2007, Vol.40, Issues 5, The Professional Voice

Otolaryngol Clin N Am
40 (2007) xi–xii
Preface
Yolanda D. Heman-Ackah, MD Robert T. Sataloff, MD, DMA

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, the
pathophysiology of abnormal voice production, and the vocal disability of
which the patient complains. The ability to assimilate each of these factors
into a treatment plan that will improve vocal function and allow the voice
professional to resume vocal performance while preserving longevity of
the voice is also important. In this issue of the Otolaryngologic Clinics
of North America, we attempt to give the practicing otolaryngologist
a framework for evaluating the vocal performer and interpreting findings
on physical examination. The importance of obtaining a thorough under-
standing of the patient’s complaints and their goals for recovery cannot
be emphasized enough. Similarly, it is extremely important to realize that
not all ‘‘pathologic’’ findings on physical examination are necessarily path-
ologic from a functional perspective for the patient. Knowing which findings
are 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 evaluation
and treatment of voice disorders, and an adequate course of voice therapy
should always be instituted before recommending surgery in all cases. Many
times, voice therapy can limit the functional disability associated with many
vocal fold lesions, paresis, and compensatory hyperfunctional behavior,
thus obviating the need for surgery. Additionally, attention should be
focused on systemic medical problems, prescription medications, over-
the-counter medications, and self-prescribed herbal remedies that may con-
tribute to vocal difficulties.
0030-6665/07/$ - see front matter Ó 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 biopsy
are over. This procedure will often lead to scar formation and a hoarse or
unacceptable voice, especially in voice professionals who are acutely aware
of subtle changes in vocal fold function. Only experienced laryngologists
should attempt surgical procedures on vocal professionals. Even a small
amount of vocal fold scarring or stiffness can be career-ending and is an un-
desirable and unacceptable outcome. Because many voice professionals do
not require surgical treatment, there are several nonsurgical therapeutic op-
tions that can and should be instituted prior to referring a voice professional
to a laryngologist for surgical rehabilitation.
A diagnostic paradigm is presented in this issue to serve as a framework
for 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 of
illnesses 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 changes
than is a nonprofessional, and will likely seek attention before the disease
process begins to manifest in other bodily systems. Thus, a high index of
suspicion and a broad knowledge base of systemic diseases that can present
as 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, medical
therapy, 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 online
version 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, MD
Robert T. Sataloff, MD, DMA
Department of Otolaryngology–Head and Neck Surgery
Drexel University College of Medicine
1721 Pine Street
Philadelphia, PA 19103, USA
E-mail addresses: phillyvoicemd@aol.com (Y.D. Heman-Ackah)
RTSataloff@phillyent.com (R.T. Sataloff)
40 (2007) 909–929
Clinical Anatomy and Physiology

of the Voice
Robert T. Sataloff, MD, DMA*,
Yolanda D. Heman-Ackah, MD,
Mary J. Hawkshaw, BSN, RN, CORLN
Department 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 all
body 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 be
considered in treating the professional voice user. It is helpful to think of
the larynx as composed of four anatomic units: skeleton, mucosa, intrinsic
muscles, and extrinsic muscles. The glottis is the space between the vocal
folds [1]. The portions of the larynx above the vocal folds are referred to
as 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). Intrinsic
muscles of the larynx are connected to these cartilages. One of the intrinsic
muscles, the thyroarytenoid, extends on each side from the arytenoid carti-
lage to the inside of the thyroid cartilage just below and behind the thyroid
prominence. 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: rtsataloff@phillyent.com (R.T. Sataloff).
910 SATALOFF et al
Fig. 1. Cartilages of the larynx. (From Sataloff RT. Professional voice: the science and art of clin-
ical care. 3rd edition. San Diego (CA): Plural Publishing, Inc.; 2006. p. 143–77; with permission.)
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 relative
angles and distances, thereby permitting alterations in the shape and tension
of 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 are
brought together in the midline and revolve over the cricoid, moving inferi-
orly and anteriorly. It seems that people use different strategies for
CLINICAL ANATOMY AND PHYSIOLOGY OF THE VOICE 911
approximating the arytenoids and that such strategies may influence a per-
son’s susceptibility to laryngeal trauma that can cause vocal process ulcers
and laryngeal granulomas.
Larynx: mucosa
The vibratory margin of the vocal fold is much more 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 tract
is 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 to
withstand the trauma of vocal fold contact. The superficial layer of the lamina
propria, 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 collagenous
fibers and is rich in fibroblasts. The thyroarytenoid or vocalis muscle makes
up the body of the vocal fold and is one of the intrinsic laryngeal muscles. The
intermediate 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 are
important in only a few situations, the surgeon, in particular, should be
aware that they exist. Particularly striking variations occur at the anterior
and posterior portion of the membranous vocal fold. Anteriorly, the inter-
mediate layer of the lamina propria becomes thick, forming an oval mass
called the anterior macula flava. This structure is composed of stroma, fibro-
blasts, and elastic fibers. Anteriorly, it inserts into the anterior commissure
tendon, a mass of collagenous fibers that is connected to the thyroid carti-
lage anteriorly, the anterior macula flava posteriorly, and the deep layer
of the lamina propria laterally. As Hirano has pointed out, this arrangement
allows the stiffness to change gradually from the pliable membranous vocal
fold 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 macula
flava. 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 the
membranous vocal fold to the slightly stiffer macula flava, to the stiffer tran-
sitional structure, to the elastic cartilage of the vocal process, to the hyaline
cartilage of the arytenoid body. It is believed that this gradual change in
stiffness serves as a cushion that may protect the ends of the vocal folds
912 SATALOFF et al
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 act
as a controlled damper that smoothes mechanical changes in vocal fold ad-
justment. This arrangement seems particularly well suited to vibration, as
are other aspects of the vocal fold architecture. For example, blood vessels
in the vibratory margin come from posterior and anterior origins and run
parallel to the vibratory margin, with few vessels entering the mucosa per-
pendicularly or from underlying muscle. The vibratory margin contains
no glands, whose presence would likely interfere with the smoothness of vi-
bratory waves. Even the elastic and collagenous fibers of the lamina propria
run approximately parallel to the vibratory margin. The more one studies
the vocal fold, the more one appreciates the beauty of its engineering.
Functionally, the five layers have different mechanical properties and
may 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 (intermediate
and 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 intermediate
and deep layers, fibroblast proliferation, or scar formation.
In addition to the five layers discussed above, recent research has shown
that there is a complex basement membrane connecting the epithelium to
the superficial layer of the lamina propria [5]. The basement membrane is
a multilayered, chemically complex structure. It gives rise to Type VII col-
lagen loops that surround Type III collagen fibers in the superficial layer
of the lamina propria. Knowledge of the basement membrane has already
been important in changing surgical technique. Additional research is likely
to 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 folds may be thought of as the oscillators of the vocal mechanism
[6]. Above the true vocal folds are tissues known as false vocal folds. Unlike
the true vocal folds, they do not make contact during normal speaking or sing-
ing. They may produce voice during certain abnormal circumstances, how-
ever. This phenomenon is called ‘‘dysphonia plica ventricularis.’’ Until
recently, the importance of the false vocal folds during normal phonation
was not appreciated. In general, they are considered to be used primarily
for forceful laryngeal closure and they may be used excessively during
914 SATALOFF et al
pathologic conditions. Contrary to popular practice, however, surgeons

should recognize that they cannot simply be removed without phonatory ef-
fects. The physics of airflow through the larynx are complex, involving vortex
shedding and sophisticated turbulence patterns that are essential to phona-
tion. The false vocal folds provide a downstream resistance that is important
in 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 of
the vocal folds (Figs. 3 and 4). All but one of the muscles on each side of the
larynx are innervated by one of the two recurrent laryngeal nerves. Because
this nerve runs a long course from the neck down into the chest and back up
to the larynx (hence the name ‘‘recurrent’’), it is easily injured by trauma,
neck surgery, and chest surgery. Such injuries may result in abductor and
adductor paralysis of the vocal fold. The remaining muscle, the cricothyroid
muscle, is innervated by the superior laryngeal nerve on each side, which is
especially 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 the
inferior 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 extension

of this nerve may also supply motor and sensory innervation to the vocal
fold. 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 for
some motor innervations of laryngeal muscles. The recurrent laryngeal
nerves branch off the vagus in the chest. On the left, the nerve usually loops
around 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 the
right side, where they are more likely to be injured during neck surgery.
There are interconnections between the superior and recurrent laryngeal
nerves, 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 are
those innervated by the recurrent laryngeal nerve (thyroarytenoid, posterior
cricoarytenoid, 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 the
vocal 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 the

vocal 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 to
the muscular process. More specifically, the superior bundles of the muscle
insert into the lateral and inferior aspects of the vocal process and run pri-
marily in a horizontal direction. The anteroinferior bundles insert into the
anterolateral aspect of the arytenoid cartilage from its tip to an area lateral
to 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 is
also known as the vocalis muscle. It contains a high percentage of slow
twitch muscle fibers. The lateral compartment has predominantly fast twitch
muscle 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 fold
edge takes on a more angular or sharp contour. It originates on the upper
lateral border of the cricoid cartilage and inserts into the anterior lateral
surface 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 providing
medial compression to close the posterior glottis. It has little effect on the
stiffness of the membranous portion. The interarytenoid muscle consists
of 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 arytenoid
into the apex of the contralateral arytenoid.
The posterior cricoarytenoid muscle abducts, elevates, elongates, and
thins the vocal fold by rocking the arytenoid cartilage posterolaterally. All
layers are stiffened, and the edge of the vocal fold is rounded. It is the second
largest intrinsic muscle. It originates over a broad area of the posterolateral
portion of the cricoid lamina and inserts on the posterior surface of the mus-
cular process of the arytenoid cartilage, forming a short tendon that covers
the 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, an
important factor in control of pitch. Contraction tends to increase vocal
pitch. 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 oblique
belly inserts into the posterior half of the thyroid lamina and the anterior
portion of the inferior cornu of the thyroid cartilage. The vertical (erect)
belly inserts into the inferior border of the anterior aspect of the thyroid
cartilage.
Intrinsic laryngeal muscles are skeletal muscles. All skeletal muscles are
composed primarily of three types of fibers. Type I fibers are highly resistant
to fatigue, contract slowly, and use aerobic (oxidative) metabolism. They have
low glycogen levels, high levels of oxidative enzymes, and they are relatively
smaller in diameter. Type IIA fibers use principally oxidative metabolism
but 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 most
larger 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 proportion
of Type IIA fibers than most other muscles. The thyroarytenoid and lateral
cricothyroid muscles are particularly specialized for rapid contraction. The
laryngeal muscles in general seem to have fiber distributions and variations
that make them particularly well suited to rapid contraction with fatigue re-
sistance [9]. In addition, many laryngeal motor units have multiple neural
innervation. There seem to be approximately 20 to 30 muscle fibers per mo-
tor unit in a human cricothyroid muscle [10], suggesting that the motor unit
size 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 fibers
have two or more nerve endplates [12]. Some fibers have as many as five
nerve endplates. Only 50% of cricothyroid and lateral cricoarytenoid muscle
fibers have multiple endplates, and multiple innervation is even less common
in 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 from
different motor neurons) [9].
Larynx: extrinsic muscles

Extrinsic laryngeal musculature maintains the position of the larynx in
the neck. This group of muscles includes primarily the strap muscles. Be-
cause raising or lowering the larynx may alter the tension or angle between
laryngeal cartilages, thereby changing the resting lengths of the intrinsic
muscles, the extrinsic muscles are critical in maintaining a stable laryngeal
skeleton so that the delicate intrinsic musculature can work effectively. In
the 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 the

vocal folds, producing regular periodicity. This phenomenon contributes
to 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 thyroid
lamina of the hyoid bone. Contraction brings the thyroid and hyoid bone
closer together, especially anteriorly. The sternothyroid muscle originates
from the first costal cartilage and posterior aspect of the manubrium of
the sternum, and it inserts obliquely on the thyroid cartilage. Contraction
of 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 inferior
belly of the omohyoid originates from the upper surface of the scapula and
inserts into the intermediate tendon of the omohyoid muscle. The superior
belly originates from the intermediate tendon and inserts into the greater
cornu of the hyoid bone. The omohyoid muscle pulls down on the hyoid
bone, 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 belly
originates from the inferior aspect of the mandible near the symphysis
and inserts into the intermediate tendon. The anterior belly pulls the hyoid
bone anteriorly and raises it. The mylohyoid muscle originates from the in-
ner aspect of the body of the mandible (mylohyoid line) and inserts into
a midline raphe with fibers from the opposite side. It raises the hyoid
bone and pulls it anteriorly. The geniohyoid muscle originates from the
mental 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 and
pulls it anteriorly. The stylohyoid muscle originates from the styloid process
and inserts into the body of the hyoid bone. It raises the hyoid bone and
pulls it posteriorly. Coordinated interaction among the extrinsic laryngeal
muscles 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 (see
Fig. 2), and possibly the sinuses shape the sound quality produced at the
level 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 are
immediately recognizable to a trained vocalist or astute critic, but they often
elude the common listener.
The tracheobronchial tree, lungs, and thorax

The lungs supply a constant stream of air that passes between the vocal
folds and provides power for voice production. Singers often are thought of
as having ‘‘big chests.’’ Actually, the primary respiratory difference between
trained and untrained singers is not increased total lung capacity, as is pop-
ularly assumed. Rather, the trained singer learns to use a higher proportion
of the air in his or her lungs, thereby decreasing his or her residual volume
and increasing respiratory efficiency [13].
The abdomen
The abdominal musculature is the so-called ‘‘support’’ of the singing
voice, although singers generally refer to their support mechanism as their
diaphragm. The function of the diaphragm muscle in singing is complex
and somewhat variable from singer to singer (or actor to actor). The dia-
phragm primarily generates inspiratory force. Although the abdomen can
also perform this function in some situations [14], it is primarily an expira-
tory-force generator. The diaphragm is co-activated by some performers
during singing and seems to play an important part in the fine regulation
of singing [15]. Actually, the anatomy of support for phonation is compli-
cated and not completely understood. The lungs and rib cage generate
passive expiratory forces under many common circumstances. Passive inspi-
ratory forces also occur. Active respiratory muscles working in consort with
passive forces include the intercostal, abdominal wall, back, and diaphragm
muscles. The principle muscles of inspiration are the diaphragm, the exter-
nal intercostal muscles that connect the bony ribs, and the interchondral
portions of the internal intercostal muscles that connect the cartilaginous
ribs. 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; latissimus
dorsi; and levatores costarum. During quiet respiration, expiration is largely
passive. Many of the muscles used for active expiration (forcing air out of
the lungs) are also used in support for singing and acting. Muscles of active
expiration either raise the intra-abdominal pressure, forcing the diaphragm
upward, or lower the ribs or sternum to decrease the dimension of the tho-
rax, or both. They include the internal intercostals that connect the bony
ribs, stiffen the rib interspaces, and pull the ribs down; transversus thoracis,
subcostal muscles, and serratus posterior inferior, all of which pull the ribs
down; 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 as
a muscle of expiration and a muscle of inspiration. The above muscles all
participate in active expiration (and support). The primary muscles of active
expiration are the abdominal muscles, however. They include the external
oblique abdominus, internal oblique abdominus, rectus abdominus, and
transversus abdominus. The external oblique is a flat broad muscle located
on the side and front of the lower chest and abdomen. On contraction, it pulls
the lower ribs down and raises the abdominal pressure by displacing abdom-
inal contents inward. It is an important muscle for support of singing and
acting 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 curl
sit-ups. Appropriate strengthening exercises of the external oblique muscles
are often inappropriately neglected in voice training. The internal oblique is
a 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 abdominal
wall inward and lowers the lower ribs. The rectus abdominus runs parallel
to the midline of the abdomen originating from the xiphoid process of the
sternum and the fifth, sixth, and seventh costal cartilages. It inserts into
the pubic bone. It is encased in the fibrous abdominal aponeurosis. Contrac-
tion of the rectus abdominus lowers the sternum and ribs and stabilizes the
abdominal wall. The transversus abdominus is a broad muscle located under
the internal oblique on the side and front of the abdomen. Its fibers run hor-
izontally around the abdomen. Contraction of the transverse abdominus
compresses the abdominal contents, elevating abdominal pressure.
The abdominal musculature receives considerable attention in vocal
training. 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 support
technique. Some experts describe positioning the abdominal musculature
under the rib cage; others advocate distension of the abdomen. Either
method may result in vocal problems if used incorrectly, but distending
the 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 considerable
effort, believing he or she is practicing good support technique, without ob-
taining the desired effect. Proper abdominal muscle training is essential to
good singing and speaking, and the physician must consider abdominal
function when evaluating vocal disabilities.
The musculoskeletal system

Musculoskeletal condition and position affect the vocal mechanism and
may 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 the
metatarsal heads (a more athletic position), alter the configuration of the
abdominal and back musculature enough to adversely influence the voice.
Tensing arm and shoulder muscles promotes cervical muscle strain, which
can adversely affect laryngeal function. Careful control of muscle tension
is fundamental to good vocal technique. In fact, some teaching methods
use musculoskeletal conditioning as the primary focus of voice training.
The psychoneurologic system

The psychologic constitution of the singer impacts directly on the vocal
mechanism. Psychologic phenomena are reflected through the autonomic
nervous 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, because
minimal 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 expression
establish the commands for vocalization. The idea of the planned vocaliza-
tion is conveyed to the precentral gyrus in the motor cortex, which transmits
another set of instructions to motor nuclei in the brainstem and spinal cord.
These areas transmit the complicated messages necessary for coordinated
activity of the larynx, thoracic, and abdominal musculature and of the vocal
tract articulators and resonators. Additional refinement of motor activity is
provided by the extrapyramidal (cerebral cortex, cerebellum, and basal gan-
glion) and autonomic nervous systems. These impulses combine to produce
a sound that is transmitted not only to the ears of listeners but also to those
of the speaker or singer. Auditory feedback is transmitted from the ear to
the cerebral cortex by way of the brainstem, and adjustments are made to
permit the vocalist to match the sound produced with the intended sound.
There is also tactile feedback from the throat and other muscles involved
in phonation that undoubtedly help in fine-tuning vocal output, although
the 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 ancillary
noise 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 folds
are in the adducted state, permitting small bursts of air to escape between
them. 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), volume
velocity of air flow at the glottis, and supraglottal pressure. The vocal folds
do not vibrate like the strings on a violin. Rather, they separate and collide
somewhat like buzzing lips. The number of times they do so in any given
second (ie, their frequency) determines the number of air puffs that escape
and, 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 fold
displacement from the midline during each vibratory cycle. The sound cre-
ated at the vocal fold level is a buzz, similar to the sound produced when
blowing between two blades of grass. This sound contains a complete set
of harmonic partials and is responsible in part for the acoustic characteris-
tics of the voice. Complex and sophisticated interactions in the supraglottic
vocal tract may accentuate or attenuate harmonic partials, acting as a reso-
nator. This portion of the vocal tract is largely responsible for the beauty
and variety of the sound produced.
Interactions among the various components of the vocal tract ultimately
are responsible for all the vocal characteristics produced. Many aspects of
the voice still lack complete understanding and classification. Vocal range
is reasonably well understood, and broad categories of voice classifications
are generally accepted. Other characteristics, such as vocal register, are con-
troversial. Registers are expressed as quality changes within an individual
voice. From low to high, they may include vocal fry, chest voice, middle
voice, head voice, falsetto, and whistle, although not everyone agrees that
all categories exist. The term modal register, used most frequently in speech
terms, 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 exact
source remains uncertain, and its desirable characteristics depend on voice
range and the type of music sung. It seems most likely that the frequency
modulations are controlled primarily by intrinsic laryngeal muscles, espe-
cially the cricothyroid and adductor muscles. Extrinsic laryngeal muscles
and muscles of the supraglottic vocal tract may also play a role. Intensity
variations may be caused by variations in subglottal pressure, glottal adjust-
ments that affect subglottal pressure, secondary effects of the frequency
924 SATALOFF et al
variation because of changes in the distance between the fundamental fre-

quency and closest formant, or rhythmic changes in vocal tract shape that
cause fluctuations in formant frequencies. When evaluating vibrato, it is
helpful 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 in
untrained voice users. This regularity seems to be one of the characteristics
perceived as a trained sound. Vibratory extent refers to deviation from the
standard frequency (not intensity variation) and is usually less than 0.1
semitone in some styles of solo and choral singing, such as Renaissance mu-
sic. For most well-trained Western operatic singing, the usual vibrato extent
at comfortable loudness is 0.5 to 1 semitone for singers in most voice clas-
sifications. Vibrato rate (the number of modulations per second) is generally
5 to 7. Rate may also vary greatly from singer to singer, and in the same
singer. Vibrato rate can increase with increased emotional content of the
material, and rate tends to decrease with older age (although the age at
which this change occurs is highly variable). When variations from the cen-
tral frequency become too wide, a wobble in the voice is perceived; this is
generally 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 mechanisms
responsible for normal vibrato. Ongoing research should answer many of
the remaining questions.
Respiration
Basic functions of the nose, larynx, and elemental concepts of inspiration
and expiration are discussed elsewhere [1]. A brief review of selected aspects
of pulmonary function is included here to assist readers in understanding the
processes that underlie support and in understanding pulmonary disorders
and their assessment.
Starting from the mouth, the respiratory system consists of progressively
smaller airway structures. The trachea branches at the carina into mainstem
bronchi, which then branch into progressively smaller bronchial passages
and 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 to
permit this exchange of gases. Air is forced out of the alveoli also to create
the air stream through which phonation is produced. Ultimately, alveolar
pressure is the primary power source for phonation and is responsible for
the 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 resistance
between the alveoli and the larynx. As the air passes from the alveoli, it en-
ters first the bronchioles, which are small, collapsible airways surrounded by
smooth muscle but devoid of cartilage. From the bronchioles, air passes to
progressively larger components of the bronchial tree and eventually to the

trachea. 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 in
the respiratory system is greatest in the alveolus (alveolar pressure) and least
at 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 between
these 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 pressure
in the alveoli (alveolar pressure) is equal to the atmospheric pressure in the
room. To fill the alveoli, the alveolar pressure must be decreased to less than
atmosphere pressure, creating a vacuum that sucks air into the lungs. To
breathe out, alveolar pressure must be greater than atmospheric pressure.
As discussed above, there are passive and active forces operative during
the inspiratory–expiratory process.
To clarify the mechanisms involved, the alveoli may be thought of as tiny
balloons. If a balloon is filled with air, and the filling spout is opened, the
elastic 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 properties
of the alveoli themselves. Alternatively, we may wrap our hands around the
balloon and squeeze the air out. This squeezing may allow us to get the air
out faster and more forcefully, and it allows us to get more of the air out of
the balloon than is expelled through the passive process alone. This process
is analogous to active expiration, which involves the abdominal, chest, and
back muscles. If we partially pinch the filling spout of the balloon, air comes
out more slowly because the outflow tract is partially blocked. The air also
tends to whistle as it exits the balloon. This situation is analogous to ob-
structive pulmonary disease, and its commonly associated wheeze. If we
try 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 analogous
to restrictive lung disease. Under these circumstances, it may also take more
pressure 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 not
ruptured. When the pressure is greater, the increased elastic recoil results
in more rapid and forceful air escape when the air is released. The pressure
inside the balloon can be increased even above its maximal elastic recoil level
simply by squeezing the outside of the balloon. This analogy is helpful in un-
derstanding the forces involved in breathing (especially expiration) and in
generating 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 speech
and singing. The elastic component of expiratory pressure (specifically, al-
veolar pressure) depends on lung volume and the elastic forces exerted by
the chest and the lungs. The lung is never totally deflated. At rest the lung
is inflated to about 40% of total lung capacity (TLC). The amount of air
in the lungs at rest is the functional residual capacity (FRC). At FRC, the
thorax (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 has
a 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 expanding
elastic forces of the thorax. The lung and thorax interact closely, and their
relative positions of contact vary constantly. This situation is facilitated by
the anatomy of their boundary zone. The inner surface of the thorax is
covered by the parietal pleura, and the lung is covered by the visceral
pleura. A thin layer of pleural fluid exists between them. Hydrostatic
forces 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 for
phonation adversely.
Thoracic and lung elastic behavior can be measured. The basic principle
for doing so involves applying pressure and noting the volume changes
caused 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 curve
is 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 the
system 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 atmospheric
pressure (and is predictable using the P/V curve). The deeper the inspiration,
the greater the difference between alveolar and atmospheric pressure, and
the 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 involves
contraction 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 compress
the abdominal contents, pushing them upward and thus making the volume
of the thorax smaller. The principle muscles involved are the internal inter-
costal muscles, abdominal, back, and other muscles, as reviewed earlier in
this chapter.
For projected phonations, such as singing or acting, airflow is achieved
through active expiration. After inspiration, elastic recoil and external forces
created 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 (at
the mouth) pressure, there is a point along that path at which the pressure
inside the airway equals the active expiratory pressure (without the elastic
recoil 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. This
physiologic collapse of the airway increases airway resistance by decreasing
the diameter of the airway. The greater the active expiratory forces, the
greater the airway compression after the EPP has been passed. Expiratory
pressure and airway compression are important for control of expiratory
airflow 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 to
continue 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 the
bronchioles are narrowed by smooth muscle contraction and airway resis-
tance in the bronchioles is increased. As the air moves from the alveoli
into the bronchioles, airway pressure diminishes more quickly than normal
and EPP may be reached closer to the alveoli and bronchioles, which col-
lapse more easily and more completely. In severe circumstances, the distal
airway 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-normal
subglottic pressure. This phenomenon can have profoundly adverse effects
on phonation.
Other lung dysfunction can also impair subglottal pressure, even if air-
way resistance is normal. The classic example is emphysema, which occurs
commonly in smokers. This condition results from damage to the alveoli
in which the alveolar walls are destroyed and elasticity is lost. Destruction
of the alveolar walls effectually causes coalescence of multiple alveoli into
one large alveolar structure, with collagen deposition and scarring in areas
where elastic fibers were once deposited. Consequently, because elastic recoil
928 SATALOFF et al
pressures are lower and the alveolar volume is greater, alveolar pressure is
decreased compared with normal. Even if the active expiratory forces are
normal, the diminished alveolar pressure results in a lower pressure gradient
between 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 circumstances
they do not help because they collapse the distal airways, trapping air in the
alveoli and diminishing subglottal pressure.
Summary
This overview highlights only some of the more important components of
lower respiratory physiology. Laryngologists should bear these principles in
mind in understanding the importance of diagnosis and treatment of respi-
ratory dysfunction in voice professionals. In patients who have ‘‘Olympic
voice demands,’’ even slight changes from optimal physiology may have
profound 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 may
be 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
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[2] Hirano M. 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.
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[3] Hirano M. 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] Hirano M, 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.
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ics. San Diego (CA): Singular Publishing Group; 1991. p. 21–7.
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[8] Sadeh M, Kronenberg J, Gaton E. Histochemistry of human laryngeal muscles. Cell Mol
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[9] Lindestad P. Electromyographic and laryngoscopic studies of normal and disturbed vocal
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[10] English ET, Blevins CE. Motor units of laryngeal muscles. Arch Otolaryngol 1969;89:
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[11] Faaborg-Andersen K. Electromyographic investigation of intrinsic laryngeal muscles in
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[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
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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, CORLN
Department 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 the

cause of voice dysfunction. Effective history taking and physical examina-
tion depend on a practical understanding of the anatomy and physiology
of voice production [1–3]. Because dysfunction in virtually any body system
may affect phonation, medical inquiry must be comprehensive. The current
standard of care for all voice patients evolved from advances inspired by
medical problems of voice professionals, such as singers and actors. Even
minor problems may be particularly symptomatic in singers and actors
because of the extreme demands placed on their voices. A great many other
patients are voice professionals, however. They include teachers, sales
people, attorneys, clergy, physicians, politicians, telephone receptionists,
and anyone else whose ability to earn a living is impaired in the presence
of voice dysfunction. Because good voice quality is so important in our
society, most of our patients are voice professionals and all patients should
be treated as such.
The scope of inquiry and examination for most patients is similar to that
required for singers and actors, except that performing voice professionals
have unique needs that require additional history and examination.
Questions must be added regarding performance commitments, professional
status and voice goals, the amount and nature of voice training, the perfor-
mance environment, rehearsal practices, abusive habits during speech and
singing, 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.
932 SATALOFF et al
essential to proper treatment selection and patient counseling in singers and

actors. Analogous factors must also be taken into account, however, for
stockbrokers, factory shop foremen, elementary school teachers, home-
makers with several noisy children, and many others. Physicians familiar
with the management of these challenging patients are well equipped to
evaluate all patients who have voice complaints.
Patient history
Obtaining extensive historical background information is necessary for
thorough evaluation of the voice patient, and the otolaryngologist who
sees voice patients (especially singers) only occasionally cannot reasonably
be expected to remember all the pertinent questions. Although some laryng-
ologists consider a lengthy inquisition helpful in establishing rapport, many
of us who see a substantial number of voice patients each day within a busy
practice need a thorough but less time-consuming alternative. A history
questionnaire can be extremely helpful in documenting all the necessary in-
formation, helping the patient sort out and articulate his or her problems
and saving the clinician time recording information. The senior author
has developed a questionnaire that has proved helpful [4]. The patient is
asked to complete the relevant portions of the form at home before his or
her office visit or in the waiting room before seeing the doctor. A similar
form 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 determined
from a glance at a completed questionnaire, however, obviating the need for
extensive writing, which permits the physician greater eye contact with the
patient and facilitates rapid establishment of the close rapport and
confidence that are so important in treating voice patients. The physician
is also able to supplement initial impressions and historical information
from the questionnaire with seemingly leisurely conversation during the
physical examination. The use of the history questionnaire has added
substantially to the efficiency, consistent thoroughness, and ease of manag-
ing these delightful, but often complex, patients. A similar set of questions is
also used by the speech-language pathologist with new patients and by many
enlightened singing teachers when assessing new students.
How old are you?

