps also may present with hoarseness, loss ofrange, breathiness, and vocal fatigue. Diplophonia may occur as noted

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


above; dyspnea can occur if the polyp is large enough to obstruct the airway.In professional voice users, the emergence of dyspnea is unlikely; thesepatients probably would seek laryngologic attention before dyspnea couldevolve. The one exception is a hemorrhagic polyp, which can occur suddenlyand be large (Fig. 4).

(Access Video on Large Obstructive Hemorrhagic Polyp in online version of this article at:


Vocal fold cysts present primarily with hoarseness, although diplophoniaalso may be a problem. Vocal fold cysts are present in the superficial laminapropria and can open into the laryngeal lumen or insert onto the vocal lig-ament. Vocal fold cysts are categorized as epidermoid (sometimes calledsquamous inclusion) cysts or mucus retention cysts [42]. Epidermoid cystsare believed to arise from traumatic introduction or ingrowth of keratininto the superficial lamina propria, secondary to phonotrauma, or to be con-genital. Mucus retention cysts more likely result from occlusion of mucusglands on the inferior surface of the vocal fold.

(Access Video on Pre-op Subepithelial/Mucous Retention Cyst in online version of this

article at: http://www.Oto.TheClinics.com.)

Clearly, vocal fold nodules, polyps, and cysts cannot be distinguished byhistory alone. VLS is the key to their diagnosis. Stroboscopy is essential toan accurate diagnosis because it allows for the assessment of vocal fold clo-sure and phase symmetry, which are not discernable in the absence of stro-boscopic light. Stroboscopy’s delineation of the mucosal wave allows thelaryngologist to assess its relationship to the mass, and, thus, whether theepithelium/basement membrane zone is involved or whether the mass liesdeeper to this. On VLS, vocal fold nodules most frequently are bilateral,

Fig. 4. Hemorrhagic polyp. Associated varices and resolving blood are seen in the left true

vocal fold. Note concomitant bilateral pseudosulcus.






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

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


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

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

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

rounding erythema are seen.


Clinical manifestations include hoarseness and instability in connectedspeech, with characteristic subepithelial nodules that appear as horizontalbars or rectangles that run perpendicular to the long axis of the vocal foldin the midmusculomembranous region. Often, these are striated in appear-ance and universally cause stiffness in vocal fold vibration with reduction inthe magnitude of mucosal wave [44,45,48]. Rheumatoid nodules and bam-boo nodes (similar lesions seen in autoimmune diseases, such as Sjogren’ssyndrome and systemic lupus erythematosus) are almost always bilateral;surrounding erythema is common, particularly during a flare-up of thesystemic disease. Rheumatoid nodules and bamboo nodes must be treatedin the context of the systemic disease. Close communication with the rheu-matologist is necessary to optimize medical therapy when conservativemeasures fail. Surgical excision or direct injection of steroids into the rheu-matoid nodules/bamboo nodes is undertaken when function demands it;however, patients must be counseled that the lesions can recur in the faceof chronic disease. Perioperative reflux treatment is imperative, and anoral steroid burst is recommended preoperatively to help abate inflamma-tion. It is not uncommon to encounter dense fibrosis around the nodulesonce they are exposed subepithelially by way of cordotomy, even with sub-epithelial injection of local anesthesia/epinephrine. Nonetheless, it is impor-tant to remove the nodule in its entirety to maximize function and minimizegrowth of persistent disease. Bilateral lesions can be addressed at one sittingbecause a superior cordotomy usually is made. Postoperative management isthe same as for other benign mass lesions.

Vocal fold scarring

Vocal fold scar is a vexing diagnosis for patients and laryngologists.Although there is no agreement on how best to manage vocal fold scar, itis agreed that treatment outcomes are fair to good, but inconsistent atbest [49–53]. This mandates continued research into the pathophysiology,histology, biology, and treatment of vocal fold scarring. A detailed discus-sion of these topics is beyond the scope of this article, and the reader isreferred to several recent reviews [50,51,53]. Nonetheless, given the potentialfor permanent voice change and the impact on patients, particularly profes-sional voice users, vocal fold scar is an area worthy of utmost attention inthe clinical and research realms.

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


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

In the vocal fold, the ‘‘normal tissue’’ destroyed by scar in varying degreeand thickness is the delicate multilayered structure composed of epithelium,superficial lamina propria, intermediate lamina propria, deep lamina prop-ria, and muscle. This fibrous insult compromises vocal fold pliability, theexact property that allows production and modulation of voice, by causingcontraction of the vocal fold cover and effecting loss of vocal fold volume[53]. The result is an increase in vocal fold stiffness and subsequent decreasein vibratory capacity [49].

(Access Video on Left Vocal Fold Scar in online version of this article at: http://www.Oto.

TheClinics.com.)

Effects on voice depend on the location of vocal fold scar relative to thevocal fold’s medial edge and midmusculomembranous region, the depth ofscar, the presence of other lesions/pathologic entities, and the patient’s innateor trained compensatory mechanisms of producing voice. Patients may de-velop a strained, harsh, or breathy voice, diplophonia, or hoarseness [49]. Inaddition to change in voice, common complaints include vocal fatigue, lossof range, and loss of stamina. These complaints also apply to sulcus vocalis.

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





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

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

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

Fig. 6. Vocal fold sulcus. (A) Longitudinal scar is seen along the superomedial edge of the right

true vocal fold. (B) On suspension microlaryngoscopy, palpation with a right-angle hook

revealed this to be a ‘‘pocket’’ sulcus, or type III sulcus. It was removed successfully with pho-

nomicrosurgical techniques.


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

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

Fig. 7. Bilateral sulcus vocalis with significant loss of superficial lamina propria, vocal fold

bowing, and lateral cricoarytenoid hyperfunction. Significant muscle tension dysphonia also

is seen on phonation.


autologous fat or fascia also can be used. Medialization thyroplasty withGore-Tex or silastic blocks also will close a glottal gap. Direct approachesto sulcus deformities that aim to address the loss of pliability include endo-scopic procedures, such as cold instrument undermining of the sulcus byway of a longitudinal epithelial cordotomy, scar release, and flap redraping;cold instrument excision of the scar, similar to the redraping procedure butwith removal of scar tissue to its depth; laser undermining with redraping;and slicing technique that involves full-thickness releasing cuts in the flapmedial and perpendicular to its longitudinal axis [56,60]. These techniquesdo not always address glottal insufficiency. Finally, other procedures that at-tempt to address lack of pliability and glottal insufficiency include those thatadd an implant to scar release or excision. These also are endoscopic proce-dures and include implantation of fat, fascia, or acellular dermis (AlloDerm)in the superficial lamina propria.

The reader is advised that none of the aforementioned procedures hasbeen performed by large numbers of surgeons or on large numbers of pa-tients. The development of multiple techniques to address sulcus reflectsour poor understanding of it and parallels the lack of consensus on howbest to address it. Continued research in this area is imperative to improvingpatient care.

Varices

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

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


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

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

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

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

also has a left vocal fold paresis.


benign lesion, this clinical finding is frequent among professional voiceusers. In Hochman and colleagues’ [67] review of 42 patients who weretreated for ectasias and varices, 39 patients (93%) had additional lesions(eg, polyps, nodules). Again, most patients were female (81%), and mostwere professional/semiprofessional voice users or students (93%). Similarly,all of the 12 patients who had microvascular lesions treated with KTP(potassium-titanyl-phosphate) laser by Hirano and colleagues [70] had asso-ciated lesions requiring surgical treatment. In our experience, it is notunusual to find vocal fold varices with other benign lesions of the vocal foldsin professional voice users. Still, it is not known whether vocal fold varicescause other benign lesions (eg, nodules or polyps) to develop, whether thepresence of a mass lesion on the vocal folds predisposes them to developingvocal fold varices, or both. It has been hypothesized that the enlargement ofvocal fold blood vessels with significant vocal use or abuse will increasevocal fold mass and stiffness, changing vocal fold vibratory patterns, possi-bly inducing vocal fold edema and subsequent mass lesion development [62].Certainly, varices and mass lesions share the common pathway of significantvocal use, as in the case of professional voice users, as well as vocal overuseor misuse in other patients.

It is difficult to know the most common symptom caused by vocal foldvarices given their relative low-documented incidence and their coexistencewith other lesions. The most common complaint among patients in Postmaand colleagues’ [66] review was hoarseness (72%), followed by decreasedvocal range (16%) and vocal fatigue (12%). Often, these symptoms are inter-mittent, varying with voice use, and are widely accepted as common by otherclinicians as well. We have had the same experience; however, we also seea number of young conservatory singers in the laryngology clinic for baselineevaluations at the recommendation of their voice teachers. These studentshave been singing through childhood and high school, often competitively.Anecdotally, most of them have signs of laryngopharyngeal reflux, andmany have varices; however, most are asymptomatic. Sataloff and colleagues[64] also observed asymptomatic patients who had vocal fold varices.

The treatment of vocal fold varices in professional voice users is the sameas that for other patients with these lesions; however, as is the case withtreating any lesion in the vocal professional, the recommendation andtiming of treatment must be individualized to account for their potentialimpact on career goals and professional obligations. Also, the varices mayneed to be treated in conjunction with other lesions. An asymptomaticisolated varix does not require active treatment, but it should be followedwith regular VLS. Patients need to be educated about the possibility of vocalfold hemorrhage, because of the fragility of these lesions, and counseled thatif any acute significant voice change occurs, especially related to voice use orupper respiratory tract infection, strict voice rest should be observed andimmediate laryngologic evaluation obtained. Symptomatic vocal fold vari-ces should be treated in a staged fashion, depending on the frequency and


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

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


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

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

Vocal fold hemorrhage

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

recurrent vocal fold hemorrhage, also has been noted by multiple investiga-tors [63,67–69]. In addition to vocal fold hemorrhage occurring in peri-menstrual women (just before or during menstruation), women inhormone supplement withdrawal, pregnant women, or women having un-dergone gynecologic surgery [63,65], other risk factors for vocal fold hemor-rhage in patients who have vocal fold varices have been identified, includingconsumption of aspirin and aspirin products, use of nonsteroidal anti-in-flammatory drugs, coumadin therapy, and upper respiratory tract infections[61–63,65,66,76]. Laryngeal trauma, whether external or internal/iatrogenic,is another cause of vocal fold hemorrhage that is rare and not specific toprofessional voice users, but something of which they should be aware sothat they take proper safety measures (wearing seatbelts in motor vehiclesand well-fitted harnesses as warranted in their work). As with vocal foldvarices, it is possible that the apparent higher incidence of vocal fold hem-orrhage in professional voice users compared with the general population issimply a reflection of the makeup of most laryngology practices and the sen-sitivity of professional voice users to changes in voice. The incidence of vo-cal fold hemorrhage in the population at large may be much higher, butunderdiagnosed.

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

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

vocal fold hemorrhages.



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

All patients who have vocal fold hemorrhage, regardless of the need foroperative treatment, require follow-up voice evaluation and voice therapy.If a vocal fold varix is identified in the hemorrhagic vocal fold, this is fol-lowed closely and patients counseled on the potential for recurrent hemor-rhage and the possibility of resection of the varix (see above).

Standing the test of time: aging and the professional voice user

Perhaps among the highest concerns of professional voice users are theeffects of age on the voice and their potential impact on career longevity.For many professional voice users, ‘‘age-related’’ voice changes may bedue to scarring or fibrovascular changes from long-term use/overuse/misuseof the voice. The resultant increase in pitch and harshness of the voice, withdecreased vocal efficiency from vocal fold stiffness, are not specific to ageand can occur in young patients. More common complaints among agingprofessional voice users include a wobbly quality to the voice, lack of clarity,singing flat, and an inability to sing softly [80]; however, more frequentlythese changes are due to deficits in overall conditioning rather than irrevers-ible aging changes in the larynx. Therefore, it is important for the laryngol-ogist to be able to differentiate between physiologic age-related changes inthe larynx and functional changes in the voice that may occur for reasonsincluding, but not limited to, senescent global deconditioning.

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


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

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

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

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


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

Many clinicians and performers also have noted coincidental improve-ments in voice when menopausal women are treated with hormone replace-ment therapy for other reasons (genital atrophy, decreased libido,osteoporosis, prevention of cardiovascular and Alzheimer’s disease, hotflashes, psychoemotional changes, insomnia). Hormone replacement therapyis not considered a primary treatment for menopause-associated dysphonia,but it has been used by some clinicians to forestall it [85,101]. Based on this,Lindholm and colleagues [85] compared the changes in measured voicevalues and subjective voice/laryngeal symptoms in postmenopausal womenwho did not undergo hormonal therapy with those using estrogen alone oran estrogen-progestin combination. Among the 42 subjects, estrogenreplacement seemed to protect against detrimental changes in fundamentalfrequency and voice quality more than the estrogen-progestin combination;women with no hormone replacement suffered the largest negative impacts.Caruso and colleagues [90] investigated the effects of estrogen replacementon laryngeal cytology in postmenopausal women. They found that laryngealand vaginal epithelial smears in women on estrogen replacement therapyhad similar minimal cytologic changes compared with those of women with-out estrogen therapy in whom both smears showed aspects of atrophy-dystrophy. This work supports the idea that hormone replacement therapymay improve voice in postmenopausal women. Laryngologists should con-sider this when caring for perimenopausal professional voice users and discussthe possibilities of hormone replacement therapy with gynecologist colleagueson a case-by-case basis. Most important, however, is that professional voiceusers entering or beyondmenopause be under the care of an experienced voiceteam that can address perimenopausal voice changes appropriately.

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


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

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

Voice overuse

One of the most common problems in professional voice users, especiallysingers and actors, is laryngitis associated with voice overuse. This is to bedistinguished from infectious laryngitis, also common in this populationduring peak performance times, which are associated with long hours,lack of sleep, and often, poor nutrition. Reflux laryngitis also may be an un-derlying problem; however, overuse in and of itself can cause dysphonia inthe singing and the speaking voice, odynophonia, loss of range, loss of clar-ity, and early vocal fatigue. This is seen frequently in performers who are onthe road and in the middle or toward the end of a rigorous concert schedule(eg, four to seven performances in a week for 6 to 16 consecutive weeks).Pop, rock, country, and musical theater singers who sing in large openvenues with variable acoustics seem, anecdotally, to be at particular riskfor the effects of voice overuse. Many performers believe that they have in-finite use of their vocal folds and do not realize that they are athletes whoneed to rest and recover after an event. Frequent high-energy performancecan result in vocal fold edema that requires more ‘‘pushing’’ over time to getthe same results; this results in a vicsous cycle phonotrauma. Any number offindings may be present on laryngoscopy. Vocal fold edema, assumed to besubacute, overlying chronic fibrovascular changes, and sulcus deformitiesare common. Varices and resolving hemorrhage may be seen.

The best treatment of this condition is relative voice rest. Sometimes,complete voice rest for a few days may be appropriate. A frank discussionwith the performer about short- and long-term goals and obligations is im-portant to developing a management strategy. If a performance is imminent,the patient has to decide how important it isdfinancially, professionally,and emotionally. The laryngologist also has to weigh in on how dangerousfurther voice use is to the patient’s long-term vocal health. Doctor’s ordersfor voice rest can be a welcome relief to a performer. Conversely, the laryng-ologist may encounter significant resistance to this recommendation. If thisis the casedand especially if a performance is of paramount importanceda short course of high-dose oral steroids (burst and taper) can be prescribed.One practical approach is to prescribe methylprednisolone at a high firstdose with rapid taper. For example, this can be methylprednisolone, 16 mg,days 1 through 3, with a rapid taper over 3 to 4 days (eg, 12 mg, days 4 and


5; 8 mg, day 6; 4 mg, day 7). Patients are cautioned to mark during rehearsalsor not sing at all and to use the voice minimally otherwise. Sometimes per-formers have to tell their audiences that they cannot sing in full voice. Finally,all patients must be counseled that the risk for vocal fold hemorrhage and tearis higher when on steroid therapy. If any sudden decrement in voice occurs,they are instructed to observe immediate full voice rest and to seek laryngo-logic evaluation as soon as possible.

The patient is reevaluated once voice rest has been prescribed for overuseand the larynx has had time to recover. Symptoms and findings on VLS aretracked. Resumption of normal practice and performance schedules needsto be undertaken with serious caution and an appreciation for the fragilityof the larynx, and it can take place once the larynx has shown signs of im-provement (decreased edema, erythema, size of varices). Performers are en-couraged to improve vocal hygiene, maintain excellent hydration, andobserve regular periods of voice rest throughout the day. Most are able toaccomplish this while meeting their professional demands. The addition ofvoice therapy is an important vehicle for teaching and reinforcing thesestrategies and is an important management option for voice overuse.

Special considerations in caring for the professional voice user

Emphasis was placed on the importance of obtaining a complete historyas well as understanding the professional voice user’s priorities to establishtrust and to facilitate comprehensive patient care. Similarly, it is importantto approach this care with a team model, including voice therapists (some-times singing and speech therapists), the singing teacher/voice coach, andother physicians who care for the patient. Many patients are otherwisehealthy and do not see other clinicians, in which case the laryngologist fre-quently plays a primary care role, tending to questions of health mainte-nance and serving as a referral base as necessary. This is particularly truefor young patients, many of whom live away from home as students or astraveling performers. Obtaining complete social histories and taking timeto educate patients about the importance of hydration, rest, and tobacco,marijuana, alcohol, and other drug avoidance are critical to comprehensivecare. Young patients also benefit from discussions regarding short- andlong-term professional goals so that they begin to develop a realistic per-spective on the impact that their voice use has on its integrity. Becausemany professional voice users have multiple physicians who care for themand several may be on multiple medications, communication with otherphysicians is critical to coordinated care.

Summary

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


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

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

Although incidence and prevalence of inflammatory processes in the lar-ynx are not well documented, they seem common in professional voiceusers; include laryngopharyngeal reflux (common), laryngitis fromvoice overuse (common), and fungal laryngitis (uncommon in general,but being recognized more frequently in patients on inhaled steroids);and warrant aggressive treatment to restore the voice.

Muscle tension dysphonia is a frequent compensatory mechanism forother processes that should be sought out if muscle tension dysphoniais identified.

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

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

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

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

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40 (2007) 1063–1080

Vocal Emergencies

Adam M. Klein, MD, Michael M. Johns III, MD*Emory University School of Medicine, The Emory Voice Center, 550 Peachtree Street,

9th Floor, Suite 4400, Atlanta, GA 30308, USA

‘‘The laryngologist should unquestionably have a thorough understanding

of the various vocal disorders which he is in a position to observe in singers,orators, and what one might call professional voice-users. He should alsoknow the therapeutic methods suitable to apply them. We are far beyond

the time when hoarseness and other manifestations observed in this cate-gory of professional voice-users were attributed to ‘‘granular’’ pharyngitisor laryngitis.’’

E.J. Moure, 1929 [1]

The evaluation and management of voice disorders has evolved into a spe-cialized, multidisciplinary, and highly technological practice since the earlypart of the twentieth century. Nonetheless, a good portion of voice care de-livery for professional voice users is performed by general otolaryngologistswho do not have an experienced speech pathologist or videostroboscopicequipment available. Even in this modern era, many situations arise wherevocal performers are being assessed by dim light reflected off a dental mir-ror, often outside the office settingdthe means by which Czermak per-formed indirect laryngoscopy in 1860 [2]. Fortunately, the improvedquality, portability, and better affordability of endoscopic technology hasallowed for better visual assessment of the larynx in the office and the field.In addition, an increased focus on vocal awareness and education in modernotolaryngology training programs has begun to close the experience gapbetween general otolaryngologists and laryngology subspecialists.

Ultimately, the optimal care of a professional voice user with a vocalemergency occurs within a setting where a full clinical voice evaluationand laryngeal examination, including videostroboscopy, can be performed.This article is designed to be a reference guide for the treatment of vocal per-formers in the acute scenario, with the hopes of facilitating optimal treat-ment for these vocal athletes in any setting.


E-mail address: [email protected] (M.M. Johns).




1064 KLEIN & JOHNS

Essentials of the history

‘‘Unquestionably the greatest of all causes of laryngeal disease is the exces-sive use of one of its normal functions, phonation. This is not surprising inview of the fact that phonation was not the primary function of the larynx;

phylogenetically it is very late. The patient with chronic laryngeal disease isalmost always a person who either talks constantly or uses his voice profes-sionally, or often, both. There is little use asking the patient if he talks

much. For some curious reason a patient who talks all the time he is awakewill insist he talks little. It is not only the singer, the lecturer, and the huck-ster who suffer from occupational abuse of the larynx. Teachers are espe-

cially frequent sufferers and persons who talk in noisy places such asfactories where machinery is running often develop chronic hoarseness.The noise incidental to our modern life is a large factor in the great and

increasing incidence of hoarseness and laryngeal disease.’’Chevalier L. Jackson, 1942 [3]

A recent review of performers with acute illness before performance foundthat nearly 75% of complaints center around vocal difficulty, with sinuscomplaints, pharyngeal irritation, and cough being the next most commonprimary symptoms [4]. As with any chief complaint, a thorough history is im-perative when managing a vocal emergency. Detailed questionnaires havebeen published previously [5]. Unfortunately, patients typically are vagueand occasionally may withhold information when describing their vocalproblems [4]. The term ‘‘hoarseness’’ is nonspecific, and the exact symptomsneed to be elucidated further with the patient. Challenging the patient to de-scribe one’s voice problem without using general terms, such as ‘‘hoarseness’’or ‘‘laryngitis,’’ is one way of extracting more information. Asking ‘‘What isyour voice doing that it should not do?’’ and ‘‘What is your voice not doingthat it should do?’’ are two useful questions to prompt the patient further.

Patients should be questioned regarding the details surrounding the onsetof the vocal disorder. Any vocal change with a sudden onset (particularly anacute change that occurs during phonation) is a red flag for a vocal foldhemorrhage or mucosal tear. This finding must be investigated furtherwith laryngeal imaging. Ask specific questions about loss of range or lossof vocal control. Loss of high range during soft singing is a sensitive indica-tor of vocal fold swelling. Increased effort in singing and delay in vocal onsetare other manifestations of vocal fold mucosal edema or lesions. Changes invocal quality, effort, endurance, and fatigue; the ability to sing or speakloudly or softly at various frequencies; or limitations in dynamic range oftengive clues that vocal fold pathology is present or developing. The symptomsof throat clearing, rhinorrhea, or coughing may represent associated condi-tions requiring medical attention, such as laryngopharyngeal reflux (LPR),allergic rhinitis, acute or chronic rhinosinusitis, or an acute upper respira-tory tract infection.

The physician should gather information regarding the patient’s level oftraining and vocal awareness. Details of vocal warm-up routines, length and

1065VOCAL EMERGENCIES

frequency of performances, and vocal obligations between events should benoted. This information will help the clinician to understand the degree ofvocal demand and what can and cannot be modified to minimizephonotrauma.

Once the parameters of the chief complaint have been established, it isimportant for the physician to understand the performance environmentand schedule. Not infrequently, these patients are seen on site, allowingfor a first-hand assessment of the performance venue. Evaluation of theacoustics, the amplification system, competing sound sources, temperature,cleanliness, air filtration system, and allergen exposures aid in understandingthe patient’s relative risk for exacerbating a voice disorder. Often, simplediscussion with the stage manager/director/sound technician yields a solu-tion for short- and long-term issues. The primary goal is to minimize laryn-geal irritants and maximize the acoustic environment (eg, quality vocalmonitors) for the performer.

The event schedule and importance of upcoming events should be closelyreviewed with the patient and their manager, if available. There are signifi-cant differences in management options if the patient is being evaluated dur-ing intermission, hours before a show, or days before a show. Howupcoming events relate to the patient’s short, medium and long-term careergoals is a vital perspective to gain for the purposes of making managementdecisions. The financial implications of missing an event or events shouldalso be taken into consideration.

Differential diagnosis of vocal emergencies in the performing artist

A wide variety of pathology can lead to acute dysphonia in performersand result in vocal emergency [6]. Box 1 lists the most common presentingdiagnoses.

Vocal fold hemorrhage

Vocal fold hemorrhages are the result of acute phonotrauma and can beconsidered a ‘‘vocal accident’’ (Fig. 1). The shearing forces within the super-ficial lamina propria layer tear the microvasculature, allowing blood tospread within Reinke’s space. The amount of blood and extent of spread de-pend on the size of the vessel, the fluid pressure within the vessel, and thecontents of Reinke’s space (eg, scar tissue may prevent spread of extravasat-ing blood). Patients commonly note sudden voice change that occurredwhile performing a strenuous vocal task. Anticoagulation (eg, aspirin, non-steroidal anti-inflammatory drugs [NSAIDs], warfarin sodium) and hor-monal changes (eg, perimenstrual) put singers at risk for the developmentof a hemorrhage [7]. Women should avoid the use of NSAIDs and aspirinin the premenstrual and menstrual periods. Identification of a vocal fold

1066 KLEIN & JOHNS

hemorrhage in the acutely dysphonic performer is extremely important andis the primary reason why laryngoscopy needs to be performed during theassessment. Vocal fold hemorrhage is treated with absolute voice rest,with or without corticosteroids, until resolution has occurred (ie, resorption

Box 1. Differential diagnosis

Vocal fold hemorrhageVocal fold mucosal tearAcute laryngitis

ViralBacterialFungalPhonotraumatic edema

Acute edema on chronic fibrovascular (subepithelial)change/preexisting lesions

Asthma exacerbationUpper respiratory tract infection

Pharyngitis, viral/bacterialRhinosinusitis, viral/bacterialBronchitis, viral/bacterial

Allergic rhinitisLPR exacerbationHormonal/endocrine changes

Fig. 1. Acute vocal fold hemorrhage. Note diffuse distribution of blood within the superficial

lamina propria (Reinke’s space) of the left true vocal fold.


or migration of blood away from the vibratory margin). This usually in-cludes cancellation of scheduled performances; thus, the otolaryngologistmust be prepared to support the patient in interactions with management.Patients need to be advised of the serious risk for scar or lesion developmentif they are to perform through a vocal fold hemorrhage.

Vocal fold mucosal tear

Mucosal tears usually result from an episode of harmful singing, yelling, orsevere coughing/retching. The overwhelming shearing forces exerted upon theepithelium and superficial lamina propria cause the tissue to literally separate(Fig. 2) [8]. The acute symptoms include immediate hoarseness, loss of range,anddiscomfort.Amucosal tearmay appear as a visible break in themucosa onstroboscopy, presenting as a jagged edge in the epithelium. Initial findings onexamination also can include vocal fold hemorrhage, edema, erythema, andstiffness on videostrobolaryngoscopy.Often, a tear can be difficult to diagnosein the acute setting, andone should have a low threshold to place a patientwiththese symptoms on absolute voice rest with close serial evaluation. If completevoice rest is followed, healing usually occurs without sequelae. If phonation orcoughing persists in the setting of a tear, the epithelium may heal to the liga-ment, creating a sulcus, or curl up on itself, resulting in an epithelial band.Both of these sequelae can result in an adynamic segment on the phonatorysurface of the true vocal fold.

Acute laryngitis

As with many upper respiratory tract infections, the cause of infectiouslaryngitis can be viral, bacterial, or fungal. Fungal laryngitis should be

Fig. 2. Acute vocal fold mucosal tear. Arrow denotes location of mucosal tear. Notice clear

break in mucosa. (Courtesy of A. Rubin, MD, St. Clair Shores, MI.)

1068 KLEIN & JOHNS

suspected in immunocompromised patients and in those on inhaled or sys-temic steroids. Regardless of the pathogen, the effect is essentially identicalin the acute setting: Reinke’s space (the superficial lamina propria layer) en-gorges with inflammatory cells, resulting in increased mass (Fig. 3). Thisprevents the vocal fold from vibrating periodically. The addition of vocalfold mass and irregular vibration creates a lower or raspy tone. In singers,this also translates into a difficulty, or an inability, in attaining higher fre-quencies because the vocal folds need to oscillate more quickly at thesepitches [9]. Intermittent voice breaks and changes in register transition areadditional symptoms. Phonotraumatic edema has the same effect, but it ismore easily treatable with conservative measures.

Relative or absolute voice rest is the mainstay of treatment, depending onthe severity of the edema. Mild to moderate edema can be treated with rel-ative voice rest and adjunctive measures noted below. Severe edema shouldbe treated with absolute voice rest. Additionally, the patient should be ad-vised against the use of NSAIDs, because there is an increased risk for vocalfold hemorrhage secondary to the fragility of the vocal fold blood vessels inthe acutely inflamed state. Appropriate antibiotics should be prescribed ifclinical suspicion for bacterial infection is present. For mild to moderate vo-cal fold edema, corticosteroids can be used acutely to treat edema effectivelyand facilitate performance. Intramuscular steroids, such as dexamethasoneand cortisone, can begin to have an effect within 1 hour; oral steroids,such as prednisone and methylprednisolone, typically produce the desiredeffect within 1 day. Patients should be reexamined before returning to

Fig. 3. Acute laryngitis. Note boggy edema and erythema of the true vocal folds with irregular

free glottal edges. Prominent varices also can be seen.


performance. Steroids have limited effect in cases of severe edema. In gen-eral, steroids should be used with caution, counseling patients regardingthe risk for vocal fold hemorrhage, mood swings, agitation, appetite change,sleep disturbance, acid reflux exacerbation, and more serious but rare risks,such as osteopenia, precipitation or worsening of diabetes, gastric or duode-nal ulcers, and avascular necrosis of the hip. Steroids should not be used inisolation without modified voice rest, defined as essential voice use only, andsupportive measures. Vocal fold tear, hemorrhage, scarring, or permanenthoarseness are risks that need to be discussed with the patient when per-forming while taking steroids. Often, the voice sounds normal, despite theacutely fragile state of the vocal folds. The otolaryngologist also needs to beaware of performers living ‘‘shot to shot,’’ using steroids as a crutch forvoice overuse or misuse. Taking a careful history about steroid use and ef-fect can give clues to this problem. Vocal rehabilitation with voice therapyhelps to free these patients from their chronic steroid use by instilling funda-mental changes in how they use their voice and maximizing vocal efficiency.

Acute edema on chronic fibrovascular change

Phonotrauma in a setting of chronic fibrovascular change often results inacute edema, which results as a consequence of the increased vocal effortnecessary to overcome the decreased pliability of the scarred regions. Thecombination of these changes results in convexities of the midmusculo-membranous true vocal folds. During phonation, these areas contact pre-maturelydresulting in an ‘‘hourglass configuration’’dand air escapesanterior and posterior to the lesions. In addition, the affected areas arestiffer than the surrounding superficial lamina propria, resulting in a differen-tial pliability between the two vocal folds and within each true vocal fold.Diagnosis is difficult without videostroboscopy, and short-term manage-ment is similar to acute laryngitis.

Upper respiratory tract infection

Viral and bacterial upper respiratory tract infections can lead indirectlyto acute vocal changes by way of localized edema, secretions, pain, throatclearing, coughing, dehydration, generalized malaise, nasal congestion, orheadaches. A careful history of onset, location, and severity of symptomsand physical examination helps make the diagnosis and treatment andshould be directed to the site of pathology. Empiric treatment with antibi-otics is warranted in cases with suspected bacterial etiology. Symptomaticrelief of nasal congestion can be achieved with the short-term use of topicalnasal decongestants (eg, oxymetazoline). Topical nasal steroid sprays alsocan be helpful in the acute setting. Oral decongestants (eg, pseudoephedrine)can be extremely drying and may have secondary deleterious effects. The useof drying agents can lead to increased shearing forces, predisposing patients

1070 KLEIN & JOHNS

to vocal fold tears, subepithelial thickening, and fibrosis. Patients should becautioned regarding the use of topical anesthetics for pharyngitis becausenumbness can lead to loss of vocal control. Vigorous hydration and modi-fied voice use is encouraged. Performance during an acute upper respiratorytract infection is discouraged.