Serious vocal endeavor may start in childhood and continue throughout
a lifetime. As the vocal mechanism undergoes normal maturation, the voice
changes. The optimal time to begin serious vocal training is controversial.
For many years, most singing teachers advocated delay of vocal training
and serious singing until near puberty in the female and after puberty and
MEDICAL HISTORY IN VOICE PROFESSIONALS 933
voice stabilization in the male. In a child who has earnest vocal aspirations
and potential, however, starting specialized training early in childhood is
reasonable. Initial instruction should teach the child to vocalize without
straining and to avoid all forms of voice abuse. It should not permit prema-
ture indulgence in operatic bravado. Most experts agree that taxing voice
use and singing during puberty should be minimized or avoided altogether,
particularly by the male. Voice maturation (attainment of stable adult vocal
quality) 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 sound
older 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 lose
elasticity, the thorax loses its distensibility, the mucosa of the vocal tract at-
rophies, mucous secretions change character and quantity, nerve endings are
reduced in number, and psychoneurologic functions change as one advances
past the midlife. Moreover, the larynx itself loses muscle tone and bulk and
may show depletion of submucosal ground substance in the vocal folds. The
laryngeal cartilages ossify, and the joints may become arthritic and stiff.
Hormonal influence is altered. Vocal range, intensity, and quality all may
be modified. Vocal fold atrophy may be the most striking alteration. The
clinical effects of aging seem more pronounced in female singers, although
vocal fold histologic changes may be more prominent in males. Excellent
male singers occasionally extend their careers into their 70s or beyond
[6,7]. Some degree of breathiness, decreased range, decreased breath
support, 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 to
separate acute from chronic dysfunction. Often an upper respiratory tract
infection sends a patient to the physician’s office, but penetrating inquiry,
especially in singers and actors, may reveal a chronic vocal problem that
is the patient’s real concern. Identifying acute and chronic problems before
beginning therapy is important so that patient and physician may have
realistic expectations and make optimal therapeutic selections.
The specific nature of the vocal complaint can provide a great deal of
information. Just as dizzy patients rarely walk into the physician’s office
complaining of ‘‘rotary vertigo,’’ voice patients may be unable to articulate
their symptoms without guidance. They may use the term ‘‘hoarseness’’ to
describe a variety of conditions that the physician must separate. Hoarse-
ness is a coarse or scratchy sound that is most often associated with
934 SATALOFF et al
abnormalities of the leading edge of the vocal folds, such as laryngitis or

mass lesions. Breathiness is a vocal quality characterized by excessive loss
of air during vocalization. In some cases it is caused by improper technique.
Any condition that prevents full approximation of the vocal folds can be
responsible, however. Possible causes include vocal fold paralysis, a mass
lesion separating the leading edges of the vocal folds, arthritis of the cricoar-
ytenoid joint, arytenoid dislocation, scarring of the vibratory margin, senile
vocal fold atrophy (presbyphonia), psychogenic dysphonia, malingering,
and other conditions.
Fatigue of the voice is inability to continue to speak or sing for extended
periods without change in vocal quality or control. The voice may show
fatigue by becoming hoarse, losing range, changing timbre, breaking into
different 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 the
time it is assumed to be attributable to muscle fatigue, which is often the
case in patients who have voice fatigue associated with muscle tension dys-
phonia. The mechanism is most likely to be peripheral muscle fatigue caused
by chemical changes or depletion in the muscle fibers. Muscle fatigue may
also 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 may
also 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 propria
or 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 recovery
between phonatory stresses, and genetic or structural tissue weaknesses
that 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 may
also be related to linear and nonlinear chaotic characteristics of the voice
signal [8]. As the voice becomes more trained, vibrations become more sym-
metrical and the system becomes more linear. In many pathologic voices, the
nonlinear components seem to become more prominent. If a voice is highly
linear, slight changes in the vibratory margin may have little effect on the
output of the system. If the system is substantially nonlinear because of vo-
cal fold pathology, poor tissue environment, or other causes, slight changes
in the tissue (eg, slight swelling, drying, surface cell damage) may cause
substantial changes in the acoustic output of the system. A butterfly effect
ensues in which vocal quality changes and fatigue occur more quickly
with smaller changes in the condition than would be seen in more linear
vocal systems.
Fatigue is often caused by misuse of abdominal and neck musculature,

oversinging, singing too loudly, or singing too long. Vocal fatigue also
may be a sign not only of general tiredness or vocal abuse, sometimes sec-
ondary to structural lesions or glottal closure problems, but also of serious
illnesses, such as myasthenia gravis. The importance of this complaint thus
should not be understated.
Volume disturbance may manifest as inability to sing loudly or inability
to sing softly. Each voice has its own dynamic range. Within the course of
training, singers learn to sing louder by singing more efficiently. They also
learn to sing softly, a more difficult task, through years of laborious practice.
Actors and other trained speakers go through similar training. Most volume
problems are secondary to intrinsic limitations of the voice or technical er-
rors in voice use, although hormonal changes, aging, and neurologic disease
are other causes. Superior laryngeal nerve paresis impairs the ability to
speak or sing loudly. This condition is a frequently unrecognized conse-
quence of herpes simplex II infection (cold sores) and Lyme disease and
may also be precipitated by any viral upper respiratory tract infection.
Most highly trained singers require only about 10 to 30 minutes to warm up
the voice. Prolonged warm-up time, especially in the morning, is most often
caused by reflux laryngitis. Tickling or choking during singing is most often
a symptom of an abnormality of the vocal fold’s leading edge. The symptom
of tickling or choking should contraindicate singing until the vocal folds have
been examined. Pain while singing can indicate vocal fold lesions, laryngeal
joint arthritis, infection, or gastric acid reflux irritation of the arytenoid
region. Pain is much more commonly caused by voice abuse with excessive
muscular activity in the neck rather than an acute abnormality on the leading
edge of a vocal fold, however. In the absence of other symptoms, these patients
do not generally require immediate cessation of singing pending medical
examination. Sudden onset of pain, usually sharp pain, while singing may
be associated with a mucosal tear or a vocal fold hemorrhage, however, and
warrants voice rest pending laryngeal examination.
Do you have any pressing voice commitments?

If a singer or professional speaker (eg, actor, politician) seeks treatment
at the end of a busy performance season and has no pressing engagements,
management of the voice problem should be conservative and designed to
ensure long-term protection of the larynx. The physician and patient rarely
have this luxury, however. Most often, the voice professional needs treat-
ment within 1 week of an important engagement and sometimes within
less than 1 day.
Younger singers fall ill shortly before performances, not because of hypo-
chondria or coincidence, but rather because of the immense physical and
emotional stress of the pre-performance period. The singer is frequently
working harder and singing longer hours than usual. Moreover, he or she
936 SATALOFF et al
may be under particular pressure to learn new material and to perform well
for a new audience. The singer may also be sleeping less than usual because
of additional time spent rehearsing or because of the discomforts of a strange
city. Seasoned professionals make their living by performing regularly,
sometimes several times a week. Consequently, any time they get sick is
likely 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 importance
of your voice quality and upcoming commitments
To choose a treatment program, the physician must understand the
importance of the patient’s voice and his or her long-term career plans,
the importance of the upcoming vocal commitment, and the consequences
of canceling the engagement. Injudicious prescription of voice rest can be
almost as damaging to a vocal career as injudicious performance. For
example, although a singer’s voice is usually his or her most important
commodity, other factors distinguish the few successful artists from the
multitude of less successful singers with equally good voices. These include
musicianship, reliability, and professionalism. Canceling a concert at the last
minute may seriously damage a performer’s reputation. Reliability is espe-
cially critical early in a singer’s career. Moreover, an expert singer often
can modify a performance to decrease the strain on his or her voice. No
singer should be allowed to perform in a manner that permits serious injury
to the vocal folds, but in the frequent borderline cases the condition of the
larynx 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 is
important, 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 use
without training or premature training with inappropriate repertoire may
underlie persistent vocal difficulties later in life. The number of years a
performer has been training his or her voice may be a fair index of vocal
proficiency. A person who has studied voice for 1 or 2 years is somewhat
more likely to have gross technical difficulties than someone who has been
studying 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 who
has had many teachers in a brief period of time commonly has numerous
technical insecurities or deficiencies that may be responsible for vocal
dysfunction, especially if the singer has changed to a new teacher within
the preceding year. The physician must be careful not to criticize the
patient’s current voice teacher in such circumstances. It often takes years of

expert instruction to correct bad habits.
All people speak more often than they sing, yet most singers report little
speech training. Even if a singer uses the voice flawlessly while practicing
and performing, voice abuse at other times can cause damage that affects
singing.
Under what kinds of conditions do you use your voice?

The Lombard effect is the tendency to increase vocal intensity in response
to increased background noise. A well-trained singer learns to compensate
for this tendency and to avoid singing at unsafe volumes. Singers of classical
music usually have such training and frequently perform with only a piano,
a situation in which the balance can be controlled well. Singers performing
in large halls, with orchestras, or in operas early in their careers tend to
oversing and strain their voices. Similar problems occur during outdoor
concerts because of the lack of auditory feedback. This phenomenon is
seen even more among pop singers. Pop singers are in a uniquely difficult
position; often, despite little vocal training, they enjoy great artistic and
financial success and endure extremely stressful demands on their time
and voices. They are required to sing in large halls or outdoor arenas not
designed for musical performance amid smoke and other environmental
irritants 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 singer
on the stage and provide auditory feedback. Determining whether the pop
singer uses monitor speakers and whether they are loud enough for the
singer to hear is important.
Amateur singers are often no less serious about their music than are
professionals, but generally they have less ability to compensate technically
for illness or other physical impairment. Rarely does an amateur suffer
a great loss from postponing a performance or permitting someone to
sing in his or her place. In most cases, the amateur singer’s best interest is
served through conservative management directed at long-term maintenance
of good vocal health.
A great many of the singers who seek physicians’ advice are primarily
choral singers. They often are enthusiastic amateurs, untrained but dedi-
cated to their musical recreation. They should be handled as amateur solo
singers, educated specifically about the Lombard effect, and cautioned to
avoid the excessive volume so common in a choral environment. One
good way for a singer to monitor loudness is to cup a hand to his or her
ear, which adds about 6 dB to the singer’s perception of his or her own voice
and can be a helpful guide in noisy surroundings [9]. Young professional
singers are often hired to augment amateur choruses. Feeling that the
professional 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 than
others in their sections. These singers should be advised to lead their section
by 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 them
recording their choral performance for their voice teacher. This approach
usually 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 conditioning
of other muscle systems is to the athlete. Proper vocal practice incorporates
scales and specific exercises designed to maintain and develop the vocal ap-
paratus. Simply acting or singing songs and giving performances without
routine studious concentration on vocal technique is not adequate for the
vocal performer. The physician should know whether the vocalist practices
daily, whether he or she practices at the same time daily, and how long the
practice lasts. Actors generally practice and warm up their voices for 10 to
30 minutes daily, although more time is recommended. Most serious singers
practice for at least 1 to 2 hours per day. If a singer routinely practices in the
late afternoon or evening but frequently performs in the morning (religious
services, school classes, teaching voice, choir rehearsals, and so forth), one
should inquire as to the warm-up procedures preceding such performances
and the cool-down procedures after voice use. Singing cold, especially early
in the morning, may result in the use of minor muscular alterations to com-
pensate for vocal insecurity produced by inadequate preparation. Such
crutches can result in voice dysfunction. Similar problems may result from
instances of voice use other than formal singing. School teachers, telephone
receptionists, sales people, and others who speak extensively also often
derive great benefit from 5 or 10 minutes of vocalization of scales first thing
in the morning. Although singers rarely practice their scales too long, they
frequently perform or rehearse excessively. This is especially true immedi-
ately before a major concert or audition, when physicians are most likely
to see acute problems. When a singer has hoarseness and vocal fatigue
and has been practicing a new role for 14 hours a day for the previous 3
weeks, no simple prescription can solve the problem. A treatment regimen
can usually be designed to carry the performer safely through his or her
musical obligations, however.
The physician should be aware of common habits and environments that
are often associated with abusive voice behavior and should ask about them
routinely. Screaming at sports events and at children are among the most
common. 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 communication
with hearing-impaired people are likely to be associated with voice abuse,
as is extensive professional voice use without formal training. The physician
should inquire about the patient’s routine voice use and should specifically
ask 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 as
weight 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 in
the tongue, neck, and larynx; inadequate abdominal support; and excessive
volume. Inadequate preparation can be a devastating source of voice abuse
and may result from limited practice, limited rehearsal of a difficult piece, or
limited vocal training for a given role. The latter error is tragically common.
In some situations, voice teachers are at fault and the singer and teacher
must 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’s
voice. Singers are habitually unhappy with the limitations of their voices.
At some time or another, most baritones wish they were tenors and try to
prove they can sing high C’s in Vesti la giubba. Singers with other vocal
ranges have similar fantasies. Attempts to make the voice something that
it 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 who
complain of voice fatigue associated with voice use, patients whose voices
are worse at the end of a working day or week, and in any patient who is
chronically hoarse. Technical errors in voice use may be the primary cause
of a voice complaint, or it may develop secondarily because of a patient’s
effort to compensate for voice disturbance from another cause.
Dissociation of one’s speaking and singing voices is probably the most
common cause of voice abuse problems in excellent singers. Too frequently,
all the expert training in support, muscle control, and projection is not
applied to a singer’s speaking voice. Unfortunately, the resultant voice
strain affects the singing voice and the speaking voice. Such damage is
especially likely to occur in noisy rooms and in cars, where the background
noise is louder than it seems. Backstage greetings after a lengthy perfor-
mance can be particularly devastating. The singer usually is exhausted
and distracted, the environment is often dusty and dry, and generally a noisy
crowd is present. Similar conditions prevail at postperformance parties,
where smoking and alcohol worsen matters. These situations should be
940 SATALOFF et al
avoided by any singer who has vocal problems and should be controlled
through awareness at other times.
Three particularly abusive and potentially damaging vocal activities are
worthy of note. Cheerleading requires extensive screaming under the worst
possible physical and environmental circumstances. It is a highly undesirable
activity 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 the
cheerleaders, and so on. Conducting, particularly choral conducting, can
also be deleterious. An enthusiastic conductor, especially of an amateur
group, frequently sings all four parts intermittently, at volumes louder than
the 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 control
after conducting a rehearsal or concert suggests voice abuse during conduct-
ing. The patient should be instructed to record his or her voice throughout the
vocal 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 has
lost 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 conductors
can generally be managed by additional training in conducting techniques and
by voice training, including warm-up and cool-down exercises.
Teaching singing may also be hazardous to vocal health. It can be done
safely but requires skill and thought. Most teachers teach while seated at the
piano. Late in a long, hard day, this posture is not conducive to mainte-
nance of optimal abdominal and back support. Usually, teachers work
with 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. Teachers
also often demonstrate vocal works in their students’ vocal ranges rather
than their own, illustrating bad and good technique. If a singing teacher
is 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 up
before beginning to teach voice lessons), voice abuse should be suspected.
Helpful modifications include teaching with a grand piano, sitting slightly
sideways on the piano bench, or alternating student position to the right
and left of the piano to facilitate better neck alignment. Retaining an accom-
panist so that the teacher can stand rather than teach from sitting behind
a 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 treatment
of 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 and
coordinated interaction of numerous physical functions. Maladies of any
part of the body may be reflected in the voice. Failure to maintain good
abdominal muscle tone and respiratory endurance through exercise is partic-
ularly harmful because deficiencies in these areas undermine the power
source of the voice. Patients generally attempt to compensate for such
weaknesses by using inappropriate muscle groups, particularly in the
neck, causing vocal dysfunction. Similar problems may occur in the well-
conditioned vocalist in states of fatigue. These are compounded by mucosal
changes that accompany excessively long hours of hard work. Such
problems may be seen even in the best singers shortly before important
performances 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 is
in most other athletic artists, and it should be prevented from the start of
one’s vocal career. Appropriate and attractive body weight has always
been valued in the pop music world and is becoming particularly important
in the opera world as this formerly theater-based art form moves to televi-
sion and film media. Attempts at weight reduction in an established speaker
or singer are a different matter, however. The vocal mechanism is a finely
tuned, complex instrument and is exquisitely sensitive to minor changes.
Substantial fluctuations in weight frequently cause deleterious alterations
of the voice, although these are usually temporary. Weight reduction pro-
grams for people concerned about their voices must be monitored carefully
and designed to reduce weight in small increments over long periods. A
history of sudden recent weight change may be responsible for almost any
vocal complaint.
Have you noted voice or bodily weakness, tremor, fatigue, or loss

of control?
Even minor neurologic disorders may be extremely disruptive to vocal
function. Specific questions should be asked to rule out neuromuscular and
neurologic diseases, such as myasthenia gravis, Parkinson disease, tremors,
other movement disorders, spasmodic dysphonia, multiple sclerosis, central
nervous system neoplasm, and other serious maladies that may present with
voice complaints.
942 SATALOFF et al
Do you have allergy or cold symptoms?

Acute upper respiratory tract infection causes inflammation of the
mucosa, alters mucosal secretions, and makes the mucosa more vulnerable
to injury. Coughing and throat clearing are particularly traumatic vocal
activities 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, resulting
in similar problems, and may actually alter the sound of a voice, especially
the 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 sound
to normal frequently result in laryngeal strain. The expert singer or speaker
should 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 tract
infections and postnasal drip, but the relevance of other maladies may not be
obvious to them. Consequently the physician must seek out pertinent history.
Respiratory problems are especially important in voice patients. Even
mild respiratory dysfunction may adversely affect the power source of the
voice [11]. Occult asthma may be particularly troublesome [12]. A complete
respiratory 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?

Any mucosal irritant can disrupt the delicate vocal mechanism. Allergies to
dust and mold are aggravated commonly during rehearsals and performances
in concert halls, especially older theaters and concert halls, because of numer-
ous curtains, backstage trappings, and dressing room facilities that are rarely
cleaned thoroughly. Nasal obstruction and erythematous conjunctivae sug-
gest generalized mucosal irritation. The drying effects of cold air and dry
heat may also affect mucosal secretions, leading to decreased lubrication,
a scratchy voice, and tickling cough. These symptoms may be minimized by
nasal breathing, which allows inspired air to be filtered, warmed, and humid-
ified. Nasal breathing, whenever possible, rather than mouth breathing, is
proper vocal technique. While the performer is backstage between appear-
ances or during rehearsals, inhalation of dust and other irritants may be
controlled by wearing a protective mask, such as those used by carpenters,
or a surgical mask that does not contain fiberglass. This practice is especially
helpful 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]. One
must be careful to avoid talking loudly and to maintain good hydration
and nasal breathing during air travel. Environmental changes can also be
disruptive. Las Vegas is infamous for the mucosal irritation caused by its
dry atmosphere and smoke-filled rooms. In fact, the resultant complex of
hoarseness, 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 substances
and conditions encountered daily. Inhalation of toxic pollutants may affect
the voice adversely by direct laryngeal injury, by causing pulmonary dysfunc-
tion that results in voice maladies, or through impairments elsewhere in the
vocal tract. Ingested substances, especially those that have neurolaryngologic
effects, may also adversely affect the voice. Nonchemical environmental pol-
lutants, such as noise, can cause voice abnormalities also. Laryngologists
should be familiar with the laryngologic effects of the numerous potentially
irritating substances and conditions found in the environment. We must
also 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 are
exposed routinely to chemicals encountered through stage smoke and pyro-
technic effects [14–16]. Although it is clear that some of the special effects
result in serious laryngologic consequences, much additional study is need
to 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 the
Journal of Singing [17]. Smoking of cigarettes, cigars, marijuana, and other
substances affects the larynx, lungs, and other body systems adversely and
should 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 avoid
milk and ice cream before performances. In many people, these foods
seem to increase the amount and viscosity of mucosal secretions. Allergy
and casein have been implicated, but no satisfactory explanation has been
established. In some cases restriction of these foods from the diet before
a voice performance may be helpful. Chocolate may have the same effect
and should be viewed similarly. Chocolate also contains caffeine, which
may aggravate reflux or cause tremor. Voice patients should be asked about
eating nuts. This question is important not only because some people expe-
rience effects similar to those produced by milk products and chocolate but
also because they are extremely irritating if aspirated. The irritation pro-
duced by aspiration of even a small organic foreign body may be severe
and impossible to correct rapidly enough to permit performance. Highly
944 SATALOFF et al
spiced foods may also cause mucosal irritation. In addition, they seem to ag-
gravate reflux laryngitis. Coffee and other beverages containing caffeine also
aggravate gastric reflux and may promote dehydration or alter secretions
and necessitate frequent throat clearing in some people. Fad diets, especially
rapid weight-reducing diets, are notorious for causing voice problems. Eat-
ing a full meal before a speaking or singing engagement may interfere with
abdominal support or may aggravate upright reflux of gastric juice during
abdominal muscle contraction.
Do you have morning hoarseness, bad breath, excessive phlegm, a lump

in your throat, or heartburn?
Reflux laryngitis is especially common among singers and trained
speakers because of the high intra-abdominal pressure associated with
proper 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 and
then go to bed with a full stomach. Chronic irritation of arytenoid and vocal
fold mucosa by reflux of gastric secretions may occasionally be associated
with dyspepsia or pyrosis. The key features of this malady are bitter taste
and halitosis on awakening in the morning, a dry or coated mouth, often
a 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 alert
to these symptoms and ask about them routinely; otherwise, the diagnosis
is overlooked because people who have had this problem for many years
or 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 voice
complaint. These symptoms may accompany infection, anxiety, various
gastroenterologic diseases, and other maladies.
Are you under particular stress or in therapy?