Allergic rhinitis

The rhinorrhea and nasal mucosal swelling associated with allergic rhini-tis can affect the vocal performer significantly, although symptoms rarelyare severe enough to warrant show cancellation. Short-term relief can beachieved with oral antihistamines and nasal decongestion, although patientsshould be warned about the drying side effects and potential sedation seenwith antihistamines. Newer antihistamines (eg, loratadine) have less anti-cholinergic side effects. Long-term treatment of allergic rhinitis with appro-priate therapy (eg, nasal steroids, oral or topical antihistamines, leukotrieneantagonists, mast-cell stabilizers, immunotherapy) should be recommendedas indicated [10].

Laryngopharyngeal reflux

Performers are particularly at risk for the development of symptomsfrom LPR [11]. Erratic dietary habits, stress, and abdominal support asso-ciated with singingdcombined with the sensitive nature of high-level vocalperformancedmake the vocal performer more susceptible to acute vocalchange from LPR. Patients should be queried regarding typical gastro-esophageal reflux disease symptoms of heartburn and regurgitation and typ-ical LPR symptoms of throat clearing, globus, cough, and postnasal drip.The threshold for treatment with dietary, behavioral, and medical therapy(proton-pump inhibitors [PPIs] and histamine-2 receptor (H2)-blockers)should be low, and the otolaryngologist should be aware that LPR maybe an exacerbant to other acute ailments, such as acute laryngitis and pho-notrauma. In the acute setting, over-the-counter antacids may be of benefit.Treating reflux acutely and aggressively with twice-daily dosing of PPIs anda nighttime dose of an H2-blocker, even in asymptomatic individuals, mayhasten recovery from an upper respiratory tract infection.

Acute asthma exacerbation

Aswith the general population, professional voice users are subject tomed-ical conditions that may affect vocal quality. Asthma can diminish vocalstrength, endurance, and quality byweakening the power source to the larynx.It is important to recognize this problem so that proper medical managementfor an acute asthma exacerbation can be instituted in a timely fashion. Inhaledsteroids in conjunction with rescue inhalers are the mainstay of treatment forreactive airway disease. The clinician and the patient need to be aware of the


deleterious effects that inhaled steroids can have on vocal foldmuscle bulk, thevoice, and the predisposition to fungal laryngitis [12]. When possible, the pa-tient should discuss using noninhaled or nebulized preparations to treatasthma acutely and chronically with his/her pulmonologist.

Functional dysphonia

Vocal performers and orators experience a significant amount of stress oranxiety, especially when nearing an event or performance. Poor vocal be-haviors, including muscle tension dysphonia, can create speaking and sing-ing difficulties that may require urgent voice therapy intervention beforevocal performance. Stage fright is a behavioral problem that is addressedbest with behavioral solutions. The anxiety associated with performanceleads to a sympathetic ‘‘fight or flight’’ response. The main adverse conse-quence for the vocal performer is overwhelming anxiety that manifests as ex-cessive laryngeal muscle tension and reduced breath support. The result isimpaired vocal performance. Intervention consists of strategies to optimizerespiration support and phonatory control, maximizing resonance, and re-assurance. Hydration and good health habits are essential adjuncts. Per-formers should be advised to avoid turning to b-blockers and anxiolytics.These medications blunt mental and physical sharpness as well as the perfor-mance edge that results from the natural sympathetic response necessary foroptimal performance. Identification of these problems and an establishedrelationship with a trained voice/singing pathologist are essential to addressthis issue adequately.

Site of the evaluation

Phone triage

As one would infer from the label ‘‘vocal emergencies,’’ such events docommand a sense of urgency. Often, the problem is not a threat to the pa-tient’s long-term vocal health, but it is a threat to one’s imminent vocalobligation. A politician who enters a debate with a weak voice or frequentthroat clearing does so at a distinct disadvantage. A lyric soprano who is un-able to lilt gracefully through her upper register will earn the label of unreli-able. Amidst the vocal crisis, the performing artist is rehearsing his/her lines,applying makeup, or resting to compensate for weeks of little or no sleep.For all of these reasons, voice professionals often phone the physicianwith the expectation that he/she will understand the predicament and pro-vide last-minute, free advice. Not infrequently, the call comes from thepatient’s manager, who attempts to convey the patient’s symptoms withlimited information, making medical management difficult.

Ideally, the otolaryngologist can overcome this obstacle by seeing thepatient in the office or, rarely, by driving to the venue to see the patient

1072 KLEIN & JOHNS

personally; this is not always possibledespecially if the patient has traveledout of the areadand treatment decisions may have to be made over thephone. One must go back to the history and extract any available datathat may give a clue as to the likely diagnosis. Was the onset of the vocaldisorder an acute event that occurred during a show? Is it part of a patternthat occurs after every show? Can the patient sing/speak at all? Is pain as-sociated with phonation? Can the patient even warm up his/her voice? Isthe patient sick?

Usually, an illness resulting in vocal difficulties is apparent. Patients com-plaining of hoarseness associated with the symptoms of rhinosinusitis or anacute upper respiratory tract infection will need over-the-counter or pre-scription medications quickly in an attempt to lessen the effect on the voiceas soon as possible, followed by a reassessment. They occasionally requesttheir ‘‘usual’’ remedy, such as steroids, NSAIDS, or vitamin B12. The issuessurrounding these medications are discussed later.

When triaging a vocal emergency over the phone, significant trust is re-quired on the part of the physician. Voice professionals have significantpressures placed upon them to proceed with the upcoming vocal obligation,which can cloud judgment. The job of the physician is to gather enough in-formation about the medical event, the details, the importance of the perfor-mance situation, and the patient’s ‘‘gut’’ feeling to provide professionalguidance. The otolaryngologist should have a low threshold to requestthat the patient be seendeither by one’s usual otolaryngologist or a col-leaguedto ensure safety of performance. Ultimately, the decision to per-form or not to perform will have to be entrusted to the patient.

On-site evaluation

The ideal setting for the evaluation of the acutely ill performer is in thephysician’s office, where the full diagnostic armamentarium is present.This is particularly true for the patient with acute voice change in whomhigh-resolution laryngeal imaging and videostroboscopy are essential for ac-curate diagnosis. Thus, in general, otolaryngologists are advised against go-ing to the site to evaluate the patient in lieu of an office visit. Circumstancesmay arise, however, when an on-site evaluation is the only option. If a pa-tient needs to be evaluated within minutes to hours before a scheduled per-formance, evaluation of the patient at the venue is better than letting thepatient risk performance when one should cancel.

On-site evaluation does allow the clinician to see the performance venueand its acoustic and environmental features. One also can request to see thetransportation vehicle, if any, which is being used for long road trips. Thismay reveal potential allergens, irritants, or other factors that can contributeto voice disorders.

There are clearly significant limitations in the ability to diagnose andtreat optimally in on-site settings. The main limitation is the lack of easily


portable laryngeal videostroboscopy and high-resolution laryngeal imagingequipment. Advancing technology is moderating this limitation, and oneshould be equipped with appropriate instruments and therapeutics (see‘‘Tools’’ section) if he/she is going to be able to provide adequate on-sitecare.

Office evaluation

The office setting offers the best facilities to optimize patient care. Thisseparates the patient from one’s stressful setting to allow for a more focusedinterview, and the otolaryngologist will have the full array of diagnostic in-strumentation to make an accurate diagnosis and guide treatment. Outsideof an insightful history and general otolaryngologic examination, videostro-boscopy is the most clinically useful tool for the acutely dysphonic per-former. Subtle vocal fold edema, lesions, glottal closure, and vocal foldmucosal pliability can be assessed clearly, and severe problems (eg, vocalfold hemorrhage) can be ruled out.

The tools you need: essential equipment to evaluate the professional

voice user

On-site location

For the unusual circumstance when an on-site evaluation is the only fea-sible option, the ‘‘doctor’s bag’’ should be equipped properly for the situa-tion. A charged otoscope and light source are essential. Nasal specula,tongue depressors, 4 � 4 gauze, various syringes and needles, topical decon-gestants and anesthetics, nonlatex gloves, head mirror or headlight, curvedcannulas, injectable steroids and vitamin B12, ear curettes, various dentalmirrors, alcohol swabs, a defogging agent, over-the-counter medications(eg, anti-inflammatories, decongestants, cough suppressant, phenylephrine,mucolytic), and antibiotic samples are the basic equipment necessary tohandle most situations.

Limitations in equipment portability are being overcome by technologi-cal advances. Flexible fiberoptic laryngoscopes are readily available, asare the portable light sources that can optimize the assessment of a vocalemergency on site; however, one should be armed with other equipment be-cause many patients will refuse the topical anesthetic (out of fear that it willaffect one’s voice or swallowing) or simply will not tolerate the nasolaryngo-scopy procedure. Rigid scopes also can be attached to portable light sourcesand are equally equipped with an eyepiece to provide direct visualization ofthe larynx. Historically, stroboscopy has not been an option, although por-table stroboscopy units are becoming available, and handheld strobe lightsare under development. The key is to have rigid or flexible endoscopy withquality illumination and, ideally, videostroboscopy to allow clear

1074 KLEIN & JOHNS

visualization of the larynx. Without this equipment, otolaryngologists arediscouraged from evaluating patients on site.

Office location

The optimal setting for the acute evaluation and management of a vocalcrisis is the medical office. Pulling the patient out of one’s element limits dis-tractions and preoccupations and aids in focusing on the matter at hand.Clearly, the availability of videostroboscopic equipment enables the laryng-ologist to improve one’s ability to accurately diagnose and, therefore, treatthe ailment. Some pathologic processes are obvious enough that a dentalmirror or flexible fiberoptic laryngoscope could reveal the pertinent findings;however, it does not provide useful information regarding the effects of thepathology on the laryngeal biomechanics and vocal fold oscillation. Inaddition, the resolution and magnification may be inadequate to revealsecondary pathologies or chronic fibrovascular changes.

Typically, the decision to purchase a videostroboscopy unit is driven byfinances; one needs to treat enough patients who have voice disorders to jus-tify the initial and maintenance costs of the equipment. One should con-sider, however, that with competition in the market growing at analarming rate, many affordable, satisfactory units are available.

Aside from proper imaging equipment, one must be prepared to treatpatients acutely, because there may be only hours before a performanceor vocal commitment. Therefore, a stock of injectable steroids and othercommonly used medications is essential. Maintaining a supply of over-the-counter remedies can help to postpone a trip to the pharmacy for theperformer or production staff until a more convenient time is available.

Evaluation and management of the acutely ill performer

Hours until show time

Thepressure of performance is transferred from the patient to the physicianin these situations. A significant amount of time, money, and effort has beeninvested in preparation for the upcoming event, and the gears are in full mo-tion. Accurate diagnosis and thoughtful management decision making is im-perative. The otolaryngologist primarily should determine if a vocal foldhemorrhage, vocal fold tear, or other significant laryngeal injury hasoccurred to warrant cancellation of the performance. Therefore, visualizingthe larynx in someway is imperative. In the absence of a show-stoppingfindingand after the most accurate possible diagnosis has been made, a frank discus-sion should occur between the patient andphysician, involving the event/showmanagement only at the patient’s discretion. This discussion should focus onwhether the patient believes that he/she will be able to perform acceptably. Ifthe patient feels that he/she simply cannot perform, then it is the physician’s


obligation to advocate for the patient. Most patients will want to perform, inwhich case supportive measures to facilitate vocal performance can bepursued.

Days until show time

The benefit of having several days to manage a vocal emergency is simplyhaving the luxury of time. Patients can be seen in the office with optimum di-agnostic equipment and the benefit of videostroboscopy. Precise diagnosisplus time for healing and therapy to take effect improve the odds of full perfor-mance at show time. The option of voice rest is opened, because many acutephonotraumatic events resolve spontaneously. If a vocal fold hemorrhagehas occurred, serial observation for resolution can be performed, and showcancellation may be avoided. The luxury of time also enables the otolaryngol-ogist to administer a larger range ofmedications. Antibiotics, steroids (if indi-cated), and supportive medications will have time to take effect. Oral steroidscan be used in lieu of intramuscular injection, and voice therapy can be enter-tained. Working with a speech pathologist with singing expertise offers thebenefit of optimizing techniques and repertoire to help set vocal limitations,prevent further phonotrauma, and optimize upcoming performances.

Weeks/months until show time

Extended time until performance allows for more involved, planned man-agement of vocal emergencies. The short-, medium-, and long-term vocalgoals can be considered and weighed into the decision-making process.The role of voice therapy to modify maladaptive vocal behaviors becomesmore important, and working with a skilled speech pathologist or singingvoice specialist should be encouraged. Disorders, such as LPR, allergic rhi-nitis, and chronic sinusitis, can be managed more effectively. Acute changescan be sorted out from chronic changes, allowing the performer to return tobaseline before returning to intense voice use.

Adjunctive medical therapy: steroids and other medications

Corticosteroids

A variety of corticosteroids can be used to treat acute vocal fold edemaarising from phonotraumatic laryngitis and acute infectious laryngitis. Judi-cious use of these medications can allow a vocal professional to perform suc-cessfully through a short period of vocal demand until a period of rest isavailable. Patients need to understand that steroids are a short-term solu-tion, cannot be used frequently with hope for significant effects, and carryrisks for significant side effects. Vocal performers who develop acute phono-traumatic laryngitis from voice abuse and misuse are most at risk for re-peated corticosteroid abuse. Steroids give the false impression that there is

1076 KLEIN & JOHNS

a quick fix for voice abuse and that the risk for chronically abusing the voiceis small. Fortunately, most performers who have acute laryngeal edema areresponsible individuals who have had the misfortune of acquiring a viral ill-ness at an inopportune time. These patients are ideal candidates for acuteuse of steroids to facilitate performance. The authors’ choice for intramus-cular corticosteroids in the acute setting is a mixture of dexamethasone,5 mg (4 mg/mL ¼ 1.25 mL) and methylprednisolone acetate (Depomedrol),100 mg (80 mg/mL ¼ 1.25 mL). The dexamethasone has onset of effectwithin an hour and lasts approximately 24 hours. Depomedrol begins totake effect within 24 hours and has effect for approximately 5 days. A shortburst and taper of oral methylprednisolone is the authors’ choice for oralsteroids. A corticosteroid dosing equivalency chart is given in Table 1.

Nonsteroidal anti-inflammatory drugs

Ibuprofen and other NSAIDs commonly are available over the counterand are taken frequently by ill performers to relieve sore throat and facialdiscomfort. Although the anti-inflammatory effect of these medicationsmay be beneficial, the risk for vocal fold hemorrhage from their anticoagu-lative properties likely warrants the use of acetaminophen as an alternative.

Decongestants

Oral decongestants, such as pseudoephedrine, are common ingredients inover-the-counter cold remedies. These medications are effective in providingnasal decongestion; however, they come with a high price of significant vo-cal fold, oral, and pharyngeal dryness, all of which can affect vocal effort[13]. Short courses of topical nasal decongestants (eg, oxymetolazone andphenylephrine) have minimal systemic side effects and are effective; how-ever, they carry the risk for rhinitis medicamentosa and should only beused for three to five consecutive days.

Antihistamines

Similar to oral decongestants, many cold remedies contain antihista-mines. These medications are effective for sneezing and symptoms of allergicrhinitis, but also have a drying effect, although less severe than with oral de-congestants. Patients should be counseled regarding these medications’ sideeffects. Nonsedating antihistamines (eg, loratadine) are more appropriate touse around performance times than are sedating antihistamines (eg,diphenhydramine).

Mucolytics

Mucolytics, such as guaifenesin, offer symptomatic relief by thinningsecretions. Short- and long-acting formulations are available. Long-acting

Table 1

Corticosteroid com

drocortisone Half-life

Agent Mineral-corticoid Plasma (min) Duration of action (h)

Short acting

Hydrocortisone 1 90 8–12

Cortisone acetat 0.8 30 8–12

Intermediate acting

Prednisone 0.8 60 12–36

Prednisolone 0.8 200 12–36

Triamcinolone 0 300 12–36

Methylprednisol 0.5 180 12–36

Long acting

Dexamethasone 0 200 36–54

Betamethasone 0 300 36–54

Commonly pres mg ¼ dexamethasone, 0.75 mg ¼ hydrocortisone (Cortef), 20 mg.

Data from Adre ouis (MO): Facts and Comparisons, Inc.; 1997. p. 122–8.

1077

VOCALEMERGENCIE

S

parison chart

Equivalent glucocorticoid

dose (mg)

Potency relative to hy

Anti- inflammatory

(Cortef, Cortisol) 20 1

e 25 0.8

5 4

5 4

4 5

one 4 5

0.75 30

0.6 30

cribed replacement steroid equivalents: prednisone, 5 mg ¼ cortisone, 25

nal cortical steroids. In: Drug facts and comparisons. 5th edition. St. L

1078 KLEIN & JOHNS

Mucinex (guaifenesin), 1200 mg twice daily, is helpful for relieving the sen-sation of excess mucus.

Other medications

Inhaled steroids are to be avoided in acute laryngitis because of theknown risk for dysphonia and fungal superinfection associated with thesemedications [14]. Many performing artists report an improved sense ofwell-being with a vitamin B12 injection intramuscularly when they are ill.The efficacy of this is unknown. Patients should be counseled that herbalremedies are not without risk and should be taken judiciously. Many vita-mins and herbs can have drying or anticoagulant properties. Likewise, innu-merable throat sprays and lozenges are available whose efficacy have notbeen proven. In general, the authors recommend that performers avoidany spray, lozenge, or liquid that gives a numb or tingling feeling in thethroat (eg, menthol- or benzocaine-containing preparations).

Humidification and hydration

The benefits of humidification and hydration cannot be overstated.Articulation and vocal fold oscillation are affected significantly by dry envi-ronments. Oral hydration and steam inhalation can help to fight the effectsof dryness in the laryngopharynx.

When to cancel a show

‘‘The importance of the singer’s voice in his long-term career plans, the im-portance of the upcoming performance, and the consequences of canceling

the concert must be seriously considered. In the frequent borderline condi-tions, the condition of the larynx must be weighed against other factors af-fecting the singer as an artist.’’

R.T. Sataloff, 1991 [15,16]

Making the recommendation for a professional singer or speaker not toperform can be an extremely difficult decision. Pressure for these individualsto perform can be extreme. The cost of canceling an event extends beyondthe large financial cost to the patient, crew, and venue. Artists and oratorsare loyal to their fan base and do not want to disappoint. Despite these pres-sures, it must be kept in mind that the treating physician is advocating forthe patient’s well-being now and in the future. Absolute indications for non-performance are acute vocal fold hemorrhage and acute vocal fold tear. De-spite the desires of the patient, recommendation should be absolute voicerest in these situations to avoid the potential of vocal fold scarring. Outsideof these situations, the decision to cancel a show is a judgment call betweenphysician and patient. The physician must decide whether the severity of the


laryngeal findings puts the patient at risk for scarring or hemorrhage while‘‘singing sick.’’ Fortunately, these circumstances arise infrequently. Addi-tionally, the patient must decide if he/she feels able to perform acceptablywell. If the patient wishes to perform, full discussion of the potential adverseconsequences of the decision (eg, permanent vocal fold scarring) has to oc-cur with the artist. If the patient does not feel that he/she is physically capa-ble of performing, it is the physician’s obligation to advocate for the patientand recommend nonperformance. The decision to recommend nonperfor-mance is rare; in a review of 40 singers with acute illness before show

No

Acutely ill vocalperformer

Significantchange in voice

quality

• Full performance • Medical evaluation and therapy as appropriate

• Evaluation by otolaryngologist in office or on-site (rarely)• Laryngoscopy (with stroboscopy, ideally): rigid transoral, flexible transnasal

Vocal foldhemorrhage or

tear?

Risk of jeopardizing career? • By suboptimal performance • By further laryngeal injury/severe laryngitis

• Non-performance • Absolute voice rest • Medical therapy as indicated• Follow up in clinic

Laryngealedema?

• Full performance • Medical therapy as indicated• Follow up by phone or in clinic

• Modified voice rest • Consider modification of performance duration/intensity• Consider corticosteroids; oral or intramuscular depending on time to performance • Medical therapy as indicated • Follow up in clinic next day following performance

Phonetriage

Yes

NoYes

Yes

No

No Mild/Moderate

Note: Individual situations vary and care should betailored to the patient’s specific needs and

circumstances

Severe

Fig. 4. Management algorithm: less than 24 hours until performance.

1080 KLEIN & JOHNS

time, cancellation of performance was necessary in only two cases [4]. Asimple algorithm for management is outlined in Fig. 4.

Summary

Acute management of vocal emergencies can be a difficult and stressfulelement of this specialty. A thoughtful history, coupled with appropriate di-agnostic instrumentation, is the cornerstone of evaluating a patient witha vocal emergency. Understanding the various causes of acute dysphoniain the performing artist, as well as awareness of the additional pressuresplaced upon performing artists, empowers the otolaryngologist to helppatients in this specialty.

References

[1] Moure E. The vocal organ in singing. Overuse and misuse of the voice. In: Jackson C,

Coates G, editors. The nose, throat and ear and their diseases. Philadelphia: W.B. Saun-

ders Company; 1929. p. 809–23.

[2] Zeitels SM. Premalignant epithelium and microinvasive cancer of the vocal fold: the evolu-

tion of phonomicrosurgical management. Laryngoscope 1995;105:1–51.

[3] Jackson C, Jackson CL. Diseases and injuries of the larynx. New York: The Macmillan

Company; 1942. 38–56.

[4] Mishra S, Rosen CA, Murry T. 24 hours prior to curtain. J Voice 2000;14:92–8.

[5] SataloffRT. Professional voice: the science and art of clinical care. SanDiego (CA): Singular

Publishing Group; 1997.

[6] Punt NA. Management of ENT disabilities of singers. Proc R Soc Med 1973;66:1073–5.

[7] Neely JL, Rosen C. Vocal fold hemorrhage associated with coumadin therapy in an opera

singer. J Voice 2000;14:272–7.

[8] Sataloff RT, Spiegel JR, HawkshawM. Acute mucosal tear and vocal fold hemorrhage. Ear

Nose Throat J 1994;73:633.

[9] Sataloff RT, Shaw A, Markiewicz A. Acute laryngitis in a professional singer. Ear Nose

Throat J 2001;80(7):436.

[10] McGrath KG, Patterson R. Allergic rhinitis jeopardizing the careers of professional singers,

justifies intense therapy. Allergy Proc 1988;9:665–7.

[11] Hone SW, Donnelly MJ, Robertson J, et al. Dysphonia and inhalation of corticoids: a pro-

spective study. Rev Laryngol Otol Rhinol (Bord) 1996;117(4):331–3 [in French].

[12] Cammarota G, Elia F, Cianci R, et al. Worsening of gastroesophageal reflux symptoms in

professional singers during performances. J Clin Gastroenterol 2003;36:403–4.

[13] Verdolini K, Titze IR, Fennell A. Dependence of phonatory effort on hydration level.

J Speech Hear Res 1994;37(5):1001–7.

[14] Gallivan GJ, Gallivan KH, Gallivan HK. Inhaled corticosteroids: hazardous effects on

voicedan update. J Voice 2006;21(1):101–11.


2:251–66.

[16] Kay M, Hicks D. Voice pathology. In: Tucker HM, editor. The larynx. New York: Thieme

Medical Publishers; 1993. p. 156–8.


40 (2007) 1081–1090

Effects of Medications on the Voice

Mona M. Abaza, MDa, Steven Levy, MDb,Mary J. Hawkshaw, BSN, RN, CORLNc,

Robert T. Sataloff, MD, DMAc,*aDepartment of Otolaryngology, University of Colorado School of Medicine,

Denver, CO 80262, USAbPhiladelphia Ear, Nose and Throat Associates, 1721 Pine Street,

Philadelphia, PA 19103, USAcDepartment of Otolaryngology-Head and Neck Surgery, Drexel University College


Otolaryngologists should be familiar with the potential side effects andinteractions of medications that are prescribed commonly to professionalvoice users. Because some of these side effects are atypical and can be psy-chiatric symptoms, their relationship to medications might not be obvious.Oropharyngeal dryness, voice changes, movement changes, mood distur-bances (eg, agitation, anxiety, depression, and mania), perceptualdisturbances (eg, hallucinations and delusions), cognitive disturbances (eg,delirium and confusion), behavioral disturbances (eg, insomnia), and druginteractions are all important possibilities of which the prudent practitionershould be aware. Drug-induced symptoms can occur even with standarddosages and at any time during the course of treatment. An awareness ofthe potential for side effects caused by adrenocorticoids, antihistamines,decongestants, antisecretory drugs, and other medications will help theclinician to avoid or detect and treat drug-induced disorders, as will anawareness of the potential for side effects caused by combinations of medi-cations. Identification of individual risk factors, such as age, preexisting or-ganic brain disease, a history of drug abuse or dependence, or coexisting orpreexisting psychiatric disorders, is important in preventing and detectingdrug-induced disorders. The drugs discussed in this article can have seriousdand even fataldinteractions with certain medications.

The combination of some of the medications prescribed by several practi-tioners, including otolaryngologists, psychiatrists, and naturopathic care givers,






1082 ABAZA et al

has the potential to enhance or interfere with the therapeutic effects of one orthe other. In addition to psychiatric side effects, other adverse reactions canoccur (eg, cardiac arrhythmias, hypertension, and local effects). Certainly, allreactions, particularly psychiatric symptoms, are not caused by medication;however, some can be a manifestation of a coexisting or preexisting psychiatricor other disorder that has been aggravated by a combination of medications.

Drug-induced psychiatric disorders

The manifestations of drug-induced psychiatric disorders can be relatedto direct drug toxicity or to interference with the brain’s metabolism of cer-tain drugs. The most common psychiatric symptoms include delirium(an acute reaction with fluctuating awareness of self and environment), con-fusion, disorientation, tremor, ataxia, andmania. Associated behavioral signsinclude increased physical activity, rapid speech, insomnia, and mood eleva-tion. Psychiatric symptoms that occur during the course of treatment alsomay be related to the medical or psychiatric condition being treated. Forexample, anxiety disorders and panic attacks are known to occur in asso-ciation with thyroid, parathyroid, and adrenocortical disorders; Langhan’scell endocrinopathies; collagen vascular disorders (eg, systemic lupus eryth-ematosus, rheumatoid arthritis, temporal arteritis, and periarteritis no-dosa); neurologic (eg, multiple sclerosis) and neurotologic (eg, Meniere’sdisease) [1]. Delusions (the perception that one’s environment and circum-stances seem unfamiliar) can occur in association with certain endocrino-pathies [1]. Derealization (the feeling that familiar events seem unreal,strange, or dream-like and that colors, objects, and shapes appear to bedistorted) and delusions have been reported in systemic lupus erythemato-sus [1].

A detailed history aids in the clinician’s assessment of each patient’s risk.The history should include the following questions:

� What prescription medications, over-the-counter (OTC) medications,and herbal remedies are the patient taking?� Are there any coexisting medical conditions?� Is there a personal or family history of a psychiatric disorder?� Is there a history of a reaction to a psychiatric drug?� Is there a history of drug or alcohol abuse?

The patient’s age also is an important factor when deciding which med-ications to prescribe. Elderly patients have a greater risk for drug-inducedpsychiatric disorders because they tend to be taking more medicationsand, therefore, are more likely to experience drug interactions. Olderpatients also tend to have other medical conditions that can prolong drugmetabolism and increase systemic drug levels.

Preexisting organic brain disease and drug abuse also can be risk factorsfor the development of psychiatric side effects. Patients who have a history

1083EFFECTS OF MEDICATIONS ON THE VOICE

of drug dependence or abuse often manifest delirium. The presence orhistory of a mood disorderddepression or maniadalso is a risk factorfor psychiatric side effects to medications [2]. Adrenocorticoids can aggra-vate or unmask depression or mania in these patients. Even a family historyof mania is a risk factor for the development of mania as a side effect [2].

Assessment of all risk factors is important because multiple factors ina particular patient can be additive. The overall low incidence of psychiatricside effects with a particular medication might increase in the presence ofother factors. An understanding of the risks in each individual patient isessential in selecting medications. Physicians should routinely ask patientsto bring in or to make a list of all medications that they have taken duringthe previous 2 months. Clinicians also should inquire if a patient has ever ex-perienced any side effects or abnormal reactions from medication (Table 1).

Side effects of specific common medications

Steroids

Adrenocorticoids are known to cause side effects. Gastrointestinal upsetand ulcers, increased appetite, mucosal drying, blurred vision, and

Table 1

Selected drugs and their possible psychiatric side effects

Drug Side effect

Adrenocorticoids Agitation, anxiety, confusion, delirium, depression,

hallucinations, mania, paranoia, psychoses, sleep

disturbances

Antihistamines and decongestants

Azatadine Agitation, anxiety, euphoria, hallucinations,

hypomania, mania, nervousness, somnolence

Loratadine Agitation, anxiety, confusion, delirium, depression,

nervousness

Fexofenadine Somnolence

Phenylpropanolaminea/guaifenesin Agitation, anxiety, nervousness

Pseudoephedrineb/guaifenesin Hallucinations

Antisecretory agents

Cimetidine Confusion, delirium, depression, hallucinations,

mania, paranoia

Famotidine Agitation, anxiety, depression, nervousness

Lansoprazole Hallucinations

Nizatidine Agitation, anxiety, nervousness, somnolence

Omeprazole Aggression, agitation, anxiety, depression,

hallucinations, hostility, nervousness, violence

Ranitidine Confusion, delirium, depression, hallucinations,

mania

a Agents containing phenylpropanolamine also can cause confusion, delirium, depression,

euphoria, hallucinations, hypomania, mania, and paranoia.b Agents containing pseudoephedrine also can cause agitation, anxiety, euphoria, hypoma-

nia, mania, nervousness, and paranoia.

1084 ABAZA et al

aggravation of blood glucose levels, particularly in diabetics, are docu-mented side effects [3]. Delirium, depression, insomnia, mania, andpsychoses are not uncommon psychiatric effects. Symptoms tend to be pro-portional in incidence to the dosage and duration of steroid use. IatrogenicCushing’s syndrome, which can be caused by long-term steroid use, also canmanifest these signs [2,4]. A personal or family history of affective mentalillness can predispose a patient to the psychiatric side effects of steroids.Some drugs, such as corticotropin, can cause an increase in endogeniscorticosteroids causing similar effects. The potential for steroid abuse inprofessional voice users cannot be overemphasized, and the side effectsshould not be dismissed as insignificant.

Treatment of side effects may need to be considered when steroid use isrequired. A concomitant use of a histamine-2 receptor antagonist(H2 blocker) or proton pump inhibitor (PPI) can assist with gastrointestinalupset. A carefully titrated insulin sliding scale can help to control bloodsugar elevation in diabetics [3]. Severe depression might require antidepres-sant treatment, and an antipsychotic medication or a mood stabilizer maybecome necessary to treat steroid-induced mania. Insomniadas an isolatedside effect or as part of a manic episodedalso could require medicalintervention.

Inhaled steroids are used primarily for respiratory disorders and presentmore local than systemic effects. Nasal steroids have had few documentedeffects on the voice; however, orally inhaled steroids have demonstratedoral candidiasis, dysphonia, pharyngitis, and cough and often are not rec-ommended for use in professional voice users unless absolutely needed forasthma control because of the common voice effects [3,5]. Ipratropium bro-mide, a nasally or orally inhaled medication used primarily for pulmonarysymptoms, has shown side effects that include hoarseness and cough. Fluti-casone, one of the more common medications used for asthma and used alsoas a primary nasal steroid, lists a prevalence of 2% for hoarseness and sorethroat for the orally inhaled preparation. Salmeterol xinafoate and flutica-sone propionate (Advair) lists the same incidence of hoarseness and throatirritation, attributing it to either drug. It does not seem to be dose depen-dent. Triamcinolone, pirbuterol acetate, and albuterol list voice changesas part of their common side effects. Voice difficulties due to lack of respi-ratory support in uncontrolled asthma need to be taken into considerationwhen evaluating the use of these medications in professional voice users.

Antihistamines and decongestants

These medications can be particularly troublesome because many antihis-tamines and decongestants can be purchased and are consumed withoutphysician supervision. Moreover, some patients do not realize that theirOTC medications include antihistamine and decongestant components;they are part of several OTC sleep aids as well. Some patients do not regard


OTC medications as ‘‘real medicines’’; therefore, they do not report them aspart of their medical history unless they are asked specifically about them.