The human voice is an exquisitely sensitive messenger of emotion. Highly
trained voice professionals learn to control the effects of anxiety and other
emotional stress on their voices under ordinary circumstances. In some
instances, 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 in
the voice. Anxiety reactions are mediated in part through the autonomic
nervous system and result in a dry mouth, cold clammy skin, and thick
secretions. These reactions are normal, and good vocal training coupled
with assurance that no abnormality or disease is present generally
overcomes them. Long-term, poorly compensated emotional stress and
exogenous stress (from agents, producers, teachers, parents, and so forth)
may cause substantial vocal dysfunction and may result in permanent
limitations of the vocal apparatus. These conditions must be diagnosed
and treated expertly. Hypochondriasis is uncommon among professional
singers, despite popular opinion to the contrary.
Recent publications have highlighted the complexity and importance of
psychological factors associated with voice disorders [18]. It is important
for the physician to recognize that psychological problems may not only
cause voice disorders but also delay recovery from voice disorders that
were 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 following
the death of a loved one. This process may be initiated even when physical
recovery is complete if an incident, such as injury or surgery, has made the
vocalist realize that voice loss is possible. Such a ‘‘brush with death’’ can
have profound emotional consequences in some patients. It is essential for
the laryngologist to be aware of these powerful factors and to manage
them properly if optimal therapeutic results are to be achieved expeditiously.
Do you have problems controlling your weight? Are you excessively

tired? 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 in
alterations of fluid content of the lamina propria just beneath the laryngeal
mucosa, which causes alterations in the bulk and shape of the vocal folds
and result in voice change. Hypothyroidism and thyroiditis are well-recog-
nized causes of such voice disorders, although the mechanisms are not fully
understood [19–23]. Hoarseness, vocal fatigue, muffling of the voice, loss of
range, and a sensation of a lump in the throat may be present even with mild
thyroid dysfunction. Even when thyroid function test results are within the
low 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 associated

with menses, recent menopause, or other hormonal changes or problems?
Voice changes associated with sex hormones are encountered commonly
in clinical practice and have been investigated more thoroughly than have
other hormonal changes [24,25]. Although a correlation seems to exist
946 SATALOFF et al
between sex hormone levels and depth of male voices (higher testosterone
and 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 singers
and tend to occur during menopause or several months after the cessation of
hormone replacement therapy. It is always important to ask a female patient
who complains of gradual onset of decreased range, increased instability,
and vocal fatigue about her menstrual and hormonal status, particularly if
she 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 the
hyoid bone and indirectly as generalized increased muscle tension. These
problems often result in decreased range, vocal fatigue, and change in the
quality or placement of a voice. Such tension often is accompanied by excess
tongue muscle activity, especially pulling of the tongue posteriorly. This hy-
perfunctional behavior acts through hyoid attachments to disrupt the balance
between the intrinsic and extrinsic laryngeal musculature. TMJ problems are
also problematic for wind instrumentalists and some string players, including
violinists. In some cases, the problems may actually be caused by instrumental
technique. 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. Auditory
feedback is fundamental to speaking and singing. Interference with this
control mechanism may result in altered vocal production, particularly if
the person is unaware of the hearing loss. Distortion, particularly pitch
distortion (diplacusis) may also pose serious problems for the singer. This
distortion seems to be attributable to aesthetic difficulties in matching pitch
and also to vocal strain, which accompanies pitch shifts [45].
In addition to determining whether the patient has hearing loss, inquiry
should also be made about hearing impairment occurring in family
members, roommates, and other close associates. Speaking loudly to
people who are hard of hearing can cause substantial, chronic vocal strain.
This possibility should be investigated routinely when evaluating voice
patients.
Have you suffered whiplash or other bodily injury?

Various bodily injuries outside the confines of the vocal tract may have
profound effects on the voice. Whiplash, for example, commonly causes
changes in technique, with consequent voice fatigue, loss of range, difficulty

singing softly, and other problems. These problems derive from the neck
muscle spasm, abnormal neck posturing secondary to pain, and consequent
hyperfunctional voice use. Lumbar, abdominal, head, chest, supraglottic,
and extremity injuries may also affect vocal technique and be responsible
for 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 whom
it was done, whether intubation was necessary, and whether the anesthesiol-
ogist reported difficulty with the intubation. It is also important to ascertain
whether voice therapy was instituted pre- or postoperatively, especially if the
lesion is commonly associated with voice abuse (vocal nodules or vocal
process granulomas). If the vocal dysfunction that sent the patient to the
physician’s office dates from the immediate postoperative period, surgical
or intubation trauma must be suspected.
Otolaryngologists frequently are asked about the effects of tonsillectomy
on the voice. Singers, especially, may consult the physician after tonsillec-
tomy and complain of vocal dysfunction. Certainly, removal of tonsils
can alter the voice [46,47]. Tonsillectomy changes the configuration of the
supraglottic vocal tract. In addition, scarring alters pharyngeal muscle func-
tion, which is trained meticulously in the professional singer. Singers must
be warned that they may have permanent voice changes after tonsillectomy;
however, these can be minimized by dissecting in the proper plane by cold
technique and minimal use of cautery, laser, or other thermal coagulation
devices to lessen scarring. The singer’s voice generally requires 3 to 6
months 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 stretch
the palatal musculature helps to limit the effects of palatal scarring. As
with 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 great
care, and the use of nonirritating plastic rather than rubber or ribbed metal
endotracheal tubes is preferred. Use of a laryngeal mask may be advisable
for selected procedures for mechanical reasons, but this device is often not
ideal for tonsillectomy and it can cause laryngeal injury, such as arytenoid
dislocation.
Surgery of the neck, such as thyroidectomy, may result in permanent
alterations of the vocal mechanism through scarring of the extrinsic
laryngeal musculature. The cervical (strap) muscles are important in
maintaining laryngeal position and stability of the laryngeal skeleton and
they should be retracted rather than divided whenever possible. A history
948 SATALOFF et al
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 should
be prohibited until pain has subsided and healing has occurred sufficiently
to allow normal support. Abdominal exercises should be instituted before
resumption of vocalizing. Singing and speaking without proper support
are often worse for the voice than not using the voice for performance at all.
Other surgical procedures may be important factors if they necessitate
intubation or if they affect the musculoskeletal system so that the person
has to change stance or balance. For example, balancing on one foot after
leg 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 the
voice. The effect of small amounts of alcohol is controversial. Although
many experts oppose its use because of its vasodilatory effect and conse-
quent mucosal alteration, many people do not seem to be adversely affected
by small amounts of alcohol, such as a glass of wine with a meal. Some
people have mild sensitivities to certain wines or beers. Patients who develop
nasal congestion and rhinorrhea after drinking beer, for example, should be
made 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 drip
or other symptoms. The drying effect of antihistamines may result in
decreased vocal fold lubrication, increased throat clearing, and irritability,
leading to frequent coughing. Antihistamines may be helpful to some voice
patients but they must be used with caution and are best taken at bedtime to
minimize daytime side effects.
When a voice patient seeking the attention of a physician is already
taking antibiotics, it is important to find out the dose and the prescribing
physician, if any, and whether the patient frequently treats himself or
herself with inadequate courses of antibiotics often supplied by colleagues.
Singers, actors, and other speakers sometimes have a sore throat shortly
before important vocal presentations and start themselves on inappropriate
antibiotic therapy, which they generally discontinue after their
performance.
Diuretics are also popular among some performers. They are often
prescribed by gynecologists at the vocalist’s request to help deplete excess
water in the premenstrual period. They are not effective in the larynx in
this scenario, because they cannot diurese the protein-bound water in the
laryngeal ground substance. Unsupervised use of these drugs may cause
dehydration and consequent mucosal dryness, placing the singer at risk for
vocal 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 do
not mention them routinely when asked whether they are taking any
medications. Vitamins and herbal supplements are also frequently not
mentioned. 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 upper
respiratory tract infections, seems to act as a mild diuretic and may lead to
dehydration and xerophonia [48]. Herbal remedies should be used by singers
with 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 can
be extremely irritating to the nasal mucosa, causes marked vasoconstriction,
and may alter the sensorium, resulting in decreased voice control and
a 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 been
reported with selective cyclooxygenase-2 inhibiting (COX-2) anti-inflamma-
tory medications, such as Celecoxib (Celebrex, Pfizer Inc., New York) and
valdecoxib (Bextra, Pharmacia Corp., New York). The effects of other
new medications, such as sildenafil citrate (Viagra, Pfizer Inc.) and medica-
tions used to induce abortion remain unstudied and unknown but it seems
plausible that these types of medications may affect voice function, at least
temporarily. Laryngologists must be familiar with the laryngologic effects of
the many substances ingested medically and recreationally.
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40 (2007) 953–969
Physical Examination of Voice

Professionals
Mary J. Hawkshaw, BSN, RN, CORLN,
Venu Divi, MD,
Yolanda D. Heman-Ackah, MD
of Medicine, 1721 Pine Street, Philadelphia, PA 19103-6771, USA
Physical examination
A detailed history frequently reveals the cause of a voice problem even
before 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 physical
condition. A patient who is extremely obese or seems fatigued, agitated,
emotionally stressed, or otherwise generally ill has increased potential for
voice dysfunction. This dysfunction could be attributable to any number
of factors: altered abdominal support, loss of fine motor control of laryngeal
muscles, 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 abdominal
musculature is suspect as cause for dysphonia. Some conditions, such as
pregnancy, are obvious; however, a sprained ankle or broken leg that re-
quires the singer to balance in an unaccustomed posture may distract him
or her from maintaining good abdominal support and thereby result in voice
dysfunction. A tremorous neurologic disorder, endocrine disturbances such
as 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 the
doctor must remain alert for conditions outside of the head and neck. If
the patient uses his or her voice professionally for singing, acting, or other
vocally 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. Even
a slight hearing loss may result in voice strain as a singer tries to balance his
or her vocal intensity with that of associate performers. Similar effects are
encountered among speakers, but they are less prominent in the early stages
of hearing loss. This observation is especially true of hearing losses acquired
after vocal training has been completed. The effect is most pronounced with
sensorineural hearing loss. Diplacusis, distortion of pitch perception, makes
vocal strain even worse. With conductive hearing loss, singers tend to sing
more softly than appropriate rather than too loudly, and this is less harmful.
During an ear, nose, and throat examination, the conjunctivae and
sclerae should be observed routinely for erythema that suggests allergy or
irritation, for pallor that suggests anemia, and for other abnormalities,
such as jaundice. These observations may reveal the problem reflected in
the vocal tract even before the larynx is visualized. Hearing loss in a spouse
or family member may be problematic also if the voice professional strains
vocally to communicate.
The nose should be assessed for patency of the nasal airway, character of
the nasal mucosa, and nature of secretions, if any. A patient who is unable
to breathe through the nose because of anatomic obstruction is forced to
breathe unfiltered, unhumidified air through the mouth. Pale gray allergic
mucosa or swollen infected mucosa in the nose suggests abnormal mucosa
elsewhere in the respiratory tract.
Examination of the oral cavity should include careful attention to the
tonsils and lymphoid tissue in the posterior pharyngeal wall and to the mu-
cosa. Diffuse lymphoid hypertrophy associated with a complaint of scratchy
voice and irritative cough may indicate infection. The amount and viscosity
of mucosal and salivary secretions also should be noted. Xerostomia is par-
ticularly important. The presence of scalloping of the lateral aspects of the
tongue should be noted. This finding is caused commonly by tongue thrust
and may be associated with inappropriate tongue tension and muscle ten-
sion dysphonia. Dental examination should focus not only on oral hygiene
but also on the presence of wear facets suggestive of bruxism. Bruxism is
a clue to excessive tension and may be associated with dysfunction of the
temporomandibular joints, which should also be assessed routinely.
PHYSICAL EXAMINATION OF VOICE PROFESSIONALS 955
Thinning of the enamel of the central incisors in a normal or underweight

patient may be a clue to bulimia. It may also result from excessive ingestion
of lemons, which some singers eat to help thin their secretions.
The neck should be examined for masses, restriction of movement, excess
muscle tension or spasm, and scars from prior neck surgery or trauma. La-
ryngeal vertical mobility is also important. For example, tilting of the larynx
produced by partial fixation of cervical muscles cut during previous surgery
may produce voice dysfunction, as may fixation of the trachea to overlying
neck skin. Particular attention should be paid to the thyroid gland. Enlarge-
ment of the gland may signal subclinical hypothyroidism or thyroiditis, both
of which can affect the vocal folds, their vibratory function, and the integrity
of the laryngeal nerves, in some cases contributing to paresis and paralysis
of the superior or recurrent laryngeal nerves. Examination of posterior neck
muscles and range of motion should not be neglected. Neck muscle spasm,
decreased range of motion, and cervical spine abnormalities can contribute
to increased neck tension and hyperfunctional voice behaviors. The cranial
nerves should also be examined. Diminished fifth nerve sensation, dimin-
ished gag reflex, palatal deviation, or other mild cranial nerve deficits may
indicate 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 and
projection in the voice. The recurrent laryngeal nerve is also affected in
some cases. More serious neurologic disease may also be associated with
such symptoms and signs.
Laryngeal examination
Examination of the larynx begins when the singer or other voice patient
enters the physician’s office. The range, ease, volume, and quality of the
speaking voice should be noted. If the examination is not being conducted
in the patient’s native language, the physician should be sure to listen to
a 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]. The
classification proposed by the Japanese Society of Logopedics and Phoniat-
rics is one of the most widely used. It is known commonly as the GRBAS
Voice Rating Scale [13].
Physicians are not usually experts in voice classification. Physicians should
at least be able to discriminate substantial differences in range and timbre,
however, such as between bass and tenor, or alto and soprano. Although
the correlation between speaking and singing voices is not perfect, a speaker
who has a low, comfortable bass voice who reports that he is a tenor may
be misclassified and singing inappropriate roles with consequent voice strain.
This judgment should be deferred to an expert, but the observation should
lead the physician to make the appropriate referral. Excessive volume or
956 SATALOFF et al
obvious strain during speaking clearly indicates that voice abuse is present
and may be contributing to the patient’s singing complaint. The speaking
voice can be evaluated more consistently and accurately using standardized
reading passages [14], and such assessments are performed routinely by
speech-language pathologists, phoniatricians, and sometimes by
laryngologists.
Any patient who has a voice complaint should be examined by indirect
laryngoscopy, at least. It is not possible to judge voice range, quality, or
other 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 be
established, however. Erythema and edema of the laryngeal surface of the
epiglottis is seen often in association with muscle tension dysphonia and
with frequent coughing or clearing of the throat. It is caused by direct
trauma 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. Stroboscopic
examination adds substantially to diagnostic abilities (Fig. 1). Another oc-
casionally helpful adjunct is the operating microscope. Magnification allows
visualization of small mucosal disruptions and hemorrhages that may be sig-
nificant but overlooked otherwise. This technique also allows photography
of the larynx with a microscope camera. Magnification may also be achieved
through magnifying laryngeal mirrors or by wearing loupes. Loupes usually
provide 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 authors
usually use a 70 laryngeal telescope, although 90 telescopes are required
for some patients. The combination of a telescope and stroboscope provides
optimal 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 the
larynx during normal phonatory gestures.
Flexible fiberoptic laryngoscopy can be performed as an office procedure
and allows inspection of the vocal folds in patients whose vocal folds are dif-
ficult to visualize indirectly. In addition, it permits observation of the vocal
mechanism 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 information
about speaking and singing techniques. The combination of a fiberoptic laryn-
goscope with a laryngeal stroboscope may be especially useful. This system
permits magnification, photography, and detailed inspection of vocal fold
motion. Sophisticated systems that permit flexible or rigid fiberoptic strobo-
videolaryngoscopy are currently available commercially. They are invaluable
assets 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 fiberoptic
laryngoscopy, accomplished by placing a laryngoscope through each nostril,
fastening the two together in the pharynx, and observing the larynx through
the eyepieces [15]. This method allows visualization of laryngeal motion in
three dimensions. It is used primarily in a research setting, however.
Rigid endoscopy under general anesthesia may be reserved for the rare
patient whose vocal folds cannot be assessed adequately by other means
or for patients who need surgical procedures to remove or biopsy laryngeal
lesions. In many cases this may be done with local anesthesia, avoiding the
need 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 larynx
and trachea. Topical anesthetics may act as severe mucosal irritants in
a small number of patients, however. They may also predispose the patient
to aspiration in the postoperative period. If a patient has had difficulty with
a topical anesthetic administered in the office it should not be used in the
operating room. When used in general anesthesia cases, topical anesthetics
should usually be applied at the end of the procedure. If inflammation oc-
curs, it will not interfere with performance of microsurgery. Postoperative
duration 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 is
an essential part of a comprehensive physical examination [2]. It is as valuable
to the laryngologist as audiometry is to the otologist [16,17]. Familiarity with
some of the measures and technological advances currently available is help-
ful. This information is covered in greater detail elsewhere [5].
958 SATALOFF et al
Strobovideolaryngoscopy
Integrity of the vibratory margin of the vocal fold is essential for the com-
plex motion required to produce good vocal quality. Under continuous
light, the vocal folds vibrate approximately 256 times per second while pho-
nating at middle C. Naturally, the human eye cannot discern the necessary
details during such rapid motion. The vibratory margin may be assessed
through high-speed photography, strobovideolaryngoscopy, high-speed
video, videokymography, electroglottography (EGG), or photoglottogra-
phy. Strobovideolaryngoscopy provides the necessary clinical information
in a practical fashion. Stroboscopic light allows routine slow-motion evalu-
ation of the mucosal cover layer of the leading edge of the vocal fold. This
state-of-the-art physical examination permits detection of vibratory asym-
metries, structural abnormalities, small masses, submucosal scars, and other
conditions that are invisible under ordinary light [18,19]. Documentation of
the procedure by coupling stroboscopic light with the video camera allows
later reevaluation by the laryngologist or other health care providers.
Stroboscopy does not provide a true slow-motion image, as obtained
through high-speed photography. The stroboscope actually illuminates dif-
ferent points on consecutive vocal fold waves, each of which is retained on
the retina for 0.2 seconds. The stroboscopically lighted portions of the suc-
cessive waves are fused visually; thus the examiner is actually evaluating
simulated cycles of phonation. The slow-motion effect is created by having
the 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 rather
than move in slow motion. In most instances, this approximation of slow
motion 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 symmetry
of movements, periodicity, glottic closure, the amplitude of vibration, the
mucosal 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 normal
variations in vibration, however. Vibrations depend on fundamental fre-
quency, intensity, and vocal register. For example, failure of glottic closure
occurs normally in falsetto phonation. Consequently, it is important to note
these 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-speed
photography, 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 true

slow 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 vocal
fold. 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 of
the presence or absence of glottal vibrations and easy determination of the
fundamental period of vibration and is reproducible. It reflects the glottal
condition 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 available
to the laryngologist, helpful in treatment of professional vocalists who have
specific voice disorders, and are useful in assessing the results of surgical
therapies. Maximum phonation time is measured with a stopwatch. The pa-
tient is instructed to sustain the vowel /a/ for as long as possible after deep
inspiration, vocalizing at a comfortable frequency and intensity. The fre-
quency and intensity may be determined and controlled by an inexpensive
frequency analyzer and sound level meter. The test is repeated three times
and the greatest value is recorded. Normal values have been determined
[13]. Frequency range of phonation is recorded in semitones and documents
the vocal range from the lowest note in the modal register (excluding vocal
fry) to the highest falsetto note. This range is the physiologic frequency
range of phonation and disregards quality. The musical frequency range
of phonation measures lowest to highest notes of musically acceptable qual-
ity. Tests for maximum phonation time, frequency ranges, and many of the
other parameters discussed later (including spectrographic analysis) may be
preserved 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 of
registers is controversial, however, and many other classifications are used.
Although the classification listed above is common among musicians, at
present 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 low
pitch, an abnormality associated with chronic voice abuse and development
of vocal nodules. This parameter may be followed objectively throughout
a course of voice therapy. Intensity range of phonation (IRP) has proved
a 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 at
a single fundamental frequency, IRP averages 54.8 dB for males and 51 dB
for females [24]. Alterations of intensity are common in voice disorders, al-
though IRP is not the most sensitive test to detect them. Information from
these 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 to
subglottal power) provides useful information but is not clinically practical
because measuring acoustic power at the level of the glottis is difficult. Sub-
glottic power is the product of subglottal pressure and airflow rate. These
can be determined clinically. Various alternative measures of glottic effi-
ciency have been proposed, including the ratio of radiated acoustic power
to subglottal power [25], airflow intensity profile [26], and ratio of the
root mean square value of the AC component to the mean volume velocity
(DC component) [27]. Although glottal efficiency is of great interest, none of
these 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 lungs
during inspiration and leaves during expiration in normal breathing; (2)
functional residual capacity, the volume of air remaining in the lungs at
the end of inspiration during normal breathing, which can be divided into
expiratory reserve volume (maximal additional volume that can be exhaled)
and residual volume (the volume of air remaining in the lungs at the end of
maximal exhalation); (3) inspiratory capacity, the maximal volume of air
that can be inhaled starting at the functional residual capacity; (4) total
lung capacity, the volume of air in the lungs following maximal inspiration;
(5) vital capacity, the maximal volume of air that can be exhaled from the
lungs following maximal inspiration; (6) forced vital capacity, the rate of
air flow with rapid, forceful expiration from total lung capacity to residual
volume; (7) FEV1, the forced expiratory volume in 1 second; (8) FEV3, the
forced expiratory volume in 3 seconds; (9) maximal mid-expiratory flow, the
mean 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 by
voice abuse, abnormal pulmonary function tests may confirm deficiencies in
aerobic conditioning or reveal previously unrecognized asthma [28]. Flow
glottography with computer inverse filtering is also a practical and valuable
diagnostic tool for assessing flow at the vocal fold level, evaluating the voice
source, and imaging the results of the balance between adductory forces and
subglottal pressure [17,29]. It also has therapeutic value as a biofeedback tool.
The spirometer, readily available for pulmonary function testing, can also
be used for measuring airflow during phonation.
Air volume is measured by the use of a mask fitted tightly over the face or
by phonating into a mouthpiece while wearing a nose clamp. Measurements
may be made using a spirometer, pneumotachograph, or hot-wire anemom-
eter. The normal values for mean flow rate under habitual phonation, with
changes in intensity or register, and under various pathologic circumstances,
were determined in the 1970s [13]. Normal values are available for adults
and children. Mean flow rate also can be measured and is a clinically useful
parameter to follow during treatment of vocal nodules, recurrent laryngeal
nerve paralysis, spasmodic dysphonia, and other conditions.
Glottal resistance cannot be measured directly, but it may be calculated
from 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 various
healthy 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 correlate
closely with maximum flow rate [30] and is a more convenient measure. Nor-
mative data determined by various authors have been published [13]. The
phonation quotient provides an objective measure of the effects of treatment
and is particularly useful in cases of recurrent laryngeal nerve paralysis and
mass 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. The
DSP Sona-Graph Sound Analyzer Model 5500 (Kay Elemetrics, Lincoln
Park, New Jersey) is an integrated voice analysis system. It is equipped
for 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. Using
the band pass filters, generalizations about quality, pitch, and loudness
can be made. These observations are used in formulating the voice therapy
treatment plan. Formant structure and strength can be determined using the
narrow-band filters, of which various configurations are possible. In clinical
settings in which singers and other professional voice users are evaluated
and treated routinely, this feature is extremely valuable. A sophisticated
voice analysis program (an optional program) may be combined with the
Sona-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 electroglottograph
may be used in conjunction with the Sona-Graph to provide some of these
voicing parameters. Examining the EGG waveform alone is possible with
this 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 in
screening for hoarse or breathy voices. In addition, computer interface ca-
pabilities (also an optional program) have solved many data storage and
file maintenance problems.
In analyzing acoustic signals, the microphone may be placed at the level
of 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 being
developed to improve the usefulness of acoustic analysis. Because of the
enormous amount of information carried in the acoustic signal, further re-
finements in objective acoustic analysis should prove particularly valuable to
the clinician.
Laryngeal electromyography
Electromyography (EMG) requires an electrode system, an amplifier, an
oscilloscope, a loudspeaker, and a recording system [32]. Needle electrodes
are placed transcutaneously into laryngeal muscles. EMG can be extremely
valuable in confirming cases of vocal fold paresis, in differentiating paralysis
from arytenoid dislocation, distinguishing recurrent laryngeal nerve paralysis
from combined recurrent and superior nerve paralysis, diagnosing other more
subtle neurolaryngologic pathology, and documenting functional voice disor-
ders and malingering. 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, even
definitions of basic terms, such as hoarseness and breathiness, are still con-
troversial. Psychoacoustic evaluation protocols and interpretations are not
standardized. Consequently, although subjective psychoacoustic analysis
of 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 GRBAS

scale using a continual line, with one end being most normal and the other
most abnormal, has been shown to produce reliable ratings that show good
intrarater and interrater reliability [33]. Grade 0 is normal, 1 is slightly ab-
normal, 2 is moderately abnormal, and 3 is extremely abnormal [13]. Grade
refers to the overall degree of voice abnormality. Roughness refers to what
many describe as raspiness, the auditory impression of an irregularly peri-
odic voice signal. Breathiness refers to the auditory perception of air leakage
or escape mixed into the voice signal. Asthenia is the perception of vocal
weakness 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 individual
in his or her normal activities of daily living has always been challenging.
Recent advances have begun to address this problem, however. Validated
instruments, such as the Voice Handicap Index (VHI) and the Voice Related
Quality of Life (VRQOL) [34] are currently in clinical use, and are likely to
be used widely in future years [35]. Current trends and future directions in
measuring 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 addressed
comprehensively even in the most recent editions (2001, 5th edition) of the
American Medical Association’s Guidelines for the Evaluation of Impairment
and Disability (The Guides). The Guides still do not take into account the
person’s profession when calculating disability. Alternative approaches
have been proposed, and advances in this complex arena are anticipated
over 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 sick
singer to perform, a brief observation of the patient’s singing may provide
invaluable information. This observation is accomplished best by asking
the singer to stand and sing scales either in the examining room or in
a 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 virtually
all other voice patients. The singer’s stance should be balanced, with the
weight slightly forward. The knees should be bent slightly and the shoulders,
torso, and neck should be relaxed. The singer should inhale through the
nose whenever possible allowing filtration, warming, and humidification
of inspired air. In general, the chest should be expanded, but most of the ac-
tive breathing is abdominal. The chest should not rise substantially with
each inspiration, and the supraclavicular musculature should not be in-
volved obviously in inspiration. Shoulders and neck muscles should not
be tensed even with deep inspiration. Abdominal musculature should be
contracted shortly before the initiation of the tone. This contraction may
be evaluated visually or by palpation (Fig. 2). Muscles of the neck and
face should be relaxed. Economy is a basic principle of all art forms. Wasted
energy and motion and muscle tension are incorrect and usually deleterious.
The singer should be instructed to sing a scale (a five-note scale is usually
sufficient) 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 position
with 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 as
the singer performs the scales, improper voice use can be confirmed by positive
evidence (Fig. 3). The position of the larynx should not vary substantially with
pitch changes. Rising of the larynx with ascending pitch is evidence of techni-
cal dysfunction. This examination also gives the physician an opportunity to
observe any dramatic differences between the qualities and ranges of the pa-
tient’s speaking voice and the singing voice. A physical examination summary
form 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 information
from 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 skills
that allow him or her to compensate safely. On the other hand, if a singer
does not sing with correct technique and does not have the discipline to
modify volume, technique, and repertoire as necessary, the risk for vocal in-
jury may be increased substantially even by mild inflammation of the vocal
folds. In borderline circumstances, observation of the singer’s technique
may greatly help the physician in making a judgment.
If the singer’s technique seems flawless, the physician may feel somewhat
more secure in allowing the singer to proceed with performance commit-
ments. More commonly, even good singers demonstrate technical errors
when experiencing voice difficulties. In a vain effort to compensate for
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.)
dysfunction at the vocal fold level, singers often modify their technique in
the neck and supraglottic vocal tract. In the good singer, this usually means
going 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 of
making the voice more secure, this technical maladjustment undermines vo-
cal efficiency and increases vocal strain. The physician may ask the singer to
hold the top note of a five-note scale; while the note is being held, the singer
may simply be told, ‘‘Relax your tongue.’’ At the same time the physician
points to the singer’s abdominal musculature. Most good singers immedi-
ately correct to good technique. If they do, and if upcoming performances
are particularly important, the singer may be able to perform with a re-
minder that meticulous technique is essential. The singer should be advised
to ‘‘sing by feel rather than by ear,’’ to consult his or her voice teacher, and
to conserve the voice except when it is absolutely necessary to use it. If
a singer is unable to correct from bad technique to good technique
966 SATALOFF et al
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.)
promptly, especially if he or she uses excessive muscle tension in the neck