Often, antihistamines are paired with sympathomimetic or parasympa-tholytic medications, which thicken and reduce mucosal secretions, causingsignificant drying and consequent voice changes and pathologies. Sedationalso is a side effect of these medications, with some preparations, such as lor-atadine and fexofenadine, causing less. Medications that contain phenylpro-panolamine, pseudoephedrine, and phenylephrine are contraindicated inpatients who are taking monoamine oxidase inhibitors (MAOIs) [2]. Thesemedications can produce dangerously high levels of norepinephrine becausethe MAOIs impair the metabolism of sympathomimetic medications [2].

Sympathomimetic medications by themselves also can cause psychiatricside effects. Young children and elderly patients who have organic brainsyndrome are the most vulnerable. It may become necessary to discontinuethe suspected culprit medication or to prescribe sedation or treatment witha high-potency antipsychotic, such as haloperidol. Low-potency antipsy-chotics, such as thioridazine or chlorpromazine, should not be taken withphenylpropanolamine because the combination can cause hypotension.

The antihistamine and anticholinergic components of a combinationantihistamine and decongestant can produce an atropine-like psychosis, typ-ically manifesting as confusion, disorientation, agitation, hallucinations,and memory deficits. Agitation can be treated with a short-acting, nonanti-cholinergic sedative, such as lorazepam. Severe agitation or psychotic symp-toms can be treated with low doses of haloperidol. Recovery of the patient’smental status following the administration of physostigmine confirms thediagnosis of atropine-like psychosis [2]. Symptoms should resolve com-pletely after the suspected medication is discontinued.

The hepatic metabolism of many medications is mediated by certaincytochrome P-450 enzymes, and the antidepressants fluvoxamine and nefa-zodone interfere with certain P-450 enzymes [6]. When these antidepressantsare prescribed with other medications that are metabolized by the sameP-450 enzymes, competition between the medications for the enzymes im-pairs the liver’s ability to metabolize each as efficiently as usual. This cancause blood levels of these medications to become dangerously high andlead to significant side effects or even a fatal reaction [6]. These antidepressantscannot be used in combination with astemizole for the same reason. Lorata-dine, fexofenadine, and cetirizine can be used with these antidepressantsbecause they are metabolized by a different cytochrome P-450 isozyme [6].

Reflux medications

Laryngopharyngeal reflux is a common disorder treated in otolaryngol-ogy [7,8]. The condition is often detected in patients who have voicecomplaints. Antisecretory medications, which decrease stomach acidproduction, are commonly used in the treatment of reflux laryngitis. The

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two primary classes of drugs prescribed for this condition are the PPIs andthe H2 blockers. The former includes agents such as omeprazole, lansopra-zole, and esomeprazole; the latter includes drugs such as famotidine, nizati-dine, ranitidine, and cimetidine. Even OTC antacids demonstrate significantside effects, including constipation, bloating, diarrhea, and a drying effect[3].

Documented side effects of PPIs include diarrhea, abdominal pain,nausea, elevation of hepatic enzymes, dry mouth, esophageal candidiasis,muscle cramps, depression, tremors, dizziness, fatigue, and headaches.H2 blockers can cause dryness, but it usually is not significant. A recentstudy from England indicated an increased risk for hip fractures withlong-term and high-dose PPIs and, to a lesser extent, H2 blockers, particu-larly in men. The investigators recommended that in patients older than 50years of age, an absorbable form of calcium should be taken with high-doseor long-term use of these medications [9].

All H2 blockers have been associated with some psychiatric side effects[2]. Although the overall prevalence of these side effects in outpatients isless than 0.2%, it is significantly higher among hospitalized patients, theelderly, the seriously ill, and patients who have hepatic or renal failure[10]. These effects of the H2 blockers vary with respect to their time of onset,but they usually resolve within 3 days of discontinuing the drug. For exam-ple, ranitidine can cause depression beginning at 4 to 8 weeks after the ini-tiation of treatment. Cimetidine was reported to cause adverse events within2 to 3 weeks and even caused delirium within 24 to 48 hours [2]. The discon-tinuation of ranitidine and cimetidine has been associated with a withdrawalsyndrome that includes anxiety, insomnia, and irritability [11]. Cimetidinecan increase the blood level and action of tricyclic antidepressants, suchas amitriptyline, doxepin, imipramine, and nortriptyline; blood levels ofthese antidepressants can reach toxic levels, resulting in tachycardia andother side effects. The inhibition of the cytochrome P-450 enzymes by rani-tidine or cimetidine also can lead to potentially dangerous side effects withcertain other cytochrome P-450 metabolized medications. Cimetidine is themore potent inhibitor of the two; ranitidine is one fifth to one tenth aspotent. Famotidine and nizatidine do not inhibit this enzyme system at all [2].

Cimetidine lengthens the half-life of the antianxiety medications cloraze-pate, chlordiazepoxide, and diazepam to a greater degree than does raniti-dine [2]. Lower dosages of these long-acting benzodiazepines should beconsidered when they are prescribed for a patient who is taking cimetidine.An alternative is to use a short-acting benzodiazepine, such as oxazepam orlorazepam. The metabolism of these short-acting antianxiety medications isnot affected by ranitidine or cimetidine [2]. Cimetidine also can increase theblood levels of serotonin reuptake inhibitors and antipsychotic medicalanticonvulsants [2,4]. Whenever possible, lower dosages of these medica-tions should be given when they are used in combination with cimetidine.The blood levels of these medications should be monitored periodically,


and their dosages should be adjusted accordingly. Another option is to usea different H2 blocker, such as famotidine or nizatidine.

Hormones

Significant voice effects have been documented with androgens and ana-bolic steroids [3]. Irreversible lowering of the fundamental pitch and coars-ening of the voice can be the result of danazol, which is commonly used inthe treatment of endometriosis and postmenopausal sexual dysfunction [12].High-dose progesterone birth control pills, generally not available in theUnited States, can cause similar androgen-like changes in the voice [13].Most low-dose contraceptives have a significantly lower chance of voicechanges, usually reversible when the medication is discontinued. Van Lierdeand colleagues [14] evaluated 24 professional voice users during the use oforal contraceptives and found no objective voice differences. Depo-Provera(medroxyprogesterone acetate) has demonstrated hoarseness as a side effect.

Estrogen replacement has become a controversial area in medicine fornumerous health reasons. In professional voice users, estrogen replacementmay help to prevent postmenopausal voice changes [3]. Low-dose progester-one supplements, such as found in Premarin, are not believed to cause sig-nificant voice changes; however, some synthetic substitutes may causeandrogenic effects [3].

Hypothyroidism, with thyroid hormone replacement, is one of the morecommon disorders found in women. Sometimes diagnosed in professionalvoice users by voice changes alone, careful monitoring of supplemental thy-roid hormone replacement can be particularly important in a professionalvoice user.

Antivirals

Antivirals are used for many disorders. Their use in chronic disease(eg, HIV and herpes) and in acute viral illnesses is common. Several of themedications cause side effects. Hoarseness, cough, pharyngitis, nervousness,muscle spasm, and tremor have been reported with zidovudine; becauseHIV disease alone can demonstrate these signs, it can be difficult to differen-tiate. More common antivirals, such as oseltamivir, have not shown docu-mented voice changes; however, swelling of the face and tongue has beenreported. Oseltamivir phosphate is not recommended in patients who haveairway disease, secondary to reports of bronchospasm and decreased lungcapacity. Amantadine hydrochloride, used in Parkinson’s disease, has antivi-ral effects with side effects of agitation, tachycardia, and xerostomia [3].

Analgesics

Aspirin, several nonsteroidal anti-inflammatory medications (NSAIDs),and acetaminophen are OTC medications that are used commonly for the

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relief of minor pain and fever. Delay in clotting is a known complication ofaspirin and all NSAIDs, so avoidance of these medications is recommendedoften for professional voice users. A low dosage of aspirin is used often forcardiac prevention and is a situation where the minimal bleeding risk likelyis outweighed by the cardiac prevention benefit. Newer cyclooxygenase-tinhibitors, now available by prescription, do not have the same bleeding is-sues or gastrointestinal upset because of a different pathway, but they dohave other significant cardiac side effects [15].

Topical anesthesia and narcotic use in professional voice users, particularlybefore a performance, should be discouraged. Narcotics can be associatedwith signs of dysarthria, in addition to mental impairment [16]. Impairmentof physical feedback of the voice by these types of agents can predispose theuser to injury and more significant long-term voice disabilities and can bemore career-ending than a performance cancellation may be.

Diuretics

Diuretics are used to eliminate fluid in medical conditions such as cardiacor renal failure. In premenstrual women, excess fluid can be found in Rein-ke’s space and other tissues because of increased circulation of antidiuretichormone. This fluid is bound and not affected by the use of diuretics. In fact,diuretics can add to the dehydration of the performer. Diuretics also areused in conjunction with other antihypertensive medications. Several angio-tensin-converting enzyme inhibitors, such as captopril and enalapril, havehad case reports of hoarseness, cough, and aphonia [17]. Careful monitoringof the voice is important when these medications are needed for other healthconcerns.

Other medications

Numerous other medications have had hoarseness reported as a sideeffect [17]. Antineoplastic agents (eg, vincristine), tricyclic antidepressants(eg, amitriptyline and nortriptyline), clonazepam (Klonopin), and ropinirolehydrochloride (Requip) are a few of the more common medications that listhoarseness as a potential side effect. The evaluation of voice changes in a per-former needs to involve a detailed review of new and old medications, aswell as dosage changes.

Homeopathic medications

The realm of homeopathic and herbal remedies is beyond the scope of thisarticle but it warrants amention. Professional singers often usewhat they viewas natural solutions to medical problems. Often, patients are reluctant toinform their physician about the use of these medications; therefore, it is


important for the otolaryngologist to stress the impact that these substancesmay have on the body andon the efficacy of othermedications.A few commonsubstances and their side effect profile are listed in Table 2.

References

[1] Othmer E, Othmer SC. The clinical interview using DSM-IV, vol. 1. Washington, DC:

American Psychiatric Press; 1994. p. 252–9.

[2] Bernstein JG. Handbook of drug therapy in psychiatry. St. Louis (MO): Mosby; 1995.

p. 370–1, 546, 353, 384, 380–1, 346, 359.

[3] SataloffRT,HawkshawMJ,Anticaglia J.Medications and the voice. In: SataloffRT, editor.

Professional voice. The science and art of clinical care. San Diego (CA): Plural Publishing;

2006. p. 905–24.

[4] Bazire S, Benefield WH Jr. Psychotropic drug directory: the mental health professionals’

handbook. West Orange (NJ): Quay Books; 1997. p. 217–36, 179, 166.

[5] Buhl R. Local oropharyngeal side effects on inhaled corticosteroids inpatients with asthma.

Allergy 2006;61(5):518–26.

[6] Stahl SM. Psychopharmacology of antidepressants. London: Dunitz Ltd.; 1997. p. 101–8.

[7] Sataloff RT, Castell DO, Sataloff DM, et al. Reflux and other gastroenterologic conditions

that may affect the voice. In: Sataloff RT, editor. Professional voice. The science and art of

clinical care. 2nd edition. San Diego (CA): Singular Publishing Group; 1997. p. 319–29.

[8] Sataloff RT, Castell DO, Katz PO, et al. Reflux laryngitis and related disorders. San Diego

(CA): Singular Publishing Group; 1999.

[9] YangY, Lewis JD, Epstein S, et al. Long term proton pump inhibitor therapy and risk of hip

fracture. JAMA 2006;296(24):2947–53.

[10] Canter TG, Korek JS. Central nervous system reactions to histamine-2 receptor blockers.

Ann Intern Med 1991;114:1027–34.

[11] Rampello L,Nicoletti G. TheH2-antagonist therapywithdrawal syndrome: the possible role

of hyperprolactinemia [Italian]. Medicina (Firenze) 1990;10:294–6.

[12] Slayden SM. Risks of menopausal androgen supplement. Semin Reprod Endocrinol 1998;

16(2):145–52.

[13] Abitbol J, Abitbol P, Abitbol B. Sex hormones and the female voice. J Voice 1999;13(3):

424–46.

[14] Van Lierde KM, Claeys S, De Bodt M, et al. Response of the female vocal quality and

resonance in professional voice users taking oral contraceptive pills: a multiparameter

approach. Laryngoscope 2006;116(10):1894–8.

Table 2

Some herbal medications side effects

Herbal medication Side effect

Echinacea Allergic response, immunosuppressive after 8 weeks of use

Ephedra Dehydration, cardiac events, stroke

Fennel Anticoagulation activity

Garlic, ginger, Ginkgo Anticoagulation activity

Ginseng Agitation, insomnia, vaginal bleeding

Licorice root Hormonal (estrogen/progesterone) activity, hypertension, reflux

Milk thistle Laxative effects

Nettles Diuretic effects

Primrose Anticoagulation activity

St John’s wort Insomnia, gastrointestinal upset, fatigue, bleeding

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[15] Marwali MR, Mehta JL. COX-2 inhibitors and cardiovascular risk. Inferences based on

biology and clinical studies. Thromb Haemost 2006;96(4):401–6.

[16] Damste PH. Changes in the voice caused by drugs. In: Meyer L, Pach HM, editors. Drug

induced diseases. Amsterdam (The Netherlands): Excerpta Medica; 1978. p. 543–8.

[17] Micromedex� healthcare series [Internet database]. Greenwood Village (CO): Thomson

Micromedex. Updated periodically.


40 (2007) 1091–1108

Vocal Fold Masses

Kenneth W. Altman, MD, PhD, FACSDepartment of Otolaryngology, The Mount Sinai School of Medicine, One Gustave L.

Levy Place, Box 1189, New York, NY 10029, USA

Althoughmany performers consider vocal foldmasses, such as nodules, thebane of their existence, it is rare that these lesions are true career-breakers. It isessential, however, that the many issues contributing to the development ofthese lesions be identified and a multidisciplinary approach instituted toobtain the best possible and most consistent outcome. In the context of theprofessional voice, lesions are generally benign and inflammatory, but profes-sional voice users often engage in carcinogenic activities, such as smoking, al-cohol abuse, and use or abuse of recreational drugs. Such behaviors increasethe risk for malignancies and the possibility of such cannot be overlooked.Also, the title of this article, vocal fold masses, has been chosen to reinforcethe concept that these inflammatory conditions add weight to the vocal foldsand impair vocal closure. This article reviews the multifactorial contributionsto voice disorders with emphasis on the pathophysiology of vocal masses, de-scribes the resulting effects on voice function, and elaborates on the types ofmasses encountered in professional voice users.

Multifactorial contributions to developing vocal masses

Voice use demands (overuse) and vocal technique (misuse) are central tothe trauma and pathogenesis of vocal fold masses in professional voiceusers. Common to performers and other professionals is a passion for com-munication that often pushes the scope of voice use relating to amount oftime, intensity, frequency of use, vocal range, and more advanced tech-niques. Young performers, in particular, usually use their voices in manydifferent roles that include self-management and day jobs also requiringtheir voices. The blossoming use of cellular telephones, especially in loudpublic environments, significantly adds to this sustained and repetitive vocaltrauma. Trauma and subsequent inflammation manifest as vocal limitations

E-mail address: [email protected]




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that frustrate the professional voice user, and there is a tendency to try toexceed these limitations.

Paying tribute to these personality factors in the pathogenesis of nodulesand polyps, Yano and colleagues 1982 [1] recognized significantly higher ex-troversion scores on Maudsley Personality Inventory in these patients. Morerecently, Roy and colleagues [2] used the Multidimensional PersonalityQuestionnaire to evaluate personality features distinct to functional dyspho-nia and those who have vocal nodules. They determined that the functionaldysphonia group was introverted, stress-reactive, alienated, and unhappy.In contrast, the vocal nodules group was considered to be socially dominant,stress-reactive, aggressive, and impulsive.

Based on the multifactorial nature of voice disorders, underlying medicalconditions,medications, and the environment add to the synergy in pathogen-esis of vocal foldmasses.With the larynx at the epicenter, the significant inter-relations of the respiratory and upper gastrointestinal tracts also predisposethe vocal folds to further damage. These contributing diseases include rhinitis,allergy, sinusitis, asthma, bronchitis, laryngopharyngeal reflux, and othersdiscussed elsewhere in this issue. Environmental factors include allergens,dust and other particulates, tobacco smoke, and a host of occupationalirritants.

Principal to medical conditions that contribute to inflammatory vocal le-sions is laryngopharyngeal reflux (LPR). There are many examples in the lit-erature; Kuhn and colleagues [3] studied 11 patients who had vocal nodulesusing 24-hour simultaneous three-site pharyngoesophageal pH monitoring.They found pharyngeal acid reflux events in 7 patients in that 24-hour pe-riod (one to four episodes) compared with 2 of 11 controls studied (oneto two episodes). In a follow-up study by Ulualp and colleagues [4], 9 pa-tients who had vocal nodules and posterior laryngitis underwent similarevaluation, in which 78% were found to have pharyngeal acid reflux (signif-icantly higher than controls). It is believed that the baseline inflammationresulting from LPR episodes predisposes the vocal folds to the stressesfrom vocal overuse and misuse.

In a series of allergy patients who had laryngeal disease, Hocevar-Boltezarand colleagues [5] found that treatment of 70 patients who had laryngitis andpositive allergy skin tests resulted in an improved outcome compared with 5patients who did not receive treatment, suggesting that hypersensitivity to in-halatory and nutritional allergens makes laryngeal mucosa more susceptibleto the adverse action of other factors. This example also reinforces the syner-gistic effects contributing to the development of vocal fold masses.

Pathophysiology, shearing stress, and compensation

Because vocal overuse and misuse are central to the development of vocalfold masses, it is important to understand how biomechanical factors work

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on the membranous vocal folds to produce such lesions. Jiang and col-leagues [6] developed a mathematical computer-based model to describethe vibratory response of the vocal folds during phonation using the finiteelement method. They found that in normal phonation, mechanical stresswas the least at the midpoint of the membranous vocal fold and highestat tendon attachments. In contrast, during hyperfunctional dysphonia therewas an increase in the second mode of vibration, resulting in incomplete ap-proximation of the vocal folds posteriorly and increased stress at the loca-tion between vibratory segments. In other words, when there wasincreased stiffness in the body of the vocal folds, the midpoint of the mem-branous vocal folds encountered higher shearing stresses.

Furthermore, when there was already a nodule or mass, it produceda high mechanical stress at its base during vibration. The authors concludedthat intraepithelial stress plays an important role in the pathogenesis of nod-ules and other masses, and that an abnormal vibratory mode may be moredamaging than a high intensity of vibration [6].

In a follow-up study using a self-oscillating model, mechanical stress wasnoted to periodically undulate with the vibration of the vocal folds, and thatvocal impact caused a jump in the normal stress value [7]. The model wasalso able to confirm that stress was significantly higher on the surface ofthe vocal folds compared with that under the surface. These models rein-force the concept of how vocal impact results in vibratory trauma to the vo-cal folds, and that stresses are compounded once a lesion is present.

Many lesions can result (at least in part) from this process, including nod-ules, polyps, and cysts, but other pathology should be considered, such asreactive lesions, intracordal scarring, feeding varices, and reparative granu-loma. The direct effect of the vocal mass is to add weight to the vocal fold,which decreases its vibratory qualities and frequency as demonstrated onstrobolaryngoscopy. There is a clinical decrease in phonatory pitch alongwith an abbreviated pitch range, as demonstrated on voice function testing.The presence of the mass causes impaired vocal phase closure during pho-nation, resulting in excess air egress. Clinically, this adds to a breathy qual-ity of the voice, but also contributes to vocal fatigue. Disruption of vocalfold vibration and phase closure often leads to phase asymmetry (dependingon the specific lesion), which adds to a grainy quality of the voice.

At this point in the development of the vocal mass, there is a self-perpet-uating cycle of inflammation and trauma. Although behavioral qualitiescontribute to the initial vocal trauma that leads to the development ofthis process, the presence of a lesion can result in compensatory muscle ten-sion in an effort to reduce excess air flow through the glottis. Altman andcolleagues [8] reviewed 150 patients who had muscle tension dysphonia, inwhich 34 had polyps, 20 had nodules, and 12 had vocal cysts. They founda significant degree of compensatory muscle hyperconstriction in this popu-lation. Nevertheless, the multifactorial contributions and spectrum of le-sions that may result emphasize the importance of strobolaryngoscopy in

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assessment and multidisciplinary approach with speech and voice therapy,medical, and surgical options.

Prevalence of vocal masses and dysphonia in voice professionals

Teachers are perhaps the largest group of voice professionals who seemto be at higher risk for the development of hoarseness and vocal masses. Sul-kowski and Kowalska [9] analyzed 1261 cases of occupational voice disor-ders referred for otolaryngologic evaluation in Poland over a 5-yearperiod. Some 66% of these patients were primary school teachers, and55% of referrals were 51 to 60 years of age. Overall, vocal nodules werefound in 4.2%. In a Finnish study, Smolander and Huttunen [10] surveyed181 teachers, of whom 42% reported frequent voice symptoms, and 10%had history of vocal nodules.

Because the evolution of these lesions is complex and the laryngologistinitially evaluates patients after they have experienced voice limitationsover a period of time, it is uncommon to have an isolated lesion withoutconcomitant or confounding findings. Similarly, nodules are often a ‘‘waste-basket’’ diagnosis for those clinicians unskilled to differentiate between nod-ules, polyps, cysts, reactive lesions, and intracordal scarring. Although itmay be a matter of semantics what to name a lesion, the description is nev-ertheless helpful in considering prognosis and therapeutic plan.

Nagata and colleagues [11] reviewed their 10-year experience with 1156patients and found 372 who had nodules and 784 who had polyps. Sataloffand colleagues [12] reviewed their experience with videostroboscopy on 377patients and found nodules in 32, polyps in 4, cysts in 8, granulomas in 3,Reinke edema in 4, and scar in 32. An in-depth discussion of these vocalfold masses follows. Discussion about each of these masses follows with rel-evance to diagnosis and prognosis.

Nodules

Vocal nodules are defined as bilateral symmetric epithelial swelling of theanterior/mid third of the true vocal folds.

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

com.)

Demographically, these are seen in children, adolescents, and predomi-nantly female adults working in professions with high voice demands. Sar-fati [13] evaluated 90 French teachers referred for vocal disorders, andpathology was found in two thirds overall, with pseudocysts or nodules inone third overall.

De Bodt and colleagues [14] characterized evolution of these nodulesfrom childhood to adolescence. They examined a group of 34 post-





mutational adolescents who had a prior diagnosis of vocal fold nodules.These nodules were still present in 47% of girls but only 7% of boys. Thedegree of dysphonia in childhood and the presence of allergy were also pre-dictors of persisting voice complaints in adolescence. This study reinforcesmultifactorial contributions to the development of these lesions, includingbehavior. The female preponderance from childhood to adolescence, cou-pled with adult female preponderance in other studies, further confirmsthat females are at particular risk. Perhaps the softer intensity of female voi-ces leads to more hyperfunction in adult professional environments withlouder background noise.

One additional note is made of preponderance of nodules in patients whohave congenital microweb. Ruiz and colleagues [15] reviewed a sample of107 patients who had vocal nodules and recognized microweb in 9.4%, al-though the presence of microweb did not affect nodule location. Althoughthis is a small portion of those patients who develop nodules, it does implythat the clinician should have a heightened awareness of the presence of mi-crowebs, which may have additional implications of treatment andprognosis.

The pathophysiology of vocal nodules relies on the mid-membranous vo-cal fold experiencing maximal shearing and collision forces. This locationcorresponds to the junction of the anterior to middle vocal folds (becausethe posterior third of the vocal folds is coupled to the vocal process of thearytenoids). This repeated collision initially results in localized vascular con-gestion with edema. Eventually hyalinization of Reinke space with thicken-ing of overlying epithelium occurs with the development of epithelialhyperplasia.

Consequently, the histology of nodules is distinct from polyps and othervocal lesions. Kotby and colleagues [16] collected 11 patients who had nod-ules (all female) to characterize this histology. Nodules are generally acellu-lar, with thickening of epithelium over a matrix with abundant fibrin andorganized collagen. Polyps also have a more pronounced epithelial reactionand a more dense fibrous stroma than polyps. Immunohistochemical char-acterization of nodules reveals a thickened basement membrane zone rich incollagen type IV and more intense fibronectin staining [17].

Patients who have vocal nodules present with chronic hoarseness, oftenwith repeated episodes of more severe voice loss. Singers may complain ofa loss of ability to sing high notes softly, with frequent voice breaks, in-creased breathiness, and vocal fatigue. Strobolaryngoscopy reveals bilateralsymmetric superficial swelling of the vocal folds at the striking zone junctionof the anterior to middle thirds (Fig. 1A). There is slightly decreased ampli-tude of the mucosal wave, but the wave is generally symmetric. Becausethere is hourglass-shaped glottal closure, there is consequently decreasedphase closure (Fig. 1B).

The mucus layer on the surface of the vocal folds is also important forlubrication and reducing friction. Patients who have vocal nodules may

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subsequently have irregular vibration of the surface mucus layer, perhaps re-sulting in drying, leading to impaired lubrication and an exacerbation of thesurface stresses leading to the formation of nodules [18]. In addition, abnor-mal or excess mucus has been anecdotally noted by the author to be respon-sible for increased voice breaks in singers when transitioning through thepassaggio (ascending glissando from the chest voice into the head voice).

When considering treatment options for a patient who has vocal nodules,it is useful to discuss with the patient a simple analogy of a carpenter usinga hammer over a long period of time without gloves. As a result, callusesform at the areas of maximal impact with the hand. Using this analogy,one may expect that conservative (nonsurgical) treatment would be applica-ble to the patient who has true vocal nodules.

Hogikyan and colleagues [19] recognized a consensus among otolaryngol-ogists, speech pathologists, and teachers of singing regarding the treatmentof singers who have nodules. Addressing voice use demands, improper tech-nique, optimizing other contributing factors, and coordinating care were be-lieved to be paramount.

Indications for microsurgical treatment include longstanding nodules,particularly when other factors, including speech therapy, have been maxi-mized, and suspicion of a primary lesion with a reactive callus on the othervocal fold. Microsurgical technique is addressed elsewhere; it is imperativeto preserve normal anatomy, keeping the plane of dissection superficial,and to minimize trauma to the lamina propria.

Polyps

Vocal polyps are unilateral, occasionally pedunculatedmasses encounteredon the true vocal fold. They occur more often in males, after intense intermit-tent voice abuse, history of aspirin or anticoagulant use, or other vocaltrauma, such as endotracheal intubation. Kotby and colleagues [16] reviewed19 patients who had polyps, of whom 16 (84%) were male. The pathophysiol-ogy is believed to be attributable to breakage of a capillary in Reinke space

Fig. 1. Vocal nodules in a classical singer (A) during inspiration, and (B) during phonation.

Note the hourglass configuration with pinpoint phase closure on strobolaryngoscopy.


(superficial lamina propria) with subsequent extravasation of blood, resultantlocal edema, and ultimate organization with hyalinized stroma.

The resulting mass may be broad-based or pedunculated, and hemor-rhagic versus nonhemorrhagic (Fig. 2).

(Access Video on Pre-op Excision of Bilateral Polyps in online version of this article at:

http://www.Oto.TheClinics.com)

Hemorrhagic polyps may also have a feeding blood vessel, or varix.

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

TheClinics.com)

Although the gross appearance may vary, the lesion is generally consid-ered to be an outpouching of inflamed and organized Reinke space. A super-ficial nonhemorrhagic, broad-based polyp may therefore be interpreted asor called a pseudocyst.

Pathologically, polyps are acellular, with thickened epithelium over su-perficial lamina propria and increased vascularity in an abundant delicatefibrin stromal matrix. They have more vasculature and less organized colla-gen than nodules, but the distinction may be difficult for the pathologist [20].Immunohistochemistry studies reveal clustered fibronectin and disruption oflaminar pattern suggesting diffuse injury in the region of the polyp [17].

On strobolaryngoscopy, vocal folds with small polyps generally have in-tact mucosal waves but phase asymmetry because of the impaired phase clo-sure and the mass effect of the polyp. Vocal folds with larger polyps havemore prominent decreased mucosal wave amplitude. Thibeault and col-leagues [21] characterized gene expression in vocal polyps compared withReinke edema. They found evidence of enhanced expression of extracellularmatrix proteins in vocal polyps corresponding to increased mucosal wavestiffness observed on strobolaryngoscopy.

Both nodules and polyps result in excess air egress during phonation (witha relatively breathy voice), and earlier vocal fatigue, frequent voice breaks in

Fig. 2. Vocal polyps. (A) Hemorrhagic. (B) Broad-based, nonhemorrhagic.






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singers, and worsening hoarseness with high-pitched soft phonation. As such,this decreased vocal efficiency with decreased mucosal wave phase closure hasbeen quantified with decreased subglottal and acoustic power [22]. Becausepolyps are asymmetric masses of the vocal folds, they are more prone to resultin chaotic vibrations and aperiodic mucosal waves [23].

In the treatment of patients who have vocal polyps, all of the factors thatcontribute to voice disorders should be addressed from a multidisciplinaryperspective, and polyps are usually addressed withmicrosurgery. An evolvingtreatment modality for particularly hemorrhagic polyps is the use of office-based technology using lasers. The wavelength of the lasers is well absorbedby hemoglobin, and damage to the epithelium is minimal. In one recent pilotstudy evaluating the use of the pulsed-dye laser (585 nm), small vascularpolyps showed greater potential for resolution over larger polyps [24].

There have also been reports (and anecdotal observation by the author ofthis article and others) that small vocal polyps may completely resolve withconservative nonsurgical treatment [25]. One would expect that smaller le-sions and those that have been present for shorter periods of time may bemore prone to regression, especially in patients who are more compliantwith treatment.

Cysts

Cysts are subepidermal epithelial-lined sacs locatedwithin the lamina prop-ria, and may be mucus retention or epidermoid in origin. Mucus retentioncysts form when a mucous gland duct becomes obstructed (usually duringanupper respiratory infection orwith overuse), retaining glandular secretions.

(Access Video on Pre-op Subepithelial/Mucous Retention Cyst in online version of this

article at: http://www.Oto.TheClinics.com.)

Epidermoid cysts develop either from congenital cell rests in the subepi-thelium of the fourth and sixth branchial arches or from healing injured mu-cosa burying epithelium.

(Access Video on Left Cyst, Right Nodule in online version of this article at: http://www.

Oto.TheClinics.com.)

A ruptured cyst may result in scarring within the lamina propria or ina sulcus. A cyst may also irritate the contralateral vocal fold, producing a -reactive lesion on that vocal fold.

The history of a patient who has a vocal cyst is similar to those of patientswho have nodules and polyps, but with less vocal limitation than expectedfrom its size. The voice often sounds diplophonic (particularly with epider-moid cysts), whereby there is great pitch instability and there is splitting ofthe fundamental frequency overtones. As with nodules and polyps, this isusually accompanied by vocal hyperfunction, which is often compensatory.







Bouchayer and colleagues [26] reviewed their experience with 157 cases ofcysts, sulci, and mucosal bridges over a 10-year period. Cysts were present in78, and more commonly in females. Female professional singers may noteincreasing vocal limitation and voice roughness when they are premenstrual[27], and there is anecdotal evidence of varying cyst size with the femalemonthly cycle. Consequently, many phonosurgeons exercise caution whenoperating on premenstrual women.

On strobolaryngoscopy, the vocal folds appear asymmetric with occa-sional evidence of the subepithelial mass (Fig. 3). Because of displacementof lamina propria, there is significant decreased or absent mucosal waveon the side of the cyst. Phase closure depends on the cyst size and whetherthere is the development of a contralateral reactive callus.

Shohet and colleagues [28] compared stroboscopic findings between cystsand polyps. They determined that the mucosal wave was the most importantparameter in differentiating cysts from polyps. They also found the mucosalwave to be diminished or absent in 100% of vocal fold cysts, and the waveto be present in 80% of polyps.

Treatment again requires a multidisciplinary approach addressing factorsthat contribute to voice disorders. Although it is imperative to respect vocallimitations, a true cyst does not resolve with conservative management. Thephonosurgical approach is discussed elsewhere in this issue, but requiresmore extensive dissection because the cyst is in the submucosal plane. Thecyst may also be associated with intracordal scarring, requiring a more elab-orate dissection. Consequently, recovery of the mucosal wave is prolongedand may never return to being completely normal.

Furthermore, leaving behind a minute fragment of epithelium in the cystsac may result in recurrence of the cyst. Some vocal professionals have beenknow to have cysts that do not cause substantial limitation to their singingcareers and have been observed without surgery. Consideration of surgery in

Fig. 3. Vocal cyst.

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a vocal professional with this complex lesion should not be taken lightly,therefore, and there should be a lengthy discussion of the risks and alterna-tives to surgery.

Reactive lesions

The presence of a unilateral vocal fold lesion results in hourglass-shapedclosure of the membranous vocal folds during phonation. Consequently,there are extra shearing forces on the contralateral vocal fold that may pro-duce a reactive callus with epithelial hyperplasia. A unilateral lesion with re-active callus formation may appear as bilateral lesions, such as nodules, thatmay confound the diagnosis, prognosis, and ultimate management.

Rosen and colleagues [29] evaluated a series of 85 patients who had bilat-eral vocal fold lesions and found 21 to have nodules and 64 to have a unilat-eral vocal fold lesion with a contralateral reactive lesion (UVFL/RL). Whencomparing patients who had nodules to those who had UVFL/RL, theyfound statistically significant differences in (1) symmetry of vocal fold vibra-tion, (2) amplitude perturbations, (3) estimated subglottic pressure, and (4)voice handicap index as tools to differentiate nodules from UVFL/RL.

It is important to distinguish bilateral lesions, such as nodules, from a pri-mary lesion with reactive callus, from the standpoint of prognosis and sur-gical planning.

(Access Video on Left Cyst, Right Nodule in online version of this article at: http://www.


Fig. 4A shows an example of a singer who has a left vocal polyp and re-active right vocal fold broad-based edema/callus. After a 1-month period ofreducing voice use, speech therapy, and treatment of LPR, Fig. 4B showssignificant improvement in the right reactive callus. As such, contralateralreactive lesions are often not removed in microsurgery for the primary le-sion, because the reactive lesion tends to resolve with conservativemanagement.

Intracordal scarring

Repeated inflammation, vocal trauma, vocal hemorrhage, and the pres-ence of an intracordal cyst predispose to scarring in Reinke space. Intracor-dal scarring is often found in association with a cyst, particularly if it isepidermoid in origin and has ruptured. Intracordal scarring may also befound after vocal surgery involving the lamina propria, with the use ofthe CO2 laser, and after repeated epithelial procedures, such as those for ma-lignancy, leukoplakia, and papilloma.

(Access Video on Left Vocal Fold Scar in online version of this article at: http://www.Oto.

TheClinics.com.)








Discussion on vocal sulcus (epithelial scarring) goes beyond the scope ofthis article, although it can certainly affect the professional voice [30].

Intracordal scarring is suspected on strobolaryngoscopy when there ismarkedly reduced or absent mucosal wave (usually asymmetric), which oftenaffects phase closure. From a professional voice standpoint, it is crucial to dif-ferentiate between an uncomplicated subepithelial cyst and an intracordalscar, because the latter is a more complex problem with worse prognosis forprofessional voice rehabilitation. A convex subepithelial fullness of the mem-branous vocal foldmaywarrant exploratorymicroflap surgery to tease out re-maining cyst sac and adynamic fibrous components. Because the extracellularmatrix components of the lamina propria largely determine the biomechanicalproperties of the vocal folds (and subsequent voice quality), there has been sig-nificant recent interest in functional soft tissue replacement substances [31].

Feeding varices and hemorrhage

Varices and ectasias of the vocal fold are aberrant vessels of the microcir-culation within the superficial lamina propria. Although they are not truemasses, they develop as a result of the same multifactorial and shearingforces that lead to masses, and they also predispose to the development ofpolyps and vocal hemorrhage. Fig. 5A and B show strobolaryngoscopicexamples of a varix and hemorrhage.

Treatment options for these aberrant vessels have traditionally includedmicrodissection and the use of the CO2 laser, which lead to an increased riskfor postoperative scarring or sulcus. More recently, there has been renewedinterest in the use of pulsed angiolytic lasers that have a wavelength withinthe specific absorption of oxyhemoglobin, because this has the potential of se-lectively ablating microvessels without damage to the overlying epithelium.Hirano and colleagues [32] demonstrated the use of the KTP laser (532 nm

Fig. 4. (A) Left vocal polyp (on right of image) with reactive callus on the right vocal fold. (B)

Resolution of the reactive callus after 1 month of voice reduction, speech therapy, and treat-

ment of LPR.

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wavelength) on 12 patients who had microvascular and hemorrhagic lesionsand found no adverse scarring or reduction in the mucosal wave postopera-tively. Zeitels and colleagues [33] also recognized the potential for the pulsedKTP and the 585-nm pulsed-dye laser in a series of 39 patients.

Granulomas

Although vocal process granulomas are not on themembranous vocal foldand often do not cause vocal symptoms, it is important for the clinician to un-derstand differences with other vocal fold masses. Vocal process granulomasoccur in response to trauma,most commonly fromLPR, exacerbating chroniccough, or throat clearing. They may also occur after endotracheal intubationresulting in contact ulceration, or by forceful glottal closure when compensat-ing for vocal paresis or presbylaryngia. Kiese-Himmel and Kruse [34] docu-mented a male predominance with 27 out of 28 patients who had contactgranuloma being male.

The granuloma may appear as solitary or bilobed (Fig. 6) and often doesnot affect mucosal wave or phase closure on strobolaryngoscopy (unlessthere is underlying vocal paresis, presbylaryngia, or sulcus).

(Access Video on Vocal Process Granuloma in online version of this article at: http://www.


Treatment relies on addressing the underlying LPR, other factors, andvocal process impact on cough or phonation. Botox to the thyroarytenoidmuscle has also been shown to be helpful in reducing the glottal impact incases refractory to LPR treatment and speech therapy. Because there isa high recurrence rate after surgical excision, surgery is reserved for casesin which the lesion is (1) enlarging; (2) compromising the voice, breathing,or swallowing; or (3) suspicious for malignancy.

Fig. 5. (A) Vocal varix, and (B) vocal fold hemorrhage (both on the patient’s right; left of the

figure)





Papilloma

Respiratory papillomatosis is an infection caused by human papillomavi-rus (HPV), which is also known tomore commonly cause cervical, vaginal, pe-nile, and anal warts. Although relatively uncommon in the larynx, it is stillconsidered to be among the most common laryngeal neoplasms. There aremore than 50 strains of HPV, but HPV 6 and 11 are among the most commonin the larynx.Aswith genitalwarts, there is an approximately 2% likelihood ofmalignant degeneration in laryngeal papilloma, most commonly found withstrains HPV 16 and 18. Once the wart is manifested, there is overall abouta 10% likelihoodof spread to the tracheaor other sites, depending on the num-ber of surgical procedures necessary to control the disease.

HPV appears as a cauliflower-like exophytic protuberance, most com-monly found at the transition between columnar and squamous epithelium(Fig. 7). Because pathologic specimens reveal multiple fronds of fibrovascu-lar stalks, papilloma also has vascular stippling on the mass. Early formsmay have a superficial spreading presentation, again with vascular stipplingseen on laryngoscopy, providing a clue to the underlying disease.

(Access Videos on bilateral papilloma in online version of this article at: http://www.Oto.

TheClinics.com.)

Strobolaryngoscopy is exceptionally helpful in making an early diagnosis,especially when recurring disease is suspected, because the mass effect ofthickened diseased epithelium can present with a decreased mucosal wave.

There are many controversies related to papilloma and HPV, includinga high prevalence of greater than 40% with HPV-positive serology but stillrelatively low overt infection rates, suggesting an important role of host im-mune recognition [35]. The many treatments for papilloma go beyond thescope of this discussion, although shaver excision and CO2 laser excisionare also used in select instances. The greater depth of penetration of the laser

Fig. 6. Left vocal process granuloma.




1104 ALTMAN

than is visibly apparent increases the risk for scarring and implantation ofthe virus (an epithelial disease) into deeper tissues of the vocal fold anduse of the CO2 laser is avoided in most centers. Pulsed-dye lasers are nowconsidered the mainstay. The emerging use of the HPV vaccine for themost common strains and cidofovir injections to control regrowth are excit-ing options for protection from acquiring the disease and for treatment.

Polypoid corditis

Polypoid corditis, vocal polyposis, and Reinke edema are terms that referto a proliferation or redundancy of the superficial lamina propria (Reinkespace). It is often seen in patients who have chronic irritant exposure,such as tobacco smoke, laryngopharyngeal reflux, and sometimes occupa-tional exposures. Polypoid corditis appears as an outpouching of the mem-branous vocal folds with an edematous, almost water-balloon appearance(Fig. 8). Strobolaryngoscopy reveals decreased mucosal wave because ofthe mass effect of the edema, often with phase asymmetry because ofball-valving and asymmetric edema. Treatment is aimed at reducing airwayobstruction while preserving voice quality. Surgically, it is paramount topreserve some epithelium and remaining superficial lamina propria so thatpatients may maintain some degree of mucosal wave postoperatively. It isalso imperative to stage procedures in patients who have bilateral diseaseto reduce the likelihood of postsurgical anterior web formation [36] Cessa-tion of smoking and control of reflux disease are important factors in pre-venting recurrence of the disease after surgical excision and should beinstituted before surgery to maximize the postoperative outcome.

Leukoplakia and dysplasia

Leukoplakia, or white plaque, refers to a spectrum of diseases affectingthe vocal fold epithelium, and includes hyperkeratosis, dysplasia, and early

Fig. 7. Vocal fold papilloma involving the left vocal fold.


verrucous changes. Overall, when leukoplakia is present there is an 8% to14% likelihood of developing malignancy in such lesions. The pathophysi-ology is still unknown, but it is likely that chronic irritation and genetic pre-disposition form a synergy in such patients. The plaque may present initiallywith subtle hyperkeratotic epithelium resulting in decreased or sluggish mu-cosal wave on strobolaryngoscopy (Fig. 9A). Progression, particularly withdysplastic or premalignant changes, may be exophytic in a surrounding bedof erythema (Fig. 9B). Microflap excision, carbon-dioxide lasers, andpulsed-dye lasers are all treatment options, but appropriate pathologic stag-ing must be performed because the visual appearance does not always cor-respond to the degree of dysplasia [37]. Treatment of hyperkeratosis andmild dysplasia is centered on eradication of disease while preserving neigh-boring normal anatomy and voice quality. Severe dysplasia and carcinomain situ must be treated more aggressively.

Fig. 8. Bilateral polypoid corditis.

Fig. 9. (A) Broad superficial leukoplakia blanketing bilateral vocal folds, and (B) discrete leu-

koplakia with severe dysplasia and microinvasion seen in a bed of erythematous vocal folds.

1106 ALTMAN

Vocal fold carcinoma

Squamous call carcinoma is by far the most common form of laryngealmalignancy. Those patients who have a history of tobacco smoking accountfor about 90% of cases, and the likelihood is far greater with a concurrenthistory of excess alcohol consumption. There are also anecdotal and indirectdata to support the role of laryngopharyngeal reflux in causing and com-pounding the development of vocal fold carcinoma. Any mass lesion in a pa-tient who has such a history should therefore raise the appropriate level ofsuspicion.

Features of squamous carcinoma include exophytic, ulcerative, and infil-trative. Consequently, one may see on strobolaryngoscopy an area of focallydecreased mucosal wave at the site of an exophytic epithelial lesion (Fig. 10).This area is distinguished from papilloma, which remains an epithelial dis-ease, whereas carcinoma tends to infiltrate into the lamina propria, account-ing for the decreased mucosal wave. Also, the fibrovascular fronds seen inpapilloma are generally softer than the exophytic mass produced in carci-noma, so carcinoma would have more of a detrimental effect on phase clo-sure seen in strobolaryngoscopy. Distinguishing carcinoma fromleukoplakia is more challenging because leukoplakia may form a continuumfrom keratosis to severe dysplasia to microinvasive disease. Nevertheless,the degree of clinical suspicion and evidence of microinvasion with focallydecreased mucosal wave should mandate further evaluation [38].

Summary

There are several vocal masses that can affect the professional voice. It isimportant to understand the multifactorial contributions and pathogenesisof each to determine prognosis. Strobolaryngoscopy plays a crucial role indifferentiating the spectrum of masses and in guiding optimal management.

Fig. 10. Vocal fold squamous cell carcinoma.


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40 (2007) 1109–1131

Vocal Fold Paresis and Paralysis

Adam D. Rubin, MDa,b,Robert T. Sataloff, MD, DMAc,*

aLakeshore Professional Voice Center, Lakeshore Ear Nose and Throat Center,

21000 East 12 Mile, Suite 111, St. Clair Shores, MI 48081, USAbUniversity of Michigan, Department of Otolaryngology–Head and Neck Surgery,

Ann Arbor, MI 48109, USAcDepartment of Otolaryngology–Head and Neck Surgery, Drexel University College


Anatomy

Recurrent laryngeal nerve

Anatomy of the larynx and related structures is discussed in detail else-where [1]. This article reviews only a few of the relationships that aremost important when evaluating vocal fold mobility disorders.

The nuclei of the recurrent laryngeal nerve (RLN) axons lie within thenucleus ambiguus in the medulla of the brainstem. The RLN axons travelwith the vagus nerve down the neck until they branch off at the level ofthe aortic arch on the left and the subclavian artery on the right. On theleft, the nerve passes inferior and posterior to the aortic arch and reversesits course to continue ly into the visceral compartment of the neck. The rightRLN loops behind the right subclavian artery and ascends superomediallytoward the tracheoesophageal groove. Both RLNs travel just lateral to orwithin the tracheoesophageal groove and enter the larynx posterior to thecricothyroid joint. The positions of the nerves in the neck make them sus-ceptible to iatrogenic injury during surgery. Low in the neck, the courseof the right recurrent nerve is more oblique, lateral, and probably moreprone to injury than the left RLN [2].

Approximately 5 out of 1000 people have a nonrecurrent laryngeal nerveon the right. A nonrecurrent laryngeal nerve occurs only on the right, except

This article is modified from: Sataloff RT. Professional voice: the science and art of clinical

care. 3rd edition. San Diego (CA): Plural Publishing, Inc. 2006. p. 871–86; with permission.






1110 RUBIN & SATALOFF

in the rare case of situs inversus. It branches from the vagus nerve at thelevel of the cricoid cartilage and enters the larynx directly, without loopingaround the subclavian artery. This anomaly occurs in conjunction with aretroesophageal right subclavian artery [2].

The RLN innervates four of the intrinsic muscles of the larynx: the thy-roarytenoid (TA), posterior cricoarytenoid (PCA), lateral cricoarytenoid(LCA), and interarytenoid (IA) muscles. Muscle innervation is unilateral ex-cept for the IA muscle, which receives contributions from both RLNs [5].The TA and LCA muscles are vocal fold adductors. Unilateral denervationof these muscles results in an inability to close the glottis with resultingbreathy voice and possible aspiration.

The PCA is the main vocal fold abductor. Paralysis of this muscle resultsin an inability to abduct during inspiration. Denervation of the PCA usuallycauses the arytenoid cartilage to subluxate anteromedially in unilateral vo-cal fold paralysis. The denervatedPCAno longer counters the anterior pullon the arytenoid cartilage by the vocal ligament [5]. If both PCA musclesare denervated, as in the case of bilateralRLNparalysis, airway obstructionmay occur.

The IA muscle is actually three muscles: the transverse arytenoideus mus-cle and two oblique arytenoideus muscles. The function of the IA muscle isnot completely understood; however, it may assist in vocal fold adductionand provide medial compression to close the posterior glottis [5].

Superior laryngeal nerve

The laryngeal nerve (SLN) branches from the vagus nerve just inferior tothe nodose ganglion, which contains the sensory cell bodies of the SLN. Thenerve travels inferiorly along the side of the pharynx, medial to the carotidartery, and splits into two branches at about the level of the hyoid bone. Theinternal division of the SLN penetrates the thyrohyoid membrane with thelaryngeal artery and supplies sensory innervation to the larynx. The externaldivision of the SLN provides motor innervation to the cricothyroid (CT)muscle. The CT muscle changes vocal fold tension by elongating the fold.It is responsible for increasing the fundamental frequency of the voice.The external division of the SLN lies close to the thyroid artery, althoughits exact relationship to the artery is variable [3,4].

Vocal fold paresis and paralysis

Vocal fold paralysis implies vocal fold immobility due to neurologic in-jury. It does not indicate complete denervation, because nonselective rein-nervation of the intrinsic laryngeal muscles may occur immediately afternerve injury without restoration of vocal fold movement. Vocal fold paresisimplies vocal fold hypomobility due to neurologic injury and may resultfrom weakness of the RLN, SLN, or both. Nerve injury may be unilateral

1111VOCAL FOLD PARESIS AND PARALYSIS

or bilateral. Vocal fold paresis may present as dysphonia, loss of the upperregister of the voice, hoarseness, breathiness, throat pain, choking episodes,or decreased vocal stamina. Laryngeal findings may be subtle and includeasymmetric vocal fold movement, bowing, and rotation of the larynx. Vocalfold paresis may also present as muscle tension dysphonia or in conjunctionwith benign vocal fold lesions, such as vocal nodules or cysts resulting fromcompensatory hyperadduction.

Recurrent laryngeal nerve paresis/paralysis

The RLN may be injured by several means, including iatrogenic or non-iatrogenic trauma, neurologic disease, tumor infiltration or compression, in-fection, collagen-vascular disease, or idiopathic disease. This event mayoccur with or without concomitant SLN injury, depending on the causeand site of the lesion. The RLN is at risk for injury during many surgicalprocedures, such as thyroid, anterior cervical spine, and thoracic surgery.The true incidence of vocal fold paralysis remains unknown. The incidenceof injury to the recurrent laryngeal nerve from thyroid surgery has beenreported as between 0.3% and 13.2%, and from anterior cervical spinesurgery as between 2% and 21.6% [6,7]. Mechanisms of iatrogenic injuryinclude intubation, transection, crush, traction, inadvertent ligature place-ment, and thermal injury.

The laryngologist must always consider unusual causes. Several neuro-logic diseases may affect vocal fold movement, including multiple sclerosis,amyotrophic lateral sclerosis, syringomyelia, myasthenia gravis, Guillain-Barre, and Parkinson disease [8–15]. Cerebrovascular accidents may resultin injury to RLN neurons, but typically other neurons are affected also.Central nervous system (CNS) tumors, such as gliomas, can cause RLN pa-ralysis, and diabetics may develop RLN neuropathy [16–19]. More unusualcases include disorders such as Gerhard syndrome, laryngeal abductorparalysis that may be familial (autosomal dominant, autosomal recessiveor X-linked inheritance and with adult onset) or acquired secondary to bul-bar lesions or neurodegenerative disease [20].

Aggressive thyroid malignancies may invade and injure the RLN. Com-pression by large thyroid goiters, benign neoplasms, and nonthyroid malig-nancies, such as the classic Pancoast tumor of the left upper lung, may alsoinjure the nerve [21].

Idiopathic vocal fold paralysis is not well understood. Some suspect aviral cause, because many patients report an upper respiratory infectionbefore the onset of vocal symptoms. There are several infectious causesthat have been reported to cause RLN paralysis, such as Lyme disease, ter-tiary syphilis, Epstein-Barr virus, and herpes [22–25]. Other causes of RLNinjury reported include systemic lupus erythematosus, patent ductus arterio-sus, mediastinal radiation, I-131 therapy, amyloidosis, Charcot-Marie-Tooth, mitochondrial disorders, porphyria, polyarteritis nodosa, silicosis,and familial hypokalemic periodic paralysis [26–36].


The natural history of vocal fold paralysis depends on the mechanismand degree of injury to the nerve. The Sunderland classification system de-scribes different degrees of nerve injury. First-degree injury means neurap-raxia. Nerve function should recover completely. Second-degree injurymeans that Wallerian degeneration has occurred distal to an injured site(axonotmesis). Second-degree injury usually occurs after a crush injuryand also results in complete recovery. Because the endoneural sheathsremain intact in a second-degree injury, synkinesis does not occur. Third-degree injury includes endoneural scarring, which can cause misdirectedregeneration. Fourth-degree injury involves scarring that may block regen-erating axons. Fifth-degree injury signifies complete transection of the nerve[37,38].

Clinically, unilateral RLN injury presents as a breathy voice. Diplopho-nia, aspiration, and dysphagia symptoms may also occur. After a few weeks,the contralateral vocal fold may compensate by adducting further to im-prove vocal quality and aspiration. Should reinnervation occur, typicallyit may not be detectable initially [39,40]. The clinical course following rein-nervation is determined by the degree of reinnervation and synkinesis.

Synkinesis

Reinnervation prevents muscle atrophy. Shindo and colleagues [40] dem-onstrated in a canine model that during the first 3 months after transectionof the RLN there is atrophy of the TA and PCA muscles. After 3 months,however, the muscle fiber diameters of the denervated muscle begin toincrease. By 9 months, the fiber diameters of the denervated muscles ap-proach those of normal muscle. Spontaneous reinnervation may occur afternerve transection and prevent muscle atrophy. The source of the reinnerva-tion is not known, but may include regenerating fibers from the transectedRLN, the SLN, cervical autonomic nerves and nerve branches innervatingpharyngeal constrictors [40].

Although reinnervation after a complete RLN transection prevents mus-cle wasting, typically it does not restore useful movement to the vocal foldbecause of synkinesis. Synkinesis results from nonselective innervation ofadductor and abductor muscles. As a result, muscles that perform oppositefunctions contract simultaneously, resulting in immobility or hypomobilityof the vocal fold [41]. The clinical picture depends on the proportion ofadductor and abductor fibers reinnervated.

Crumley [39] describes a classification system for laryngeal synkinesis. InType I synkinesis, or ‘‘favorable synkinesis,’’ there is little or no vocal foldmovement. The patient’s airway and voice are fairly normal, however.Types II, III, and IV are considered ‘‘unfavorable synkinesis.’’ A spasticvocal fold that may twitch without control characterizes type II. Voice qual-ity is poor. In type III synkinesis there is tonic adduction of the vocalfold. This adduction results in a reasonable voice, but the airway may be


compromised. Type IV synkinesis involves tonic abduction of the vocal foldresulting in a breathy voice and greater risk for aspiration. Type III synki-nesis probably results from greater reinnervation of the LCA in comparisonwith the PCA fibers, whereas in Type IV the opposite likely occurs.

Superior laryngeal nerve paresis/paralysis

Superior laryngeal nerve paresis or paralysis may be caused by variousconditions. Iatrogenic trauma during thyroidectomy has been historicallyaccepted as the most frequent cause of SLN paralysis [42,43]. In 1980,Adour and colleagues [44] reported that SLN palsy was part of a combinedcranial polyneuropathy attributable to viral infections. Similarly, Dursunand colleagues [45] suggested that viral infections, such as herpetic coldsores and upper respiratory infections, are commonly associated with thiscondition. A likely explanation is that infections lead to viral neuritis, result-ing in SLN damage. To the best of our knowledge, this retrospective reviewincluded the largest population of confirmed SLN paresis and paralysis inthe medical literature. Of the total sample (n ¼ 126), 118 patients (93.6%)reported a viral infection immediately before the sudden onset of vocal im-pairment. Some of the patients used aspirin to relieve pain or fever accom-panying acute infection. In some patients aspirin ingestion probablycontributed to vocal fold hemorrhage, which resulted in further voice dys-function. Often, several months elapsed after the causative infection beforethe patients sought medical attention. Before the diagnostic examination,these patients attributed the symptoms of SLN damage to upper respiratoryinfections. The development of compensatory mechanisms, such as muscletension dysphonia (MTD), which subjectively improved voice quality, some-times resulted in further delays in seeking treatment. As expected, singerswere more aware of their symptoms than nonsingers, and delay in seekingattention tended to be shorter in this population. This observation was con-firmed in a study by Eckley and colleagues [46] that demonstrated that voicerange measurement is a useful parameter for analyzing the effects of SLNparesis or paralysis on voice and may also be used for measuring outcomefollowing voice therapy. The effects of SLN paresis on vocal range helpexplain the sensitivity of professional voice users (especially singers) to theeffects of the condition. Laboratory investigations performed during se-lected patient evaluations often demonstrated increased serum titers indicat-ing herpesvirus types I and II and antibodies to influenza type A and othercommon viruses. This evidence suggested infection at some undeterminedtime in the past.

There were 8 patients in Dursun’s [45] study who had iatrogenic causes,such as thyroid surgery or external trauma. Such findings suggest that iatro-genic trauma can also cause isolated SLN paresis. Extreme care must betaken, particularly during thyroid surgery, to protect the external branchof the SLN in the pole of the thyroid, where it descends close to the thyroid


vessels. Jansson and colleagues [47] performed pre- and postoperative elec-tromyography (EMG) on 20 patients undergoing thyroid surgery. Nine pa-tients had postoperative SLN paresis by EMG. Additionally, 3 patients whohad goiters had preoperative SLN paresis, which worsened postoperatively.Some 58% of the SLN pareses were present at 1 year follow-up, althoughmost cases had some nerve recovery. To avoid harming the SLN during thy-roid surgery, some authors recommend ligating distal branches of the thy-roid artery as close to the thyroid capsule as possible, whereas others suggestidentification of the external branch of the SLN to prevent injury [48]. Lesscommon causes have also been reported, including neurologic disorders, an-terior approach to the cervical vertebrae during surgery, carotid endarterec-tomy, nonsurgical trauma, and Reye syndrome [42,47,48].

The clinical manifestations of SLN paresis and paralysis are variable. Thevariability relates to different degrees of impairment, other associated pa-thologies, and the voice needs and awareness of each patient. Normally,the CT muscle contracts briskly in falsetto, vocal inflection, and modal pho-nation to increase tension in the vocal fold [49]. In SLN paresis and paral-ysis, the loss of this function may lead to lowered pitch, a more monotonevoice, and poor vocal performance, especially at higher pitches [42,45]. SLNparesis and paralysis may cause vocal fatigue, hoarseness, impairment ofvolume, loss of upper range, loss of projection, and breathiness. Vocal fa-tigue may be caused by the additional effort required to raise vocal pitchand to project, by hyperfunctional compensatory gestures, or by pathologicneuromuscular fatigue in cases of marked paresis. The clinical manifesta-tions of SLN paresis or paralysis, particularly loss of upper range, aremore troublesome in singers and professional speakers. These patients oftendevelop MTD to generate a stronger voice. In Dursun’s [45] series, 23.8% ofthe patients had MTD that seemed to be compensatory. It must be remem-bered that SLN paresis may be the underlying cause of voice misuse andconsequent structural lesions.

Although not a commonly described finding, choking with or without re-gurgitation and throat clearing may also occur especially if there is associ-ated neuralgia, hypoesthesia, or paresthesia. Anesthesia of the upperlaryngeal space suggests injury to the internal branch of the SLN. The ab-sence of anesthesia does not always rule out SLN paresis or paralysis, how-ever, because the external branch may be the only affected portion.Although anesthesia usually is not seen even with complete paralysis ofthe SLN, subtle decreased ipsilateral gag (hypesthesia) is fairly common.

Indirect laryngoscopy or mirror examination may or may not reveal vo-cal fold abnormalities. A strong activation of the normal CT muscle mustoccur to cause laryngeal tilt toward the weak side, another sign of unilateralSLN paresis [50]. Flaccidity of the affected vocal fold may cause irregularvertical movements during respiration, which in turn causes various config-urations of the glottis. A bowed vocal fold may be evident in SLN paresis orparalysis. These vocal folds are slightly concave, and glottic closure is


usually incomplete. This finding may be associated with other coexistingconditions, however, such as recurrent laryngeal nerve paresis or paralysis,advanced age, or other neurologic disorders [51].

Several authors have discussed the position of the vocal folds and glotticconfiguration in SLN paresis and paralysis. The studies reflect differentopinions [50,52–54]. Contraction of a normal CT muscle rotates the poste-rior commissure toward the inactive side, which causes the paralyzed vocalfold to shorten and form an obliquely shaped glottis [49,50,55–57]. Athinned, shortened, and bowed vocal fold and an oblique glottis deviatingto the paralyzed side are most consistent signs described in previous reports[42,43,57,58]. These are evident only in some cases of unilateral paralysis,however, and in the authors’ experience the lack of these signs does notrule out paralysis or paresis. Moreover, these findings may be observed ifCT contractions are weak or if the patients have MTD, which involvesnot only the hyperadduction of the normal vocal fold but also anterior–posterior compression of the glottis [54,59]. Vocal fold lag (sluggish motion)during phonation requiring rapidly repeated adduction is the most consis-tent and easily observed sign of SLN paresis or paralysis.

Evaluation

Evaluation of vocal fold paralysis or paresis begins with a history andphysical examination. The history should define the main complaints andsymptoms of the patient and likely cause of the hypomobility. One shouldinquire about previous surgeries, prolonged intubations, and trauma. Acomplete medical history should be taken, including a thorough neurologicreview of systems, smoking and alcohol history, and other questions to eval-uate for possible malignancy. Questions pertaining to possible infectiouscauses should be asked, and a thorough vocal history should be taken todefine the patient’s vocal habits and needs.

The physical examination should include a complete head and neck ex-amination, with particular attention to examination of the cranial nerves.The laryngologist should assess the patient’s gag reflex and palatal move-ment to evaluate vagus nerve function. If the patient has a unilateral highlesion of the vagus nerve, the palate deviates to the intact side. The physicianshould listen carefully to the patient’s voice, and the larynx should be visu-alized. A mirror examination should be performed first, followed by laryn-goscopy with either a rigid or flexible endoscope, or both. The voice shouldbe evaluated during various phonatory tasks at several frequencies and in-tensities, as discussed elsewhere [60]. The laryngologist should look forasymmetric movement, vocal fold bowing, horizontal and vertical positionof the vocal folds, and tilting of the posterior larynx. The presence of struc-tural lesions and signs of laryngopharyngeal reflux disease can be observedalso. Video documentation is important. Even thorough, routine


otolaryngologic examination generally is not sufficient for establishing a di-agnosis in these patients, however.

Patients who have vocal fold paralysis deserve comprehensive evaluation.Strobovideolaryngoscopy and various objective evaluations are extremelyhelpful in diagnosis, treatment planning, and assessment of treatment effi-cacy. They are reviewed in other publications [61]. Laryngeal EMG is help-ful in confirming clinical impressions, and in detecting abnormalities inother laryngeal nerve–muscle complexes that may be missed because of dis-tortion related to the most severe injury. For example, in a total right recur-rent nerve paralysis, a left laryngeal nerve paresis is considerably lessobvious than usual. Such information is important in designing optimaltherapy, however. We have found laryngeal EMG to be a practical and in-valuable component of the voice evaluation, as have other authors [62,63].

Each vocal fold is moved by many intrinsic laryngeal muscles. Thesemuscles permit adduction, abduction, and longitudinal tension of the vocalfolds. The laryngeal nerves supply the cricothyroid muscle, which is the pri-mary structure responsible for increasing longitudinal tension. Maintainingstretch of the vocal fold is extremely important for pitch control, volume,and stability during soft singing, especially from the upper mid-range andhigher. The recurrent laryngeal nerves innervate all of the other intrinsicmuscles of the larynx. Paralysis or paresis may involve one or both vocalfolds, although only one vocal fold is involved in the vast majority of cases[64]. When the recurrent laryngeal nerve is paralyzed, the vocal fold appearsto stand still, except for slight respiratory motion. The ability to alter longi-tudinal tension is maintained, however. The vocal processes are thereforeusually at the same level, and even the paralyzed side lengthens as pitch isincreased. Consequently, if the normal vocal fold can cross the midline farenough to reach the paralyzed vocal fold, compensation is possible and glot-tic closure and reasonably good phonation can be achieved. The normal vo-cal fold can only compensate in the horizontal plane, however. It cannotmove ly or inferiorly to meet the injured side if laryngeal nerve paralysisis present and has resulted in differences in vocal fold height. Over time, at-rophy of the thyroarytenoid may occur, making even horizontal compensa-tion more difficult.