and ineffective abdominal support, it is generally safer not to perform
with even a mild vocal fold abnormality. With increased experience and
training, 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, applying
them to other patients is relatively easy if the laryngologist takes the time
to 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 voice
is advisable in most cases and essential before any surgical intervention. The
author routinely uses strobovideolaryngoscopy for diagnosis and documenta-
tion in virtually all cases along with many of the objective measures discussed.
Pretreatment testing is extremely helpful clinically and medicolegally.
Additional examinations
A general physical examination should be performed whenever the
patient’s systemic health is questionable. Debilitating conditions, such as
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 of
movement disorders and of serious neurologic disease. Dysarthria is a defect
in rhythm, enunciation, and articulation that usually results from neuro-
muscular impairment or weakness, such as may occur after a stroke. It
may 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 motor
neuron or primary muscle disorders, such as myasthenia gravis and tumors
or strokes involving the brainstem nuclei. Spastic dysarthria occurs in upper
motor neuron disorders (pseudobulbar palsy), such as multiple strokes and
cerebral 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 Gilles
de la Tourette disease, or dystonic, as in chorea and cerebral palsy. Mixed
dysarthria occurs in amyotrophic lateral sclerosis (Lou Gehrig disease).
The preceding classification actually combines dysphonic and dysarthric
characteristics but is useful clinically. The value of a comprehensive neuro-
laryngologic evaluation [40] cannot be overstated. More specific details of
voice changes associated with neurologic dysfunction and their localizing
value are available elsewhere [41–43].
It is extremely valuable for the laryngologist to assemble an arts-medicine
team that includes not only a speech-language pathologist, singing voice
specialist, acting voice specialist, and voice scientist, but also medical
colleagues 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 disorders
is 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 and
productive growth of voice as a subspecialty.
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Neurolaryngologic Evaluation
of the Performer
Adam D. Rubin, MDa,b,*
a
Lakeshore Professional Voice Center, Lakeshore Ear, Nose and Throat Center,
21000 E. Twelve Mile Road, Suite 111, Saint Clair Shores, MI 48081, USA
b
Department 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 neural
network is responsible for ensuring that the larynx performs its main
functions: providing and protecting the airway, producing cough and Val-
salva, and producing voice. The complexity is greater considering all of
the other muscles of support and articulation that need to be coordinated
during voice and speech production. Human beings have more voluntary
control over the laryngeal and articulating muscles than other animal
species. Although more primitive visceromotor pathways are involved,
particularly with more cathartic vocal functions, human voice production
is marked by greater cortical control [1]. As with other voluntary motor
systems, 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
Upper motor neurons relay signals from the cortex to lower motor neurons
in 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 movement
is 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: rubinad@sbcglobal.net
972 RUBIN
production, however, with the left primary motor cortex playing a more dom-
inant role [3,4]. The right motor cortex likely plays an important role in the
prosody, or melody, of speech [5].
The cell bodies of the laryngeal nerves lie within the nucleus ambiguus in
the medulla. In addition to upper motor neuron input, these lower motor
neurons receive input from other brainstem nuclei, including the nucleus
tractus solitarius and nucleus parabrachialis. This complex network of inter-
connections integrates afferent input and modifies reflexes. Other synapses
occur from neurons in the periaqueductal gray matter, the final pathway
of the visceromotor system, and are likely involved in the cathartic functions
of voice, such as during crying or screaming [1,4]. The lower motor neuron is
the final common pathway to the target muscle [1].
Extrapyramidal system
Upper and lower motor neurons are part of the pyramidal system and
control voluntary movement. The basal ganglia and cerebellum are part
of the extrapyramidal system. The extrapyramidal system is important in
controlling gross motor function. It inhibits erratic movements and helps
maintain muscle tone. The basal ganglia inhibit the rapid firing of motor
neurons (the ‘‘release phenomenon’’). They receive input from most cortical
areas and send output to areas of the frontal cortex involved with planning
movement. The cerebellum improves accuracy of movement by comparing
central motor commands with sensory input from the periphery [2]. It is
likely involved in vocal self-monitoring and fine-tune adjustments in pitch
and airflow [1]. Neurodegenerative processes involving the extrapyramidal
system 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 of
the target muscle. This synapse is called the neuromuscular junction. The
neurotransmitter acetylcholine is released from the nerve terminal and
triggers 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 branches
from the vagus within the superior mediastinum and loops around the aortic
arch on the left and subclavian artery on the right. It travels back superiorly
within or just lateral to the tracheoesophageal groove until it enters the
larynx posterior to the cricothyroid joint. The SLN branches off the vagus
nerve just inferior to the nodose ganglion. The nodose ganglion contains
the sensory cell bodies of the SLN. The SLN travels inferiorly along the
side of the pharynx, medial to the carotid artery, and splits into two
branches at about the level of the hyoid bone. The internal division of the
NEUROLARYNGOLOGIC EVALUATION OF THE PERFORMER 973
SLN penetrates the thyrohyoid membrane with the superior laryngeal artery
and supplies sensory innervation to the larynx. The external division of the
SLN 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 receives
contributions from both RLNs [6]. The TA and LCA muscles are vocal fold
adductors. Unilateral denervation of these muscles results in an inability to
close the glottis, with resulting breathy voice and possible aspiration [7].
The PCA is the main vocal fold abductor. Paralysis of this muscle results
in an inability to abduct during inspiration. When both PCA muscles are
denervated, airway obstruction may occur. Denervation of the PCA may
cause the arytenoid cartilage to subluxate anteromedially in unilateral vocal
fold paralysis. The denervated PCA no longer counters the anterior pull on
the 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 branches
into an internal and external division. The internal division of the SLN
penetrates the thyrohyoid membrane with the superior laryngeal artery
and supplies sensory innervation to the larynx. The external division of
the SLN provides motor innervation to the cricothyroid (CT) muscle. Un-
opposed CT muscle contraction lengthens the vocal fold, increasing tension
and thus the fundamental frequency of the voice [7].
Although the intrinsic laryngeal muscles are classically described as
abductors and adductors, their functions are more complex. Antagonistic
muscles contract simultaneously during normal vocal function. For example,
unopposed TA contraction results in shortening of the vocal fold. It acts
synergistically with the CT muscle to affect vocal fold tension [8]. CT muscle
function may also depend on the position of the vocal fold at the time of
contraction. It may be active with some voice production regardless of pitch
variation. Different patterns of intrinsic muscle activation are seen depending
on the purpose of motion. For example, different muscles may be activated or
deactivated during adduction or abduction depending on whether the motion
occurs during cough, respiration, or voice production. The CT muscle is active
during abduction with sniff, but not respiration [1,8].
Manifestations of neurologic disease

Neurologic disorders may affect voice and speech production in several
ways. Central injury may affect initiation, coordination, and quality of voice
and speech. Direct effects on the larynx can affect glottic closure patterns
and efficiency along with laryngeal muscle tone. Denervation of muscles
involved in the support mechanism of the voice, such as the diaphragm or
chest wall musculature, affects voice strength and quality. Dysfunction of
974 RUBIN
oropharyngeal musculature may affect resonance. A palatal paralysis results

in a more hypernasal voice. Impairment of cranial nerve V, VII, or XII func-
tion can affect articulation. Findings on general neurologic and laryngeal
examination depend on which nerves are involved and where the disorder
affects the neuromuscular pathway (Table 1).
Motor neuron diseases

Motor neuron diseases may result from degeneration of upper motor
neurons, lower motor neurons, or both. When both upper and lower motor
neurons are involved, the diagnosis of amyotrophic lateral sclerosis (ALS)
or Lou Gherig’s Disease is made [9]. ALS is fatal, usually from respiratory
failure, but the clinical course is variable. Other examples of upper motor
neuron disease processes include progressive lateral sclerosis and pseudobul-
bar palsy. Primary lateral sclerosis typically involves destruction of upper
motor neurons only. The diagnosis is typically made after 4 years of
predominantly upper motor neuron involvement [10]. Pseudobulbar palsy
results from interruption of bilateral corticospinal tract axons from other
disease processes, such as stroke, multiple sclerosis, or tumor, as opposed
to 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, and
spinal muscle atrophy. Progressive bulbar palsy is essentially ALS affecting
only the cranial nerves. Progressive spinal atrophy includes several autoso-
mal-recessive disorders that involve degeneration of the anterior horn cells
of the spinal cord. Although some forms present in adulthood, many present
in 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, Spastic vocal fold paralysis/
rigidity, positive Babinski paresis, spastic dysarthria,
sign, myoclonus laryngeal myoclonus
Lower motor neuron Weakness, flaccidity, Flaccid vocal fold paralysis/
fasciculations paresis, glottic insufficiency,
hypernasal speech, flaccid
dysarthria
Extrapyramidal Tremor (pill-rolling in Vocal fold bowing, mid-fold
Parkinson’s disease), insufficiency, tremor,
dystonia, dyskinesia, laryngeal dystonia,
dysdiadochokinesia dysdiadochokinesia
Peripheral nerve Weakness, atrophy, sensory Hypomobility, immobility,
deficits ?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 voice
that might be misconstrued as spasmodic dysphonia. Patients may suffer
from intermittent laryngospasm. Spasticity of oral musculature results in
strained, effortful dysarthria. Myoclonus may occur. Extremity involvement
may be noted. A positive Babinski reflex is a classic finding of upper motor
neuron disease [9,11].
Lower motor neuron processes result in flaccid paralysis, muscle atrophy,
and fasciculations. Patients may develop weak, breathy voices, bowing of
the vocal folds, and poor cough. Palatal involvement may lead to nasal
regurgitation and hypernasal speech. Pharyngeal musculature involvement
leads to oropharyngeal dysphagia. Tongue and facial muscle involvement
leads to slurred speech and oral dysphagia. With poor oral motor function,
pharyngeal squeeze, and glottic incompetence, these patients are often at
significant 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 may
result from ischemia (secondary to thrombosis or hypotension) or hemor-
rhage. Unilateral cortical strokes are unlikely to result in complete vocal
fold paralysis because of bilateral cerebral innervation of the laryngeal
nerves. Brainstem stroke may cause vocal fold paralysis if disruption of
the nucleus ambiguus or corticobulbar fibers synapsing with the nucleus
ambiguus occurs. Isolated vocal fold paralysis secondary to stroke is rare.
Wallenberg syndrome or lateral medullary syndrome results from occlusion
of the posterior inferior cerebellar artery. It may result in some combination
of 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]. Stroke
patients often are debilitated, which also contributes to poor voice quality.
Abnormal body positioning and strength contribute to vocal problems. In
addition, these patients often have significant dysphagia and are at high
risk 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 movement
disorder resulting from degeneration of dopamine-secreting cells within the
substantia nigra of the brainstem. This process results in loss of the neural
pathways through the basal ganglia that are involved in control of move-
ment. Classic findings include tremor, rigidity, bradykinesia, and postural
instability.
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 and
speech manifestations. Patients who have Parkinson’s disease often have
soft, 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 dysarthria
and dysphagia. Characteristic laryngeal signs include vocal fold bowing,
glottic insufficiency, and slow vibration. The glottic insufficiency and poor
breath support attributable to debilitation and chest wall rigidity result in
a 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, and multisystem
atrophy. These disease processes are usually more rapidly progressing and less
responsive to medication. In addition, patients who have multisystem atrophy
are 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 other
dystonias, 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 mixed
dysphonias 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 have
AbSD have spasms of the PCA muscle with voiceless consonants, resulting
in 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 of
laryngeal muscle action [5,21]. Laryngeal tremor may be present in addition
to the dystonia. The combination of tremor and dystonia is referred to as
dystonic tremor. These entities can be difficult to distinguish at times [22].
Spasmodic dysphonia might also be difficult to distinguish from muscle
tension dysphonia or other functional dysphonias.
Laryngeal tremor
Vocal tremor presents as nearly regular oscillations of the laryngeal and
pharyngeal musculature.
(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 as

a 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. Tremor
may also be seen with and is often difficult to distinguish from spasmodic
dysphonia [22]. When laryngeal tremor is present, a thorough neurologic
evaluation 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 usually
a manifestation of essential tremor, one of the most common causes of voice
tremor. It may be the only manifestation, but typically the extremities are
involved also. The voice is affected in approximately 20% of cases of essential
tremor [24]. In addition to the intrinsic laryngeal muscles, the extrinsic laryn-
geal muscles, pharyngeal muscles, and muscles of respiration may be involved.
The pathophysiology of tremor is incompletely understood. Electromyograph
studies have demonstrated that various laryngeal muscles may oscillate at dif-
ferent frequencies, suggesting multiple foci of central stimulus, or peripheral
contribution to the oscillatory pattern by a reflex arc. In addition, there may
be 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 is
bilateral, although it may occur unilaterally. Palatopharyngeal myoclonus
may produce slow, regular voice arrests that may be missed in running
speech. It may also be triggered by speech and result in more rapid, dramatic
voice arrests [26]. Myoclonus is believed most commonly to arise from
dysfunction 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 muscle
weakness exacerbated by repetitive use and improved with rest. Antibodies
are 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
978 RUBIN
to move more briskly and then appears more sluggish in comparison with
the contralateral side) [5,11,28]. Patients may also suffer from dysphagia
and dysarthria.
Peripheral nerve
Peripheral nerve injury, specifically to the vagus nerve or the recurrent or
superior laryngeal nerve branches, typically presents with absent or sluggish
vocal fold movement. Proximal vagal injuries may also present with palatal
and pharyngeal paralysis. Clinically, unilateral RLN paralysis typically
presents 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 modal
phonation to increase tension in the vocal fold [31]. The inability to increase
vocal tension results in poor vocal performance, especially at higher pitches
[29,30]. The clinical manifestations specific to SLN paralysis are likely more
troublesome for singers and professional speakers [5,7]. Moreover, the
internal division of the SLN carries afferent fibers from the larynx to the
central nervous system. This afferent input likely plays a role in vocal
control and modulation [8].
More subtle paresis of the SLN or RLN may cause numerous voice
complaints, including vocal fatigue, hoarseness, impairment of volume,
loss of upper range, loss of projection, and breathiness. Vocal fatigue may
be caused by the additional effort required to raise vocal pitch and project,
and by hyperfunctional compensatory gestures. Patients who have either
RLN or SLN paresis often develop a compensatory, hyperfunctional
MTD to generate a ‘‘stronger’’ voice [32].
Other symptoms may occur with injury to the vagus or the laryngeal
nerve branches. Hypoesthesia of the supraglottic larynx suggests injury to
the 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 or
contribute to chronic cough, globus, or laryngeal pain syndromes [35,36].
Dysphagia often occurs with vocal fold paralysis and paresis. Patients
may aspirate, particularly if there is significant pharyngeal involvement. In-
jury to the SLN may result in dysphagia by several mechanisms. Injury to
the internal division results in loss of afferent input to the swallowing center
in the brainstem. In addition, recent evidence has suggested that the external
division 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 the
severity of injury. A vocal fold paralysis results in absent motion on the
affected side. Vocal fold paresis may be more subtle. Vocal fold lag, or
sluggishness, is the most common sign. This lag may only become apparent
with repetitive tasks that cause the patient to fatigue. Asymmetry in motion
should raise suspicion of a paresis, but does not always indicate which
nerves in particular are involved [38–40]. Supraglottic hyperfunction is often
present in patients who have paresis and may make the examination more
difficult to interpret. Efforts to try to relax or ‘‘unload’’ the hyperfunction
may help in determining which muscles are affected. Asymmetry may be
present in patients who have muscle tension dysphonia without paresis.
Vocal fold tone is variable after injury to the recurrent laryngeal nerve
and depends on the degree of reinnervation. Reinnervation prevents muscle
atrophy. Spontaneous reinnervation may occur after nerve transection. The
source of the reinnervation is not known, but may include regenerating
fibers from the transected RLN, the SLN, cervical autonomic nerves, and
nerve branches innervating pharyngeal constrictors [41].
Should reinnervation occur after nerve transection, it is usually not
detectable for about 4 months [41,42]. The clinical course after 4 months
is determined by the degree of reinnervation and synkinesis. Although
reinnervation after a complete RLN transection prevents muscle wasting,
typically it does not restore useful movement to the vocal fold because of
synkinesis. Synkinesis results from nonselective reinnervation of adductor
and abductor muscles. As a result, muscles that perform opposing functions
contract simultaneously, resulting in immobility or hypomobility of the
vocal fold. The clinical picture depends on the proportion of adductor
and abductor fibers reinnervated and the ability of the contralateral vocal
fold to compensate by crossing the midline of the glottis [6,7].
Myopathy
Myopathies may be inherited or result from metabolic or inflammatory
processes [43]. Isolated laryngeal myopathy is rarely reported, although
chronic steroid inhaler use has been insinuated as a cause [44]. Laryngeal
findings include loss of muscle tone and hypomobility. These findings are
similar to those that may be seen with motor neuropathy. Some have sug-
gested that myopathy is underdiagnosed as a laryngeal disorder, because
we tend to think more about nerve injuries when we see weak, flaccid vocal
folds [44].
Neurolaryngologic evaluation
A thorough neurologic evaluation should be routine for any patient
presenting with voice complaints. A thorough history should be performed,
including presenting symptoms, rapidity of onset, progressive nature, and
inciting or precipitating factors, such as a URI or neck surgery. Specifics
about the patient’s voice complaints should be elicited. For example, does
the patient complain of raspiness, breathiness, loss of range, vocal
980 RUBIN
instability, air hunger, or fatigability? Given the close interrelationship of

voice, swallowing, and airway function, questions should address these is-
sues also. Laryngospasm, although often caused by reflux, may also occur
with neurologic disease [45]. Patients should be asked about dysphagia,
choking, cough, and airway obstruction. A complete neurologic review of
systems and family history should be obtained.
The general appearance of the patient can give clues as to underlying
neurologic disease. Abnormal posturing, muscle tone, gait, and extremity
or head tremor should be noted. Listening to voice and speech patterns is
critical. 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. Attention
should 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, whereas
abductory SD presents as breathy breaks during voiceless consonants of
the 60 to 69 tasks. Mixed SD has intermittent spasms during both, whereas
functional disorders are usually pressed through the entirety of each of the
vocal 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 caricature
voicing 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 musculature
may 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’s
disease [5,8,16,17].
Oral motor function should be assessed closely. The tongue should be
inspected for atrophy, strength, ‘‘bag of worm’’ fasciculations, and symme-
try in motion. Symmetry in palatal elevation and gag reflex should be
tested. Unilateral palatal paralysis suggests a high vagal lesion, whereas
asymmetry in gag may suggest a glossopharyngeal nerve paresis. Palatal
myoclonus may be observed. Systemic neurologic examination should be
performed when there is suspicion of a more diffuse neurodegenerative
process.
Endoscopic visualization of the larynx is a critical part of the evaluation

of any patient who has a voice complaint. A dynamic voice assessment is
best performed with a flexible rhinolaryngoscope to allow the patient to
be in as physiologic positioning as possible to evaluate the movements of
the larynx and vocal tract during unaltered vocal posturing. Rigid videostro-
boscopy is essential to look for vibratory abnormalities and to assess
discrepancies in vocal process height. Protrusion of the tongue during rigid
videostroboscopy creates a nonphysiologic position for vocalization and
therefore is less useful at assessing for fine movement abnormalities of the
larynx than is the flexible rhinolaryngoscope.
The patient should be asked to perform various vocal tasks (Table 2) to
observe 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/ are
particularly helpful in unmasking mild PCA paresis. Repeated rapid pho-
nation on /i/ with a complete stop between each phonation during the
task /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 is
analogous 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
982 RUBIN
(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 help
distinguish lag resulting from a true paresis from asymmetry created from
supraglottic muscle tension. The open laryngeal posture during whistling
provides particularly good visibility of rapid vocal fold motions for easier
assessment of asymmetries in vocal fold mobility [7].
A glissando maneuver, asking the patient to slide slowly from his or her
lowest to highest note and then slide back down is invaluable for assessing
SLN function. If a superior laryngeal nerve is injured, longitudinal tension
does not increase as effectively on the abnormal side, disparities in vocal fold
length 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 finding
of rotation of the posterior larynx to the side of SLN injury is likely to occur
only 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 the
work environment. Singers should be asked to demonstrate their vocal
range, whereas professional speakers or teachers should give a sample of
their day-to-day vocal demands. This gives more insight to the patient’s
capability of performing in the workplace and reveals how much he or
she is compensating to meet these vocal demands.
Other studies
Laryngeal electromyography
Laryngeal electromyography (LEMG) evaluates the integrity of the
nerves and muscles of the larynx. Although its usefulness remains unproven
by evidence-based data, it remains the most objective means of evaluating
neuromuscular function of the larynx. In addition to identifying RLN or
SLN paresis, it is useful for evaluating lower and upper motor neuron
disorders, neuromuscular junction disorders, prognosis for recovery of vocal
fold paralysis, differentiation of paralysis and arytenoid fixation, differenti-
ation of malingering and psychogenic dysphonia, basal ganglia disorders,
laryngeal dystonias and tremors, and myopathic disorders. Edrophonium
chloride may be administered to test for myasthenia. Repetitive nerve
stimulation and single-fiber EMG may also be useful [7,18]. For many of
the 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 Botox
in the treatment of spasmodic dysphonia [43,48–54]. Diagnostic LEMG may
be useful in helping to confirm the presence of dystonia and in identifying
which muscles are most involved [39]. Some have suggested its usefulness
for identifying muscles most affected by laryngeal tremor to target Botox

therapy [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 if
a paresis is present, however, the examiner might predict the nerve or side
involved incorrectly. A recent study by Rubin and colleagues [38] demon-
strated that 25% of the time a unilateral mild paresis was suspected in
patients who had mobile vocal folds on endoscopic examination, laryngeal
EMG disagreed with the side of paresis predicted. In addition, in some cases
in which the laryngeal examination was believed to be normal, LEMG
demonstrated bilateral paresis. The failure to predict paresis on examination
in these cases was likely because movement was fairly symmetrical because
both sides were affected [38]. Heman-Ackah and Barr found that LEMG
agreed 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 patients
who had vocal fold paresis. They found 40% had both RLN and SLN
involvement, whereas 60% had involvement of either the RLN or SLN.
LEMG can be helpful for management of patients who have movement
abnormalities on examination. Voice therapy routines can be created to
focus on strengthening muscles specifically affected by the paresis. For
example, for isolated SLN injury, exercises such as a glissando in thirds
or fifths can be performed to strengthen the cricothyroid muscles, taking
care 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 unilateral
paresis may benefit from bilateral thyroplasty if a bilateral paresis is noted
on LEMG. Also, one might choose to medialize a patient with injection lar-
yngoplasty at the time of mass excision should the patient have significant
paresis. By revealing an underlying neurologic problem, the LEMG may
bring insight and comfort to a patient who eventually requires a surgical
procedure for glottic insufficiency and to the voice team that has been
unable 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 skull
base through the mediastinum is essential. If the paralysis involves recurrent
and superior laryngeal nerves or if there are other neurologic findings, intra-
cranial studies should be considered as well. Because of the seriousness of
missing intracranial lesions, many physicians obtain MRI with and without
gadolinium 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
984 RUBIN
if motor neuron disease or other central nervous system processes are

suspected.
Serology
Serologic testing may be appropriate in some cases. For example, if
myasthenia 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 patients
who have myasthenia gravis. In these patients, weakness typically affects
neck and respiratory muscles [55]. Myasthenia symptoms may be isolated
to the larynx, but serologic tests are often negative.
Although the usefulness of serologic testing in patients who have vocal
fold paralysis is controversial, certain tests may be useful, particularly
when the history is suggestive. Some serologic tests to consider include:
thyroid function tests, thyroid antibodies, autoimmune labs (eg, anti-nuclear
antibodies, rheumatoid factor, erythrocyte sedimentation rate), tests for
tertiary syphilis and Lyme disease, fasting blood glucose, cholesterol, and
triglycerides.
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 identifying
the presence of laryngeal sensory deficits, evaluating aspiration risk, plan-
ning swallowing therapy, and providing strategies to enable patients to eat
the 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 additional
information concerning sensory deficits that can contribute to dysphagia
and aspiration risk. Air pulses are delivered by way of a port in a flexible
laryngoscope (or sheath over a flexible laryngoscope) to mucosa innervated
by the internal division of the superior laryngeal nerve. Sensory capacity is
measured 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 FEESST
or MBS. In stroke patients managed by FEESST, however, the incidence
of aspiration pneumonia was significantly lower than in those managed by
MBS [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 paresis