When the superior laryngeal nerve is involved, longitudinal tension is im-paired and the vocal fold may be bowed or sagging. Consequently, it typi-cally lies in a lower plane, and compensation is difficult. This finding isespecially true if both recurrent and laryngeal nerves are paralyzed, butproblems occur even with isolated laryngeal nerve paralysis in the presenceof abduction and adduction. Bilateral laryngeal nerve paralysis is oftenmore difficult to diagnose and is probably missed frequently. Patients whohave this condition have a ‘‘floppy’’ epiglottis, rendering their larynges dif-ficult to see. Their vocal quality, volume, and pitch range are impaired. It isoften particularly helpful to confirm a clinical impression of bilateral laryn-geal nerve paralysis through EMG.


Briefly, if vocal fold paralysis seems to occur below the level of the no-dose ganglion, complete evaluation from the skull base through the chest(including the thyroid) is essential. This localization can usually be madereliably in isolated unilateral recurrent laryngeal nerve paralysis. If the pa-ralysis is complete (recurrent and ) or if there are other neurologic find-ings, intracranial studies should be performed also. Occasionally, centraldisease (especially multiple sclerosis) can produce unexpected neurologicsigns, and if no cause is found after a paralyzed recurrent laryngeal nervehas been thoroughly evaluated, addition of a MRI of the brain and otherstudies should be considered. Because of the seriousness of missing intra-cranial lesions, many physicians obtain MRI of the brain and 10th cranialnerve with enhancement in all cases and this practice certainly is notunreasonable.

A few clinical maneuvers are useful for making paresis more apparent.Repeated maneuvers alternating a sniff with the sound /i/ are particularlyhelpful in unmasking mild PCA paresis. Repeated rapid phonation on /i/with a complete stop between each phonation frequently causes increasedvocal fold lag as the pathologic side fatigues more rapidly than the normalside. Other rapidly alternating tasks are helpful also, including /i/-/hi/-/i/-/hi/-/i/-/hi/. and /pa/-/ta/-/ka/-/pa/-/ta/ka/-pa/ta/ka/.. The vocalfold lag is sometimes easier to see during whistling. Laryngeal posture dur-ing this maneuver provides particularly good visibility of rapid vocal foldmotions. A glissando maneuver, asking the patient to slide slowly fromhis or her lowest to highest note and then slide back down, is invaluablefor assessing SLN function. The vocal process should be observed undercontinuous and stroboscopic light. If a laryngeal nerve is injured, longitu-dinal tension does not increase as effectively on the abnormal side, dispar-ities in vocal fold length are apparent at higher pitches, and the vocalfolds may actually scissor slightly with the normal fold being higher.

(Access Video on Normal neurolaryngeal examination in online version of this article at:


Appropriate laboratory studies should be considered to rule out specificcauses of vocal fold paresis and paralysis. Thesemay include tests for syphilis,Lyme disease, diabetes, thyroid dysfunction, collagen vascular disease, myas-thenia gravis, thyroid neoplasm, and other conditions. In addition to testinggag reflex, more quantitative sensory testing may be helpful.

Treatment

Treatment of unilateral vocal fold paralysis is designed to eliminate aspi-ration and improve the voice. When there is no aspiration, treatment de-pends on the patient’s need and desire for improved voice quality. It iswell recognized that recovery of laryngeal nerve function is common if the




injury was not caused by transection of the nerve. Even when the nerve istransected, some innervation may occur. Consequently, it is best to delaysurgical intervention for approximately 1 year, if possible, unless the nerveis known to have been divided or resected. This plan does not mean thattreatment should be delayed, however, but only irreversible surgery. Thecollaboration of an excellent speech-language pathologist is invaluable.

Voice therapy

Objective voice analysis, assessment, and therapy by speech-language pa-thologists specializing in voice are helpful in virtually all patients who havedysphonia. Voice therapy is invaluable in the management of vocal fold pa-resis and paralysis. In all cases, the speech-language pathologist can providedetailed preoperative and postoperative assessment. Such assessment is of-ten of diagnostic value. It is also of great help to the surgeon in objectivelyevaluating the efficacy of treatments. In addition, voice therapy sometimesavoids the need for surgery, saving the patient from exposure to unneces-sary surgical risks. Heuer and colleagues [65] studied 19 female patientsand 22 male patients who had unilateral recurrent nerve paralysis andfound that after excellent voice therapy, 68% of the female patients and64% of the male patients considered their voices satisfactory and electednot to have surgery. Final outcome satisfaction data were similar for surgi-cal and nonsurgical patients. Even when surgery is eventually required, pre-operative voice therapy helps the patient while surgical decisions arepending, provides training for optimal postoperative phonation, and pre-pares the patient psychologically for surgery with the knowledge that every-thing possible has been done to avoid unnecessary operative intervention.This strategy results in patient cooperation, motivation, and understandingthrough educated participation in the voice restoration process. The impor-tance of this factor should not be overlooked in the art of medicine andmedicolegal prudence.

In people who have unilateral vocal fold paralysis, initial assessment notonly quantitates and documents vocal dysfunction but also explores a widerange of potentially useful compensatory strategies. In addition, the speech-language pathologist identifies spontaneous compensatory behaviors thatmay be counterproductive. For example, although speech pathology text-books generally classify and treat vocal fold paralysis as a hypofunctional dis-order, undesirable compensatory hyperfunctional behavior is common inthese patients [66,67]. This behavior is responsible for most of the voice strain,neck discomfort, and fatigue that may accompany unilateral vocal fold paral-ysis. Such gestures often can be eliminated even during the first assessment andtrial therapy session, increasing vocal ease and endurance.Moreover, if the as-sessment reveals improved voice with a different pitch, training in safe pitchmodification in combinationwith other techniquesmay also provide rapid im-provement. Indeed, under good guidance, therapy sometimes produces


astonishingly rapid improvements in voice quality despite persistence of theneurologic deficit. In any case, initial assessment is worthwhile to documentvocal condition before surgery is considered and to get an estimate of howmuch the patient’s voice can be improved without surgery.

Most often, initial assessment results in modest but noticeable improve-ment in voice quality and subjectively important improvement in ease andendurance. Generally, several therapy sessions are needed to optimize vocalfunction. The speech-language pathologist provides patients with educa-tional information about the workings of phonation, about their specific ab-normality, and about vocal hygiene. The importance of and rationale fortherapy are also explained. Therapy is directed toward avoidance of hyper-functional compensation and progressive development of optimal breath-ing, abdominal support, and intrinsic laryngeal muscle strength andagility. Training includes head and neck muscle relaxation exercises, aerobicconditioning, abdominal and thoracic muscle strength and control exercises,attention to respiration, and various voice exercises that build limb strengththrough multiple repetitions with light weights. Forced adduction exercises,often recommended in speech pathology texts, such as pushing or pulling onchairs, must be avoided or monitored closely and used with extreme cau-tion. Although such exercises are still in fairly common use, other tech-niques may be more effective and have less potential for harm. Whenavailable, traditional voice therapy combined with a few expert singing les-sons may expedite improvement. This plan is analogous to including jog-ging or running in a rehabilitation program aimed at improving limbstrength for walking.

Like surgery, therapy is least successful in combined paralysis. In mostpatients who have unilateral vocal fold paralysis, therapy results in improve-ment. In many cases, the improvement is sufficient for the patients’ needs.When the patient has complied with voice therapy, improvements havereached a plateau, and they feel that their voice quality is not satisfactory,surgery may be indicated.

If preoperative voice therapy has been optimal and if surgery has beensuccessful, the postoperative voice therapy course should be short. Never-theless, the patient is working with a ‘‘new voice.’’ At least a few sessionswith a speech-language pathologist generally help the patient apply effectiveprinciples learned in preoperative therapy. It is particularly important forthe voice therapist and speech-language pathologist to monitor the patient,avoiding development of abusive habits and stressing the importance of vo-cal hygiene measures. At the conclusion of therapy, objective voice measuresshould be repeated.

If the patient is interested in optimizing voice quality, it is reasonable tocontinue therapy as long as it continues to produce voice improvement. Thisjudgment is usually made jointly by the patient, speech-language patholo-gist, and laryngologist. In most patients who have had good preoperative


voice therapy, this juncture or goal is reached within 1 to 3 months aftersurgery.

Bilateral vocal fold paralysis creates much greater problems; this is true forbilateral recurrent, bilateral , or bilateral combined nerve paralysis, or combi-nations thereof. There is still no satisfactory treatment of bilateral recurrentnerve paralysis. Frequently, this condition leaves the patient in the uncomfort-able position of choosing between good voice and tracheotomy, or a good air-way and bad voice. Therapy may provide some help to these patients, but it israrely definitive. It is hoped that laryngeal pacing can provide a solution tothese problems, as discussed later in this article. If so, there is an importantrole of the voice therapist following pacemaker implantation.

Surgical therapy

The two main surgical options for patients who have unilateral vocal foldparalysis are medialization and reinnervation. The most common and im-portant techniques for surgical management of patients who have vocalfold paresis and paralysis are discussed in the article on voice surgery by Sa-taloff and colleagues elsewhere in this issue [68]. In this article we have in-cluded only a brief overview of some of these procedures and havehighlighted discussions of techniques of reinnervation, gene therapy, and la-ryngeal pacing that are not discussed comprehensively elsewhere in this is-sue. Medialization procedures include injection laryngoplasty andlaryngeal framework surgery. Several materials have been injected to medi-alize the vocal fold and improve glottic competence. These include polyte-trafluoroethylene (commonly known as Teflon, E.I. DuPont Nemous andCompany, Wilmington, Delaware), absorbable gelatin powder (Gelfoam,Pharmacia, Kalamazoo, Michigan), fat, collagen, dermal collagen, hydrox-ylapatite, and others. Teflon used to be the most popular choice; however, ithas few (if any) indications today. The senior author (RTS) has not usedTeflon since 1988. Teflon is permanent and leads to a chronic granuloma-tous inflammatory response [69]. Teflon can also migrate and may evenspread to other parts of the body [70]. Teflon granulomas are difficult to re-move and often result in a poor vocal outcome [61].

Gelfoam is used as a temporary measure, typically when future return ofvocal fold function is possible but the patient needs or wants immediatesymptomatic improvement. Gelfoam is absorbed within 3 months. If vocalfold function has not returned by then, the surgeon must decide whether re-injection or a more permanent procedure is warranted.

Fat is resorbed partially within 3 to 4 months [70], but improvement maybe permanent. Autologous fat is harvested easily using liposuction or by di-rect excision and generally allows the vocal fold to maintain normal vibra-tory qualities.

Allogeneic, autologous, and bovine collagen have been used to medializeparalyzed vocal folds [69,71]. Collagen incorporates into host tissue [69].


Some report collagen lasting as long as 3 years. Collagen may be injectedinto the vocal ligament. It softens scar tissue and can improve the vibratoryqualities of the vocal fold.

Medialization

Type I thyroplasty was popularized by Isshiki and colleagues [72]. Aryte-noid adduction surgery was designed by Isshiki and colleagues [73] also toimprove closure of the posterior glottis. Some laryngologists believe that af-ter a long duration of vocal fold paralysis, the cricoarytenoid joint scars andbecomes fixed. In this case, the ankylosis must be addressed for a medializa-tion procedure to be effective [74]. Several animal and cadaver studies sug-gest that the cricoarytenoid joint remains normal for as long as 17 yearsafter RLN injury, however [75,76].

Reinnervation

Several reinnervation procedures for the paralyzed vocal fold have beendescribed using the ansa cervicalis [74], phrenic nerve [77,78], preganglionicsympathetic neurons [79], hypoglossal nerve [80], and nerve–muscle pedicles[74,77–82]. The main purpose of reinnervation procedures is to preventdenervation atrophy of laryngeal muscles. Crumley [74] reports improvedvocal quality and restoration of the mucosal wave after reinnervation usingthe ansa cervicalis. The ansa cervicalis provides weak tonic innervation tothe intrinsic laryngeal muscles. Reinnervation of the TA muscle restores ten-sion resulting in a more normal mucosal wave. Reinnervation of the PCAand LA muscles stabilizes the arytenoids and prevents inferior displacementof the vocal process, which may occur in some patients. Crumley [74] reportsadditionally that the ansa cervicalis–RLN anastomosis is particularly usefulin cases of synkinesis after nerve injury resulting in jerky movements of thevocal folds. Although there is still synkinesis after ansa–RLN anastomosis,the weak tonic innervation supplied by the ansa produces a vocal fold that isless spastic.

Attempts to design reinnervation techniques that might avoid synkinesisand restore movement to the paralyzed vocal fold have been reported[83,84]. Hogikyan and colleagues [85] examined muscle-nerve-muscle neu-rotization in the cat. In this technique, the paralyzed thyroarytenoid muscleis reinnervated by way of axons that sprout from the contralateral, inner-vated TA muscle through an interposed nerve graft. The authors demon-strated histologic and EMG evidence of this specific reinnervationpathway in more than half the cats used. Actual return of vocal fold adduc-tion was demonstrated in one cat. This technique of motion-specific reinner-vation is promising for restoration of physiologic movement after vocal foldparalysis.


Tucker [81] has reported improvement in voice quality and restoration ofadduction of the unilateral paralyzed vocal fold after nerve–muscle pedicletransfer. This technique involves implanting a piece of strap muscle inner-vated by nerve terminals from the ansa cervicalis into one of the denervatedlaryngeal muscles, usually the LCA or TA [82,86]. Tucker [86] also reportsbetter vocal quality in patients who have unilateral vocal fold paralysis whenthey are treated with nerve–muscle pedicle and medialization, than whentreated with medialization alone.

Bilateral vocal fold paralysis

Although voice quality is typically good in the presence of bilateral vocalfold paralysis (BVFP), airway patency is jeopardized by the paramedianposition of the vocal folds. Tracheotomy may be required acutely, followedby surgery to improve the size of the glottic airway. Surgical techniques aredesigned to lateralize one or both vocal folds to improve airway patency andassist with decannulation. Voice quality is impaired when the paralyzed vo-cal fold is lateralized. The most important of these techniques are reviewedelsewhere [68].

Cordotomy and arytenoidectomy with or without suture lateralization ofthe vocal fold are the most commonly performed lateralization proceduresto treat bilateral vocal fold paralysis [87]. These procedures are typically per-formed endoscopically with use of the CO2 laser. The advantages of usingthe CO2 laser include arguably increased precision through the narrow en-doscope and improved hemostasis requiring less need for tissue manipula-tion [88]. Potential complications include granuloma formation, scar,chondritis, and endotracheal tube fire. Patients should be put on antirefluxmedication preoperatively to reduce the risk for scar and granuloma forma-tion [88,89].

Good results have been reported using the above techniques. Efforts con-tinue to improve lateralization techniques. Cummings and colleagues [90]have developed a polyethylene device with a double-helix screw that engagesand lateralizes the vocal fold. The authors have reported in animals, prom-ising potential advantages of this new device including more control of thelateralization process and adjustability to fine-tune voice and airway results.

Several reinnervation procedures to the PCA muscle have been described[77,79,81]. Given its inspiratory activity, the phrenic nerve is an obvious can-didate for anastomosis. Despite animal models, however, there has been noreported clinical success with such a technique [91]. Tucker [81] has reportedairway improvement and return of abductor function after nerve–musclepedicle transfer. Such success has not been universal, however [92].

The use of botulinum toxin injection in the treatment of bilateral paral-ysis has been explored in animal models [93,94]. Injection of toxin into thecricothyroid muscle results in decreased tension in the vocal fold and subse-quent lateralization with airway improvement. The author (RTS) has also


used botulinum toxin injections in the adductor muscles (TA and LCA) forbilateral severe paresis to eliminate synkinesis and permit unopposed actionof the PCA to abduct the vocal folds.

When both vocal folds are paralyzed in the cadaveric position, as froma high vagal lesion, the airway may be fine, but voice and swallowing maybe impaired. In this setting, unilateral or bilateral medialization proceduresmay be useful.

Laryngeal pacing

Functional electrical stimulation (FES) of the larynx, or laryngeal pacing,continues to be explored as a potential therapeutic option for unilateral andbilateral paralysis [91,94–102]. FES systems have been used to restore motorfunction to patients who have spinal cord injury, to control heart rhythms incardiac disease, and to restore sensory function (cochlear implant, for exam-ple) [91].

Unlike cardiac pacemakers, laryngeal pacers require an efferent and anafferent limb. An afferent limb is needed to provide information to enableeffective timing of muscle contracture [95]. For example, in the setting ofunilateral vocal fold paralysis (UVFP), if the paralyzed side is stimulatedto adduct when the innervated side is abducted, this does not result in im-provement of glottic competence or voice. In the setting of BVFP, firingof the phrenic nerve, a change in intrathoracic pressure, or chest wall expan-sion can provide the afferent input signaling inspiration [91,96]. This activityresults in stimulation of the PCA muscles to abduct the vocal folds. In thesetting of UVFP, the contralateral TA or LCA muscles are the best candi-dates for afferent input [97].

The efferent limb of the system may be connected to a nerve, either thevagus or RLN if it is still intact [91], to the nerve of a nerve–muscle pedicle[95], or to the denervated muscles themselves [91,98,99]. After an RLN tran-section, axons may fail to regrow through a neurorrhaphy or other reinner-vation procedure. By placing the electrodes in the denervated musclesthemselves, the system would bypass this potential pitfall. In addition, func-tioning of the system would not rely on regeneration of axons.

Several animal studies have been performed to explore the ideal param-eter settings for laryngeal pacemakers. These parameters differ dependingon where electrodes are placed and what muscles are being stimulated[91,100]. In the canine PCA muscle, the optimal stimulation frequency is be-tween 60 and 90 Hz and the optimal pulse duration is 2.0 milliseconds. Stim-ulation intensities up to 6 V are tolerated without tissue damage. In a modelof canine UVFP, maximal adduction was achieved with stimulation intensi-ties from 3 to 7 V, pulse duration of 0.5 milliseconds, and frequencies from84 to 100 Hz [97]. In human patients who had vagal nerve stimulators placedfor intractable seizures, abduction was noted at 20 Hz, whereas 40 Hz wasrequired for adduction. Pulse duration of 3 milliseconds and stimulation


intensities of 3 mA were used for all patients [101]. Some implantations oflaryngeal pacers have been done in patients who have bilateral vocal foldparalysis. More than one half of the patients have been decannulated. Pa-tients must turn on the device manually and train themselves to breath syn-chronously with the device. In the future, pressure-sensing devices may beadded to stimulate abduction with inspiration [102].

Gene therapy

Gene therapy may offer future treatment options for recurrent laryngealnerve injury. Several growth factors have been identified that promote neu-ronal survival and sprouting. Delivery of genes encoding such growthfactors into host tissue may protect against neuronal degeneration and stim-ulate regeneration after nerve injury. Shiotani and colleagues [103] deliveredthe gene for IGF-I in a nonviral vector to the rat thyroarytenoid muscleafter RLN transection. Rats who received the gene demonstrated greaterreinnervation and less muscle atrophy than rats who did not receive thetreatment.

Viral vectors carrying gene products can be delivered to the CNS by ret-rograde transport after peripheral injection into nerve or muscle. Rubin andcolleagues [104] demonstrated that delivery of viral vectors to the CNS ispossible through the recurrent laryngeal nerve. This technique could be use-ful in the treatment of neurodegenerative diseases, such as amyotrophic lat-eral sclerosis, or for RLN injury with a partially intact nerve.

Vocal fold paralysis in children

Vocal fold paralysis represents 10% of congenital anomalies of the lar-ynx, second only to laryngomalacia [105,106]. It is also the second mostcommon cause of neonatal stridor [105,107].

The most common cause of pediatric vocal fold paralysis is controversial.CNS anomalies are the most common causes of bilateral vocal fold paralysis[105]. Of these, Arnold-Chiari malformation is the most common [105,108].This anomaly involves herniation of the cerebellum and brainstem becauseof an abnormally small posterior fossa and results in either unilateral or bi-lateral paralysis. Some controversy exists as to whether the reason for para-lysis is increased intracranial pressure secondary to hydrocephalus orpressure on the vagus nerve exerted by the herniating central nervous systemtissue [105,109]. Other causes of vocal fold paralysis in children include birthtrauma, iatrogenic injury, blunt trauma, mediastinal masses, cardiac anom-alies, and other neoplasms [105,108,110].

Stridor is the most common sign of unilateral vocal fold paralysis(UVFP) or bilateral vocal fold paralysis (BVFP) in children. UVFP alsomay present as a breathy cry, feeding difficulties, and aspiration. Bilateral


vocal fold paralysis typically presents with airway obstruction and aspira-tion. Evaluation for vocal fold paralysis includes a complete history, carefullistening to the airway and child’s cry, full head and neck examination withparticular attention to the neurologic exam, fiberoptic examination of theairway, direct laryngoscopy and bronchoscopy to assess cricoarytenoid jointfunction and to look for other anomalies, and MRI from the brain and skullbase through the mediastinum. EMG is used at some centers [111].

Recovery rates for pediatric vocal fold paralysis have been reported from16% to 64%. Function may return after 6 weeks to 5 years [105]. Childrenwho have UVFP can be observed in most cases, although occasionally a tra-cheostomy may be warranted. Positioning maneuvers can be performed totry to prevent aspiration. Type I thyroplasty has been performed in somecases [112]. BVFP typically requires urgent airwaymanagement and tracheot-omy. Lateralization procedures, such as arytenoidectomy or cordotomy, maybe performed if bilateral paralysis does not recover [105,107].Many otolaryn-gologists recommend waiting at least 12 months before surgery, but this too iscontroversial [107]. EMG may provide prognostic information [105].

Arytenoid dislocation/subluxation

Arytenoid dislocation or subluxation, although frequently unrecognized,is not a rare entity. Arytenoid dislocation is frequently mistaken for vocalfold paralysis. It is extremely important for the otolaryngologist to be awareof this condition, because it can usually be treated successfully if diagnosedpromptly. When missed or misdiagnosed as vocal fold paralysis, surgical re-pair becomes more difficult, although not impossible as previously believed[113–118]. Understanding the complex anatomy and embryology of thearytenoid helps clarify the condition [119].

Traditionally, arytenoid dislocation has been suspected by history andabsence of the jostle phenomenon present in many cases of unilateral vocalfold paralysis. Often it is not diagnosed until direct laryngoscopy revealsimpaired passive mobility of the vocal fold. Preoperative differentiationbetween vocal fold paralysis and arytenoid dislocation should be possiblein virtually all cases. If not considered specifically, however, it is oftenmissed. Disparity in height between the vocal processes is much easier tosee in slow motion under stroboscopic light at various pitches. In posteriordislocations, the vocal process is higher on the abnormal side. In anteriordislocations, the vocal process is lower on the involved side. In either case,the injured vocal fold may move sluggishly or may be immobile. Rarely, ab-duction and adduction may appear almost normal under continuous light.Video documentation of the preoperative and postoperative appearancecan prove particularly helpful in cases of arytenoid dislocation, becausemany of these patients are involved in litigation related to their injuries.

The most valuable tests are the stroboscopic examination to visualize dif-ferences in vocal process height; CT scan, which may image the arytenoid


dislocation and reveal clouding or obliteration of the cricoarytenoid jointspace; and laryngeal EMG to differentiate an immobile dislocated arytenoidjoint from vocal fold paralysis. Airflow analysis is also helpful in document-ing changes.

Although surgical reduction of a dislocated arytenoid may rarely be im-possible even in early cases, it is worth attempting in all patients beforetreatment with vocal fold injection, adduction/rotation, or other surgery.Even many months after injury it has been possible to move the arytenoidenough to bring the vocal process back to normal height and allow goodapproximation with the mobile vocal fold.

Summary

Vocal fold paralysis and paresis remain incompletely understood phe-nomena. Although evaluation techniques continue to improve, we still diag-nose many cases as idiopathic. Although current surgical techniques enableus to improve voice, swallowing, and airway, we have not been able torestore useful movement consistently to the paralyzed vocal fold. With thedevelopment of new diagnostic and surgical techniques, we will continueto improve our understanding and treatment of the paralyzed or pareticvocal fold.

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40 (2007) 1133–1149

Voice Therapy for the Professional Voice

Sarah L. Schneider, MS, CCC-SLP,Robert T. Sataloff, MD, DMA*

Department of Otolaryngology–Head and Neck Surgery, Drexel University College


The practice of speech-language pathology includes prevention, habilita-tion, and rehabilitation of communication, swallowing, or other upper aero-digestive disorders; elective modification of communication behaviors, andenhancement of communication [1]. The American Speech-Language-Hearing Association (ASHA) states that the speech-language pathologistshould provide prevention, screening, consultation, assessment, treatment,intervention, management, counseling, and follow-up services for speech,voice, language, swallowing, cognition, and sensory awareness for commu-nication, swallowing, and upper aerodigestive functions. In the area of treat-ing voice disorders, the speech-language pathologist is concerned not withdiagnosis and treatment of laryngeal diseases or other physiologic disorders,but rather with understanding, analyzing, and modifying vocal function.

If, perceptually, the voice is within normal limits for the patient and isbeing produced in a reasonably efficient, nonabusive manner, then interven-tion by a speech-language pathologist need not be conducted. It is notwithin the speech-language pathologist’s scope of practice to provide specialtraining that develops range, power, control, stamina, and the esthetic qual-ity required for artistic expression. The speech-language pathologist is con-cerned with the voice that presents with a current or potential problem,identifying and analyzing the problem, and then helping the voice user mod-ify vocal behaviors to use the vocal mechanism with optimal efficiency. Inthe case of the professional voice user, increased demand and expectationsfor voice quality may be present and should be considered when judgingnormalcy of the voice. Responsibilities in ameliorating voice problems

This article is taken in part from Marx Schneider SL, Sataloff RT. Speech language inter-

ventiondvoice therapy. In: Merati A, Bielamowicz S, editors. Textbook of laryngology. 1st

edition. San Diego (CA): Plural Publishing, Inc.; 2007.






1134 SCHNEIDER & SATALOFF

include: analyzing vocal behaviors perceptually and objectively; analyzingvocational, educational, and psychologic factors that may interact withvocal behaviors and precipitate, maintain, or exacerbate vocal difficulty;and designing and implementing an individual program for modifying vocalbehaviors [2].

Similar to physicians and their subspecialites, speech-language patholo-gists vary in their backgrounds and experience in the treatment of voicedisorders. Furthermore, the curricula that speech-language pathologistscomplete during education and training vary widely and typically only ad-dress normal and disordered voice production at a general level. Curriculararely provide education or knowledge about the professional voice. Beforemaking a referral to a speech-language pathologist for voice therapy, there-fore, his or her background and training should be considered.

This article focuses on the speech-language pathologist’s treatment ofvoice disorders with special emphasis on the treatment of professional voiceusers. There are many factors to consider when working with professionalvoice users. The following is not meant to be an inclusive list but is intendedmerely to provide a framework of key considerations. Evaluation and treat-ment of a professional voice user requires increased sensitivity from the cli-nician. At first, when listening to the patient’s voice, it may sound normal.Sounding normal is relative, however. The professional voice user typicallyhas increased awareness of minute changes in the voice production andquality. A speech-language pathologist must therefore be ‘‘super sensitiveto super speaking.’’ The goals of the professional voice user or performerare typically different from those of a nonperformer and must be consideredas such. With that in mind, it is important to learn the patient’s expectationsand provide a realistic perspective on the possible outcome of therapy basedon the diagnosis and response to trial therapy techniques during the initialassessment.

Further consideration must be given to body and self-awareness issues inperformers versus nonperformers. Body and self-awareness, in this sense, re-fers to the patient’s awareness of his or her own behaviors and the ability tomake changes as instructed. Professional voice users may have increasedawareness of vocal behaviors, depending on their previous depth of training.Body and self-awareness are important skills to develop or maximize in thevoice user. They aid the patient in developing, recognizing, and maintainingtechniques for efficient voice use.

Environmental contributions also should be noted. As a professionalvoice user, the patient may be in detrimental performance situations thatmay not be obvious to a treating clinician. These may include poor acousticswhile performing, interference of costumes and clothing, positional factors,and so forth, which can be significant contributing factors to suboptimalvoice performance. The clinician must therefore ask specific questionsor even attend a rehearsal or performance to make a complete assessmentof conditions.

1135VOICE THERAPY FOR THE PROFESSIONAL VOICE

Psychologic factors also commonly contribute to voice problems. Thevoice can be described as an emotional part of each person. Studies by Fo-nagy, described by Sundberg [3], have indicated that articulatory and laryn-geal structures and respiratory muscle activity patterns change in relation to10 different emotions. This finding indicates an emotional/psychologic con-nection to the voice. Psychologic factors may be related to the patient’sresponse to the voice disorder and its effect on his or her life. Or, the voicedisorder may be the manifestation of a larger psychological issue that iscausing a voice disorder, as in psychogenic voice disorders. In either case,treatment should be tailored to the needs of each patient with careful historytaking and thorough examination. The speech-language pathologist may actas a patient advocate speaking with the physician and acting as a catalyst fora referral to the appropriate psychologic professional as deemed necessaryby the physician.

Emotional factors also can affect the patient’s overall response to thevoice disorder. Is the patient able to cope with the voice disorder? Howwill it affect his or her current life, voice demand and expectations, and ca-reer? Are past vocal experiences, the diagnosis, or other people’s responsesaffecting therapy sessions or outcomes [4]? These basic questions should beaddressed with the patient.

Treating voice patients requires the interaction of many disciplines. Pa-tients and clinicians alike benefit from a team approach to the voice patient’scare. Treatment by an interdisciplinary team is important when treatinganyone who has a voice disorder and crucial when treating the professionalvoice user. The members of the team may include a laryngologist, speech-language pathologist, singing voice specialist or singing teacher, acting voicespecialist, voice researcher or scientist, singing coach, or psychologist (Table 1).Relationships with other arts medicine specialists are also important, includingneurologists, pulmonologists, gastroenterologists, endocrinologists, physiat-rists, psychiatrists, and others.

In some centers the interdisciplinary team may be in one facility, but notalways. Whenever possible, it is beneficial for voice therapy and singingvoice therapy to be completed by two different professionals. When this oc-curs adequate time is spent on both areas of the voice, the clinicians canwork together to target areas in the speaking and singing voice, and eachclinician can advise the patient within the area in which they are working,regardless of the individual background. If team members are not withinthe same facility it is important to build relationships within the communityto maximize patient care.

In specific cases other specialists may be included in the interdisciplinaryteam. The voice researcher or scientist can provide valuable insight and per-spective regarding the care of a voice patient because of his or her specificknowledge and skill set in acoustic measurement and voice production. Re-ferral to a singing voice coach may also be useful following rehabilitationwork with the speech-language pathologist and singing voice specialist.


The singing voice coach is a valuable aid in the development of artistic styleand repertoire for the voice user. A psychologist or psychiatrist may provevaluable in a team setting, providing the patient with counseling for themanagement of emotional reactions to the voice disorder along with psycho-logic issues that may have contributed to its occurrence. In addition, a phys-iatrist may offer contributions in the way of addressing areas of tension orother injury throughout the body.

Regarding the interdisciplinary team, singing and acting voice specialists,in addition to the singing coach, have no formal licensing or certificationboard. It is therefore important to understand that resources from commu-nity to community can vary widely, as can the backgrounds and knowledgeof various voice professionals. For example, singing and acting voiceteachers and coaches are not trained to work with the injured voice andtherefore may not have experience in this area. Singing voice specialistsand acting voice specialists are experienced teachers who have acquiredsuch training, usually through apprenticeships.