to determine if LEMG is warranted in patients who have asymmetric but
mobile vocal folds. More than 90% of patients who had a normal EGG
waveform despite asymmetry in vocal fold motion had a normal LEMG.
A normal EGG waveform thus had a negative predictive value of greater
than 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 whose
livelihood is not so dependent on their voices. As a result, the performer
who has early underlying neurologic disease may present to the laryngolo-
gist before presenting to the neurologist. The laryngologist therefore has
to be aware of the vocal manifestations of neurologic disease. Unfortu-
nately, other manifestations of the disease may become of higher priority
for the patient’s well-being, but vocal problems are still likely to weigh
heavily on the performer’s mind and quality of life.
Performers who have vocal fold paralysis may need urgent intervention
to help them return to work. Early voice therapy is important to avoid
the development of hyperfunctional compensatory habits that could be
difficult to break if nerve function returns. In some cases, voice therapy
can provide enough improvement in the voice that surgery can be avoided.
Injection laryngoplasty is an excellent option when it is unclear if nerve
function will return. Extra care must be taken to avoid superficial injection
into Reinke space, which impedes mucosal wave and delays vocal optimiza-
tion. Laryngeal framework surgery is appropriate after 1 year from time of
injury or if nerve recovery is not expected (eg, after nerve transection).
Expectations should be tempered depending on the vocal demands of
each 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 if
the nerve is not transected). For instance, the soprano who has a thyroid
nodule 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 the
potential risks need to be weighed and presented to the patient so that he
or she can make the best informed decision possible.
Treatment of the performer who has a subtle vocal fold paresis is more com-
plex, particularly if the performer is able to obtain glottic closure. Voice com-
plaints are often multifactorial and nonspecific. It is often difficult to be certain
that 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 vocal
fold of a performer. Performers seldom have baseline examinations (when
986 RUBIN
they are not having problems) for comparison. If one excises a mass before
treating all other potential contributing factors, one risks making the voice
worse. The same is true when approaching a suspected paresis.
History is helpful, but still not always completely enlightening. For
instance, voice change after thyroid or neck surgery without any evidence
of mucosal or vibratory abnormality is likely caused by nerve injury. The
same could be said for symptoms starting after an upper respiratory
infection [32]. Unfortunately, evaluation often reveals other pathology,
such as edema or a mass. Conservative management, particularly in subtle
cases, 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 and
more immediate effects, however, to meet their obligations.
The future
Current treatment options for vocal fold paresis, paralysis, and other
neurologic disorders are suboptimal. We still are unable to restore
movement 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 restoring
useful vocal fold motion after paralysis. Innovative techniques have been
suggested, 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 assessment
of any patient who has voice complaints. Voice changes may be the initial
presentation of neurologic disease. The otolaryngologist must be familiar
with laryngeal neuroanatomy and laryngologic manifestations of neurologic
disorders. Collaboration with a neurologist is essential when systemic or
central neuromuscular disease is suspected. The otolaryngologist can play
an important role in the care of patients who have voice, swallowing, and
airway issues resulting from neurodegenerative disease.
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40 (2007) 991–1001
and 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 in

known manners, not all patients who have the same vocal pathology exhibit
the 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 larynx
and vocal tract. More importantly, the unaided human eye is unable to vi-
sualize the vibratory patterns of the true vocal folds during phonation. This
inadequacy may lead to inappropriate management decisions. Strobovideo-
laryngoscopy and laboratory vocal testing are most valuable to the voice
specialist in this clinical scenario [1,2].
Recognition of the advantages and disadvantages of current diagnostic
techniques allows for optimal appreciation and instrumentation selection
for supplemental diagnostic laryngeal testing. Although it is agreed that
there is no one gold standard algorithm for the diagnostic process of a pa-
tient who has a voice disorder, most practitioners would agree that some
additional laboratory testing is indicated in most patients. This article
discusses current diagnostic techniques available for physiologic vibratory
testing and anatomic and functional assessment of the vocal tract.
True vocal fold vibration is a complicated physiologic function, the ob-
servation of which far outreaches the visual capabilities of the human eye
with a normal light source. The human adducted vocal folds cyclically
E-mail address: gaelyn.garrett@mcmail.vanderbilt.edu (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 be
observed and processed. Stroboscopy capitalizes on the inherent optic prop-
erties of our visual organ and exploits the limitations of observation of the
unaided eye. According to Talbot’s law, the human eye can perceive no
more than five distinct images per second. Each image therefore lingers
on the retina for approximately 0.2 seconds after exposure. Stroboscopic
flashes make the vocal folds appear to slow down by advancing the light
pulse through successive glottal cycles in percentage increments. Individual
still images are recorded at selected points from sequential vibratory cycles
and 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 to
a phenomenon called persistence of vision. Additional instrumentation
added 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 vocal
fold 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 yet
popularized, by Bozzini in 1806 when he constructed an angled speculum
with a mirror insert that was meant to examine various body cavities, includ-
ing the human larynx. It was not until 1854 that indirect laryngoscopy gained
wider acceptance when Manuel Garcia, a Spanish-born voice teacher who had
a limited gag reflex, first visualized his larynx with a small dental mirror using
sunlight as a light source. In 1895, Oertel followed suit and was credited with
creating the first laryngostroboscope. His device consisted of a variable-speed
perforated disc that was interspersed between a light source and the practi-
tioner’s head mirror [5,6]. Since that time, strobovideolaryngoscopy has
evolved into finely controlled, high-intensity light sources with fiberoptic endo-
scopes or distal camera scopes coupled with analog or digital recording
devices.
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 examination
may be performed by transnasal flexible laryngoscopy with distal chip tech-
nology or perorally with a rigid angled telescope. Video cameras are now
available in single-chip and three-chip versions. A single-chip camera uses
a 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 and
higher resolution. Analog or digital recording technologies are then used for
image capture, documentation, and reproduction [3,7].
STROBOVIDEOLARYNGOSCOPY AND LABORATORY EVALUATION 993
The illusion of apparent slow motion of the vibrating vocal folds during
strobovideolaryngoscopy evolves from the collection of several sequential
still images of the folds at selected time intervals during repeated glottal cy-
cles at a given vibratory frequency. This illusion is called the stroboscopic
glottal 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, known
as asynchronization. This feature of stroboscopy is producible through tech-
nological communication between the microphone and the strobe light
source. By synchronizing the stroboscopic flashes to the fundamental fre-
quency of the vibrating vocal folds, a perceptual stopped image or standstill
of the vocal folds is produced. An asynchronized mode is generated by cal-
ibrating the stroboscopic flashes at a consistent frequency slightly different
than the produced phonatory fundamental frequency. This variation allows
successive light impulses to strike at different phases of the vibratory cycle
and 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 operation
of 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 of
the upper and lower lips during an approximation phase of the cycle [2,3,7].
The strobovideolaryngoscopic examination is most clinically useful to the
practitioner when a standard protocol is used for the acquisition of the data
and its interpretation. Phonatory tasks during the examination should be
performed at low, normal, and high pitches and in the range of the speaking
or singing problem area, if known. Once recorded, a standardized approach
to the interpretation of the examination allows consistency in diagnosing
and 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 is
arguably 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 often
addressed include symmetry, periodicity, mucosal wave ratings, amplitude
of vibration, shape and contour of the glottal margin, and glottic closure.
Particular attention is also given to any adynamic segments and the presence
or absence of vertical phase difference [2,6,7]. Vocal fold symmetry remains
intact in the absence of abnormalities along the glottal margin. Periodicity
refers 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 same
with 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 phase
difference, which is created normally by the presence of an upper lip and
lower 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 amplitude
occur 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 be
a valuable tool for the diagnosis of laryngeal pathology given the detailed
physical examination it provides of the vocal tract and the vibratory margin
of 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, which
are frequently unilateral, have asymmetric vibration and variable periodicity
depending on the size and shape of the polyp. Mucosal wave can be absent
because 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 can
have the greatest adverse effect of the nonneoplastic lesions on the vibratory
characteristics. Mucosal wave is frequently absent and aperiodic if present.
A change in diagnosis and altered assessment of vocal pathology based on
the strobovideolaryngoscopic findings can occur in 10% to 30% of cases
[4,8]. Furthermore, abnormal findings have been reported in up to 58% of
healthy, asymptomatic professional singers stressing the importance of
screening examinations for certain populations of patients [9].
Strobovideolaryngoscopy is not a test to be done in the absence of other
clinical data. It is only a valuable complement to a thorough vocal history
and 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 records
an entire vibratory cycle and provides detailed cycle-to-cycle variations.
Even with this limitation, strobovideolaryngoscopy remains an invaluable
tool in the diagnostic armamentarium of the voice specialist.
Glottography
Glottography is a general technique that monitors the vibration of the
vocal folds by the transmission of a probe signal from one side of the larynx
to the other. The probe signal itself can be directed in either a vertical plane
or horizontal plane. Current probing signals most commonly used in glot-
tography include electrical current flow, light transmission, and ultrasonic
waves. The time variation of the glottis combined with laryngeal tissues
that are in constant partial stages of contact during phonation modulates

the probe’s properties. This modulation is then detected and recorded sup-
plying immediate objective data in the form of graphic displays that can be
clinically 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 also
provides a possible objective method that can be used to evaluate and detect
vocal fold pathology. Overall, glottography provides some clinical data
about vocal fold vibration. This technique fails to determine the vibration
capacity of an individual vocal fold or diagnose individual laryngeal lesions
without 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 being
a moderately good conductor of electricity. It is performed by placing two
electrodes above the thyroid laminae on the external neck and measuring
the impedance between them with a high-frequency, low-current signal.
Ohm’s law states that a current must flow through a system if its resistance
is to be measured. Based on this law, when the vocal folds are touching
a greater current flows through them compared with when they are open.
The electroglottographic signal represents the contact area between the
two vocal folds and can be used to determine when the vocal folds are closed
and how fast they are closing [10–13]. This characteristic contrasts with pho-
toglottography (PGG), which gives information about the separation of the
vocal 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 past
two decades have commented on the shape of the EGG waveform as it relates
to the underlying physiology of vocal fold vibration. Interpretation of EGG
waveforms remains controversial, however, especially as it relates to analyzing
vocal 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 to
be an effective tool for verifying information from the EGG waveform with
stroboscopic images [12,14]. Also, recent research is moving toward standard-
ization of normal EGG measurements with the goal of allowing this test to
serve as a reference for the diagnosis and follow-up of dysphonic patients [15].
There are limitations of EGG. The most obvious one for the voice specialist
is that it cannot be used with all dysphonic subjects. Patients who have a uni-
lateral vocal fold paralysis have a considerably diminished or absent signal
because of lack of good contact of the vocal folds. Obese or thick necks
may impede proper placement of the electrodes or hinder the electrical current
resulting 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 may
act like a shutter through which light can pass in proportion to the degree
of opening of the vocal folds. Light is usually directed transnasally from
above the glottis and is detected by an optoelectronic device over the skin
of the trachea immediately beneath the vocal folds. The external photosen-
sor then converts the light intensity absorbed into electric voltage, which can
be recorded and converted into a graphic display. The direction of the light
path 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 the
external neck with the photosensor in the opposite complementary position.
Typically, for the best functional examination with the additional advantage
of simultaneous laryngeal observation, a transnasal flexible laryngoscope is
used as the light source with the photosensor placed externally on the neck.
PGG gives some clinical data during the open phase of phonation with
two 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 the
validity of the quantitative information obtained from this technique. These
are 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 hypopharynx
and supraglottis during different vowel productions. Overall, the PGG
waveform is considered complementary to the EGG signal [10,11,13].
Ultrasound glottography
Ultrasound glottography (UGG) is a technique in which ultrasonic waves
are constantly applied across the laryngeal area of the neck during phonation.
The border between the vocal fold surface and the glottal air is determined by
the difference in acoustic impedance between two media (air and soft tissue).
Like all ultrasound studies, it is based on the frequency shift produced when
a continuous ultrasonic beam is reflected back from or transmitted through
a tissue medium. In UGG, a narrow-beam ultrasound transducer is placed ex-
ternally on one side of the neck near the larynx with a receiver on the other
side. The ultrasonic signal is aimed at the air tissue interface of the glottis.
Air is an extremely poor ultrasound transmission medium and therefore when

the 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 glottography
then displays an open–closed pattern that corresponds to the open and closed
phases of phonation. Unfortunately, the space resolution of ultrasound glot-
tograms is not very high and therefore few reports are available regarding
voice function. Nonetheless, it remains a noninvasive means of laryngeal
monitoring and combined with newer technological advances may hold
promise for future clinical voice research [10,11,13].
Videokymography
Videokymography is a laboratory technique that was developed as
a 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 and
scanning of the endoscopic image to a rapid repetition of a single line. Each
new scan of the same line is stacked on top of the others from superior to
inferior so that a screen image is built up with time represented in the
vertical direction. The line scan camera therefore records a small area of
the vocal fold in a real-time fashion while it vibrates and allows for subtle
aperiodic irregularities or phase asymmetries to be observed and doc-
umented. A major shortcoming of this technique is that any movement
of either the larynx or endoscope during signal acquisition changes the locus
being observed. Also, the line image produced is not a complete image of the
larynx. Some training is also required for interpretation of the examination
results. Although still regarded as mainly an experimental technique for
laboratory voice testing, new generation digital videokymographic systems
are currently being developed in hopes of becoming an important tool for
routine clinical laryngeal examination [10,16,17].
High-speed photography and digital imaging

High-speed photography and digital imaging are laboratory techniques
that were developed to overcome the limitations of strobovideolaryngoscopy.
As previously discussed, stroboscopy is a technique that produces a virtual
slow-motion image of the larynx from the summation of images obtained
from several glottal cycles. The clinical use of this technique is based on vocal
tract pathology being periodic and stable at a given phonatory frequency.
Dysphonic patients suffering from aperiodic phonatory disorders may not
completely benefit from the examination, therefore. High-speed photography
and digital imaging overcome these limitations by providing real-time images
of successive glottal cycles of the larynx during phonation.
High-speed photography requires several expensive pieces of equipment

that require technical expertise for proper operation. The main piece of
equipment is a camera capable of taking pictures at a rate of 3000 to
4000 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 the
camera 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-speed
photography using a laryngeal mirror has provided valuable information
about vocal function when used in a clinical setting.
High-speed digital imaging has seen recent activity over the last several
years with the development of new camera image sensor systems with in-
creased image resolution combined with improved computer processing
speed and storage capacity. The technique uses standard rigid endoscopes
to record full images of the superior surface of the larynx at sampling rates
from 1000 to 8000 frames per second. The recorded images are typically in
black and white and can be played back in ultraslow motion for clinical
analysis. 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 in
few studies being performed regarding the application of this modality in di-
recting patient care. From a research standpoint, high-speed digital imaging
has been used to identify characteristics of normal and abnormal vocal fold
vibration. Digitization of the images enables accurate quantification of vocal
fold vibrating parameters not possible with strobovideolaryngoscopy. High-
speed digital imaging has also been used to examine the basic physiology of
different 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 for
estimated measurements of glottal parameters, including scarring and other
elastic 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 injection
materials. More widespread clinical use of high-speed digital imaging in the
future is expected as the cost of the instrumentation decreases.
Acoustic voice measurements

Phonatory tasks for normal and dysphonic patients may be obtained for
objective 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 the
voice specialist, including the VisiPitch (Kay Elemetrics Corporation) in-
strument. This equipment is most useful for obtaining fundamental frequency
and vocal intensity and can provide other measures of speech parameters also.
In addition, numerous computer programs, some used in conjunction with
strobovideolaryngoscopy, also exist. Computerized Speech Lab (CSL, Kay
Elemetrics Corporation, Lincoln Park, New Jersey), CSpeech, and Dr. Speech
Science (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-mentioned
parameters and are relatively simple to use. Research suggests that although
these systems are not necessarily comparable in absolute figures, their judg-
ment against normative data is typically similar. Ambulatory monitoring of
the dysphonic patient in the form of miniature accelerometers placed on the
anterior neck has also been reported and may show future promise in the clin-
ical assessment and management of voice disorders [13,20,21].
Speech spectrograms represent a measure of the vibratory characteristics of
the 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 be
taken to use the same vowel while comparing spectrograms of a patient to
eliminate the vocal tract as a variable and therefore allow independent analy-
sis of the vocal folds. The most useful measure from a speech spectrogram is
the harmonics-to-noise ratio (signal-to-noise ratio). It represents a ratio of the
energy 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 is
decreased 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 produce
higher-quality spectrograms at a greater expense [13].
Perturbation measures rely on the inherent ability to determine an accurate
fundamental frequency and are usually measured using sustained vowel frag-
ments. Dysphonic voice samples are often only marginally periodic at best and
are often difficult to obtain. Furthermore, most dysphonias are multifactorial
in nature and often times show variability at different points in a patient’s vo-
cal range. Connected speech may overcome some of these obstacles and there-
fore be a more appropriate stimulus for the dysphonic patient because it is
more representative of functional vocal productions over a broader vocal
range. An inherent difficulty with the analysis of connected speech by typical
perturbation methods as previously mentioned is that these measures are
influenced by intonation and other modulation effects. Long-term average
speech spectrum (eg, spectral tilt) and derivations of the spectrum such as
cepstral peak prominence overcome these difficulties. These measures do
not 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 transformation
of the spectrum of the signal, better correlate with perceptual measures of
overall dysphonia compared with more traditional measures of periodicity
or perturbation [22]. Special software is needed to complete these measures
and 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 is
often difficult to measure. Factors such as the severity of the voice disorder
and the vocal needs of the patient are central to the determination of how
the dysphonia alters his or her physical, social, and emotional well-being.
Two well-known instruments that quantify the psychosocial consequences
of voice disorders are the Voice-Related Quality of Life Measure and the
Voice Handicap Index. Both instruments have been shown to be valid and
reliable as a vocal quality-of-life measure [25,26]. They allow for subjective
perceptual analysis of a given clinical intervention by the voice specialist
and are a low burden in a population of patients who have a diverse group
of voice disorders [27]. One drawback of all outcome instruments for
dysphonia is the large number of questions that need to be answered to receive
a complete score. Recently, the development and validation of the Voice
Handicap Index-10 has been introduced as one instrument that may decrease
this burden [28]. Overall, outcome instruments for vocal quality of life are
important indices of patient functional capacity that enhance the voice
specialist’s ability to successfully treat patients who have voice disorders.
Summary
Laboratory and strobovideolaryngoscopy voice evaluation are important
parts of the clinical work-up of the dysphonic patient. When selected appro-
priately with appreciation of their limitations, the techniques discussed
afford the voice specialist the opportunity to make informed diagnostic
decisions 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
a
b
Department of Neurology, Thomas Jefferson University, Jefferson Medical College,
Philadelphia, PA, USA
c
Department 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 is
easy to perform, well-tolerated, and presents minimal risks to patients. It
is 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 mechanical
disorders. It is also useful in establishing prognosis in laryngeal nerve palsies
and for guidance during the injection of botulinum toxin in the treatment of
spasmodic dysphonia. Judgements regarding when to use LEMG, selection
of muscles to be studied, and the choice of EMG techniques depend upon
a comprehensive history and physical examination. LEMG requires expert
interpretation, 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 respect
to its exterior [1–3]. This electrical potential difference is called the resting
membrane 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: phillyvoicemd@aol.com (Y.D. Heman-Ackah).
1004 HEMAN-ACKAH et al
motor neurons it is about 70 millivolts. The resting membrane potential

reflects 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 and
the extracellular compartment has a high concentration of sodium and chlo-
ride, a gradient that is maintained by active transport over the cell
membrane.
With the application of an appropriate stimulus, nerves and muscles gen-
erate action potentials. The action potential is a fast and transient reversal
of the membrane potential caused by a temporary change in membrane per-
meability. The action potential is generated by depolarization of the cell
membrane to the membrane threshold potential. This action potential is
propagated along the fiber without decrement [4,5].
The motor unit consists of a single lower motor neuron and the muscle
fibers that it innervates. It, therefore, includes the cell body of the lower
motor neuron in the spinal cord, its axon with its terminal arborization,
the neuromuscular junctions, and all the muscle fibers innervated by
them. Every muscle unit has an innervation ratio, which is a measure of
the total number of muscle fibers in the muscle to the total number of motor
axons innervating that muscle. The innervation ratio in small muscles, such
as 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 that
perform fine motor movements typically require low innervation ratios.
Muscles with high innervation ratios are typically involved in more gross
motor movements. The individual muscle fibers belonging to a given motor
unit 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 in
myofibrillar adenosine triphosphatase (ATPase), whereas Type 2 fibers are
rich 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 fiber
so that a muscle fiber may change its histochemical characteristics when re-
innervated by motor neuron from a different motor unit type. Type 1 muscle
fibers are best suited for producing sustained, low-intensity muscle contrac-
tions; Type 2 fibers are best suited for short bursts of high intensity muscle
contractions [7]. In the spinal cord, smaller motor neurons innervate Type 1
fibers and large motor neurons innervate Type 2 fibers. Smaller motor neu-
rons are typically activated at low muscle tension; therefore, they are the
first 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 at
a lower rate, typically less than 20 Hz; large motor neurons are capable of
LARYNGEAL ELECTROMYOGRAPHY 1005
firing at rates as high as 100 Hz. With aging, there is a significant loss of
motor neurons in the anterior horn cells, which causes an increase in the
innervation ratio of the surviving units [8].
The electrodiagnostic apparatus

Bioelectrical potentials from the muscles or nerves being examined are
detected by an active recording electrode connected to a differential ampli-
fier with a typical common mode rejection ratio of 100,000:1 and a high
input 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 EMG
machine is typically set at 10 Hz to 10,000 Hz. The reference electrode is also
connected to the amplifier. The signal of interest is measured as the potential
difference between the active and reference electrodes. The patient must be
grounded to reduce the risk for electrical injury and 60 Hz interference. The
electrodiagnostic signal is displayed on a cathode ray oscilloscope in real
time and can be heard through a loudspeaker. The amplified signal can
then 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 also
possible. In modern systems, the amplifier signal is also connected to an
analog-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 stimulator
incorporated into the system that is connected to the microprocessor and
the oscilloscope so that it can trigger the recording system when stimulation
is provided. The ability of an amplifier to reject common mode signals is
indicated 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, which
means that unequal potential differences between the two inputs of the
amplifier 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 many
advantages, including permitting simultaneous, multichannel recording, but
EMG systems are fairly expensive. For otolaryngologists who plan to use
laryngeal EMG for needle guidance when injecting botulinum toxin or for
occasional diagnostic purposes, less expensive, conveniently portable
systems 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 connected
to a computer to provide a visual display. Such compact devices are also
valuable for bedside, in-patient testing of patients who have laryngeal
trauma in whom differentiation between arytenoid injury and vocal fold
paralysis is necessary. They are especially convenient during evenings and

weekends, 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. Most
ABR units can be used (sometimes with minor modifications) for single-
channel EMG recordings. Although such devices can be used for specific
clinical indications when formal EMG cannot be performed, they should
be used in addition to, not in place of, a sophisticated, multichannel
EMG system for diagnostic testing.
Electrodes
The flow of current in biologic tissues occurs as a result of the movement
of ions. In electronic systems, it is caused by the movement of electrons. The
conversion 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 penetrate
the surface. Although they are noninvasive, they are the least selective elec-
trode type. Surface electrodes are used in the study of nerve conduction
velocity and neuromuscular transmission. The potential that is recorded rep-
resents the sum of all individual potentials produced by the nerve or muscle
fibers 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 needle
electrode consists of a hollow steel needle; a silver, steel, or platinum wire
runs through the needle, which is insulated fully except at the tip. The
potential difference between the outer shaft of the needle, which serves as
a local reference electrode, and the tip of the wire is measured by connecting
it to one side of the differential amplifier. Because the electrode cannula acts
as a shield, the electrode has directional recording characteristics that are
controlled 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 those
recorded with concentric needle electrodes, primarily because more muscle fi-
bers are within the zone of detection and there is less cancellation because of
potentials being recorded from the cannula of the electrode. The reference
electrode 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 grounded
and the two internal wires are each connected to one side of the differential
amplifier so that the potential difference between the two wires is measured.
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 recording range of the bipolar electrode is restricted to the area between
the two wires within the shaft, which makes it unsatisfactory for many rou-
tine clinical purposes. The potentials are shorter and lower in voltage than
those recorded with concentric needle electrodes [11].
With single-fiber EMG, a fine wire that is capable of recording a single
muscle fiber action potential is embedded at the tip of a needle shaft that
acts 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 as
a barb, stabilizing the position of the electrode in the muscle. Obviously,
these electrodes cannot be repositioned once they have been placed, but
they bend easily and can thus be withdrawn without difficulty. Hooked
wire electrodes are extremely well tolerated and can be left in place for
long 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. 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.)
the procedure is generally not very painful, and because local anesthesia
may alter results (especially in the cricothyroid muscle), local anesthesia is
not used. A surface electrode is used as the ground electrode, and a reference
(also surface) is placed on the cheek. For diagnostic purposes, routinely we
test cricothyroid, thyroarytenoid, and posterior cricoarytenoid muscles. In
some 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, electrical
recordings may be coordinated with acoustic data. Blitzer and colleagues
observed that the normal delay between the onset of the electrical signal
and the onset of the acoustic signal (0–200 milliseconds) can be increased
to a delay of 500 milliseconds to 1 second in patients who have spasmodic
dysphonia [12,13].
After cleaning the skin with alcohol, the needle electrode is inserted into
the muscle belly. The cricothyroid (CT) notch is the anatomic reference for
needle insertion. To locate the CT notch, the patient’s neck is extended and
the cricoid cartilage is identified. Immediately above the cricoid cartilage is
a small depression, which is the CT notch (also known as the CT space) and
the 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 evaluated
by inserting the needle approximately 0.5 cm from the midline and angled
laterally 30 to 45 (Fig. 3). The needle first passes through the sternohyoid
muscle. The CT muscle is approximately 1 cm deep. To validate the position
of the electrode, the patient is asked to phonate /i/ at a low pitch and then
asked to raise the pitch. If the electrode is in a normal CT muscle, the EMG
activity 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. 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 insertion
of the electrode generally indicates that the needle has penetrated the airway
and is causing irritation of the mucosa. In that case, the needle should be
withdrawn and reinserted. The position of the needle is validated by asking
the 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 in
the lateral cricoarytenoid muscle there is an increase and rapid drop-off in
EMG activity.
The posterior cricoarytenoid muscle (PCA) can be accessed by rotating
the 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 cricoid
cartilage posteriorly. The latter technique is successful usually only in
non-ossified larynges, such as those of young women. The PCA lies lower
in the neck than many physicians realize; inserting the electrode too high
is a common reason for difficulty in locating the PCA. Position is confirmed
through detection of increased EMG activity during sniffing, and with much
less EMG activity during swallowing and phonating the sound /i/. Thyroar-
ytenoid, posterior cricoarytenoid, lateral cricoarytenoid, and interarytenoid
electrodes 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 capacity
coupling. This current leakage may lead to death or injury in a patient by
causing 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 the
needle is introduced into the muscle. This activity should last no more than
several hundred milliseconds. This burst of electrical activity results from
the needle itself having some electrical energy that, when placed near the
muscle membrane, causes a relative change in the surrounding electrical
energy.
If the electrical charges surrounding the muscle membrane are unstable,