The interdisciplinary approach to the treatment of voice disorders isincreasingly important. Professional organizations are recognizing the de-velopment of these specialized relationships. ASHA has worked in conjunc-tion with the National Association of Teachers of Singing and the Voice andSpeech Trainers Association to present a joint statement, ‘‘The role of thespeech language pathologists, the teacher of singing, and the speaking voicetrainer in voice habilitation’’ [5]. This statement is intended to encourage

Table 1

A typical interdisciplinary team

Title Role

Laryngologist Primary medical member of the team; responsible for

diagnosis and medical/surgical intervention

Speech-language pathologist Conducts evaluation and treatment of the voice

problem by promoting efficient use of the vocal

mechanism

Singing voice specialist Develops singing technique and singing voice

production; may be beneficial to a nonsinger in

teaching more efficient breathing and coordination

with voicing that can be carried over into speaking

Acting voice specialist Focuses on honing vocal skills, such as projected

speech, and communication skills as they relate to

vocally demanding professions; typically used once

a patient has become efficient in speaking voice

production with a speech-language pathologist

The patient The most important member of the team; the patient

must be motivated to participate in therapy,

knowledgeable about the voice disorder and

techniques for treatment as instructed by the

clinician, and involved in therapy decision- making

and planning


interdisciplinary treatment of voice disorders and to encourage professionalsworking with voice patients to work within the scope of practice and lawsregarding treatment. It is important for professionals to stay within thebounds of their knowledge and remain within their area of expertise.ASHA has also worked with the Speech, Voice, and Swallowing Subcom-mittee of the American Academy of Otolaryngology–Head and Neck Sur-gery to generate a joint statement, ‘‘The use of voice therapy in thetreatment of dysphonia’’ [6]. This statement recognizes the importance ofvoice therapy in conjunction with medical and surgical management intreating voice disorders as supported by clinical research and expert experi-ence. These statements should be used to advocate for speech pathologyservices to benefit the patients treated and the field as a whole.

Voice evaluation

The initial voice evaluation should include a thorough review of case his-tory, performance of objective and subjective evaluation, trial therapy, andassembling initial impressions and recommendations. This evaluation pro-vides the clinician with baseline information about vocal function, patientstimulability and possible therapy techniques and approaches, expectationsof the voice user, and information from which to draw conclusions regard-ing success of therapy and possible outcomes.

Case history

A thorough case history should be elicited from the patient beginningwith the onset and development of the voice problem and the circumstancesunder which it ensued. The patient’s previous or current medical diagnosesand treatments should be reviewed. The duration of the voice disorder andits constancy are also important factors. In some cases, voice problems canbe intermittent over many years with the patient not having pursued treat-ment until the problem worsened significantly. Knowing this informationcan give the clinician perspective on the patient’s overall voice disorder.Whether or not the patient had received voice therapy previously shouldbe documented. If so, when the treatment took place, its duration, tech-niques used, and whether previous treatment was effective should noted.These factors can indicate how receptive the patient will be to further inter-vention and how he or she will likely respond to different voice therapytechniques.

A complete inventory should be taken regarding vocal hygiene, includinghydration and intake of drying agents; engagement in phonotraumaticbehaviors, including yelling, shouting, loud talking, coughing, and throatclearing; exposure to other irritants, including smoking, exposure to second-hand smoke, and stage smoke; and behavioral factors that may include sleeppatterns, overall rest, and environmental factors. In addition, vocal


demands should be reviewed and the patient should provide examples ofvoice use during a typical day. Throughout this inventory, the patientshould explain the primary vocal complaints so as to provide the clinicianwith a possible starting point for intervention. The patient’s initial concernsare addressed immediately and this may increase his or her motivation tocontinue therapeutic intervention.

Special factors must be considered when eliciting a history from a profes-sional voice user. Learning vocal complaints as they relate to the perfor-mance voice can be helpful. The clinician should inquire about the historyof professional voice use, whether it be singing, acting, public speaking, ora combination thereof. The clinician should also ask about the genre of mu-sic the patient is singing, voice classification, performance venues, and thesize of his or her typical audience, if any. Knowing the extent of the profes-sional voice user’s vocal training is also valuable, particularly when and howlong he or she has studied, the specific school of training, and whether he orshe is studying currently. This process provides information about the typesof vocal techniques the patient may already use or be aware of, or those thatmay need to be developed or reworked further.

The clinician should request that the patient share his or her professionalgoals and expectations for voice. Ideally, voice therapy should be tailored toaccommodate the patient’s professional and career goals concurrently withsatisfying the clinician’s therapeutic objectives. Even though the singingvoice specialist typically performs a more thorough evaluation of the com-plaints of a singer, the speech-language pathologist can play an importantrole in singing voice rehabilitation and development. The clinician can useknowledge of a patient’s background, education, and experience to assistin development of efficient daily speaking voice and in articulating therelationship between daily speaking routines and singing or stage voice.

Objective evaluation

Gathering and analyzing objective voice data is a crucial part of thecomplete voice evaluation. Completing pre- and posttherapy voice measurescan supply objective data to assist in predicting therapy outcomes, to use inresearch, and to provide tangible voice statistics for use by insurancecompanies. The objective voice evaluation is discussed further in the articleabout laboratory and strobovideolaryngoscopy evaluation elsewhere in thisissue.

Subjective voice evaluation

RespirationThe respiratory system is the source of power for voice production. Many

voice problems can be related to poorly coordinated breathing. The clinicianshould pay special attention to the manner in which the voice user inhalesand then exhales air to produce voice during the evaluation. Observation


of the patient’s breathing pattern should be completed during reading andconversational speech. Breathing patterns that may be inefficient for voiceproduction include clavicular breathing, upper thoracic breathing, or a com-bination of the two. So-called ‘‘diaphragmatic breathing’’ can be the mostefficient breathing pattern because it tends to provide optimal balance ofinspiratory and expiratory muscle use. Speaking on residual air, shortnessof breath while speaking, gasping for air during inhalation, forced exhala-tion, or decreased airflow during phonation are also common indicatorsof vocal misuse.

PhonationPhonation is defined as the production of sound at the level of the vocal

folds. A perceptual evaluation of phonation (vocal quality, loudness andpitch) during reading and conversation should be completed. Vocal qualitycharacteristics may include: hoarseness, breathiness, roughness, raspiness,vocal fry, diplophonia, voice breaks, pitch breaks, and others. Vocal inten-sity or loudness should be judged as appropriate, increased, or decreased forthe particular setting. The pitch of the patient’s voice should be judged asappropriate, high, or low for the age and gender. In addition, the frequencyof hard glottal attacks should be assessed.

ResonanceVocal resonance refers to the way sound is shaped acoustically as it

travels through the vocal tract. Phonation begins at the level of the vocalfolds and moves up through the pharynx, oral cavity, and nasal cavity.Frontal resonance or forward focus of sound is ideal for most efficient voiceproduction. It optimizes acoustics of the vocal tract while balancing oro-nasal resonance. The use of resonant voice therapy, which places emphasison frontal tone focus, can increase perceived vocal loudness levels, whichthen may allow the voice to be heard better in noisy situations without ex-cessive strain. Various resonance patterns may be observed while makinga perceptual judgment of the voice, including oral, oropharyngeal, nasal, na-sopharyngeal, and hypopharyngeal.

PostureBody posture, how the body is held up against gravity, can have a direct

effect on respiration, phonation, and resonance. Posture is a complicatedinteraction of muscle groups throughout the body. There are multiple disci-plines that target body work to improve posture and overall wellness, in-cluding Alexander, Feldenkrais, Pilates, and Rolf [2]. Posture should beassessed paying attention to placement of the hips, spine, shoulders, neck,head, jaw, and even tongue while at rest and in movement. Posture may beassessed statically in the sitting or standing position and in movement whilewalking, running, dancing, teaching, and so forth. Considerations should bemade to observe the patient during activities in which they engage daily.


A brief explanation may be given to the patient so that posture can bebetter understood. While sitting, posture can be described as the feet restingflat on the ground, knees at a 90� angle, hips at a 90� angle, shoulders abovethe hips, and ears above the shoulders. The chin should be in a neutralposition with the crown of the head as the uppermost point. At rest, thetongue maybe resting on the alveolar ridge or behind the bottom incisorsand the jaw should be released. Postural adjustments should not produce stiffmovement but should allow for relaxation within a position. Abnormal pos-tures that negatively influence efficient voice production may include, but arenot limited to: posteriorly tilted hips, a c-shaped spine, arching the lower back,high shoulder placement, rounded shoulders, forward chin placement, ele-vated chin placement, clenched jaw, or retracted tongue. Small adjustmentsmade in posture may allow the larynx to relax in the anterior neck, permit eas-ier breathing, and subsequently result in more coordinated voice production.

ArticulationA global assessment of articulation should be completed judging clarity

and accuracy of articulatory movement for intelligible speech production.

ProsodyProsody may have a subtle affect on voice production and should be

assessed generally paying attention to the rhythm, fluency, rate, pauses,and intonation or inflection patterns used.

Muscle tensionMuscle tension can have an adverse affect on voice production causing

vocal fatigue, pain, or changes in the ease and quality of voice production.Locating these areas of tension is vital in breaking patterns of tension andretraining efficient muscle patterns. Box 1 provides examples of generaland specific areas where tension may occur.

Laryngeal palpation provides valuable information regarding specificareas of tension that may include the suprahyoid area, the strap muscles,and other related structures. The base of tongue should also be palpatedto assess the presence and degree of tension. Digital manipulation and laryn-geal massage of the extrinsic laryngeal musculature can provide the clinicianwith valuable information regarding tension. As demonstrated by NelsonRoy, manual laryngeal musculoskeletal tension reduction may yield imme-diate improvement in vocal quality or an identifiable release in laryngealtension [7]. These changes are useful in providing the patient with anidentifiable vocal change or release of tension and may indicate the patient’sresponsiveness to therapeutic intervention.

Oral mechanism examinationA general assessment of oral and facial structure and function should be

completed to rule out abnormalities or asymmetries in strength, range of


motion, and coordination that may impact functional communication.Structures include the face, mouth, dentition, tongue, and hard and softpalate. Abnormalities may indicate neurologic problems that warrantfurther evaluation.

Trial therapyDuring the initial evaluation, a period of trial therapy should be com-

pleted using facilitators to improve ease and quality of voice production.The facilitators are used to assess the patient’s stimulability for improve-ment in voice production. Throughout the trial therapy period, the clinicianattempts to provide the patient with a demonstration of possible improve-ment in voice production that should in turn increase motivation and feel-ings of therapeutic success. While completing facilitating techniques theclinician should gain information about the patient’s self-awareness of exist-ing habits and of changes in voice production that may occur. Judgmentscan also be made by the clinician about the patient’s ability to learn newtechniques, their willingness to comply with voice therapy, and the overallappropriateness for therapy. A statement of prognosis for outcomesthrough voice therapy should also be made.

Box 1. Identifying areas of tension

TongueAnteriorBase of tongue

JawMasseterTemporomandibular joint

Laryngeal tensionIntrinsic laryngeal muscles

Anterior/posterior neckStrap musclesSuboccipital area, posterior cervical musclesSternocleidomastoid muscle

ShouldersHigh shoulder postureTightness/stiffnessWinged scapulae

Upper chestAnterior/posterior chest musclesClavicular area


Impressions/recommendationsA complete voice evaluation provides the clinician with baseline data

regarding voice production and the patient’s view of his or her voice disor-der, in addition to allowing the speech-language pathologist to developan impression of the cause or contributing factors in the cause of the voicedisorder. The review of vocal hygiene, vocal demand, and overall voice useprovides the clinician with a place to begin educating the patient about hisor her voice. Although the trial therapy portion identifies facilitators forimproved ease or quality of voice production, it also provides an appropri-ate starting point for therapeutic intervention.

When a general impression has been formulated by the clinician, it shouldbe discussed with the patient. The clinician should indicate to the patientwhether a course of voice therapy is recommended and what the expecta-tions for follow-up sessions should be. The goals of therapy should thenbe discussed with the patient and consideration should be given at thattime to the patient’s personal goals. Once the goals are delineated, otherreferrals may be made, including singing intervention, physical therapy,and so forth. It should be clear to the patient the expectations for therapeu-tic intervention, including clinician recommendations; the approximatelength of the therapy in months, weeks, or sessions; and how often the ses-sions should be scheduled (weekly, biweekly, monthly). The patient alsoshould be aware that home practice is a crucial part to success in therapy.The clinician teaches the patient tools and provides support to improvevocal efficiency and carryover of efficient voice use. It is the patients’ respon-sibility to attend sessions, complete home practice, and work to carry overefficient voice use in their everyday lives, with the clinician’s guidance so thattherapy goals can be met and independence in efficient voice use can beachieved.

Therapy

Initially goals for therapy must be set forth. When treating the profes-sional voice user the ultimate long-term goal is to produce an excellentspeaking voice. The means to reach this goal is to increase vocal efficiencyduring speaking. The therapy techniques that are presented can be used toaddress behavioral voice problems that may include organic or structuralchanges that have taken place on the vocal folds.

Currently, in the speech pathology literature, therapy outcomes data arelimited. The therapy techniques discussed in this section are effective basedon clinical experience. Research has been referenced throughout this chapteras appropriate. Further outcomes research is still needed in this area,however.

Therapy begins with educating the patient. A brief overview of the anat-omy and physiology of voice production should be introduced and discussedwith the patient; including coordinating breathing, phonation, and


balancing oronasal resonance. This explanation should provide the patientwith a foundation for understanding voice production and the primaryfocus of voice therapy. Vocal hygiene should be addressed and improvedto eliminate vocal stressors and promote an optimal environment for im-proving vocal ease and quality. Furthermore, the voice user must be madeaware of vocal habits that promote abuse or misuse of the vocal mechanismand should be provided with alternatives to abusive vocal behavior.

Voice conservation strategies should be taught to the patient in an at-tempt to manage voice use on a daily basis. Vocal exercises should thenbe introduced and practiced to begin retraining muscle patterns for voiceproduction. The vocal exercises work to maximize efficiency of the vocalmechanism and promote carryover of targeted voice use into daily activities.Body and self-awareness should be targeted from the onset of therapy topromote carryover of the efficient voice learned during therapy.

Areas of tension and postural misalignment can have an adverse effect onefficient voice production. Areas of muscle tension were identified during theinitial evaluation and should be addressed throughout therapy. The patientshould be taught a daily routine for stretches and massage. Table 2 providesexamples of exercises to target specific areas of muscle tension.

Laryngeal massage may be taught to the patient and completed indepen-dently, outside the therapy setting. Postural alignment should also be

Table 2

Exercises to decrease muscle tension

Sites of tension Sample exercises (partial list)

Tongue

Anterior Tongue stretches

Base of Tongue Manual tongue stretch

Base of tongue massage

Jaw

Masseter Massage

Temporomandibular joint Jaw stretch

Tension/relaxation awareness exercises

Laryngeal Tension

Intrinsic laryngeal muscles Digital manipulation of the suprahyoid

area and thyrohyoid muscle

Breathy, sighing

Gentle scales and glides

Anterior/posterior neck

Strap muscles Massage

Suboccipital area, posterior cervical muscles Neck stretches

Sternocleidomastoid muscle

Shoulders/upper chest

High shoulder posture Shoulder shrugs

Tightness/stiffness Shoulder rolls

Winged scapulae Massage

Anterior/posterior chest muscles

Clavicular area


addressed with special attention given to hip angle and shoulder and headplacement. Slight misalignments in posture can cause increased muscle ten-sion. For example, elevated chin placement tightens laryngeal and neckmuscles or an arched lower back makes relaxing the abdomen for lowerabdominal breathing difficult.

Facilitators for breath control and support

Because respiration is the power source for phonation, the patient mustbe taught to balance inspiratory and expiratory muscles for efficient breath-ing. Exercises for breath management may start with a simple explanation ofthe respiratory system. This explanation may include a description of theexpansion of the lungs and diaphragm with subsequent expansion of therib cage and abdominal area during inhalation. As exhalation takes placethese areas begin to slowly deflate. Expiratory muscles may be engagedbut should not be hyperfunctioning. The patient must understand that itis possible to coordinate breathing and vocalization without hyperfunc-tional muscle use.

Appropriate terminology should be used when teaching a new breathingpattern secondary to learned responses that many adults have to phrasessuch as ‘‘take a deep breath.’’ When a patient is asked to do this, the stom-ach pulls in, the shoulders and chest rise and the patient holds his or herbreathe. Phrases such as ‘‘expand for inhalation’’ versus ‘‘take a deepbreath’’ and ‘‘release/deflate for exhalation’’ or ‘‘engage the abdomen duringexhalation’’ rather than pushing or pulling in may be used. In addition, theimage of a newborn baby during quiet breathing with the belly rising oninhalation and falling on exhalation may elicit understanding of the targetbreathing pattern.

While establishing a more efficient breathing pattern, the patient may beplaced in multiple positions to experience the targeted feeling of expansionduring inhalation and active deflation during exhalation. Positions may in-clude lying on the floor in the supine or prone position and concentrating onexpansion of the lower rib cage and abdomen during inhalation and thenslowly releasing air during exhalation. These two positions, with the helpof gravity, provide tactile feedback during expansion and deflation. Theyalso aid in decreasing shoulder and upper thoracic movement while breath-ing. These strategies alter respiratory function, however, and should be usedcautiously and with knowledge of their purposes and limitations. Anotheruseful technique is instructing the patient to bend over at the waist witharms extended to a chair or table so that his or her back is parallel withthe floor. The patient is instructed to expand the abdomen during inhalationand feel the abdomen actively deflate during exhalation. These breathingtechniques and positions are not meant to be sustained but to increasebody awareness of an efficient pattern of breathing that can be appliedduring daily activities. As the patient and clinician work through the


therapeutic hierarchy and gradually introduce simple to complex exercisesthe patient should be instructed to use the new breathing patterns for shortperiods multiple times throughout the day while breathing quietly and alsowhile talking, as appropriate.

Facilitators for increasing airflow during phonation

Once an efficient breathing pattern can be replicated, breathing and voic-ing should be paired together, cueing the patient to produce voicing duringexhalation. It is important that the patient understand that inhalationbefore phonation is as important as releasing air during exhalation to pro-duce phonation. To achieve appropriate airflow during phonation, musclehyperfunction must be eliminated from the vocal tract by various exercises.

The yawn-sigh may be used to promote active inhalation while decreasingmuscular tension in the throat. It also creates increased oral space by liftingthe soft palate. The increased oral space and sensation of open throat shouldbe maintained during exhalation while producing a sigh. The patient may becued to place the tongue in a relaxed position behind the bottom incisors tomaintain oral space. When the targeted yawn-sigh can be replicated consis-tently, the yawn can then be down-sized to an open-mouthed inhalation andvoicing during exhalation may be shaped into words, phrases, and so forth.

The stretch and flow therapy technique, originally developed by R.E.Stone, focuses on increasing ease and quality of voice production by increas-ing airflow during phonation. The patient is asked to use a strip of tissuedraped over his or her finger to provide a visual cue for airflow. The patientis instructed to blow a passive airstream onto the tissue, which should feeleasy. Confirm this feeling with the patient. Once a consistent, passiveairstream is achieved, the patient is instructed to add his or her voice ona /u/ vowel while maintaining the airstream. The patient should producea smooth, air-filled, easy voice. This voice may sound slightly more air-filledthan normal. The initial goal is to slightly overexaggerate the airflow duringthe exercise, so ultimately the ease of voice production is maintained andairflow can be normalized. Each trial should be modified until the targetedvoice is achieved. The air-filled, easy /u/ is then used as a facilitator intowords, phrases, sentences, and so forth, through the therapeutic hierarchy.When the patient can produce the targeted voice consistently using the facil-itator, its use should be gradually eliminated until the targeted voice can beproduced consistently independent of the facilitator.

Lip trills or tongue-out trills are other facilitators to coordinate airflowand phonation. For lip trills, which are made using airflow to vibrate thelips, the patient is instructed to expand during inhalation and producea lip trill with only airflow while exhaling. If this is difficult the patientmay place his or her index finger on each cheek and slightly press forwardreleasing any lip tension. The patient may also be cued not to clench hisor her back molars together. When the patient is consistent with production


of the lip trill with air only, he or she is instructed to add voicing.Consistency should be developed on one pitch and through a range ofpitches. Once this is completed, the lip trill may be used as a facilitator ininitial /br/ words, phrases, and so forth. Similarly, with the tongue-out trillthe patient should relax the tongue over the bottom lip, expand duringinhalation, and produce a tongue-out trill without voicing during exhala-tion. This facilitator requires that the tongue and jaw be relaxed and airflowcoordinated to produce the targeted tongue-out trill. When consistency isachieved, voicing should be added and developed at one pitch and througha range of pitches. The tongue-out trill can then be used as a facilitator intoopen vowels, words, phrases, etc. When the targeted voicing is achieved theuse of the facilitator should be faded out.

When evaluating coordination of airflow and phonation, hard glottalattacks (abrupt adductions of the vocal folds on words with an initial vowel)should be addressed. Voicing should be initiated with airflow rather thanabrupt adduction of the vocal folds. This issue can be addressed by targetingcoordination of airflow and phonation. Easy onset exercises should be com-pleted beginning with discrimination tasks so the patient is able to identifyhard glottal attacks. Minimal pairs should then be used (ie, hear/ear, hat/at).The patient should be made aware of the abduction of the vocal folds duringan /h/ and their closure during the voiced cognate. Cueing may be requiredto ensure inhalation before each trial for optimal air supply throughoutvoicing. The patient is then instructed to maintain the open feeling duringthe /h/ into the voiced cognate without producing an /h/ sound. Complex-ity should be increased as appropriate. The above-mentioned exercise ad-dresses vowel-initiated words that begin a word or group of words to besaid using one breath. When a vowel-initiated word is found within a breathgroup, linking should be used. Linking is used to connect the last sound ofthe word previous to the vowel-initiated word. For singers or musicians itmay be described as tying the words together, just as notes on the staffmay be tied in legato.

Facilitators for oral resonance

To achieve an optimal balance of oronasal resonance, a relaxed vocaltract must be maintained in addition to maintaining breath support andappropriate airflow during phonation. In many hyperfunctional voice users,it is difficult to achieve forward tone focus secondary to reduced space in theoral cavity that may be caused by increased tongue or jaw tension. To in-crease oral space it may be beneficial to increase soft palatal lift, addressjaw tension through stretches and massage, and decrease tongue retractionthrough stretches and tongue-relaxation exercises.

Resonance exercises may include the use of a hum to achieve improvedbalance of oronasal resonance. The patient should be cued to maintainoral space, which may be achieved by creating space in between the back


molars to release jaw tension and maintaining relaxed tongue placementbehind the lower front incisors and away from the roof of the mouth. Thepatient is instructed to inhale and exhale while producing a hum, or hum-sigh on a descending glide, with the lips barely touching. The patient’s atten-tion should be brought to the targeted frontal tone focus and buzz on thelips. This buzz can provide tactile feedback for the patient in working tomaintain frontal focus while increasing complexity of trials. If the patienthas difficulty achieving a hum without pressing, he or she may be cued torelease air through the nose and maintain a consistent airstream. Whenthe targeted hum is achieved consistently, it should be used as a facilitatorinto vowels, words, phrases, and so forth. Eventually use of the facilitatorshould be minimized and then eliminated.

Honking is used as an effective facilitator for developing awareness andmaintenance of balanced oronasal resonance. Honking is completed bypinching the nose while phonating on any vowel. The patient is cued to al-low the sound to resonate in his or her nose and release airflow through themouth. Tactile feedback should be provided with vibration or buzz at thenasal bridge. When the patient is able to achieve consistent voicing andawareness of the buzzing, words and phrases may be spoken using the honk-ing as a facilitator. The word or phrase may be spoken while occluding thenose and then repeated after releasing the nose maintaining airflow andfrontal focus of the sound production. When consistency of voice produc-tion is achieved, the use of the facilitator should be gradually eliminated.

There are multiple other resonance exercises, including the use of the/f/ and /v/ or /s/ and /z/ sounds. This exercise, as with others mentioned,combines the use of abdominal breathing, use of a continuous airstream,and frontal tone focus. Initially, the /f/ or /s/ sound is used to establisha consistent stream of air coming past the lips. The patient is instructedto expand and make an /f/ with the back molars parted and the top teethbarely touching the bottom lip. Following the trial, confirm the feeling ofair past the lips. The patient is then instructed to use the same airflowand breath support and produce a /v/ sound. A buzz should be felt onthe lower lip during this trial and should be confirmed with the patient. Ifthe patient has difficulty achieving the buzz, recheck jaw tension and oralspace. Production of a /v/ sound should become consistent and then maybe used as a facilitator into /v/ words, phrases, and so forth. The /v/may then be used as a facilitator into words and phrases that do not beginwith /v/. Use of the facilitator should eventually be faded out.

There are four elements of voice production: respiration, phonation, res-onance, and amplification. There are multiple facilitators that target eachelement. Choosing an appropriate therapeutic facilitator can be challenging.Clinical judgment should be applied when choosing therapeutic techniquesand modifications should be made for patients as needed. When choosinga facilitator, consider the patient’s primary complaints, the perceptual andacoustic evaluation of his or her voice, and the physiology of the patient’s


current voice production versus the targeted efficient voice production. Theclinician should be aware of the benefits and limitations of each facilitatorand choose appropriately to maximize the patient’s voice output and poten-tial for improved voice production.

Summary

There are multiple factors that affect voice production. When evaluatingand treating professional voice users who have voice disorders, these factorsmust be taken into careful consideration. Expert listening and managementskills must be used while staying within the scope of practice as a speech-lan-guage pathologist. A multidisciplinary approach to the care of professionalvoice users is crucial to care for this population. Professional relationshipsshould be cultivated to maximize care for the patient and promote contin-ued learning in our respective fields. Each voice user is unique and the ther-apy plan and treatment should be treated as such. When developinga therapy plan, the voice user’s previous experience should be taken intoconsideration and addressed in therapy, as appropriate.

Further readings

Benniger MS, Jacobson BH, Johnson AF. Vocal arts medicine. New York: Thieme Medical

Publishers, Inc.; 1994.

BooneDR. Is your voice telling on you?How to find and use your natural voice. SanDiego (CA):

Singular Publishing Group, Inc.; 1994.

Colton R, Casper J. Understanding voice problems. Baltimore (MD): Williams &Wilkins; 1990.

Johnson AF, Jacobson BH. Medical speech–language pathology a practitioner’s guide. 2nd edi-

tion. New York: Thieme Medical Publishers, Inc.; 2007.

McCoy S. Your voice: an inside view multimedia voice science and pedagogy. Princeton (NJ):

Inside View Press; 2004.

Merati AL, Bielamowicz SA. Textbook of laryngology. San Diego (CA): Plural Publishing, Inc.;

2007.

Rosen DC, Sataloff RT. The psychology of voice disorders. SanDiego (CA): Singular Publishing

Group, Inc.; 1997.

Rubin JS, Sataloff RT, KorovinGS. Diagnosis and treatment of voice disorders. 3rd edition. San

Diego (CA): Plural Publishing; 2005.

Stemple JC. Voice therapy clinical studies. 2nd edition. San Diego (CA): Singulair Publishing

Group, Inc.; 2000.

ZemlinWR. Speech andhearing science: anatomy andphysiology. EnglewoodCliffs (NJ):Allyn&

Bacon; 1998.

References

[1] American Speech-Language Hearing Association. Scope of practice in speech language

pathology. Rockville (MD): American Speech-Language Hearing Association; 2001.

[2] Sataloff Robert T. Professional voice: the science and art of clinical care. 3rd edition. San

Diego (CA): Plural Publishing; 2005.


[3] Sundberg J. The science of the singing voice. DeKalb (IL): Northern Illinois University Press;

1987. p. 146–56.

[4] Smith E, Verdolini K, Gray S, et al. Effects of voice disorders on quality of life. J Med Speech

Lang Pathol 1997;4:223–44.

[5] American Speech-Language- Hearing Association. The role of the speech language patholo-

gist, the teacher of singing, and the speaking voice trainer in voice habilitation [technical re-

port]. Rockville (MD): American Speech and Hearing Association Ad Hoc Joint Committee

with the National Association of Teachers of Singing and the Voice and Speech Trainers

Association; 2005.

[6] American Speech-Language- Hearing Association. The use of voice therapy in the treatment

of dysphonia [technical report]. Rockville (MD): American Speech-Language-Hearing

Association and the American Academy of Otolaryngology–Head and Neck Surgery; 2005.

[7] Roy N, Leeper HA. Effect of the manual laryngeal musculoskeletal tension reduction

technique as a treatment for functional voice disorders: perceptual and acoustic measures.

J Voice 1993;7:242–9.


40 (2007) 1151–1183

Voice Surgery

Robert T. Sataloff, MD, DMA*,Mary J. Hawkshaw, BSN, RN, CORLN,

Venu Divi, MD, Yolanda D. Heman-Ackah, MDDepartment of Otolaryngology–Head and Neck Surgery, Drexel University College of

Medicine, 1721 Pine Street, Philadelphia, PA 19103, USA

There have been many advances in microsurgery for voice professionalsover the last three decades. Driven by a greater understanding of the anat-omy and physiology of phonation, most of the advances provide greatersurgical precision through improved exposure and more delicate ins-trumentation. Laryngologists who perform laryngoscopic surgery shouldbe familiar with the current state-of-the-art and should use the latest tech-niques and technology for all voice patients and particularly for voiceprofessionals.

Laryngeal surgery may be performed endoscopically or through an exter-nal approach. To provide optimal care, laryngologists must be familiar withthe latest techniques in both approaches. Modern microsurgery of the voiceis referred to widely as ‘‘phonosurgery,’’ although von Leden introducedthat term originally in 1963 for procedures designed to alter vocal qualityor pitch [1]. ‘‘Voice surgery’’ is a better term for delicate, precise laryngealsurgery in general, although the term ‘‘phonomicrosurgery’’ has becomewidely used. It is usually performed using the microscope, with small, mod-ern instruments, and with great respect for the induplicatable anatomiccomplexity of the vibratory margin of the vocal fold.

Most surgical procedures for voice disorders can be performed endoscop-ically, obviating the need for external incisions and minimizing the amountof tissue disruption. Although endoscopic microsurgery seems intuitivelymore conservative, this supposition holds true only when the equipment


clinical care. 3rd edition. San Diego (CA): Plural Publishing, Inc.; 2006. p. 1137–214; with

permission.

* Corresponding author. Drexel University College of Medicine, 1721 Pine Street,

Philadelphia, PA 19103-6771.





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provides good exposure of the surgical site and the abnormality can betreated meticulously and thoroughly with endoscopic instruments. When en-doscopic visualization is not adequate because of patient anatomy, diseaseextent, or other factors, the surgeon should not compromise the results oftreatment or risk patient injury by attempting to complete an endoscopicprocedure. In such patients, it may be safer to leave selected benign lesionsuntreated or to treat the pathology through an external approach.

Patient selection and consent

Before performing voice surgery, it is essential to be certain that patientselection is appropriate and that the patient understands the limits andpotential complications of voice surgery. Appropriate patients for voicesurgery not only have voice abnormalities but also want to change theirvoice quality, effort, or endurance. For example, not all people who have‘‘pathologic’’ voices are unhappy with them. Sports announcers; female trialattorneys with gruff, masculine voices; and others sometimes consult a phy-sician only because of fear of cancer. If there is no suspicion of malignancy,restoring the voice to ‘‘normal’’ (eg, by evacuating Reinke’s edema) may bea disservice and even jeopardize a career. Similarly, it is essential to distin-guish accurately between organic and psychogenic voice disorders beforeembarking upon laryngeal surgery. Although a breathy voice may be causedby numerous organic conditions, it is also commonly found in people whohave psychogenic dysphonia. The differentiation may require a skilled voiceteam.

Although all reasonable efforts should be made to avoid operative inter-vention in professional voice users (particularly singers), there are timeswhen surgery is appropriate and necessary. The decision depends ona risk–benefit analysis. If a professional is unable to continue his or hercareer, and if surgery may restore vocal function, surgery should not bewithheld. Making such judgments can be challenging. A rock or pop singerwho has a vocal fold mass may have satisfactory voice quality with onlyminimal technical adjustments. Pop singers perform with amplification,obviating the need to sing loudly and to project the voice in some cases(depending on the artist’s style). Such a patient may be able to ‘‘workaround’’ pathology safely for many years. In some classical singers, evenminor pathology may be disabling. For example, if a high soprano special-izing in Baroque music develops a mild to moderate superior laryngeal nerveparesis, she may experience breathiness and instability. If she gives in to thetemptation to compensate by slightly retracting her tongue and lowering herlarynx, the breathiness will be controlled because of increased adductoryforces, but she will lose the ability to perform rapid, agile runs and trills.Similar problems may occur from compensatory maladjustments in re-sponse to other lesions, such as vocal fold cysts. In such instances, the artist

1153VOICE SURGERY

may be served better by surgical correction of the underlying problem thanby long-term use of hyperfunctional compensation (ie, bad technique) thatcan cause other performance problems and vocal fold pathology. The pa-tient must understand all of these considerations, including the risks of sur-gery. The patient needs to acknowledge the risk that any voice surgery maymake the voice worse permanently and must consider this risk acceptable inlight of ongoing vocal problems.