such as occurs during early nerve and muscle injuries, the insertional activity
is prolonged. With late nerve and muscle injuries, healing sometimes results
in replacement of normal muscle with scar tissue or fat, which insulates the
remaining 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 that
signal the muscle to contract. Spontaneous electrical activity occurs in a se-
verely denervated muscle with unstable electrical charges. The presence of
spontaneous activity implies that the muscle is degenerating or that the
nerve has been injured and the process that caused the injury is ongoing.
This finding is true in muscles throughout the body, including those in the
larynx [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 the
nerve to the muscle. This degree of denervation occurs only with severe
nerve injury, and the presence of spontaneous activity indicates a poor
prognosis for recovery. Once regeneration begins, the muscle begins to re-
ceive electrical impulses from the regenerating nerve and the spontaneous
activity ceases.
Waveform morphology
Waveform morphology refers to the shape, amplitude, and duration of the
motor unit potentials, which are the electrical signals captured by EMG. The
normal laryngeal motor unit potential is biphasic; that is, it has an upward
positive 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 the
strength of the muscle fibers innervated by one nerve ending. The duration
of the motor unit potential reflects the velocity of the neural input, which
is influenced by insulation of the nerve. Nerves that are insulated well and
have an intact and functioning sheath are able to transmit electrical impulses
faster 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. Under
normal circumstances, this is biphasic. The waveform morphology of the
motor unit potential provides information regarding likelihood of recovery.
After injury, the nerve undergoes a process of denervation followed by
regeneration. The length of time that denervation and regeneration occur
can vary from one situation to another and can last for periods of weeks
to months each. It is unknown what determines the degree of denervation
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.)
or regeneration in any given nerve. During denervation, there is no neural

input into the muscle and thus no abnormal waveforms are produced. Ab-
normal motor unit potential morphologies are produced during the period
of regeneration.
During the early phases of regeneration, tiny nerves begin to course back
into 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 produces
motor 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 recent
nerve injury.
As the regeneration progresses, the nerves become healthier and better
insulated through regrowth of their sheaths, and the muscle fibers become
stronger and gain more mass. Not all of the nerve fibers regenerate. Those
neurons that regenerate branch more than before the injury to innervate as
many muscle fibers that lack innervation as possible. The motor unit poten-
tials that are produced as a result of this ongoing regeneration have greater
amplitudes than normal (because of the greater number of muscle fibers in
the motor unit), are polyphasic (because of changes in the muscle membrane
potentials), and have a prolonged duration (because of changes in the mye-
lin sheath and nerve conduction velocity). These motor unit potentials are
usually described as being polyphasic or as giant polyphasic potentials; their
presence implies an old nerve injury.
If the nerve is uninjured and the muscle is damaged, the morphology of
the 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
in the muscle membrane are abnormal, resulting in a polyphasic shape. The

amplitude, which reflects the decreased muscle mass and force of contrac-
tion, is decreased.
Recruitment
Recruitment refers to the serial activation of motor units during increased
voluntary muscle contraction. Normally, as the intensity of the muscle con-
traction increases, the motor units have increased activity and new motor
units are recruited to maintain the strength of the contraction. This process
is seen on LEMG as an increase in the number and density of motor unit
potentials (Fig. 5). This density of motor unit potentials is the recruitment.
Recruitment thus reflects the degree of innervation, which is a reflection of
the number of active nerve fibers within a given muscle.
Common abnormal electromyography findings

Increased insertional activity occurs when the burst of electrical potential
produced by insertion or movement of the needle electrode in the muscle
lasts more than several hundred milliseconds. This finding is an indication
of muscle membrane instability and occurs in myopathic and neurogenic
processes. Insertional activity also can be reduced, indicating loss of muscle
fiber and replacement of it by fibrotic tissue or lipoid degeneration. This
process 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 muscle
action potentials with a typical amplitude of several hundred microvolts
and 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 has
occurred. Rarely, it can be seen in myopathic processes also. A positive
sharp wave is characterized by a large positive deflection of several hundred
microvolts lasting less than 2 milliseconds, followed by a negative deflection
of 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 machine
gun 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 waves
indicates 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 bizarre
configuration. The discharge rate is anywhere between 5 and 100 Hz, with
Fig. 5. (A) Maximal contraction, normal recruitment pattern. (B) Maximal contraction; motor unit
recruitment decreased approximately 30%. (C) Maximal contraction; motor unit recruitment de-
creased approximately 50%. (From Sataloff RT, Mandel S, Heman-Ackah Y, et al. Laryngeal elec-
tromyography. 2nd edition. San Diego [CA]: Plural Publishing, Inc.; 2006. p. 81–2; with permission.)
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.)
an amplitude of 100 mV to 1 mV. This abnormality indicates chronicity, and

it can be observed in neuropathic and myopathic processes.
Myotonic potentials (Fig. 8) are repetitive discharges at rates of 20 to
150 Hz and amplitudes of 20 mV to 1 mV, with the appearance of fibrilla-
tion potentials or positive sharp waves. The amplitude and the frequency
of the potentials wax and wane, which causes a characteristic ‘‘dive
bomber’’ sound in the loudspeaker of the EMG machine. These potentials
occur spontaneously with insertion of the needle, with percussion of the
muscle, or with voluntary contractions. They indicate muscle membrane
instability 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. 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.)
myotonia, such as myotonic dystrophy. Rarely, they can be observed in

chronic neurogenic and myopathic processes, such as fibromyalgia without
clinical myotonia.
Lower motor neuropathy

During minimal voluntary muscle contraction, the morphology of the
motor unit potential is evaluated. Abnormalities are characterized by
changes 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). During
early reinnervation, the amplitude is decreased and, when reinnervation is
completed, 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 any
muscle motor unit, and their distances from the neuromuscular junction
vary, 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 motor
units overlap, creating an interference pattern. Potentials that can be iden-
tified visually and audibly during weak contraction overlap during stronger
contraction; therefore, some fading can result in a recruitment pattern in
which some of the spikes appear to be lost. By looking at, or listening to,
the EMG signal, a skilled electromyographer can determine the condition
of the muscle. For example, under normal circumstances, the interference
pattern described above is present. In complete paralysis, initially there is
electrical silence; however, positive sharp waves or fibrillation potentials
generally appear within a few weeks. Reinnervation is characterized by
larger motor units with polyphasic, high-amplitude, and long-duration
responses. There is usually loss of motor units following paralysis, which
results in decreased recruitment (a less dense interference pattern). In
Fig. 9. Differences in the appearance of the motor unit potential in diseases. (From Sataloff RT,
neuropathic processes, there is decreased recruitment, with a few motor

units firing at high frequency and a decreased interference pattern (Fig. 11).
Myopathy
In a myopathic process, there is rapid and early recruitment with a low
voltage, 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 increased
number of phases and decreased amplitude.
Upper motor neuropathy

In upper motor neuron disorders, the insertional activity is normal. The
amplitude and duration of the motor unit potential are normal, and there
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.)
are no excessive polyphasic motor units. Recruitment is decreased. The

firing 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 function
with EMG in patients who have upper motor neuron disorders.
Basal ganglia disorders

The insertional activity is normal in basal ganglia disorders. Abnormal
spontaneous 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.)
potentials, indicating failure of complete relaxation of the muscle. There

may 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 have
voice tremor [21]. Stuttering may also be associated with tremor-like
EMG activity [22].
Laryngeal dystonia (spasmodic dysphonia)

In laryngeal dystonia, there are intermittent sudden increases in muscle
activity coinciding with momentary voice rest [13,23,24]. The EMG can
be helpful in differentiating adductor versus abductor or mixed dystonias
[25]. Rodriguez and colleagues [26] found abnormal activity in 81.3% of
patients who have spasmodic dysphonia but found no EMG abnormality
predictive of severity. LEMG is used routinely to guide botulinum injection
in 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 muscles
affected most by the dystonia, thereby guiding therapeutic intervention.
Laryngeal myasthenia
In myasthenia gravis (MG), the insertional activity is normal. There is no
abnormal spontaneous activity. With minimal muscle contraction, the motor
unit 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 stimulation
studies are usually abnormal and reveal a lack of increased recruitment
with each repetitive stimulation. Myasthenia gravis can be a cause of intermit-
tent and fluctuating hoarseness and voice fatigue. Laryngeal manifestations
may be the first and only sign of systemic myasthenia gravis [29]. Laryngeal
MG may occur with systemic MG or as a focal disorder similar to ocular MG.
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 electrical
shocks and recording the neuromuscular response by EMG. Because of its
easy, subcutaneous access, the nerve stimulated is often the spinal accessory
nerve 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 during
repetitive 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 units

that were previously recruited are unable to be actively and continually
recruited during repetitive stimulation. That they were able to be recruited
initially and give normal waveform morphology implies that the nerve fi-
bers themselves are intact and that the muscles are able to respond to
an 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 of
information across the neuromuscular junction that is only apparent when
the system is stressed. If the laryngeal evaluation is abnormal, or if there
are other abnormalities noted during the LEMG, then Tensilon (edropho-
nium chloride, Hoffman-LaRoche, Inc., Nutley, New Jersey) testing may
be performed. Repetitive stimulation testing is contraindicated in patients
who have pacemakers.
Tensilon is an anticholinesterase that inhibits acetylcholinesterase at the
neuromuscular junction, resulting in increased exposure of the muscle recep-
tors to acetylcholine during neural stimulation. In normal muscles, this has
little effect on muscle activity. In muscles with decreased numbers of avail-
able receptors for acetylcholine (as occurs with myasthenia), in those with
increased activity of acetylcholinesterase, or in those with decreased release
of acetylcholine from the nerve ending, the presence of Tensilon results in
increased 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 contraction
and 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 30
seconds. 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 have
had such reactions, the test may be repeated 30 minutes after administration
of atropine sulfate. In patients who have inaccessible veins, Tensilon may be
given as an intramuscular injection. Tensilon testing can also be performed in
children, 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 times
for emergency rescue. Tensilon also contains sodium sulfite. Allergic reac-
tions to sulfites can occur and are more common in patients who have
asthma than in others. The safety of Tensilon for use during pregnancy or
lactation has not been established. Use of Tensilon in pregnant women
and nursing mothers is relatively contraindicated.
Summary
LEMG is easy to perform and well tolerated in the office setting with
minimal risks. It is useful in the evaluation of numerous laryngeal disorders,
allowing clinicians to differentiate among upper motor neuron, lower motor
neuron, peripheral nerve, neuromuscular junction, myopathic, and mechan-
ical disorders. It is also useful in establishing prognosis in laryngeal nerve
palsies and for guidance during the injection of botulinum toxin in spas-
modic dysphonia. Our experience and that of others are similar to that of
Koufman and colleagues, who reported 415 LEMG studies, 83% of which
revealed a neuropathic process [30–32]. They reported unexpected findings
in 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 laryngologist
and a skilled laryngeal electromyographer is an invaluable and essential
asset to the voice care team. There is a striking paucity of evidence-based
research to confirm or refute scientifically and incontrovertibly the value
of LEMG for most of the purposes for which we use and recommend it,
however [33]. Additional prospective, controlled LEMG research should
be encouraged and supported, and should be used to formulate formal prac-
tice guidelines for clinical use of LEMG.
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[33] Sataloff RT, Mandel S, Mann EA, et al. Practice parameter: laryngeal electromyography (an
evidence based review) report of the quality standard subcommittee of the American Acad-
emy of Neurology in collaboration with the American Academy of Otolaryngology – Head
and Neck Surgery, the American Academy of Physical Medicine and Rehabilitation, the
American Association of Electrodiagnostic Medicine and the Voice Foundation. Manu-
script in Preparation, 2002.
40 (2007) 1025–1061
Common Diagnoses and Treatments

in Professional Voice Users
Ramon A. Franco, MD*, Jennifer G. Andrus, MD
Division of Laryngology, Massachusetts Eye & Ear Infirmary,
Department of Otology and Laryngology, Harvard Medical School,
243 Charles Street, Boston, MA 02114, USA
Common problems among all patients with vocal difficulties seen by the
laryngologist also are common among professional voice users. These in-
clude laryngopharyngeal reflux, muscle tension dysphonia, fibrovascular
vocal fold lesions (eg, nodules and polyps), cysts, vocal fold scarring, and
changes in vocal fold mobility. Microvascular lesions and their associated
sequelae of vocal fold hemorrhage and laryngitis due to voice overuse are
more common among professional voice users. Much more common among
professional voice users is the negative impact that voice problems have on
their ability to work, on their overall sense of well-being, and sometimes on
their very sense of self. In diagnosing voice disorders in professional voice
users, clinicians must possess and clearly convey an understanding of this
important truism, which will facilitate trust, confidence, and the opportunity
to treat the patient. This article reviews the diagnosis and treatment options
for common problems among professional voice users, emphasizing the im-
portance of gaining insight into the ‘‘whole’’ patient and of developing indi-
vidualized management plans.
History and physical examination

The history and physical examination are addressed at length elsewhere
in this issue; however, a few key points are worth mentioning here as
well. First, because of the critical role that the voice plays in the livelihood
of a professional voice user and the frequent association of the voice as a ma-
jor component of one’s identity, changes in voice frequently create signifi-
cant anxiety for these patients. This anxiety, a fear of the unknown, and
a swarm of emotions commonly accompany professional voice users to
E-mail address: ramon.franco@meei.harvard.edu (R.A. Franco).
1026 FRANCO & ANDRUS
the laryngologist’s office and may be barriers to the patient’s ability to

clearly describe the problems he/she is having with the voice. Patient ques-
tionnaires can help to overcome this difficulty and facilitate an efficient visit.
They are invaluable. The patient can be asked to fill out a history intake
form in the waiting room, along with the voice-related quality of life
(VRQOL) survey and a voice outcome survey. In addition to defining the
effects of the voice problem on the patient’s functional capacity, the surveys
are helpful for tracking the voice problem and the effect of therapy on it.
Second, the history will help to establish the acuity or chronicity and se-
verity of the problem. Along with symptoms, past medical/surgical history,
allergies, and medications, particular attention should be paid to the social
history, including place of residence; student or employment status; current
and previous tobacco, alcohol, and drug use; exposure to second-hand
smoke or chemical irritants/pollutants; and water, caffeine, carbonated bev-
erage, chocolate, peppermint, and fatty/spicy/acidic food consumption.
Changes in a patient’s routine (eg, time of day one practices, performance
venue, consumption of caffeinated beverages) often yield important infor-
mation. The history also gives clues as to what endoscopy may show. Clini-
cians are encouraged to use the history to help guide the physical
examination, but are cautioned to keep an open eye for unsuspected diagno-
ses. Similarly, history and physical examination together will help the clini-
cian to develop a differential diagnosis. More often than not, multiple
entities contribute to one symptom complex, so the laryngologist is cau-
tioned not to look for ‘‘the’’ single unifying diagnosis. Thinking about laryn-
geal pathology in terms of acute versus subacute versus chronic problems
may be more useful than a traditional schema of vascular, inflammatory,
traumatic, autoimmune, iatrogenic, neoplastic, or congenital problems.
Nonetheless, the clinician is reminded that professional voice users are sub-
ject to the same possibilities as are other patients; therefore, neoplastic and
autoimmune processes, for example, should not be overlooked.
Third, many, if not most, pathologic entities in the larynx occur on a con-
tinuum and are dynamic given the demands on the professional voice user’s
‘‘instrument.’’ Ongoing, long-term (if not lifelong) voice use in any number
of performance venues constantly subjects the larynx to insults, such as
phonotrauma, reflux, second-hand (or first-hand) smoke, and chemical ex-
posures, often under suboptimal conditions (poor acoustics, arid atmo-
sphere, and concomitant physical demands, such as dancing). Any one
condition is likely to wax and wane in severity depending on the patient’s
general health, vocal demands, rehearsal and event schedule, performance
venues, and the subsequent diet and lifestyle that ensue. Among the most
important of the laryngologist’s tasks are eliciting these details, educating
patients about ways to meet their professional demands while maximizing
vocal hygiene, and supporting them in their efforts.
Finally, laryngologists frequently see professional voice users for a second
or third opinion after they have been evaluated by other otolaryngologists.
COMMON DIAGNOSES 1027
Sometimes the patient is in denial and does not want to believe what another
clinician has diagnosed or does not want to pursue the recommended treat-
ment options. Another frequent scenario is that the patient has been told
that he/she has a normal larynx and that nothing on examination can
explain the symptoms. In these cases, it is especially important to elicit a
detailed history and to be clear about what bothers the patient about the
voice. Sometimes edema from laryngopharyngeal reflux masks a mass lesion
or hyperfunction is so severe that the vocal folds are not seen easily on
fiberoptic evaluation. Flexible distal-chip laryngoscopes are providing ex-
aminations superior to fiberoptic laryngoscopy and approximating rigid lar-
yngoscopy, such that subtle findings now are being noted that may not have
been seen without this technology. Of utmost importance, it is essential to
listen to the patient, to acknowledge that something is wrong, even if the ex-
act diagnosis is not obvious, to take a team approach with a voice therapist,
and to ‘‘stick’’ with the patient until a diagnosis and treatment plan are
formed and executed.
Voice problems in professional voices users: diagnoses and treatment

options
Laryngopharyngeal reflux
Laryngopharyngeal reflux is the retrograde movement of gastric contents
(acid and enzymes, such as pepsin) into the laryngopharynx leading to
symptoms referable to the larynx, hypopharynx, and nasopharynx (Fig. 1)
[1]. Typical laryngopharyngeal reflux symptoms include dysphonia, globus
pharyngeus, mild dysphagia, chronic cough, excessive throat mucus, and
Fig. 1. Laryngopharyngeal reflux. Note diffuse periarytenoid and postcricoid edema, vocal fold
edema, and pseudosulcus (the appearance of a ‘‘second’’ vocal fold inferior to the true vocal
fold due to edema). The larynx is wet appearing; copious, thick mucus is not seen in this patient
as in others.
nonproductive chronic throat clearing [2]. In singers, voice changes, such as

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

reflux severity index, a self-administered nine-item survey (scored from 0
to 5), the investigators documented improvements in the reflux finding score
and the reflux severity index with twice daily proton-pump inhibitor (PPI)
therapy [10].
The 24-hour dual-sensor pH/impedance probes are considered by many
to be the gold standards for diagnosing laryngopharyngeal reflux. Often,
the pharyngeal probe is the key to making the diagnosis, because the esoph-
ageal probe results may be ‘‘normal.’’ The sensitivity of single-probe esoph-
ageal pH monitoring for laryngopharyngeal reflux was 62% in one study,
with a positive predictive value of only 49%. Pharyngeal pH/impedance
monitoring can increase the diagnostic accuracy of laryngopharyngeal reflux
dramatically; however, as a diagnostic, pH-metry is expensive and not
widely available. Conversely, despite superior sensitivity and specificity for
acid reflux events over physical examination findings, the dual pH probe
could not predict the severity of the patients’ reflux symptoms or signs in
a 2002 study [11]. The investigators provided several reasons for the lack
of ability of the pH probe to separate patients who did and did not have lar-
yngopharyngeal reflux. They postulated that so little acid exposure is needed
to cause laryngopharyngeal reflux that it may not register as positive during
the limited 24-hour study. The 69% reproducibility of pharyngeal pH mon-
itoring seen in another study that they cited may indicate that a 24-hour test-
ing period is too short to accurately estimate what is going on the rest of the
time [12]. The investigators also considered that there might have been an-
other source for the irritation that was attributable to laryngopharyngeal re-
flux. Impedance testing may provide even better information for the
diagnosis of laryngopharyngeal reflux, especially when done in combination
with pH-metry. Most important in the interpretation of these tests is assess-
ing the patterns of pH and pressure changes, whether they correspond with
each other, and if they occur in the supine or upright positions. Finally, lar-
yngopharyngeal reflux also can be diagnosed by symptomatic improvement
after empiric treatment with high-dose twice-daily proton pump inhibitors.
Laryngopharyngeal reflux and gastroesophageal reflux disease differ in
their symptom complexes, largely because of differences in the epithelium
and physiology of the larynx and esophagus. A full discussion of the topic
is beyond the scope of this article; the reader is referred to additional re-
sources to explore these differences and recent research in the area [13,14].
The mechanism of laryngopharyngeal reflux, however, is important to con-
sider in the context of treating professional voice users with the disorder, as
their understanding of the problem likely will improve its treatment. Lar-
yngopharyngeal reflux is postulated to cause laryngeal symptoms in two
ways: directly and indirectly [6]. According to the direct theory, refluxate di-
rectly irritates the laryngeal mucosa through the action of the caustic mate-
rial resting on the tissues. This causes tissue edema, which is responsible for
most laryngopharyngeal reflux symptoms. In the indirect theory, refluxate
does not make it onto the laryngeal tissues, but rather evokes laryngeal re-
flexes by irritating other structures, such as the esophagus, that then incite
a vagally mediated response (ie, chronic cough, asthma-like symptoms
through bronchoconstriction). Regardless of the pathway, factors such as
the resting tone of the upper esophageal sphincter and lower esophageal
sphincter, the duration and the amount of intra-abdominal pressure eleva-
tion, and the volume of stomach contents during exertion are important
in the creation of the refluxate bolus [6]. Considering all of the possible con-
tributors to laryngopharyngeal reflux guides its treatment, a multiarmed
pathway directed at diet changes, lifestyle/behavior modifications, medical
intervention, and, occasionally, surgery.
The multimodality treatment for managing laryngopharyngeal reflux ad-
dresses upper and lower esophageal sphincter tone, the presence of acid in
the stomach, stomach acid production, and mechanical increases in intra-
abdominal pressure. Thus, diet modifications include avoidance of sub-
stances that decrease upper and lower esophageal sphincter tone, such as
alcohol, peppermint, fatty foods, chocolate, and caffeine. It is stressed to pa-
tients that even ‘‘decaffeinated’’ products and many herbal teas contain caf-
feine; reading labels to assure that goods are ‘‘caffeine-free’’ is important.
Carbonated beverages, even without alcohol or caffeine, will cause belching
and lead to stomach refluxate contacting the laryngopharynx. Additionally,
patients are advised to avoid acidic foods, which directly irritate the hypo-
pharynx and cause inflammation. These include most fruits (especially citrus
and pineapple), tomatoes, jams and jellies, barbecue sauces, and most salad
dressings. Spicy foods (hot mustards, curry, hot peppers/hot sauce) are sim-
ilarly irritating. Behavior modifications play a large role in the management
of laryngopharyngeal reflux. It must be stressed to patients that a little com-
mon sense can go a long way in limiting the detrimental effects that laryng-
opharyngeal reflux can have on the voice. Stomach distension increases the
likelihood of regurgitation of contents into the esophagus and above. Pa-
tients are encouraged to eat smaller meals throughout the day, rather
than a few large meals, and to avoid being supine within 3 hours of eating.
Raising the head of the bed by placing the frame on blocks, placing the box-
spring mattress on blocks inside the bed frame, or using a wedge under the
mattress also is recommended (especially if pH-metry and impedance testing
demonstrate significant reflux events while supine). Increased intra-abdom-
inal pressure also increases the likelihood of reflux events, so patients are
counseled to avoid exercise, heavy lifting, and bending over within several
hours of eating. Professional voice users, in particular, are advised to avoid
singing/performing within 2 to 3 hours of a meal. These modifications can
be difficult for professional voice users to make, especially those who are
singing and performing evening events (concerts, shows) on the road, during
which days are long and a routine is hard to establish. Nonetheless, vigilant
attention to diet and lifestyle changes can result in marked improvement in
symptoms.
Although some patients’ laryngopharyngeal reflux is responsive to diet

and behavior modifications alone, most require medication to achieve the
best result. It is well accepted among laryngologists that medical manage-
ment of laryngopharyngeal reflux requires more aggressive and more pro-
longed treatment than does gastroesophageal reflux disease [1]. High-dose
PPI treatment is recommended for at least 6 months, with twice-daily PPI
dosing because none of the delayed-release PPIs exert acid suppression for
more than 16.8 hours [15,16]. Patients must know to take PPIs on an empty
stomach, followed in 30 minutes by a meal. This maximizes efficacy by ac-
counting for the natural physiology of the PPI mechanism of action [17].
Taking PPIs on an empty stomach allows for faster transit to the small
bowel, prompt absorption, and the development of maximal plasma levels.
Eating causes stomach distension and the activation of proton pumps. These
activated proton pumps are turned off by PPIs by the irreversible inhibition
of acid secretion that occurs when maximal plasma levels of the PPIs are
achieved immediately before the meal. Some patients manifest nocturnal
acid breakthrough with nocturnal cough or morning hoarseness. This is ad-
dressed best with the addition of high-dose histamine-2 blockers, such as ra-
nitidine, 300 mg orally, nightly before bed.
It takes a minimum of 6 to 8 weeks to achieve reduction in symptomsd
and although some patients note a difference in the first few days of vigilant
therapydall should be counseled to be patient and diligent with the treat-
ment plan. It takes 6 months or longer for the laryngeal findings of laryng-
opharyngeal reflux to improve [1,10,18]. The reflux severity index and reflux
finding score can be used to assess treatment efficacy, although patient his-
tory is adequate. Professional singers are especially sensitive to subtle
changes in voice and so recognize when small changes in diet, stress, or rou-
tine exacerbate their laryngopharyngeal reflux. Once laryngopharyngeal
reflux is controlled well, some patients slowly can reintroduce a few re-
flux-exacerbating foods or begin to wean off PPIs; however, patients should
be counseled to keep track of their symptoms, and laryngologists should be
liberal about represcribing twice-daily PPIs at the slightest sign of return of
laryngeal signs or symptoms.
Rarely, a patient will be unresponsive or inadequately responsive to diet
changes, behavior modifications, and maximum pharmacotherapy. Some
patients have a good initial response that is maintained for some months
but ‘‘backslide’’ over time, despite adherence to their diet and behavior
changes. Many of these patients develop a relative tolerance to the specific
PPI that they are taking, and a change from one specific medication to an-
other seems to reestablish efficacy. Sometimes, two or three changes in med-
ication are necessary to obtain the best response or the least disturbing side
effect profile; however, some patients, despite all best efforts, remain symp-
tomatic. This group should be referred to a gastroenterologist and a general
surgeon for evaluation of refractory reflux and possible fundoplication.
Eliminating much of the morbidity associated with the traditional open
approach, laparoscopic fundoplication frequently is successful [19,20].

Young, thin patients who have severe reflux may be particularly well served
by fundoplication.
Finally, transnasal esophagoscopy (TNE) is recommended as a screening
tool for evaluating the esophagus in patients who have long-standing, se-
vere, or refractory laryngopharyngeal reflux or complicated gastroesopha-
geal reflux disease. This awake, nonsedated procedure can be performed
in the office with topical anesthesia alone, biopsy can be performed as nec-
essary, any abnormalities identified can be documented, and gastroenterol-
ogy consultation can be obtained as warranted. TNE is a high-yield
diagnostic tool that aids the laryngologist/otolaryngologist in providing
comprehensive care for one’s patients [21–23].
Fungal laryngitis
Historically, fungal laryngitis was considered an opportunistic infection
in immunocompromised hosts indicative of likely invasive local or pulmo-
nary fungal disease, if not systemic fungal disease (Fig. 2). Isolated laryngeal
disease was believed to be exceedingly rare, and suspicion of laryngeal dis-
ease nearly always prompted investigation for systemic disease and possible
immunosuppression [24]. In studies that diagnosed fungal laryngitis by cul-
ture or biopsy, the causative organism usually was candida species (ie, Can-
dida albicans) [24,25]. Other known pathogens include Blastomyces
(common in the Eastern United States and Midwest), Histoplasma (endemic
to the Ohio and Mississippi River Valleys), and Coccidioides (found in the
Southwestern United States and the cause of ‘‘Valley fever’’) [25,26].
More recently, fungal laryngitis has been recognized as a local superficial in-
fection of the supraglottis or true vocal folds in immunocompetent hosts
Fig. 2. Fungal laryngitis. White fungal plaques on an erythematous base are seen in the mid-
musculomembranous region of both vocal folds. Fungal laryngitis also can manifest as multiple
punctate white plaques throughout the larynx.
with risk factors that compromise mucosal barrier integrity [26–28]. These
include laryngopharyngeal reflux, smoking, and the use of inhaled steroids
[26–29]. Prolonged antibiotic use and radiation also have been identified
as risk factors [26,27].
Patients with any of the above noted risk factors, diabetes mellitus, nutri-
tional deficits, on immunosuppressive therapy, or in an immune-suppressed
state who present with dysphonia, dysphagia, odynophagia, pain, or a sensa-
tion of ‘‘burning in the throat’’ should be suspected of having fungal laryn-
gitis [26–28]. The astute clinician who is aware of these risk factors will ask
about associated symptoms and whether the onset of the symptoms corre-
sponded to changes in risk factor profile (eg, a new inhaled steroid, a recent
illness, uncontrolled blood glucose levels). Then, the clinician will look for
signs on laryngoscopy that are indicative of fungal laryngitis: leukoplakia,
white or gray pseudomembrane adherent to mucosa, mucosal edema and er-
ythema, mucosal ulceration, and contact bleeding. Findings often mimic
that of early oral thrush; however, the lack of white plaques, or leukoplakia,
in the presence of diffuse erythema can be caused by fungal laryngitis. The
laryngologist also must look for other lesions. Malignancy should be in the
differential diagnosis, especially in the smoking population.
Diagnosis in these patients commonly rests on clinical suspicion based on
history, risk factors, laryngoscopy findings, and response to empiric treat-
ment with oral antifungal agents [28]. Patients who fit the clinical picture
of fungal laryngitis can be treated with oral fluconazole for 3 weeks (200 mg
on day 1, followed by 100 mg daily on days 2 through 21) in conjunction
with nystatin swish and swallow (100,000 units/mL at 10 mL three times
daily for 7 to 10 days). Some clinicians treat with nystatin for 3 weeks first,
followed by fluconazole if there is no response; others use only fluconazole
[26,28]. Although fluconazole is known to increase liver enzymes, Stone and
Anderson [28] do not routinely check liver function tests. Patients who have
hepatic disease can be treated with nystatin as a first-line agent and referred
to their primary care physician for evaluation of their candidacy for sys-
temic antifungal treatment if they fail to respond appropriately. Because an-
tifungal treatment often is concomitant with antireflux treatment, response
to therapy can be multifactorial. If there is any question about the diagnosis
of fungal laryngitis, should symptoms/signs not resolve, or should malig-
nancy be a significant concern, a definitive diagnosis can be obtained with
laryngeal brushings and culture or biopsy. This can be accomplished with
in-office transnasal flexible laryngoscopy and biopsy through a working
channel on the endoscope. Often, periodic acid-Schiff or methenamine silver
stains are necessary to see fungal elements on histopathologic evaluation
[26,27]. Some patients who have fungal laryngitis with severe dysphagia
also may have esophageal candidiasis. If this is suspected, TNE is recom-
mended to examine the esophagus and to obtain biopsies as necessary. Pa-
tients who have severe dysphonia and pain also may present with significant
honey-colored crusts in the larynx in addition to multiple white plaques over
erythematous bases and edema. In these patients, a bacterial superinfection

can be presumed present, and oral clindamycin, 600 mg three times daily (or
similar antibiotic with gram-positive and anaerobic coverage) for 3 weeks,
added to the antifungal therapy. Again, this is an empiric treatment; cultures
are not obtained at initial evaluation. These patients usually do not respond
to antifungals alone.
The literature does not reflect the number of professional voice users who
have asthma or other obstructive pulmonary disease who have been on in-
haled steroids at any point. Considering the broad definition of ‘‘profes-
sional voice user,’’ however, it is not difficult to imagine that this number
could be significant. Therefore, laryngologists are obligated to seek this his-
tory and communicate with the prescribing physician about possible alter-
natives to inhaled steroids for patients who develop fungal laryngitis. It is
not always possible to wean patients off inhaled steroids, in which case short
holidays from steroid use may be in order, with or without low-dose prophy-
lactic antifungal use (eg, nystatin or mycelex troches). The use of a spacer
with the inhaler should be recommended [28]. Patients also must gargle
with water and rinse the oral cavity/oropharynx after each inhaler use.
Muscle tension dysphonia

Muscle tension dysphonia is a form of voice use/misuse/abuse character-
ized by excessive muscular effort and usually by pressed phonation [30].
(Access Video on Supraglottic Hyperfunction in online version of this article at: http://
www.Oto.TheClinics.com.)
Other common clinical features include an abnormally low-pitched

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

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

Just as muscle tension dysphonia is increasingly recognized as a compen-
satory mechanism for underlying organic, and sometimes multiple, vocal
fold disorders, vocal fold paresis is receiving more attention as a common

problem that causes dysphonia. Paralleling the paradigm shift in laryngolo-
gists’ thinking about muscle tension dysphonia, more focus is being placed
on ‘‘looking’’ for vocal fold paresis as a contributing factor to changes in
voice and in the development of hyperfunction.
Dysphonia was universally present in 50 consecutive patients diagnosed
with vocal fold paresis by Koufman and colleagues [39] in a retrospective
review. The next most common symptoms were effortful phonation and vo-
cal fatigue (76%), diplophonia (40%), and odynophonia (12%). Similar
symptoms were described by other investigators [40,41]. Decreased projec-
tion and decreased range also are symptoms of vocal fold paresis. Laryngeal
findings on transnasal flexible laryngoscopy and VLS included unilateral hy-
pomobility (50%), unilateral vocal fold bowing (36%), bilateral bowing
(22%), bilateral hypomobility (8%), and axial rotation (8%). Muscle ten-
sion patterns were nearly universally observed as anterior–posterior com-
pression or false vocal fold compression. Hypomobility and bowing can
be subtle, and abduction can be affected more frequently and more notice-
ably than adduction.
Once vocal fold paresis is suspected based on history and examination,
the clinician must decide whether laryngeal electromyography (LEMG) is
indicated. This determination must be made on a case-by-case basis. Cer-
tainly, the diagnosis of vocal fold paresis rests on LEMG, because asymme-
tries in arytenoid movement are normal in some patients (ie, there is no
decrement in the neuromuscular activity of the larynx) [39]. Differences in
arytenoid movement seen on physical examination cannot be used alone
to diagnose vocal fold paresis; however, the clinician is obligated to consider
the physical findings as well as their impact on function. Although some pa-
tients who have LEMG-diagnosed paresis are symptomatic enough to war-
rant surgical therapy, many, including professional voice users, are able to
function well without surgery. Conversely, even those able to function with-
out surgical intervention may benefit from voice therapy, which can be
guided by LEMG results. Before performing LEMG, it is important to eval-
uate with the patient whether LEMG results will influence clinical decision
making. It is not surprising for a professional voice user to opt out of a di-
agnostic procedure if it yields a choice between surgical or nonsurgical man-
agement when the patient is ‘‘not ready’’dmentally or functionallydto
consider a surgical procedure. This clinical situation is not unusual and em-
phasizes the importance of assessing with the patient how limiting the voice
change is.
If it makes sense to perform an LEMG, it should be performed at a sep-
arate visit, after which findings are reviewed briefly with the patient before
complete electromyographic analysis. Review of final results is reserved for
a follow-up visit, during which therapeutic options for treating the vocal
fold paresis are presented, if warranted. Concomitant vocal fold pathology
must be uncovered and considered in the overall management plan.
Treatment options for vocal fold paresis include no treatment with observa-
tion for resolution or progression, voice therapy alone, and injection aug-
mentation or medialization laryngoplasty, preceded and followed by voice
therapy. Koufman and colleagues [39] performed laryngoplasty or lipoinjec-
tion in 54% of the aforementioned subjects, with significant improvement
achieved in 85%. Medialization techniques are covered at length elsewhere
in this issue (see the article about voice surgery).
Superior laryngeal nerve (SLN) paresis deserves special mention because
it may have devastating effects on singers, given the impact that it has on
modulating pitch in the upper range. If loss of high range is among a singer’s
complaints and hypomobility in one vocal fold is seen on examination or if
symptoms do not improve on maximal laryngopharyngeal reflux therapy
with singing therapy in the case of symmetric movement, LEMG is indi-
cated to elucidate whether the SLNs are intact. If isolated SLN paresis is
present without vocal fold bowing or signs that vocal fold augmentation/
medialization will be helpful, it is important to provide voice therapy to
avoid development of muscle tension dysphonia, to encourage appropriate
changes in repertoire, and to provide hope to the patient that the vocal
fold paresis may be postviral with potential for resolution. This last point
of management is critical: first, patients often are able to cope better with
the idea of a temporary disability; second, if the disability is permanent,
time in voice therapy and modifying repertoire will be well spent.
Benign vocal fold masses: nodules, polyps, and cysts

Vocal fold masses are discussed in detail elsewhere in this issue. Here, the
similarities and differences in the symptoms, diagnosis, and treatment of vo-
cal fold nodules, polyps, and cysts are presented in brief. Dysphonia is the
most common presenting symptom of benign vocal fold masses. The astute
clinician may develop some hypotheses as to which type of mass is present
on the vocal fold based on specific voice changes, such as loss of range in the
high frequencies (commonly associated with nodules) or diplophonia due to
a difference in vibratory frequency of the vocal folds (often associated with
a unilateral process, such as a polyp). The wise clinician is ever mindful that
more than one pathologic process or more than one type of mass can be
present. Obtaining a good history is important to help define the cause of
the problems that the patient is having with the voice, which helps guide
the development of an individualized management strategy.
Vocal fold nodules are considered the most common vocal fold lesions in
children and adults. They are common among professional voice users as well,
especially when one includes in the definition of vocal fold nodules early fibrovas-
cular changes (subtle irregularities of the medial vocal fold edges in the mid-mus-
culomembranous region) that are associated with significant voice use.
(Access Video on Nodules in online version of this article at: http://www.Oto.TheClinics.
com.)
Vocal fold nodules (Fig. 3) are the end result of subepithelial scar depo-
sition, primarily changing the mass and stiffness of the vocal fold cover, with
little effect on the body [42]. Vocal fold nodules frequently interfere with
vocal fold closure, so hoarseness and breathiness are common symptoms.
Because of the loss of vocal fold pliability that occurs as the subepithelial
scar increases in size, and because of the increased size of the persistent
gap as the result of premature contact with incomplete closure, there is a de-
crease in range and stamina with an increase in vocal fatigue. Nonetheless,
the presence of nodules does not imply a change in vocal functioning in all
patients. Vocal fold nodules may have been present since childhood, and
many singers function exceedingly well with them. The presence of vocal
fold nodules on the vocal folds is not always compromising.
Vocal fold polyps, another form of subepithelial fibrosis and deposition,
are histologically similar to vocal fold nodules, but differ in that they are
unilateral. Vocal fold polyps also may present with hoarseness, loss of
range, breathiness, and vocal fatigue. Diplophonia may occur as noted
Fig. 3. Vocal fold nodules. (A) The lesions are bilateral. (B) Premature contact is seen on VLS.
above; dyspnea can occur if the polyp is large enough to obstruct the airway.
In professional voice users, the emergence of dyspnea is unlikely; these
patients probably would seek laryngologic attention before dyspnea could
evolve. The one exception is a hemorrhagic polyp, which can occur suddenly
and be large (Fig. 4).
(Access Video on Large Obstructive Hemorrhagic Polyp in online version of this article at:
Vocal fold cysts present primarily with hoarseness, although diplophonia

also may be a problem. Vocal fold cysts are present in the superficial lamina
propria and can open into the laryngeal lumen or insert onto the vocal lig-
ament. Vocal fold cysts are categorized as epidermoid (sometimes called
squamous inclusion) cysts or mucus retention cysts [42]. Epidermoid cysts
are believed to arise from traumatic introduction or ingrowth of keratin
into the superficial lamina propria, secondary to phonotrauma, or to be con-
genital. Mucus retention cysts more likely result from occlusion of mucus
glands on the inferior surface of the vocal fold.
(Access Video on Pre-op Subepithelial/Mucous Retention Cyst in online version of this
article at: http://www.Oto.TheClinics.com.)
Clearly, vocal fold nodules, polyps, and cysts cannot be distinguished by

history alone. VLS is the key to their diagnosis. Stroboscopy is essential to
an accurate diagnosis because it allows for the assessment of vocal fold clo-
sure and phase symmetry, which are not discernable in the absence of stro-
boscopic light. Stroboscopy’s delineation of the mucosal wave allows the
laryngologist to assess its relationship to the mass, and, thus, whether the
epithelium/basement membrane zone is involved or whether the mass lies
deeper to this. On VLS, vocal fold nodules most frequently are bilateral,
Fig. 4. Hemorrhagic polyp. Associated varices and resolving blood are seen in the left true
vocal fold. Note concomitant bilateral pseudosulcus.
sessile to raised to discretely nodular lesions along the medial edge of the vo-
cal folds, in the midmusculomembranous region (junction of the anterior
one third and posterior two thirds of the entire vocal fold). Pronounced
vibration of the vocal folds anterior to the nodules is seen frequently [42].
In many cases, there is incomplete closure of the folds and in severe situa-
tions, persistent anterior and posterior glottic gaps; the resultant ‘‘hour-
glass’’ configuration is classic. Vocal fold polyps are more frequently
unilateral, broad-based sessile lesions that can be clear, white, or reddish,
small or large, and can be pedunculated (small sessile lesions are more com-
mon) [42]. Changes in vocal fold stiffness attributable to vocal fold polyps
depend on the histologic type: gelatinous polyps, with loose edematous
stroma, tend to decrease vocal fold stiffness, whereas telangiectatic polyps,
with fibrin collections in the stroma, tend to increase vocal fold stiffness.
Changes in the affected vocal fold often cause changes in the horizontal
and vertical phase symmetry of the two vibrating folds; a polyp on one vocal
fold can cause traumatic polypoid or fibrovascular changes in the contralat-
eral fold, if not scarring. Again, incomplete closure is common. Finally, vo-
cal fold cysts generally are unilateral and are distinctly subepithelial.
Sometimes a discrete intracordal mass can be appreciated. Epidermoid cysts
tend to bulge on the superior and medial aspect of the midmusculomembra-
nous region. On phonation, the epithelium often can be seen moving over
the cyst, so that it appears like an ‘‘egg in soup.’’ Mucus retention cysts
occur most frequently on the inferior aspect of the vocal fold because the
medial edge is devoid of mucus glands. Edema of the contralateral fold or
a contact nodule may be seen. Phase asymmetry dominates VLS, given
the increased stiffness of the cover, and contralateral traumatic changes
are common [42]. Notably, despite the excellent resolution of VLS, it can
be impossible to fully understand the nature of a vocal fold mass without
the higher magnification and tactile evaluation by way of palpation achiev-
able during suspension microlaryngoscopy. Similarly, if therapeutic suspen-
sion microlaryngoscopy is undertaken to treat a benign mass, additional
mass/vascular lesions not seen on VLS may be revealed. This possibility
should be discussed with patients who decide to undergo surgery, so that
occult masses discovered at that time can be addressed.
Treatment of benign vocal fold masses depends on a patient’s symptom
complex. If laryngopharyngeal reflux is present, it should be treated first,
as should muscle tension dysphonia. A course of voice therapy will address
vocal behaviors in the speaking and singing voice to which the development
of the mass or muscle tension dysphonia may be attributed. Goals of ther-
apy are to maximize vocal efficiency, thereby reducing the vibratory trauma
that underlies and exacerbates the masses [43]. Although voice therapy alone
cannot cure vocal fold nodules (ie, make them disappear in entirety), the
surrounding edema may reduce significantly with changes in vocal hygiene.
Return to near-normal function is possible, although some professionals will
continue to notice limitations in the voice and, thus, require surgery. Vocal
fold polyps and vocal fold cysts also should be treated with an initial course
of voice therapy to optimize vocal hygiene; however, in these cases, voice
therapy less often accomplishes significant recovery of function, and surgery
is almost always required if associated symptoms are significant. Precise
phonomicrosurgical excision of the lesions, with every effort to preserve as
much normal tissue (epithelium and superficial lamina propria) as possible,
remains the surgery of choice for symptomatic benign lesions. Specifics of
technique are addressed elsewhere in this issue. Following an immediate
postoperative course of voice rest ranging from 4 to 14 days, voice therapy
is mandatory to achieve the best functional results.
The special case of rheumatoid nodules and bamboo nodes is considered
here briefly (Fig. 5). First, obtaining the history of rheumatoid arthritis, or
any other/additional autoimmune disease, is critical during the interview
process for any complaint. If this history is obtained, the laryngologist
should note all current and previous medications used to treat the disorder
and the name and contact information for the patient’s rheumatologist. Sec-
ond, it is important to know how well controlled the patient’s autoimmune
disease is and whether he/she can correlate any changes in voice with
changes in the severity of autoimmune disease. Vocal fold lesions related
to rheumatoid arthritis and autoimmune disease are rare, as are their de-
scriptions in the literature [44]; however, laryngeal involvement in rheuma-
toid arthritis is well documented and may be present in most patients who
suffer from that disease [44–47]. The cricoarytenoid joint, which is diarthroi-
dal, like the interphalangeal joints in the distal extremities, is involved most
commonly. Laryngeal manifestations of rheumatoid arthritis in the cricoar-
ytenoid joint include dysphonia, odynophonia, dysphagia, dyspnea, and
throat pain. If nodules are present in rheumatoid arthritis or autoimmune
disease, vocal roughness is a frequent complaint, as is intermittent aphonia.
Fig. 5. Rheumatoid nodules. Bilateral, horizontal-appearing intracordal masses with subtle sur-
rounding erythema are seen.
Clinical manifestations include hoarseness and instability in connected

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

Vocal fold scar is a vexing diagnosis for patients and laryngologists.
Although there is no agreement on how best to manage vocal fold scar, it
is agreed that treatment outcomes are fair to good, but inconsistent at
best [49–53]. This mandates continued research into the pathophysiology,
histology, biology, and treatment of vocal fold scarring. A detailed discus-
sion of these topics is beyond the scope of this article, and the reader is
referred to several recent reviews [50,51,53]. Nonetheless, given the potential
for permanent voice change and the impact on patients, particularly profes-
sional voice users, vocal fold scar is an area worthy of utmost attention in
the clinical and research realms.
Scar is derived from the Greek eschara (scab) and is defined as ‘‘fibrous
tissue replacing normal tissues destroyed by injury or disease’’ [54]. Causes
of vocal fold scar are diverse and include inflammatory, neoplastic, trau-
matic, and iatrogenic entities [49]. Although the incidence and epidemiology
of vocal fold scar are not well documented in the general population or pro-
fessional voice users, one can imagine that inflammatory and iatrogenic
causes are the most common among professional voice users. In addition
to vocal misuse and abuse (which predispose to fibrovascular change and
mass lesions, themselves associated with scar), laryngopharyngeal reflux,

bacterial laryngotracheitis, and prior aggressive endolaryngeal surgery are
associated with vocal fold scar [49,53,55]. Sulcus vocalis is a specific entity
often considered under the ‘‘umbrella’’ of vocal fold scar, because it, too,
consists of fibrous tissue replacing normal tissue in the vocal fold. Sulcus
vocalis is discussed further in this section.
In the vocal fold, the ‘‘normal tissue’’ destroyed by scar in varying degree
and thickness is the delicate multilayered structure composed of epithelium,
superficial lamina propria, intermediate lamina propria, deep lamina prop-
ria, and muscle. This fibrous insult compromises vocal fold pliability, the
exact property that allows production and modulation of voice, by causing
contraction of the vocal fold cover and effecting loss of vocal fold volume
[53]. The result is an increase in vocal fold stiffness and subsequent decrease
in vibratory capacity [49].
(Access Video on Left Vocal Fold Scar in online version of this article at: http://www.Oto.
TheClinics.com.)
Effects on voice depend on the location of vocal fold scar relative to the
vocal fold’s medial edge and midmusculomembranous region, the depth of
scar, the presence of other lesions/pathologic entities, and the patient’s innate
or trained compensatory mechanisms of producing voice. Patients may de-
velop a strained, harsh, or breathy voice, diplophonia, or hoarseness [49]. In
addition to change in voice, common complaints include vocal fatigue, loss
of range, and loss of stamina. These complaints also apply to sulcus vocalis.
Sulcus vocalis is a linear invagination of epithelium along the medial edge
of the vocal fold into or beyond the superficial layer of the lamina propria.
Sulcus vocalis can extend into the intermediate or deep layer of the lamina
propria or to the vocalis muscle. Depth of migration generally correlates
with symptom severity, as well as the prognosis for successful treatment.
Ford and colleagues [56] developed a classification scheme for sulcus defor-
mities, which is helpful in thinking about their effect on the mucosal wave.
Types I and II sulcus vocalis are longitudinal depressions in the epithelium,
generally extending the length of the musculomembranous vocal fold (from
vocal process to anterior commissure), and they differ only in depth of pen-
etration. Type I sulcus vocalis extends into the superficial lamina propria
only, but does not reach the vocal ligament (intermediate and deep layers
of the lamina propria, the transition layer); type II sulcus vocalis extends
to or beyond the vocal ligament, causing loss of superficial lamina propria.
Type III sulcus vocalis is a deep, focal indentation of epithelium on the
medial surface of the vocal fold that does not extend its entire length, but
often resembles a ‘‘pit’’ or pocket (Figs. 6 and 7). In our experience, kera-
totic debris frequently accumulates in type III sulcus vocalis, such that ini-
tial evaluation in the clinic may raise the question of an intracordal cyst
because they are shallow, cause minimal loss of superficial lamina propria,
and generally result in only mild change of the mucosal wave. Type I sulcus
Fig. 6. Vocal fold sulcus. (A) Longitudinal scar is seen along the superomedial edge of the right
true vocal fold. (B) On suspension microlaryngoscopy, palpation with a right-angle hook
revealed this to be a ‘‘pocket’’ sulcus, or type III sulcus. It was removed successfully with pho-
nomicrosurgical techniques.
vocalis has been termed ‘‘physiologic sulcus.’’ Types II and III sulcus vocalis
are considered pathologic; type II also is referred to as ‘‘sulcus vergeture.’’
The key to diagnosing vocal fold scar or sulcus vocalis is a thorough
history (including specific vocal complaints and surgical history) and
physical examination, the most important aspect of which is VLS. VLS
features include asymmetric amplitude of vibration, the scarred side hav-
ing reduced or absent amplitude of vibration and loss of mucosal wave
(which may be focal or diffuse); incomplete glottic closure requiring
high pressure to sustain phonation given significant stiffness; and nonvi-
brating segment in the affected vocal fold that prevents mucosal wave
propagation [49].
Ventricular hyperfunction may or may not be seen, but usually appears
as the glottal gap increases in size. A complete voice evaluation with aero-
dynamic and acoustic batteries is imperative once vocal fold sulcus/sulcus
Fig. 7. Bilateral sulcus vocalis with significant loss of superficial lamina propria, vocal fold
bowing, and lateral cricoarytenoid hyperfunction. Significant muscle tension dysphonia also
is seen on phonation.
vocalis has been identified so that effects of therapy, whether medical or