Even in the best hands, an undesirable scar may develop, resulting in per-manent hoarseness. The patient must be aware that there is a possibility thatthe voice may be worse after surgery. Other complications must also be dis-cussed, including complications of anesthesia, dental fracture, recurrence oflaryngeal lesions, airway compromise, and vocal fold webbing. In additionto the hospital’s standard surgical consent, we provide patients with addi-tional written information before surgery. The patient keeps one copy ofthe ‘‘Risks and Complications of Surgery’’ document, and one signedcopy remains in the chart. Specialized informed consent documents areused for other treatments, such as injection of cidofovir, topical applicationof mitomycin-C, injection of collagen, and injection of botulinum toxin,even though such documents are not required. If medications are used fortreatment (rather than research) and are off-label uses of medicinesapproved by the FDA for other purposes, their use does not require institu-tional review board approval. We believe it is helpful and prudent to providepatients with as much information as possible and to document that theyhave been so informed.

It is often helpful for the laryngologist, speech-language pathologist,singing voice specialist, and patient to involve the patient’s singing teacherin the decision-making process. Everyone must understand the risks of sur-gery and the risk involved in deciding against surgery and relying upon tech-nical maladjustments. In many cases, there is no ‘‘good’’ or ‘‘right’’ choice,and the voice care team must combine expertise with insight into the careerand concerns of each individual patient to help the voice professional makethe best choice.

Documentation

Preoperative objective voice assessment and documentation are essential inaddition to routine documentation of informed consent discussions. A high-quality recording of the patient’s voice must be done before surgery. Auditorymemories of physicians and patients are not good in general, and the doctorand postoperative professional voice user are often surprised when they com-pare postoperative and preoperative recordings. Frequently, the preoperativevoice is worse than either person remembers. In addition, such documentationis invaluable for medical–legal purposes. Photographs or videotapes of thelarynx obtained during strobovideolaryngoscopy are helpful. Complete

1154 SATALOFF et al

objective laboratory voice assessment and evaluation by a voice team shouldbe performed. Proper documentation is essential for assessing outcomes, evenfor the physician who is not interested in research or publication.

Timing of voice surgery

The time of voice surgery is important and can be challenging in profes-sionals who have demanding voice commitments. Many factors need to betaken into account, including the menstrual cycle, pre- and postoperativevoice therapy, concurrent medical conditions, psychologic state, and profes-sional voice commitments.

Hormonal considerations may be important, especially in female patientswho have symptomatic laryngopathia premenstrualis. In patients who haveobvious vocal fold vascular engorgement or who have a history of premen-strual vocal fold hemorrhages, it may be better to avoid elective surgeryduring the premenstrual period. Except in patients in whom surgery isintended to treat vessels that have hemorrhaged repeatedly and that areonly prominent before menses, it may be best to perform surgery betweenapproximately days 4 and 21 of the menstrual cycle. Although it seems un-necessary to time surgery in this way for all patients, the issue has not beenfully studied.

Timing of surgery with regard to voice therapy and performance commit-ments can be difficult in busy voice professionals. The surgeon must be care-ful to avoid letting the patient’s professional commitments and pressuresdictate inappropriate surgery or surgical timing that is not in the patient’sbest interest. For example, some professional voice users push for early sur-gery for vocal nodules and promise to appear for voice therapy after a busyconcert season ends. This is not appropriate because therapy may cure thenodules and avoid surgical risks altogether. Professional commitments oftenrequire that appropriate surgery be delayed until a series of concerts or therun of a play is completed. In treating vocal fold cysts, polyps, and otherconditions, such delays are often reasonable. They are made safer throughongoing voice therapy and close laryngologic supervision. Sometimesindividualized treatments may help temporize. For example, aspiration ofa cyst as an office procedure can provide temporary relief from symptoms,although the cyst is likely to return and require definitive surgery.

At least a brief period of preoperative voice therapy is helpful. Even whentherapy cannot cure a lesion, it ameliorates the abuses caused by compensa-tory hyperfunction, and good preoperative therapy is the best postoperativevoice therapy. It is also invaluable in educating the patient about vocal func-tion and dysfunction and in making sure that he or she is fully informedabout surgery and other options. After surgery, voice therapy is medicallynecessary for many conditions. It is important to long-term surgical out-come to time surgery so that the patient is able to comply with postoperativevoice rest and postoperative rehabilitation.

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Many other conditions must be taken into account when deciding uponthe timing of voice surgery. Concurrent medical conditions, such as allergiesthat produce extensive coughing or sneezing (which may injure vocal foldsafter surgery), a coagulopathy (even temporary coagulopathy from aspirinuse), and other physical factors may be important contributors to voice re-sults. Psychologic factors should also be considered. The patient must un-derstand the risks and complications of surgery and be as psychologicallyprepared as possible to accept them and to commit the therapeutic and re-habilitation process. Sometimes psychologic preparation requires a delay insurgical scheduling to allow time for the patient to work with the voice team.There are few indications for benign voice surgery that contraindicate adelay of several weeks. It is generally worth taking the time to optimizethe patient’s comfort and preparedness. Realistic, committed collaborationby the patient is invaluable in achieving consistent, excellent surgical results.

Voice cosmesis: the ‘‘voice lift’’

In the modern communication age, the voice is critical in projecting im-age and personality and establishing credibility. Until recently, voice has notreceived enough attention from the medical profession or from the generalpublic. Most people (doctors and the general public) do not realize that any-thing can be done to improve a voice that is unsatisfactory or even one thatis adequate but not optimal.

Some techniques for voice improvement date back centuries. Singers,actors, and public speakers have sought out ‘‘voice lessons’’ for centuries.Recently, techniques for voice improvement have expanded and improvedand have become practical for many more people.

Vocal weakness, breathiness, instability, impaired quality, and othercharacteristics can interfere with social and professional success. Manyproblems (eg, breathiness, softness, instability, tremor, and change in habit-ual pitch) are commonly associated with aging. For most people, these vocalcharacteristics, which lead people to perceive a voice (and its owner) as‘‘old’’ or ‘‘infirm,’’ can be improved or eliminated.

The first step for anyone seeking voice improvement is a comprehensivevoice evaluation. Often, voice problems that one may ascribe to aging or togenetic makeup are caused or aggravated by medical problems. The possi-bilities include such conditions as reflux, low thyroid function, diabetes,and tumors. Sometimes, voice deterioration is the first symptoms of a seriousmedical problem, so comprehensive medical evaluation is essential beforetreating the voice complaints.

Once medical problems have been ruled out or treated, the next step forvocal habilitation or restoration is a program of therapy or exerciseprovided by a multidisciplinary team that incorporates the skills of a laryng-ologist, a speech-language pathologist, and an acting-voice specialist. Thetraining involves aerobic conditioning to strengthen the power source of

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the voice. In many cases, neuromuscular retraining (specific guided exercise)is sufficient to improve vocal strength and quality, eliminate effort, and re-store youthful vocal quality. Doing so is important not only for singers andother voice professionals (eg, teachers, radio announcers, politicians, clergy,salespeople, and receptionists) but also for almost everyone. This is espe-cially true for elderly persons. As we age, our voices get softer and weaker,and at the same time our spouses and friends lose their hearing. This makesprofessional communication and social interaction difficult, especially innoisy surroundings, such as cars and restaurants. When one has to worktoo hard to communicate, it is often related to vocal deficiencies. When ex-ercises and medications alone do not provide sufficient improvement, manypatients elect voice surgery in an attempt to strengthen their vocal qualityand endurance and to improve their quality of life.

Several procedures can be used to strengthen weak or injured voices. Theselection of the operation depends on the individual’s vocal condition as deter-mined by a voice team evaluation, physical examination including strobovi-deolaryngoscopy, and consideration of what the person wants. Care mustbe taken to ensure that patient expectations are realistic. Inmost cases, surgeryis directed toward bringing the vocal folds closer together so that they closemore firmly. This eliminates the air leak between the vocal folds that occursas a consequence of vocal atrophy from aging (atrophy or wasting of vocalnodules or other tissues) or as a result of paresis or paralysis (partial injuryto a nerve from a viral infection or other causes). In some cases, the operationis done by injecting a material through the mouth or neck into the tissuesadjacent to the vocal folds to ‘‘bulk up’’ the vocal tissues and bring the vocalfolds closer together. This is called ‘‘injection laryngoplasty’’ and is performedusually using fat, collagen, or hydroxyapatite. This operation is sometimesdone in the operating room under local anesthesia and, in selected patients,in the office with only local anesthesia. Alternatively, the problem can becorrectedbyperforming a thyroplasty.This operation involvesmaking a smallincision in the neck. The skeleton of the voice box is entered, and the laryngealtissues are compressed slightly using Gore-Tex or silastic implants. Thisprocedure is generally done under local anesthesia with sedation. All of theseprocedures usually are performed on an outpatient basis.

Recovery usually takes days to weeks, depending on the procedure. Anyoperation can be associated with complications. Rarely, the voice can bemade worse. The most likely complication is that voice improvement isnot sufficient or that it does not last over time. When this problem occurs,it can be corrected by ‘‘fine tuning’’ through additional injections or surgicaladjustment of the implant. Usually, satisfactory results are achieved the firsttime.

Voice rehabilitation through medical intervention and therapy/exercisetraining is appropriate for anyone who is unhappy with his or her vocal qual-ity (so-called ‘‘voice lift surgery’’) and is suitable for almost anyone who doesnot have major, serious medical problems (eg, end-stage heart disease) and is

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not on blood thinner medication that cannot be stopped safely for surgery, solong as that person has realistic vocal goals and expectations. ‘‘Voice lift’’surgery should be thought of as a comprehensive program stressing medicaldiagnosis and physical rehabilitation, not as surgery alone.

Thyroplasty

Another excellent approach to medialization is type I thyroplasty. Thisprocedure was popularized by Isshiki and colleagues [2] in 1975, althoughthe concept had been introduced early in the century by Payr [3]. Thyro-plasty is performed under local anesthesia. In classical thyroplasty, withthe neck extended, a 4- to 5-cm incision is made horizontally at the midpointbetween the thyroid notch and the lower rim of the thyroid cartilage. A rect-angle of thyroid cartilage is cut out on the involved side. It begins approx-imately 5 to 7 mm lateral to the midline and is usually approximately 3 to5 mm by 3 to 10 mm. The inferior border is located approximately 3 mmabove the inferior margin of the thyroid cartilage. Care must be taken notto carry the rectangle too far posteriorly, or it cannot be displaced medially.The cartilage is depressed inward, moving the vocal fold toward the midline.The wedge of silicone is then fashioned to hold the depressed cartilage inproper position. Since Isshiki’s original description, many surgeons havepreferred to remove the cartilage. Most preserve the inner perichondrium,although techniques that involve incisions through the inner perichondriumhave been used successfully. Surgeons have used various other materials,including autologous cartilage, hydroxyapatite, expanded polytetrafluoro-ethylene, and titanium [4–10].

Various additional technical modifications have been proposed as thistechnique has become more popular, and several varieties of preformedthyroplasty implant devices have been introduced commercially. Many ofthese modifications have proven helpful, especially techniques that obviatethe need to carve individualized silicone block implants, a technique thatis often challenging for inexperienced thyroplasty surgeons. The siliconeblock modifications described by Tucker [11] are also useful, particularlythe technique of cutting out a portion of the prosthesis to allow for theplacement of a nerve-muscle pedicle. We have generally abandoned all ofthese techniques except during revision cases in favor of Gore-Tex in thelarynx as reported by Hoffman and McCulloch [8]. Since then, several re-ports have documented its efficacy, and others are in preparation [12–14].Gore-Tex is easy to place and adjust and can be contoured to compensatefor vocal fold bowing and a variety of irregular laryngeal configurations.

Our preferred technique is slightly different from procedures publishedpreviously.

Access Videos on Gore-tex Thyroplasty and on Post-op Thyroplasty One Year in online

version of this article at: http://www.Oto.TheClinics.com.



1158 SATALOFF et al

One of the major advantages of Gore-Tex is that it can be placed througha minithyrotomy, obviating the need to traumatize or transect strap mus-cles. A 2-cm horizontal incision is made centered in the midline in a skincrease near the lower third of the vertical dimension of the thyroid cartilage.The cartilage is exposed in the midline, and the perichondrium is incised andelevated. A 4-mm diamond bur is used to drill a 4-mm minithyrotomy. Itsanterior border is located approximately 7 mm from the midline in femalepatients and 9 mm from the midline in male patients, and its inferior marginis approximately 3 to 4 mm above the inferior border of the thyroid carti-lage. The inner perichondrium is left intact. A fine elevator, such as a Wood-son elevator or Sataloff Thyroplasty Elevator (Medtronics Xomed,Jacksonville, FL), is used to elevate the perichondrium posteriorly. It isimportant that minimal elevation be performed. A small pocket, only 2 to3 mm in width, parallel to the inferior border of the thyroid cartilage is suf-ficient. This is substantially different from the extensive elevation performedduring traditional thyroplasty. If the perichondrium is elevated excessively,it is difficult to control the position of the Gore-Tex. Any additional eleva-tion is accomplished by the Gore-Tex during insertion. Gore-Tex is then lay-ered through the thyrotomy incision and adjusted to optimize phonation.This procedure is performed under local anesthesia with sedation, and vocalfold position can be monitored by flexible laryngoscopy during the opera-tion continuously during medialization or by checking the final positionvisually at the conclusion of the operation. Once Gore-Tex has beenpositioned optimally, it is cut a few millimeters outside the thyrotomy.For closure, some surgeons use perichondrial flaps that are repositionedand sutured. Alternatively, the thyrotomy can be filled with a few dropsof cyanoacrylate, which forms a customized button-like seal with a small in-ner flange of cyanoacrylate, and with a wick of Gore-Tex in the center of thecyanoacrylate the cyanoacrylate block. This prevents extrusion of the Gore-Tex, and the cyanoacrylate ‘‘button’’ and Gore-Tex are removed easilywhen revision surgery is necessary by pulling on the end of the Gore-Texthat extends a few millimeters beyond the cyanoacrylate. Gore-Tex thyro-plasty is so expeditious and atraumatic that it can be performed bilaterallyat the same sitting. This is done commonly to treat vocal fold bowing frombilateral superior laryngeal nerve paresis and other causes and to treat pres-byphonia refractory to voice therapy. Bilateral thyroplasties can be accom-plished ordinarily in less than 1 hour. A small drain usually is placed at theconclusion of the procedure and removed on the first postoperative day. Inmany cases, the procedure is performed as outpatient surgery, althoughovernight observation is appropriate if there is vocal fold swelling or con-cern about airway compromise.

There have been no studies documenting the efficacy of the routine use ofsteroids or antibiotics in thyroplasty surgery. Many surgeons use both rou-tinely. Sixty milligrams of prednisone taken the night before surgery canhelp to minimize intraoperative edema, improving the accuracy of implant

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placement and vocal fold medialization, and thus, the final voice outcome.In our practice, we have encountered only one infection after thyroplastyin over 20 years, and that was believed to be due to contaminated suturesrecalled by the manufacturer shortly after that operation. Because a foreignbody is implanted during thyroplasty, many surgeons prefer to give antibi-otics prophylactically.

Revision thyroplasty is a more complex matter. Most thyroplasties thathave required revision have been performed originally using a silastic blockor one of the preformed, commercially available implants. During these ini-tial operations, a large thyroplasty window was created, and perichondriumwas elevated. Removing the silastic block and replacing it with Gore-Texgenerally does not prove satisfactory. Gore-Tex position cannot be con-trolled well because of the postsurgical anatomy. In general, we prefer to re-vise such cases by carving a new silastic block or by modifying the prosthesisthat had been placed originally. If revision is being performed because of in-sufficient medialization, it is sometimes possible to elevate the anterioraspect of the prosthesis and layer Gore-Tex medial to it. Such cases areuncommon. More often, it is necessary to incise the fibrotic capsule in theregion of the inner perichondrium with an electric cautery (which often pro-duces momentary discomfort for the patient) and to create a new prosthesis.The most common problems that require revision are undermedialization,resulting in persistent glottic insufficiency, excessive anterior medializationresulting in strained voice, excessively high placement of the original pros-thesis, and inappropriate patient selection. Undermedialization can be cor-rected by underlaying Gore-Tex or creating a larger prosthesis as discussedpreviously or endoscopically by injecting fat or collagen. Excessive anteriormedialization is corrected by reshaping the prosthesis. In such cases, theoriginal implant is usually too thick and placed too far anteriorly. Exces-sively high placement is often associated with a cartilage window that is con-siderably higher than the desirable 3 to 4 mm above the inferior border ofthe thyroid cartilage. When additional cartilage is removed to place theprosthesis at the desired height, cartilage deficiency from the original oper-ation often leaves the prosthesis unstable. In such cases, the implanteddevice should be secured to the thyroid cartilage by sutures. In fact, whenusing an implant other than Gore-Tex for primary or revision surgery, wesecure the prosthesis to cartilage with Prolene sutures to prevent migrationor extrusion.

Another common reason for revision is inappropriate patient selection. Ifthere is a large, symptomatic posterior glottal gap, thyroplasty alone is ofteninsufficient. Procedures to alter arytenoid cartilage position are necessary inmany such cases. Failure to recognize this need and to perform the appro-priate operation initially may lead to a need for revision surgery that in-cludes arytenoid repositioning procedures. Apart from malposition of theimplant, type I thyroplasty is generally uncomplicated. Successful thyro-plasty improves vibratory function [15].

1160 SATALOFF et al

If thyroplasty is complicated by hemorrhage with superficial hematomaalong the vibratory margin or by infection vocal fold stiffness with perma-nent dysphonia can result. Hemorrhage and edema also can produce airwayobstruction. Weinman and Maragos [16] reported on 630 thyroplasty proce-dures. Seven of their patients required tracheotomy. Five of 143 patientswho underwent arytenoid cartilage adduction in association with thyro-plasty required tracheotomy. In the experience of Weinman and Maragos,the median interval from surgery to tracheotomy was 9 hours, with five ofthe seven patients requiring airway surgery within 18 hours after thyroplasty[16,17]. Although in most series airway obstruction has not been common,this complication and the need for tracheotomy are possible.

Occasionally, singers and actors inquire about surgery for pitch alter-ation. Laryngeal framework surgery has proven successful in altering pitchin specially selected patients, such as those undergoing gender reassignmentsurgery. These operations do not provide consistently good enough voicequality to be performed on a professional voice user for elective pitchchange. In addition, considerably more than habitual fundamental fre-quency is involved in the perception of voice classification, and other impor-tant factors (such as the center frequency of the singer’s formant) are notmodified by laryngeal surgery.

Indirect laryngoscopic surgery

Laryngoscopic surgery is generally performed through direct laryngos-copy. Indirect laryngoscopic surgery has been performed for many yearsand has value in some circumstances. It permits gross biopsy of lesions un-der local anesthesia; removal of selected foreign bodies; and injection of fat,collagen, and other substances. In patients who have cervical pathologywhose neck does not flex or extend enough to permit rigid direct laryngos-copy, indirect laryngoscopic surgery may provide a safe alternative to exter-nal surgery.

For indirect laryngoscopic surgery, the patient is generally seated. Topi-cal anesthesia is applied and may be augmented by regional blocks. The lar-ynx is visualized with a laryngeal mirror, a laryngeal telescope, or a flexiblefiberoptic laryngoscope. When surgery is performed solely for injection (eg,fat or collagen), an external or transoral technique may be used. Externalinjection may be performed by passing the needle through the cricothyroidmembrane and into the desired position lateral to the vocal fold or throughthe thyroid lamina usually near the midpoint of the musculomembranousvocal fold, about 7 to 9 mm above the inferior border of the thyroid carti-lage. Transoral injection has been used more commonly (Fig. 1), and thetransoral technique is also suitable for biopsy and other procedures. Assis-tance is required. The patient’s tongue is held with gauze, as for routine in-direct laryngoscopy. Cooperative patients may be asked to hold the tonguethemselves. Angled instruments designed specifically for indirect

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laryngoscopic surgery are passed through the mouth and guided visually.Only a surgeon who is skilled in the necessary maneuvers should performthe procedure. The advantages of this technique include relatively easy ac-cess in anyone whose larynx can be visualized with a mirror, avoidance ofthe need for an operating room procedure, and ready availability when de-lays in getting to a hospital and waiting for an operating room might causeserious problems. The procedure also has disadvantages. Precise control isnot as good as that accomplished with microlaryngoscopy under sedationor general anesthesia, intraoperative loss of patient cooperation may resultin injury, and the ability to handle complications such as bleeding andedema is limited. Nevertheless, at times the procedure is invaluable, and itshould be in the armamentarium of the laryngologic surgeon.

Direct laryngoscopy

Suspension microlaryngoscopy is the standard technique for endoscopiclaryngeal surgery. The concept of direct laryngoscopy was introduced byGreen [18] in 1852 using sunlight and supported later by Brunings [19]. Thehistory of phonomicrosurgery is reviewed in greater detail elsewhere[1,20,21].Many laryngoscopes are available.An instrument should be selectedfor each patient that provides excellent exposure of the vocal folds, internallaryngeal distension, and minimal distortion of the area of surgical interest.

In addition to choosing an appropriate laryngoscope, it is important tounderstand principles of suspension and of internal distention and externalcounterpressure. In most cases, the laryngoscope should provide visualiza-tion of only the entire vocal fold and should distend the false vocal foldsand larynx in a way that optimizes visualization. Rarely, distension of thefalse vocal folds is not desirable, and a laryngoscope positioned in the val-lecula (eg, the Lindholm; Karl Storz, Culver City, CA) provides an

Fig. 1. (Left) After topical anesthesia, the patient firmly holds his tongue extended while the

mirror and indirect needle are positioned. (Right) The patient phonates a falsetto /i/as the nee-

dle is inserted for injection. Similar positions may be used for biopsy and foreign body removal.

(From Sataloff RT. Professional voice: the science and art of clinical care. 3rd edition. San

Diego (CA): Plural Publishing, Inc.; 2006; with permission.)

1162 SATALOFF et al

alternative. This is the exception rather than the rule. In addition to internaldistention, external counterpressure is important. Gentle pressure over thecricoid cartilage often can produce dramatic improvement in laryngeal visu-alization through the laryngoscope. Traditionally, a resident, nurse, or anes-thetist has been asked to provide the counterpressure. It is better to use1 inch tape that extends from one side of the headrest of the bed to the otherand holds steady pressure on the larynx, maintaining the desired position.

There can be a disadvantage to counterpressure. Although it improvesvisibility (especially anteriorly), it introduces laxity in the vocal folds thatmay distort slightly the relationships between pathology and normal tissue.Hence, an appropriate compromise must be achieved in each case tooptimize visibility of the area of interest without introducing excessive dis-tortion. Readers interested in additional information regarding counterpres-sure and the forces involved in laryngoscopy are advised to consult otherliterature [22,23].

Anesthesia

Local anesthesia

Local anesthesia with sedation is desirable in some cases for endoscopiclaryngeal surgery, especially if fine adjustments of vocal quality are to bemade, as during injection for vocal fold paralysis or reduction of a dislocatedarytenoid cartilage. Many techniques of local anesthesia are used. They in-volve a variety of systemic, topical, and regional medications. The techniquedescribed below has proven most effective in our experience but should beconsidered only one of many options. In rare instances, direct laryngoscopymay be performed without operating room support and with topical anes-thesia alone.

Generally, procedures are performed in the operating room with moni-toring and sedation. Intravenous sedation is administered before anestheticapplication. We prefer a sedative that produces amnesia, such as propofol ormidazolam. The oral cavity is sprayed with a topical anesthetic. Cetacaine,4% Xylocaine, 0.5% Pontocaine, cocaine, and others have given satisfac-tory results. Topical anesthetic is routinely supplemented with regionalblocks and local infiltration. Bilateral superior laryngeal nerve blocks areachieved using 1% Xylocaine with epinephrine 1:100,000. Superior laryn-geal nerve block is accomplished by injecting 1 to 2 mL of 1% Xylocaineinto the region where the nerve penetrates the thyrohyoid membrane, ante-rior to a line between the greater cornu of the thyroid cartilage and thegreater cornu of the hyoid bone. Glossopharyngeal nerve blocks are placedusing 2 mL of 1% Xylocaine with epinephrine 1:100,000 in the lateral oro-pharyngeal wall, a few millimeters medial to the midportion of the posteriortonsillar pillar on each side. The tongue base is then infiltrated with 2 to4 mL, using a curved tonsil needle and metal tongue depressor. Anesthesia

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is concluded with intratracheal topical application of 4 mL of 4% topicalXylocaine administered through a midline injection in the cricothyroidmembrane (after anesthetizing the skin with 1% Xylocaine with epinephrine1:100,000 or by spraying topical anesthetic between the vocal folds if theycan be visualized easily using a metal tongue blade). Although this anes-thetic procedure can be performed rapidly, patients frequently have diffi-culty managing secretions by the time the anesthesia has been applied.Suction should be available.

The adequacy of anesthesia application can be tested by placing a metaltongue depressor against the tongue base and lifting it anteriorly and infe-riorly, simulating laryngoscope pressure and placement, while the hypo-pharynx is suctioned. If anesthesia is adequate, these maneuvers shouldnot disturb the patient. Throughout the application of anesthesia, the phy-sician and anesthesiologist should maintain verbal contact with the patient,carefully control the airway, and monitor vital signs including blood oxygensaturation. If adequate topical and regional anesthesia cannot be establishedor if adequate sedation cannot be achieved safely, the procedure should bediscontinued or general anesthesia should be induced. The patient and theanesthesia team should be prepared for possible use of general anestheticin all cases.

Most laryngeal procedures can be performed safely under local anesthesia.This choice provides the opportunity to monitor voice during the procedureand protection from the risks of endotracheal intubation. There are disadvan-tages. When maximal precision is necessary, the motion present during localanesthesia may be troublesome. Greater accuracy is enhanced by generalanesthesia with paralysis. The safety of local anesthesia during some casesof endolaryngeal surgery is questionable. In addition to mechanical surgicalproblems, in some patients who have cardiac or pulmonary problems, the re-spiratory suppression caused by sedationmaybemore hazardous than generalanesthesia. In addition, local anesthetics may produce side-effects. These mayinclude mucosal irritation and inflammation (contact dermatitis) that maycause erythemaandpruritus, vesiculation andoozing, dehydrationofmucosalsurfaces or an escharotic effect (especially from prolonged contact), hypersen-sitivity (rash), generalized urticaria (edema), methemoglobinemia, and ana-phylaxis. Safety for use during pregnancy has not been established for mosttopical anesthetics used commonly in laryngology, and they should be usedonly under pressing clinical circumstances during the first trimester of preg-nancy. Methemoglobinemia may be a frightening complication of local anes-thesia. Methemoglobin is also called ferric protoporphyrin (IX globulin) andferrihemoglobin because the iron in methemoglobin is trivalent (or ferric) in-stead of divalent (ferrous). Methemoglobinemia produces cyanosis, althoughskin discoloration is usually the only symptom of acquired methemoglobine-mia.Arterial blood gas analysis confirms the presence ofmethemoglobin. Thiscondition can be induced by any amine-type local anesthetic. Prilocaine andbenzocaine are the drugs implicated most commonly [24]. Infants may be

1164 SATALOFF et al

more susceptible, but the condition may occur in patients of any age. Methe-moglobinemia is a misnomer because the pigment is intracellular and is notfound in the plasma. Methemoglobincythemia would be more accurate, butmethemoglobinemia is used commonly.Methemoglobinemia is treated by in-travenous administration of methylene blue, although the condition is not lifethreatening and resolves spontaneously. The notion that local anesthesia ispreferable to general anesthesia should be viewed with skepticism. The choicedepends on the patient, the lesion, the surgeon, and the anesthesiologist.

General anesthesia

Probably the most important consideration in general anesthesia forvoice patients is the choice of the anesthesiologist. Laryngologists perform-ing voice surgery must insist on the collaboration of an excellent anesthesi-ologist who understands vocal fold surgery and the special needs of voicepatients. Those of us who work in teaching institutions recognize that med-ical students and first-year anesthesia residents need to practice intubation.This need should not be met on patients undergoing surgery for voice im-provement, especially professional voice users. When a gentle, skilled, wellinformed anesthesiologist and laryngologist collaborate, the choice of anes-thetic depends solely on the patient and lesion, and safe effective surgery canbe performed. Such teamwork benefits the laryngologist, anesthesiologist,hospital, and especially the patient, and every effort should be made to es-tablish the necessary professional collaboration.

The choice of agents for general anesthesia is beyond the scope of this ar-ticle. In general, the regimen includes the use of a short-term paralytic agentto avoid patient motion or swallowing. Intubation and extubation should beaccomplished atraumatically, using the smallest possible endotracheal tube.Most laryngeal endoscopic procedures are short in duration, and a 5.0 mminner diameter endotracheal tube is generally sufficient, even for most mod-erately obese patients. The laser may be used during many procedures, andit is best to use a laser-resistant endotracheal tube in such cases.

Antireflux medications are prudent, especially in patients who havesymptoms and signs of reflux. Reflux may occur under anesthesia even inpatients who do not have significant clinical reflux. The combination ofacid exposure and direct trauma from the endotracheal tube can lead to la-ryngeal mucosal injury. Intravenous steroids (eg, 10 mg of dexamethasone)may be helpful in minimizing inflammation and edema and in protectingagainst cellular injury. Intravenous steroids should be used at the surgeon’sdiscretion if there is no contraindication.

Endotracheal intubation provides the safest, most stable ventilationunder general anesthesia, and it generally provides adequate visibility. Insome cases, even a small endotracheal tube may interfere with surgery.Alternatives include general anesthesia without intubation and with jet ven-tilation or intermittent apnea. Laryngeal microsurgery without intubation

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was reported by Urban [25]. The technique involves intravenous thiopental,100% oxygen by mask initially, and manually controlled oxygen insuffla-tion. Few anesthesiologists are comfortable with this technique, and the ox-ygen insufflation can be an inconvenience during surgery.

Venturi jet ventilation can be a useful technique. Anesthetic and oxygencan be delivered through a needle placed in the lumen of the laryngoscope,through a ventilation channel in specially designed laryngoscope channels,through a catheter just above or below the vocal folds (such as the Hun-sicker catheter [Medtronics-Xomed, Jacksonville, Florida]), or througha Carden tube [26]. We use the Hunsicker catheter because of its easy place-ment, security, and laser resistance and because the jet ventilation initiatesbelow the vocal folds. This seems to cause less mechanical interference atthe vibratory margin during surgery. The catheter must be placed betweenthe vocal folds carefully by an expert anesthesiologist or the laryngologistand removed carefully to avoid intubation and extubation trauma as mightbe caused by placement of any endotracheal tube. During any surgery thatuses jet ventilation, it is essential that the surgeon be a knowledgeable, co-operative part of the anesthesia team. The airway must remain unobstructedfor expiration. If the laryngoscope moves or is removed and obstructs theairway without a warning to the anesthesia team, pneumothorax may result.

Intermittent apnea is another alternative to intubation when the presenceof the endotracheal tube would otherwise obstruct the surgical field. In sucha case, the anesthesiologist ventilates the patient with a mask or with a smallendotracheal tube to reach an O2 saturation of 100%. Once 100% O2

saturation is reached, the endotracheal tube or mask is withdrawn, andthe surgeon operates on the larynx while the patient is apneic. The O2

saturation is monitored carefully, and when the O2 saturation drops to95%, the surgeon stops operating, and the patient is ventilated via maskreplacement of the endotracheal tube. It is preferable to use an endotrachealtube for ventilation because the patient does not have to be taken out oflaryngeal suspension to resume ventilation. Instead, the endotracheal tubeis placed over a 0� laryngeal telescope and introduced into the larynx underdirect visual guidance through the rigid suspended laryngoscope. Thisallows maximal time for performing surgery during the apneic periods,which, depending on the pulmonary health of the patient, can last for5 to 7 minutes each. Additionally, time is not lost in resuspension andreobtaining exposure, which can be a frustrating consequence of choosingmask ventilation with intermittent apnea.

All the care exercised in gentle intubation may be for naught unlesssimilar caution is exercised during extubation. The most common errorduring extubation is failure to fully deflate the endotracheal tube cuff.This may result in vocal fold trauma or arytenoid cartilage dislocation.The anesthesia team should be aware of these potential problems. Thesurgeon should be present and attentive during intubation and extubationto help minimize the incidence of such occurrences.

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Anesthesia is a prime concern during nonotolaryngologic surgery involv-ing general surgeons and other surgical subspecialists. Laryngologists arefrequently called on for guidance by professional voice users, surgeons,and anesthesiologists. The anesthesiologist must appreciate that the patientis a voice professional and ensure that intubation and extubation are per-formed by the most skilled anesthesiologist available. In addition, anesthe-siologists must temper their tendency to use the largest possible tube. Thereare few procedures that cannot be performed safely through a 6.5-mm innerdiameter or smaller endotracheal tube, and many can be performed withmask anesthesia or a Brain laryngeal mask without intubating the larynx.Alternatives to general anesthesia should be considered, such as spinalblocks, regional blocks, and acupuncture. Many procedures commonlydone under general anesthesia with intubation can be performed equallywell using another technique. After surgery, postoperative voice assessmentby the anesthesiologist, patient, and operating surgeon is essential. If voiceabnormalities are present (other than very mild hoarseness that resolveswithin 24 hours), prompt laryngologic examination should be arranged.

Instrumentation

Microlaryngeal surgery uses magnification, usually provided by an oper-ating microscope that is used through a rigid direct laryngoscope [27]. Mag-nifying laryngeal telescopes are also invaluable for assessing vocal foldpathology and mapping lesions for surgery. Four-millimeter and 10-mm0� and 70� telescopes (Karl Storz, Culver City, California) and 30� and120� telescopes are useful in some circumstances. Laryngeal telescopes allowthe surgeon to visualize lesions in great detail to appreciate the limits oflesions in three dimensions better than can be accomplished through a micro-scope and to visualize obscure areas such as the laryngeal ventricle (Fig. 2).

Fig. 2. (A) 0� showing right vocal fold mass. (B) 70� reveals right vocal fold mass located

mostly on the upper half of the vibratory margin with feeding vessels and ectasias apparent.



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When laryngeal telescopes are not available, urologic rigid cystoscopes areequivalent alternatives.

A technique known as ‘‘contact endoscopy’’ has been used by gynecologicsurgeons for many years. Its value in microlaryngeal surgery was recognizedby Andrea [28]. This technique uses a vital staining agent, such as methyleneblue. Contact endoscopy permits visualization of the cellular nature and theintegrity of vocal fold epithelium at any point along the vocal fold. Cell nu-clear characteristics are visible, and specific borders between pathologic, tran-sitional, and normal epithelium can be defined, permitting precise surgicalintervention. Although this technique is relatively new and requires additionalstudy and experience, it seems to be valuable in selected cases.

Delicate microsurgery requires sharp, precise, small instruments. The fewheavy cupped forceps and scissors that constituted a laryngoscopy traythrough the early 1980s are no longer sufficient. It is now possible to obtainmicrolaryngeal instruments that look like ear instruments on long handles.Instruments should be long enough to be manipulated easily in the laryngo-scope but not so long that they bump into the microscope. They shouldinclude scissors (straight, up-biting, curved left, and curved right), smallgrasping cupped forceps (straight, up-biting, right, and left), larger cuppedforceps (straight and up-biting, at least), alligator forceps (straight, right,and left), scalpel, retractors, ball dissectors (straight, oblique, and right-angled), mirrors for reflecting lasers, and suctions. Cutting instrumentsshould be sharp at all times. Suctions should be thumb controlled, of severalsizes, and should include open tip and velvet eye designs. A suction/cauterytip may be valuable occasionally and should be available, as should cottoncarriers. Nonreflective instruments with laser-resistant coating may beadvantageous in some situations. In addition, there have been importantadvances not only in cold instrumentation, but also in powered instrumen-tation and surgical laser technology (eg, CO2, Yag, pulsed-dye) with whichall microlaryngoscopic surgeons should be familiar [29].

Powered laryngeal surgery is a relatively new concept, although poweredsurgery for other areas of the body has been used for many years [30].Acoustic neuroma surgeons have used powered instruments such as theHouse-Urban Rotary Dissector (Urban Engineering, Burbank, California)for three decades, arthroscopic knee surgeons use powered instruments reg-ularly, and powered instruments have been important to functional endo-scopic sinus surgery. Their role in laryngeal surgery is not defined, butpowered laryngeal surgery is useful in the treatment of conditions such asselected papillomas and neoplasms. The most commonly used powered la-ryngeal instrument is the Medtronic-Xomed XPS Power System (Jackson-ville, Florida) with disposable laryngeal shaver blades. To use poweredinstruments safely, it is important to understand the blades and instrumentsettings. For example, to debulk a large, exophytic, or fibrous lesion, the tri-cut laryngeal blade is used at 3000 rpm with suction set at a medium vacuumsetting. To remove papilloma near the vibratory margin or anterior

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commissure in a controlled fashion, it is more appropriate to use a 3.5-mmlaryngeal skimmer blade at 500 rpm in the ‘‘oscillate’’ mode with the suctionset at a low vacuum setting. Although some surgeons prefer using poweredinstruments under endoscopic control rather than using a microscope, wegenerally prefer using a microscope to permit binocular vision and bimanualmanipulation. Surgeons should have endoscopes available and be comfort-able with their use. In some cases, difficult anatomy precludes visualizationof certain regions of the larynx, especially at and above the anterior commis-sure with the operating microscope. In such cases, the best way to removepathology may be with the use of a 70� telescope for visualization and a pow-ered skimmer blade for resection. Delicate microdissection is the mostcontrolled and appropriate technique for removing most benign lesions,such as cysts and polyps from the vibratory margin of the vocal fold.Powered instruments, used properly, allow precision and may be helpfulespecially for selected papillomas and neoplasms.

Laryngeal microsurgery

Submucosal infusion, hemorrhage control, steroid injection

The concept of laryngeal infusion was introduced in the 1890s for thepurpose of anatomic studies [31,32]. The technique has been used for a vari-ety of purposes, including infusion of steroids to disrupt adhesions in vocalfold scar, placement of collagen along the vibratory margin, and separatingbenign and malignant lesions from underlying structures. The technique hasbeen become more popular among clinicians since the 1990s [33,34].

Submucosal infusion may be appropriate for a variety of vocal foldmasses, but it has disadvantages as well as advantages. Infusion usually isperformed using a solution made by combining 9 mL of sterile saline with1 mL of epinephrine 1:1000 (a 1:10,000 dilution). A small amount of thismixture is infused submucosally using a 30-gauge needle to increase the fluidcontent of the superficial layer of the lamina propria, to separate the under-surface of the lesion more clearly from the vocal ligament, and to help definethe vocal ligament more clearly. In lesions such as sulcus vocalis, vocal foldscar, and papilloma, this technique is extremely helpful. In other lesionssuch as small vocal fold cysts, it may obscure the pathology, making surgerymore difficult. When used in appropriate cases, the epinephrine causes vaso-constriction and helps minimize bleeding. When bleeding occurs, it can becontrolled in most cases with topical application of epinephrine 1:1000 ona small cottonoid. Rarely, cauterization with a laser or cautery is required.Infusion of saline and epinephrine does not have to be limited to the vocalfold. Infusion can be performed in the false vocal fold and lateral to the ven-tricle. This infusion technique can be successful in everting the ventricle intothe surgical field, providing direct access to lesions that involve the deep re-cesses of the laryngeal ventricle.

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In some cases, submucosal infusion may be performed with a substanceother than saline with epinephrine. For example, if the surgeon plans to in-ject steroid in a patient who has scar or sulcus, the steroid may be used forinfusion initially. It is as effective as saline and epinephrine in defining thelesion and tissue planes, but it does not provide an equally good vasocon-strictive effect. The efficacy of steroid injection in the vocal folds is un-known. Some surgeons use it regularly. Others are concerned that it mayresult in muscle atrophy. If steroid injection is used, it is important forthe surgeon to use an aqueous solution, not an oil-based preparation. Oneof the authors (RTS) recommends against using steroid suspensions thatare ‘‘milky-colored,’’ such as Kenalog (Westwood Squibb, Buffalo, NewYork). Occasionally, the white suspended particles can precipitate andform a plaque that takes months to resolve. Precipitation and the formationof plaques have not been encountered with steroid solutions, which aretypically clear liquids such as dexamethasone. Cidofovir can also be usedsparingly as the infusion material in patients who have papilloma.

Vocal fold cysts (with an overview of the evolution of voice microsurgery)

When submucosal cysts cause symptoms sufficient to warrant surgery, itis essential to resect them without damaging adjacent normal tissue. Laryn-geal microflaps were once advocated as the preferred method of accomplish-ing this goal, but that recommendation has changed. Management of vocalfold cysts provides a good window into the evolution of voice surgery.

Vast improvements in surgical care of vocal fold abnormalities occurredin the 1980s and 1990s. These changes have resulted largely because ofadvances in knowledge of the anatomy and physiology of the vocal tract,technologic developments that have improved our ability to examine andquantify voice function, and the availability of better surgical instruments[35–37]. Because the human is the only species with our layered laminapropria structure, there is no experimental animal for vocal fold surgery.Therefore, surgical advances have been based largely on anecdote andcommon sense. Consequently, it is essential to reevaluate results continuallyand to consider changing pronouncements about optimal techniques, espe-cially when research provides important new information.

Through the mid 1970s (and later in some centers), the operation of choicefor benign vocal fold pathology was ‘‘vocal cord stripping,’’ an operationabandoned except perhaps in selected cases of laryngeal cancer. Until themid 1970s, the available facts led us to believe that the operation made sense.Not knowing the complexity of the anatomy of the vibratory margin, we rea-soned that the mucosa of the vocal fold edge had become deranged. If we re-moved it, it seemed probable that the healing process would replace diseasedmucosa with new, healthy mucosa. Mucosal healing in the oral cavity andelsewhere in the upper respiratory tract was rarely a problem; so, why shouldthere be a problem on the vocal folds? We had no explanation for the

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patients who seemed to have normal vocal folds but terrible voices after thisoperation, and we tended to diagnose their persistent dysphonia as psycho-genic. In retrospect, knowing what we do now about vocal fold anatomy andphysiology, we have no explanation for the fact that so many of those pa-tients were not permanently hoarse. Nevertheless, the beginning of the endof vocal fold stripping came in 1975 when Hirano [35] described the anatomyof the vocal fold, which led to a better understanding of vocal fold scar for-mation and the development of surgical techniques to try to avoid it.

Hirano demonstrated that the vocal fold consisted of an epithelium; su-perficial, intermediate, and deep layers of the lamina propria; and thyroar-ytenoid muscle. He pointed out that fibroblasts capable of producing scarwere numerous, primarily in the intermediate and deep layers of the laminapropria and the muscle. Most benign vocal fold pathology is superficial.Moreover, research from numerous centers highlighted the importance ofthe complex mucosal wave created during phonation [37–43]. Consequently,although delicate microsurgery had been advocated by a small number offar-sighted laryngologists in the past, the need for this approach to voicesurgery quickly became generally accepted [44]. Eventually, surgeons beganto think of the anatomy and function of the vocal fold and of pathology inlayers and to conceptualize surgery in layers. This paradigm resulted in thecurrent concepts and techniques of phonomicrosurgery, which are designedto remove the pathology without disturbing adjacent normal tissue.

Vocal fold microsurgery developed rapidly in the 1980s and became thenew standard of care. It was based on the notion that surgery should be de-signed to remove pathology without promoting scar formation (ie, withoutstimulating fibroblasts in the intermediate layer of the lamina propria ordeeper). With this goal in mind, it seemed reasonable to protect the interme-diate layer of lamina propria by preserving mucosa along the vibratory mar-gin. If mucosa were absent, then the intermediate layer of lamina propriawould be traumatized directly by contact with the contralateral vocal foldduring phonation or swallowing. This contact trauma was prevented by el-evating a microflap, resecting submucosal lesions, and replacing the mucosa(Fig. 3). This technique was proposed first in 1982 and was published andillustrated in 1986 [44]. It has been recommended by numerous other au-thors since that time [44–49]. This technique was attractive because the vocalfolds looked ‘‘healed’’ almost immediately. This surgical concept was basedon reasoning, not on research. Although this is unfortunate, in many ways itis unavoidable. In the absence of an animal model with a layered laminapropria, we have little alternative. Nevertheless, although it may not be rea-sonable to perform prospective, randomized human research on microsurgi-cal techniques, at the least we are obligated to look closely and critically atour results to see whether our common sense is producing consistently fa-vorable outcomes in our patients. Laryngeal microflap surgery was a greatimprovement over vocal fold stripping. Since laryngologists began operatingwith delicate, small instruments and handling tissues gently, we have seen

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far fewer cases of permanent dysphonia from extensive vibratory marginscar. Nevertheless, the results of microflap surgery were not uniformly pleas-ing. Many were excellent (as were the results of some vocal fold strippingsyears ago), but careful strobovideolaryngoscopic analysis and voice assess-ment showed too many cases in which the final outcome was inexplicablynot perfect. Despite what seemed to be technically flawless operations,a small number of patients had severe, prolonged stiffness for many monthsafter vocal fold surgery, and critical analysis revealed permanent stiffnesseven in some patients who were happy with their voice results. Moreover,some of this stiffness was located anterior and posterior to the region ofthe mass in areas that had been normal preoperatively. This critical assess-ment of surgical results led to the uneasy feeling that we were still doingsomething wrong. The problem became clear immediately with the base-ment membrane research of Gray [50].

Fig. 3. Microflap procedure, as illustrated by Sataloff [45] in Cummings and colleagues [4]. In

this technique, a superficial incision is made in the superior surface of the true vocal fold (A).

Blunt dissection is used to elevate the mucosa from the lesion (B), minimizing trauma to the

fibroblast-containing layers of the lamina propria. Only pathologic tissue is excised under direct

vision (C). Mucosa is reapproximated (D) without violating the leading edge. We do not

recommend this technique. (From Sataloff RT. Professional voice: the science and art of clinical

care. 3rd edition. San Diego (CA): Plural Publishing, Inc.; 2006; with permission.)

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Before Gray’s landmark discovery, microflap surgery made sense. Now,it usually does not. Gray demonstrated a complex basement membranestructure between the epithelium and superficial layer of the lamina propria.Moreover, he illustrated that the epithelium and basement membrane areattached to the superficial layer of the lamina propria through an intricateseries of type VII collagen loops. These loops emanate from and return tobasement membrane cells. Type III collagen fibers of the superficial layerof the lamina propria pass through them. This highly sophisticated architec-tural arrangement is probably variable from person to person and perhapsfrom family to family. Basement membrane structures and the integrity oftheir attachments are probably related to numerous vocal fold functions, in-cluding wound healing, if we can extrapolate from basement membrane be-havior elsewhere in the body. Hence, when we elevate microflaps, we are notsimply manipulating structurally insignificant tissue. Rather, we are rippingapart delicate, functionally important anatomic structures.

Armed with this new anatomic knowledge and evidence that previoussurgical results had not been consistently as good as desired, revised com-mon sense suggested that the destruction of normal tissue structures in-volved in elevating microflaps probably rendered this techniquecounterproductive. Consequently, in the latter part of 1991, ‘‘traditional’’microflap surgery was abandoned by many surgeons. Since that time,many surgeons have limited surgery strictly to the region of pathology with-out elevating or disturbing any surrounding tissue. Masses are excised withthe smallest possible amount of their overlying mucosa, or a mini-microflapis elevated directly over the lesion (Fig. 4) [51].

Access Video on Pre-op Subepithelial/Mucous Retention Cyst, on Post-op Subepithelial/

Mucous Retention Cyst and on MDL with Excision Subepithelial/Mucous Retention Cyst in

online version of this article at: http://www.Oto.TheClinics.com.

In this technique, a small mucosal incision is made anteriorly, superiorly,and posteriorly underlying the vocal fold mass. Gentle retraction is accom-plished with a small suction on the surface of the lesion, and blunt dissectionis used to separate the mass from the lamina propria, reflecting it medially.The mass is then excised with all of its overlying mucosa or preferably re-taining a small inferiorly based medial flap of mucosa. This is generallyeasy to do once the mass has been reflected medially because the mucosais stretched because of the lesion. The micro-miniflap is a small, mediallybased pedicled flap. It should not be confused with Dedo and Sooy’s [52]much larger ‘‘micro-trap-door flap’’ for use in supraglottic stenosis orwith Ossoff and colleague’s larger ‘‘serial micro-trap-door flaps’’ used forsubglottic stenosis [53,54].

Good, prospective scientific data comparing vocal fold stripping andmicroflap and mini-microflap surgery are not available. Initial anecdotalimpressions and the data presented on excision of 96 vocal fold masses in60 patients (49 of them singers) [51] provide convincing evidence that




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mini-microflap surgery and limited mass excision with overlying mucosa(without disturbing any adjacent tissue) (Fig. 5) provide substantially betterresults than the microflap surgery advocated originally by us. There is lessextensive and prolonged postoperative stiffness with this procedure thanwas encountered after some cases of microflap surgery. Mini-microflap sur-gery is recommended for excision of vocal fold submucosal and epithelialcysts, polyps, and similar lesions. When a mini-microflap cannot be created,resection of the mass with the smallest possible amount of overlying mucosashould be performed.

Vocal fold polyps and nodules

Like the vocal fold masses discussed previously, vocal fold polyps andnodules should be removed conservatively to preserve normal mucosa andshould remain superficial to the intermediate layer of the lamina propria.

Fig. 4. (A) In elevating a mini-microflap, an incision is made with a straight knife at the junction

of the mass and normal tissue. Small vertical anterior and posterior incisions may be added at the

margins of the mass if necessary, usually using a straight scissors. (B) The mass is separated by

blunt dissection, splitting the superficial layer of the lamina propria and preserving it as much

as possible. This dissection can be performed with a spatula, blunt ball dissector (illustrated),

or scissors. (C) The lesion is stabilized, and a scissors (straight or curved) is used to excise the le-

sion, preserving asmuch adjacentmucosa as possible. The lesion acts as a tissue expander, and it is

often possible to create an inferiorly based mini-microflap. (D) The mini-microflap is replaced

over the surgical defect, establishing primary closure and acting as a biological dressing. (From

Sataloff RT. Professional voice: the science and art of clinical care. 3rd edition. San Diego

(CA): Plural Publishing, Inc.; 2006; with permission.)

1174 SATALOFF et al

Access Videos on Pre-op Excision Bilateral Polyps, on Post-op Excision Bilateral Polyps,

and on MDL with Excision Bilateral Vocal Fold Polyps in online version of this article at: http://

www.Oto.TheClinics.com.

This is accomplished best by using the mini-microflap technique. The le-sion is excised entirely with sharp instruments, rather than by tearing themucosa using cupped forceps. Nodules rarely require surgery. If they arediagnosed correctly, more than 90% resolve or become asymptomaticthrough voice therapy alone. Those that persist in causing symptoms de-spite voice therapy should be removed with little or no trauma to the sub-jacent superficial layer of the lamina propria. Many vocal fold polyps areaccompanied by an obvious central blood vessel that extends from the su-perior surface of the vocal fold. Occasionally, feeding vessels may coursealong the vibratory margin or originate below the vocal fold edge. Promi-nent feeding vessels should be cauterized with a carbon dioxide laser (at 1W, 0.1 single pulse second, 30 mj, defocused) or resected to help prevent re-current hemorrhage and polyp formation (Fig. 6). We prefer resection inmost cases. The polyp can then be removed from the vibratory margin

Fig. 5. (A) An incision is made on the superior surface of the vocal fold at the junction of the

lesion and normal mucosa. (B) Blunt dissection with the scissors is used to split the superficial

layer of lamina propria. The force of the side of the scissors is directed toward the base of the

lesion and the glottis, not laterally toward the vocal ligament. (C) The lesion is stabilized (not

retracted) with heart-shaped forceps and excised without adjacent normal tissue. A small mu-

cosal gap results, but this usually heals well. (From Sataloff RT. Professional voice: the science

and art of clinical care. 3rd edition. San Diego (CA): Plural Publishing, Inc.; 2006; with

permission.)





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with traditional instruments (Fig. 7) or laser. We use cold instruments, butthe laser can be used safely [28].

Varicosities and ectatic vessels and vocal fold hemorrhage

Ectatic blood vessels and varicosities are usually asymptomatic. Occa-sionally, they require treatment. Usually, this is due to repeated submucosalhemorrhage emanating from the enlarged, weakened blood vessel. Morerarely, it is due to dysphonia caused by engorgement of the blood vessel af-ter the exercise of voice use (just like the veins that pump up in arms afterexercise) and that change the mass of the vocal fold. This is a proven butuncommon cause of voice fatigue.

In patients who have recurrent hemorrhage from a varicose or ectatic ves-sel or voice dysfunction resulting from small vessel enlargement, vaporiza-tion of the abnormal vessels was once the treatment of choice and may beindicated in some cases. This is performed using a carbon dioxide laser, us-ing defocused 1-watt laser bursts interrupted with single pulses at 0.1 sec-ond, 30 mj, and icing the vocal fold with an ice chip or cottonoid soakedin ice water. Care should be taken not to permit heat transfer to the inter-mediate or deep layers of the lamina propria. Protection may be accom-plished by submucosal infusion and by directing the laser beamtangentially for blood vessels directly on the vibratory margin so that the di-rect impact of the laser beam is not aimed at the vibrating surface. In somecases, the mucosa may be gently retracted using alligator forceps with a cot-tonoid along the superior surface, stretching blood vessels onto the superior

Fig. 6. The feeding vessel of a hemorrhagic polyp may be treated with a 1-watt defocused laser

burst of short duration to cauterize the vessel and prevent recurrent hemorrhage. The polyp can

then be removed from the leading edge with scissors, avoiding the risk of laser injury to the

vibratory margin. (From Sataloff RT. Professional voice: the science and art of clinical care.

3rd edition. San Diego (CA): Plural Publishing, Inc.; 2006; with permission.)

1176 SATALOFF et al

surface where they may be vaporized more safely over the body of the thy-roarytenoid muscle. If the vessel is positioned over the lamina propria suchthat laser vaporization cannot be performed safely, delicate resection of thevessel with preservation of adjacent mucosa has proven successful (Fig. 8).This approach is similar to that used for symptomatic varicose vessels else-where in the body, and its rationale, technique, and results were reviewed byHochman and colleagues [55] in 1999. Thirty-four of the 42 patients re-ported were women, 84% of the patients who had documented hemorrhageswere women, and 39 of 42 of the patients were singers.

Most ectasias and varices are located in themiddle of themusculomembra-nous vocal fold, usually on the superior surface. This observation has been re-ported previously [56,57]. It was noted that 66% of the varices and ectasias

Fig. 7. (A) The old technique of grasping the lesion with a cupped forceps and evulsing the

lesion from the vocal fold is not sufficiently precise. It allows for tearing of the mucosa beyond

the necessary area of excision. Instead, the lesion may be grasped with a delicate forceps (B) or

preferably stabilized with a fine suction (C). The lesion should not be retracted medially with

forceps because this tents the mucosa and often results in excessive excision. The mucosa is

cut sharply rather than ripped (D), limiting resection to the area of pathology. Even with small

lesions, but especially with larger lesions, it is often helpful to bluntly separate the lesion from

the underlying lamina propria with a blunt dissector (E) or spreading with scissors (F). This

must be done superficially, and any pressure should be directed medially (toward the portion

being resected). Care should be taken not to traumatize the intermediate layer of the lamina

propria. Reinke’s space is not rich in fibroblasts (although it contains some), and using this

technique permits resection of the diseased tissue only while minimizing the chance of scarring.



1177VOICE SURGERY

occurred in the region of the superior and lateral extent of the mucosal wave.This is probably the point at which maximum sheering forces are generated inthe superficial layer of the lamina propria because the mucosal wave reachesits superior/lateral endpoint, decelerates quickly, and reverses direction to be-gin the closing phase of the oscillatory cycle. We speculate that this whiplash-like effect and the limitation of the microvasculature by the basement mem-brane of the epithelium are probably responsible for the preponderance ofhemorrhages, ectasias, and varices that occur on the superior and lateral sur-faces near the middle of the musculomembranous portion of the vocal fold.The middle segment of the musculomembranous portion of the vocal fold isreferred to as the striking zone [55]. It is believed that chronic mechanicaltrauma to themicrovasculature is responsible for the development varicositiesand ectasias and that direct collision forces are responsible formost of the vas-cular abnormalities that occur on themedial surface of the vocal fold. The factthat somany such abnormalities are on the superior surface rather than on thevibratory margin probably is due to the fact that the maximum sheeringstresses during oscillation are on the superior surface. Because of the whip-lash-like mechanism of injury, superficial vessels are more likely to be injuredthan deeper vessels. This is convenient because the superficial nature facili-tates surgical management. In a series of 42 patients for whom sufficient pre-operative and postoperative data were available, mucosal vibration remainedthe same or improved in all patients who underwent excision of ectasias orvarices using cold instruments [55].

This had not been the experience with laser management of similarlesions in earlier years before this technique was developed. Although theresection of vessels is preferred in most cases, laser cauterization shouldbe considered, particularly for lesions far lateral to the vibratory margin.

Fig. 8. Ectasia. (A) Technique for elevating and resecting a varicose vessel. A superficial incision

is made in the epithelium adjacent to the vessel using the sharp point of the vascular knife or a mi-

croknife (illustrated). (B) The 1-mm right angle vascular knife is inserted under the vessels and

used to elevate it. It may be necessary to make more than one epithelial incision to dissect the de-

sired length of the vessel. (C) Once the pathologic vessel has been elevated, it is retracted gently to

provide access to its anterior and posterior limits. These can be divided sharply with a scissors or

knife (bleeding stops spontaneously) or divided and cauterized with a laser as long as there is no

thermal injury to adjacent vocal ligament. (From Sataloff RT. Professional voice: the science and

art of clinical care. 3rd edition. San Diego (CA): Plural Publishing, Inc.; 2006; with permission.)

1178 SATALOFF et al

Regardless of location, the importance of avoiding trauma to adjacenttissues cannot be overstated.

In patients who have extensive hemorrhage distorting a vocal fold, anincision along the superior surface with evacuation of the hematoma mayexpedite healing. In general, this is not necessary. If the bulging vocal foldhas not flattened satisfactorily through resorption of the hematoma withina few days after the hemorrhage, evacuation may be considered. Surgery in-volves suction evacuation of the hematoma through a small incision on thesuperior surface. Vocal fold hemorrhage is discussed in detail elsewhere [58].

Reinke’s edema

Surgery for bilateral Reinke’s edema should be started with only one vo-cal fold operated on in one sitting in most cases, although this practice re-mains controversial. The vocal fold may be incised along its superiorsurface, and the edematous material may be removed with a fine suction(Fig. 9). Redundant mucosa may be trimmed, and mucosa should be reap-proximated. Care must be exercised to avoid resecting too much mucosa.The second vocal fold may be treated similarly after the first vocal foldhas healed. The voice improvement that follows unilateral evacuation ofReinke’s edema is often surprisingly good, and patients frequently electto leave the other vocal fold undisturbed.

There is a more important reason for staging surgery for Reinke’s edema.Occasionally, surgical treatment for this condition results in a stiff vocalfold, sometimes even adynamic, even though this complication theoreticallyshould be rare with the technique advocated. Nevertheless, it can occur even

Fig. 9. (A). Bulky vocal fold showing Reinke’s edema (small dots) in the superficial layer of the

lamina propria. (B) Incision in the superior surface opens easily into Reinke’s space. (C) Using

a fine-needle suction, the edema fluid is aspirated (arrows). (D) The mucosal edges are

reapproximated, trimming redundant mucosa if necessary. (From Sataloff RT. Professional


Inc.; 2006; with permission.)

1179VOICE SURGERY

when surgery has been performed well. If it occurs on one side and there isReinke’s edema on the other side, the polypoid side usually compensates.Voice quality is generally satisfactory, and (most importantly) phonationis not effortful. If stiffness occurs bilaterally, the voice is hoarse and requireshigh phonation pressures. Patients are unhappy not only with voice quality,but especially with the fatigue that accompanies increased effort required toinitiate and sustain phonation. Under these circumstances, they often feelthat they are worse than they were with untreated Reinke’s edema. If sur-gery is staged so that healing can be observed on one vocal fold beforesurgery is performed on the second vocal fold, this situation can be avoidedin nearly all cases.

Granulomas and vocal process ulcers

Vocal fold granulomas may occur anywhere within the larynx, but mostcommonly they occur in the region of the vocal processes or elsewhere onthe cartilaginous portion of the larynx. They may be unilateral or bilateral.‘‘Granuloma’’ is a misnomer because these irregular, friable lesions are in-flammatory and contain fibroblasts, collagenous fibers, proliferated capillar-ies, leukocytes, and sometimes ulceration. In most cases, they are associatedwith laryngopharyngeal reflux, but voice abuse, premature vocal processcontact caused by lateral cricoarytenoid muscle dominance, and other fac-tors may play a role. These lesions should be differentiated from neoplasmsand true granulomas, which are caused by conditions such as tuberculosisand sarcoid.

Treatment begins with excellent control of laryngopharyngeal reflux andvoice therapy. Botulinum toxin injections into the lateral cricoarytenoidmuscles may be helpful. The pulse dye laser is effective in some patients.When surgical excision is required, injury to the perichondrium should beavoided.

Sulcus vocalis and vocal fold scar

Sulcus vocalis is seen as a longitudinal groove along the vibratory marginof the vocal fold. In sulcus vocalis, the superficial layer of lamina propria isabsent, although it may be relatively thin, and the epithelium is adherent tothe vocal ligament, preventing a mucosal wave. Sulcus vergeture has a simi-lar appearance, but the ‘‘groove’’ or stria along the edge of the vocal fold isnot associated with the absence of the superficial layer of lamina propria,and the vocal fold is not adynamic in the area of this sulcus vergeture,although the mucosal wave may not be normal.

Ford and colleagues [59] have classified sulcus into three types. Type Isulcus is ‘‘physiologic.’’ It is a visual abnormality only and causes no pho-natory dysfunction. It can be observed in approximately 10% of the popu-lation. Type II sulcus is associated with a deficiency (but not absence) of

1180 SATALOFF et al

superficial lamina propria and corresponds with sulcus vergeture. The slightimpairment of mucosal wave may cause dysphonia, particularly in high-pitched voices. Type III sulcus is a true sulcus vocalis, with complete absenceof the superficial lamina propria.

Type I sulcus requires no treatment. Type II sulcus may respond to voicetherapy. When therapy is insufficient, vocal fold medialization is often ade-quate. Relieving glottic insufficiency and permitting firm vocal fold contactoften allows the focal folds to compensate and produce good voice, withoutsurgery on the vibratory margin. Type III sulcus is also treated with voicetherapy to eliminate compensatory hyperfunction, but therapy alone israrely adequate. Surgery is generally necessary to restore the mucosalwave and eliminate glottic insufficiency.

The principles of surgery for sulcus vocalis and vocal fold scar are thesame and are discussed in greater detail in other literature [60,61]. Theseconditions present with two problems: glottic insufficiency and impairedmucosal wave. Glottic insufficiency can be improved by medialization sur-gery (injection or thyroplasty). Restoration of the mucosal wave is morechallenging. It may be accomplished by resecting the sulcus, approximatingthe mucosal edges and implanting fat; elevating the sulcus and implantingfat or another substance; or through multiple incisions (essentially multipleZ-plastys) along the vibratory margin as suggested by Pontes [62].

Other abnormalities

Numerous other pathologic abnormalities may occur in the larynx.Detailed information on these subjects may be found elsewhere [36].

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