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

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

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

users. In Hochman and colleagues’ [67] review of 42 patients who were
treated for ectasias and varices, 39 patients (93%) had additional lesions
(eg, polyps, nodules). Again, most patients were female (81%), and most
were professional/semiprofessional voice users or students (93%). Similarly,
all of the 12 patients who had microvascular lesions treated with KTP
(potassium-titanyl-phosphate) laser by Hirano and colleagues [70] had asso-
ciated lesions requiring surgical treatment. In our experience, it is not
unusual to find vocal fold varices with other benign lesions of the vocal folds
in professional voice users. Still, it is not known whether vocal fold varices
cause other benign lesions (eg, nodules or polyps) to develop, whether the
presence of a mass lesion on the vocal folds predisposes them to developing
vocal fold varices, or both. It has been hypothesized that the enlargement of
vocal fold blood vessels with significant vocal use or abuse will increase
vocal fold mass and stiffness, changing vocal fold vibratory patterns, possi-
bly inducing vocal fold edema and subsequent mass lesion development [62].
Certainly, varices and mass lesions share the common pathway of significant
vocal use, as in the case of professional voice users, as well as vocal overuse
or misuse in other patients.
It is difficult to know the most common symptom caused by vocal fold
varices given their relative low-documented incidence and their coexistence
with other lesions. The most common complaint among patients in Postma
and colleagues’ [66] review was hoarseness (72%), followed by decreased
vocal range (16%) and vocal fatigue (12%). Often, these symptoms are inter-
mittent, varying with voice use, and are widely accepted as common by other
clinicians as well. We have had the same experience; however, we also see
a number of young conservatory singers in the laryngology clinic for baseline
evaluations at the recommendation of their voice teachers. These students
have been singing through childhood and high school, often competitively.
Anecdotally, most of them have signs of laryngopharyngeal reflux, and
many have varices; however, most are asymptomatic. Sataloff and colleagues
[64] also observed asymptomatic patients who had vocal fold varices.
The treatment of vocal fold varices in professional voice users is the same
as that for other patients with these lesions; however, as is the case with
treating any lesion in the vocal professional, the recommendation and
timing of treatment must be individualized to account for their potential
impact on career goals and professional obligations. Also, the varices may
need to be treated in conjunction with other lesions. An asymptomatic
isolated varix does not require active treatment, but it should be followed
with regular VLS. Patients need to be educated about the possibility of vocal
fold hemorrhage, because of the fragility of these lesions, and counseled that
if any acute significant voice change occurs, especially related to voice use or
upper respiratory tract infection, strict voice rest should be observed and
immediate laryngologic evaluation obtained. Symptomatic vocal fold vari-
ces should be treated in a staged fashion, depending on the frequency and
severity of symptoms and on the evolution of the lesion (ie, change in their
size or number). Medical treatment almost always includes aggressive
treatment of laryngopharyngeal reflux, because it is nearly ubiquitous
among professional voice users. Decreasing reflux-associated vocal fold
edema should reduce the resultant increase in vocal fold mass, which likely
predisposes the patient to develop or exacerbate varices as increased effort is
made to produce voice. Decreasing reflux-associated mucus may decrease
throat clearing and its resultant trauma. A three-armed antireflux protocol,
including diet changes, behavior modification, and PPIs, is imperative.
Maintaining adequate hydration also is important. Some investigators
also institute mucolytic therapy as necessary [66]. The second major step
in medical therapy is to obtain a comprehensive voice evaluation, including
an acoustic and aerodynamic test battery and flexible and rigid video
endoscopy with and without stroboscopy. This will be used to tailor individ-
ualized voice therapy to optimize vocal technique and minimize vocal
trauma in the speaking and singing voice. Baseline voice evaluation and
voice therapy also are critical to obtain should surgical intervention be
required later.
The most widely accepted indication for surgical treatment of vocal fold
varices is recurrent vocal fold hemorrhage in patients who have an identifi-
able varix in the vocal fold sustaining this injury and who have a resultant
irreversible unacceptable change in the voice [61–63,65–67,69,70]. As with
surgery for most benign laryngeal disease, patients must be counseled of
the risk involved in the surgery, which can be voice and career saving, but
nonetheless is elective. Other indications for surgery were outlined nicely
by Postma and colleagues, [66] however, some laryngologists may think of
these as relative indications for surgery. These indications include enlarge-
ment of the varix, development of a mass in conjunction with a varix or
hemorrhage, or unacceptable dysphonia secondary to persistent vibratory
abnormality seen on serial VLS after maximal medical and voice therapy.
One successful approach prioritizes the patient’s self-assessment of vocal
function and commitment to good vocal hygiene and technique. If vocal
hygiene and technique are sufficiently good and consistent, but vocal func-
tion is inadequate, other lesions have been treated or excluded, and medical
therapy has failed, surgery should be offered to the patient. If all of these
criteria are met, but there are other mass lesions that require treatment,
these should be treated operatively at the same time as treating the vocal
fold varices. Most important, as emphasized by other investigators, consent
must be obtained to treat/excise any mass lesions newly discovered on
suspension microlaryngoscopy that by size, position, or character could
be affecting the voice [67,70]. The decision to treat bilateral vocal fold
lesions in one or two stages is made intraoperatively and depends on the
lesions’ locations relative to each other and to the medial edge of the mid-
musculomembranous region. A two-stage approach is selected if there is
considerable risk for postoperative apposition of the operative sites and,
thus, risk for web formation, or if extensive work in the superficial lamina
propria may compromise function after bilateral surgery.
Techniques for surgical treatment of vocal fold varices have evolved over
time, paralleling the development of direct laryngoscopy, laser technology,
and microsurgical instrumentation. Baker [61] described ‘‘picking’’ off the
prominent vessel without ‘‘biting’’ into the vocal fold by way of direct
laryngoscopy. Cold instruments were used to remove vocal fold varices up
until the development of the CO2 laser, after which it was used on low-
power settings and with defocused spot sizes and short single pulses to
ablate vocal fold varices [62,63,67,69]; however, with concern for thermal
damage to the vocal fold, the CO2 laser fell out of favor, and microsurgical
technique has been used more routinely [67,69,70]. This technique involves
making several epithelial cordotomies directly overlying the varix, meticu-
lously dissecting it away from the surrounding superficial lamina propria,
then excising it with scissors or microforceps, applying epinephrine-soaked
pledgets to achieve hemostasis, and allowing the cordotomies to heal pri-
marily [67]. More recently, angiolytic lasers have been used to treat vocal
fold varices, primarily in conjunction with other lesions (ie, polyps, nodules)
[70,71]. The senior author routinely uses the 585-nm pulsed-dye laser (Pho-
togenica SV, Cynosure, Littleton, Massachusetts) at 500 to 700 millijoules
(mJ), to treat vocal fold varices and ‘‘normal’’-appearing vocal fold vessels
that seem to ‘‘feed’’ a lesion when performing surgery for mass lesions
[72,73]. The pulsed angiolytic lasers are safe and provide precise ablation
of vocal fold vessels. Further basic science and clinical research with long-
term patient follow-up is required to define the best role for the pulsed-
dye laser (PDL) and KTP lasers in the treatment of vocal fold varices and
other laryngeal processes. There are more data in the literature to support
PDL use than to support the KTP laser [71–74]. Retrospective evaluations
of both lasers are ongoing, and prospective studies are in order.
Vocal fold hemorrhage

Vocal fold hemorrhage is a laryngologic emergency that warrants imme-
diate strict voice rest for 7 to 14 days and VLS to document the effects on
the mucosal wave (Fig. 9). Most frequently, patients note a sudden signifi-
cant change in the voice with increased voice use or vocal abuse (singing
or public speaking for prolonged or intense periods, yelling) or in associa-
tion with upper respiratory tract irritation and inflammation (coughing,
sneezing) [61,63,65,68,69,75–79]. Rarely, subtle chronic change in the voice
may be the presenting symptom of vocal fold hemorrhage [65,69,77]. Vocal
fold hemorrhage usually occurs in one vocal fold, although bilateral
vocal fold hemorrhage has been reported [63,65]. The demographics of vocal
fold hemorrhage parallel those of vocal fold varices: vocal fold hemorrhage
is more common in professional voice users and in women. A strong corre-
lation between hormonal imbalance and vocal fold hemorrhage, especially
Fig. 9. Vocal fold hemorrhage sequelae. Fibrotic vocal folds after multiple recurrent bilateral
vocal fold hemorrhages.
recurrent vocal fold hemorrhage, also has been noted by multiple investiga-
tors [63,67–69]. In addition to vocal fold hemorrhage occurring in peri-
menstrual women (just before or during menstruation), women in
hormone supplement withdrawal, pregnant women, or women having un-
dergone gynecologic surgery [63,65], other risk factors for vocal fold hemor-
rhage in patients who have vocal fold varices have been identified, including
consumption of aspirin and aspirin products, use of nonsteroidal anti-in-
flammatory drugs, coumadin therapy, and upper respiratory tract infections
[61–63,65,66,76]. Laryngeal trauma, whether external or internal/iatrogenic,
is another cause of vocal fold hemorrhage that is rare and not specific to
professional voice users, but something of which they should be aware so
that they take proper safety measures (wearing seatbelts in motor vehicles
and well-fitted harnesses as warranted in their work). As with vocal fold
varices, it is possible that the apparent higher incidence of vocal fold hem-
orrhage in professional voice users compared with the general population is
simply a reflection of the makeup of most laryngology practices and the sen-
sitivity of professional voice users to changes in voice. The incidence of vo-
cal fold hemorrhage in the population at large may be much higher, but
underdiagnosed.
Most professional voice users who experience sudden decrement in the
voice self-impose voice rest and seek laryngologic evaluation. Voice rest is
believed to minimize the potential for further bleeding into the affected vocal
fold as well as the potential for trauma to the opposite vocal fold during
phonation. If seen in the immediate hours after hemorrhage, the vocal
fold may be bulging with blood/hematoma; after several days, it usually flat-
tens, but remains red; with time, blood is metabolized, and the color changes
from red to yellow because of hemosiderin staining and eventually back to
white. At any time after vocal fold hemorrhage, before complete resolution,
VLS reveals vocal fold stiffness and decreases in the amplitude and
magnitude of the mucosal wave [65,68,69]. Most investigators recommend 7

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

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

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

paralysis.
Despite the best voice training, professional voice users are not immune
to the development of disease in the middle and older years. Thus, the lar-
yngologist is obligated to keep a broad differential diagnosis in mind while
treating this select group of aging patients. Most presbyphonic patients will
benefit from voice therapy [80]. Specific vocal fold pathology can be treated
surgically as indicated.
Voice overuse
One of the most common problems in professional voice users, especially
singers and actors, is laryngitis associated with voice overuse. This is to be
distinguished from infectious laryngitis, also common in this population
during peak performance times, which are associated with long hours,
lack of sleep, and often, poor nutrition. Reflux laryngitis also may be an un-
derlying problem; however, overuse in and of itself can cause dysphonia in
the singing and the speaking voice, odynophonia, loss of range, loss of clar-
ity, and early vocal fatigue. This is seen frequently in performers who are on
the road and in the middle or toward the end of a rigorous concert schedule
(eg, four to seven performances in a week for 6 to 16 consecutive weeks).
Pop, rock, country, and musical theater singers who sing in large open
venues with variable acoustics seem, anecdotally, to be at particular risk
for the effects of voice overuse. Many performers believe that they have in-
finite use of their vocal folds and do not realize that they are athletes who
need to rest and recover after an event. Frequent high-energy performance
can result in vocal fold edema that requires more ‘‘pushing’’ over time to get
the same results; this results in a vicsous cycle phonotrauma. Any number of
findings may be present on laryngoscopy. Vocal fold edema, assumed to be
subacute, overlying chronic fibrovascular changes, and sulcus deformities
are common. Varices and resolving hemorrhage may be seen.
The best treatment of this condition is relative voice rest. Sometimes,
complete voice rest for a few days may be appropriate. A frank discussion
with the performer about short- and long-term goals and obligations is im-
portant to developing a management strategy. If a performance is imminent,
the patient has to decide how important it isdfinancially, professionally,
and emotionally. The laryngologist also has to weigh in on how dangerous
further voice use is to the patient’s long-term vocal health. Doctor’s orders
for voice rest can be a welcome relief to a performer. Conversely, the laryng-
ologist may encounter significant resistance to this recommendation. If this
is the casedand especially if a performance is of paramount importanced
a short course of high-dose oral steroids (burst and taper) can be prescribed.
One practical approach is to prescribe methylprednisolone at a high first
dose with rapid taper. For example, this can be methylprednisolone, 16 mg,
days 1 through 3, with a rapid taper over 3 to 4 days (eg, 12 mg, days 4 and
5; 8 mg, day 6; 4 mg, day 7). Patients are cautioned to mark during rehearsals
or not sing at all and to use the voice minimally otherwise. Sometimes per-
formers have to tell their audiences that they cannot sing in full voice. Finally,
all patients must be counseled that the risk for vocal fold hemorrhage and tear
is higher when on steroid therapy. If any sudden decrement in voice occurs,
they are instructed to observe immediate full voice rest and to seek laryngo-
logic evaluation as soon as possible.
The patient is reevaluated once voice rest has been prescribed for overuse
and the larynx has had time to recover. Symptoms and findings on VLS are
tracked. Resumption of normal practice and performance schedules needs
to be undertaken with serious caution and an appreciation for the fragility
of the larynx, and it can take place once the larynx has shown signs of im-
provement (decreased edema, erythema, size of varices). Performers are en-
couraged to improve vocal hygiene, maintain excellent hydration, and
observe regular periods of voice rest throughout the day. Most are able to
accomplish this while meeting their professional demands. The addition of
voice therapy is an important vehicle for teaching and reinforcing these
strategies and is an important management option for voice overuse.
Special considerations in caring for the professional voice user

Emphasis was placed on the importance of obtaining a complete history
as well as understanding the professional voice user’s priorities to establish
trust and to facilitate comprehensive patient care. Similarly, it is important
to approach this care with a team model, including voice therapists (some-
times singing and speech therapists), the singing teacher/voice coach, and
other physicians who care for the patient. Many patients are otherwise
healthy and do not see other clinicians, in which case the laryngologist fre-
quently plays a primary care role, tending to questions of health mainte-
nance and serving as a referral base as necessary. This is particularly true
for young patients, many of whom live away from home as students or as
traveling performers. Obtaining complete social histories and taking time
to educate patients about the importance of hydration, rest, and tobacco,
marijuana, alcohol, and other drug avoidance are critical to comprehensive
care. Young patients also benefit from discussions regarding short- and
long-term professional goals so that they begin to develop a realistic per-
spective on the impact that their voice use has on its integrity. Because
many professional voice users have multiple physicians who care for them
and several may be on multiple medications, communication with other
physicians is critical to coordinated care.
Summary
Multiple diagnoses may be present simultaneously in the professional
voice user. Each needs to be considered in the context of the other,
such that treatment of one problem does not ignore the influence of
others on its resolution.
The presence of a benign vocal fold lesion in a professional voice user
does not mandate treatment if it is not compromising function. Surgi-
cal treatment of asymptomatic benign vocal fold lesions in professional
voice users with the goal of preventing a problem must be approached
with caution, because any trauma to the vocal fold cover by intubation
or surgical instrumentation, including lasers, can change the voice.
Although incidence and prevalence of inflammatory processes in the lar-
ynx are not well documented, they seem common in professional voice
users; include laryngopharyngeal reflux (common), laryngitis from
voice overuse (common), and fungal laryngitis (uncommon in general,
but being recognized more frequently in patients on inhaled steroids);
and warrant aggressive treatment to restore the voice.
Muscle tension dysphonia is a frequent compensatory mechanism for
other processes that should be sought out if muscle tension dysphonia
is identified.
Vocal fold paresis can cause glottal insufficiency and subsequent breath-
iness. It is diagnosed best by LEMG and can be treated in a stepwise
fashion with voice therapy and augmentation.
Vocal fold scar is associated with long-term voice use or frequent phono-
trauma, resulting in stiff vocal folds, increase in fundamental fre-
quency, and roughness. Treatment is controversial.
Vocal fold varices are seen more frequently in professional voice users
than in nonprofessional voice users and are more frequent in women
than in men. They generally do not require treatment unless recurrent
hemorrhage occurs.
Voice changes as related to age, menopause, and voice overuse are of par-
ticular relevance to professional voice users. Understanding these areas
of laryngology is important to the continuity of care provided to these
patients by the laryngologist.
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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 also
know 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’’ pharyngitis
or 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 early
part of the twentieth century. Nonetheless, a good portion of voice care de-
livery for professional voice users is performed by general otolaryngologists
who do not have an experienced speech pathologist or videostroboscopic
equipment available. Even in this modern era, many situations arise where
vocal 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 improved
quality, portability, and better affordability of endoscopic technology has
allowed for better visual assessment of the larynx in the office and the field.
In addition, an increased focus on vocal awareness and education in modern
otolaryngology training programs has begun to close the experience gap
between general otolaryngologists and laryngology subspecialists.
Ultimately, the optimal care of a professional voice user with a vocal
emergency occurs within a setting where a full clinical voice evaluation
and 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: michael.m.johns@emoryhealthcare.org (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 in
view of the fact that phonation was not the primary function of the larynx;
phylogenetically it is very late. The patient with chronic laryngeal disease is
almost 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 awake
will 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 as
factories 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 found
that nearly 75% of complaints center around vocal difficulty, with sinus
complaints, pharyngeal irritation, and cough being the next most common
primary symptoms [4]. As with any chief complaint, a thorough history is im-
perative when managing a vocal emergency. Detailed questionnaires have
been published previously [5]. Unfortunately, patients typically are vague
and occasionally may withhold information when describing their vocal
problems [4]. The term ‘‘hoarseness’’ is nonspecific, and the exact symptoms
need 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 is
your voice doing that it should not do?’’ and ‘‘What is your voice not doing
that it should do?’’ are two useful questions to prompt the patient further.
Patients should be questioned regarding the details surrounding the onset
of the vocal disorder. Any vocal change with a sudden onset (particularly an
acute change that occurs during phonation) is a red flag for a vocal fold
hemorrhage or mucosal tear. This finding must be investigated further
with laryngeal imaging. Ask specific questions about loss of range or loss
of 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 onset
are other manifestations of vocal fold mucosal edema or lesions. Changes in
vocal quality, effort, endurance, and fatigue; the ability to sing or speak
loudly or softly at various frequencies; or limitations in dynamic range often
give clues that vocal fold pathology is present or developing. The symptoms
of 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 of
training and vocal awareness. Details of vocal warm-up routines, length and
VOCAL EMERGENCIES 1065
frequency of performances, and vocal obligations between events should be

noted. This information will help the clinician to understand the degree of
vocal demand and what can and cannot be modified to minimize
phonotrauma.
Once the parameters of the chief complaint have been established, it is
important for the physician to understand the performance environment
and schedule. Not infrequently, these patients are seen on site, allowing
for a first-hand assessment of the performance venue. Evaluation of the
acoustics, the amplification system, competing sound sources, temperature,
cleanliness, air filtration system, and allergen exposures aid in understanding
the patient’s relative risk for exacerbating a voice disorder. Often, simple
discussion 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 vocal
monitors) for the performer.
The event schedule and importance of upcoming events should be closely
reviewed 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. How
upcoming events relate to the patient’s short, medium and long-term career
goals is a vital perspective to gain for the purposes of making management
decisions. The financial implications of missing an event or events should
also be taken into consideration.
Differential diagnosis of vocal emergencies in the performing artist

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

Vocal fold hemorrhages are the result of acute phonotrauma and can be
considered a ‘‘vocal accident’’ (Fig. 1). The shearing forces within the super-
ficial lamina propria layer tear the microvasculature, allowing blood to
spread 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 the
contents of Reinke’s space (eg, scar tissue may prevent spread of extravasat-
ing blood). Patients commonly note sudden voice change that occurred
while 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 development
of a hemorrhage [7]. Women should avoid the use of NSAIDs and aspirin
in the premenstrual and menstrual periods. Identification of a vocal fold
1066 KLEIN & JOHNS
Box 1. Differential diagnosis

Vocal fold mucosal tear
Acute laryngitis
Viral
Bacterial
Fungal
Phonotraumatic edema
Acute edema on chronic fibrovascular (subepithelial)
change/preexisting lesions
Asthma exacerbation
Upper respiratory tract infection
Pharyngitis, viral/bacterial
Rhinosinusitis, viral/bacterial
Bronchitis, viral/bacterial
Allergic rhinitis
LPR exacerbation
Hormonal/endocrine changes
hemorrhage in the acutely dysphonic performer is extremely important and

is the primary reason why laryngoscopy needs to be performed during the
assessment. Vocal fold hemorrhage is treated with absolute voice rest,
with or without corticosteroids, until resolution has occurred (ie, resorption
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 otolaryngologist
must be prepared to support the patient in interactions with management.
Patients need to be advised of the serious risk for scar or lesion development
if they are to perform through a vocal fold hemorrhage.
Vocal fold mucosal tear

Mucosal tears usually result from an episode of harmful singing, yelling, or
severe coughing/retching. The overwhelming shearing forces exerted upon the
epithelium and superficial lamina propria cause the tissue to literally separate
(Fig. 2) [8]. The acute symptoms include immediate hoarseness, loss of range,
and discomfort. A mucosal tear may appear as a visible break in the mucosa on
stroboscopy, presenting as a jagged edge in the epithelium. Initial findings on
examination also can include vocal fold hemorrhage, edema, erythema, and
stiffness on videostrobolaryngoscopy. Often, a tear can be difficult to diagnose
in the acute setting, and one should have a low threshold to place a patient with
these symptoms on absolute voice rest with close serial evaluation. If complete
voice rest is followed, healing usually occurs without sequelae. If phonation or
coughing 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 phonatory
surface of the true vocal fold.
Acute laryngitis
As with many upper respiratory tract infections, the cause of infectious
laryngitis 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 identical
in the acute setting: Reinke’s space (the superficial lamina propria layer) en-
gorges with inflammatory cells, resulting in increased mass (Fig. 3). This
prevents the vocal fold from vibrating periodically. The addition of vocal
fold 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 these
pitches [9]. Intermittent voice breaks and changes in register transition are
additional symptoms. Phonotraumatic edema has the same effect, but it is
more easily treatable with conservative measures.
Relative or absolute voice rest is the mainstay of treatment, depending on
the severity of the edema. Mild to moderate edema can be treated with rel-
ative voice rest and adjunctive measures noted below. Severe edema should
be treated with absolute voice rest. Additionally, the patient should be ad-
vised against the use of NSAIDs, because there is an increased risk for vocal
fold hemorrhage secondary to the fragility of the vocal fold blood vessels in
the acutely inflamed state. Appropriate antibiotics should be prescribed if
clinical suspicion for bacterial infection is present. For mild to moderate vo-
cal fold edema, corticosteroids can be used acutely to treat edema effectively
and facilitate performance. Intramuscular steroids, such as dexamethasone
and cortisone, can begin to have an effect within 1 hour; oral steroids,
such as prednisone and methylprednisolone, typically produce the desired
effect 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 regarding
the 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 in
isolation without modified voice rest, defined as essential voice use only, and
supportive measures. Vocal fold tear, hemorrhage, scarring, or permanent
hoarseness are risks that need to be discussed with the patient when per-
forming while taking steroids. Often, the voice sounds normal, despite the
acutely fragile state of the vocal folds. The otolaryngologist also needs to be
aware of performers living ‘‘shot to shot,’’ using steroids as a crutch for
voice overuse or misuse. Taking a careful history about steroid use and ef-
fect can give clues to this problem. Vocal rehabilitation with voice therapy
helps 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 in
acute edema, which results as a consequence of the increased vocal effort
necessary to overcome the decreased pliability of the scarred regions. The
combination 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 escapes
anterior and posterior to the lesions. In addition, the affected areas are
stiffer 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 indirectly
to acute vocal changes by way of localized edema, secretions, pain, throat
clearing, coughing, dehydration, generalized malaise, nasal congestion, or
headaches. A careful history of onset, location, and severity of symptoms
and physical examination helps make the diagnosis and treatment and
should be directed to the site of pathology. Empiric treatment with antibi-
otics is warranted in cases with suspected bacterial etiology. Symptomatic
relief of nasal congestion can be achieved with the short-term use of topical
nasal decongestants (eg, oxymetazoline). Topical nasal steroid sprays also
can be helpful in the acute setting. Oral decongestants (eg, pseudoephedrine)
can be extremely drying and may have secondary deleterious effects. The use
of drying agents can lead to increased shearing forces, predisposing patients
1070 KLEIN & JOHNS
to vocal fold tears, subepithelial thickening, and fibrosis. Patients should be

cautioned regarding the use of topical anesthetics for pharyngitis because
numbness can lead to loss of vocal control. Vigorous hydration and modi-
fied voice use is encouraged. Performance during an acute upper respiratory
tract infection is discouraged.
Allergic rhinitis
The rhinorrhea and nasal mucosal swelling associated with allergic rhini-
tis can affect the vocal performer significantly, although symptoms rarely
are severe enough to warrant show cancellation. Short-term relief can be
achieved with oral antihistamines and nasal decongestion, although patients
should be warned about the drying side effects and potential sedation seen
with 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, leukotriene
antagonists, mast-cell stabilizers, immunotherapy) should be recommended
as indicated [10].
Laryngopharyngeal reflux
Performers are particularly at risk for the development of symptoms
from LPR [11]. Erratic dietary habits, stress, and abdominal support asso-
ciated with singingdcombined with the sensitive nature of high-level vocal
performancedmake the vocal performer more susceptible to acute vocal
change 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 may
be 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 and
a nighttime dose of an H2-blocker, even in asymptomatic individuals, may
hasten recovery from an upper respiratory tract infection.
Acute asthma exacerbation

As with the general population, professional voice users are subject to med-
ical conditions that may affect vocal quality. Asthma can diminish vocal
strength, endurance, and quality by weakening the power source to the larynx.
It is important to recognize this problem so that proper medical management
for an acute asthma exacerbation can be instituted in a timely fashion. Inhaled
steroids in conjunction with rescue inhalers are the mainstay of treatment for
reactive airway disease. The clinician and the patient need to be aware of the
deleterious effects that inhaled steroids can have on vocal fold muscle bulk, the
voice, and the predisposition to fungal laryngitis [12]. When possible, the pa-
tient should discuss using noninhaled or nebulized preparations to treat
asthma acutely and chronically with his/her pulmonologist.
Functional dysphonia
Vocal performers and orators experience a significant amount of stress or
anxiety, 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 before
vocal performance. Stage fright is a behavioral problem that is addressed
best with behavioral solutions. The anxiety associated with performance
leads 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 is
impaired vocal performance. Intervention consists of strategies to optimize
respiration 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 for
optimal performance. Identification of these problems and an established
relationship with a trained voice/singing pathologist are essential to address
this issue adequately.
Site of the evaluation

Phone triage
As one would infer from the label ‘‘vocal emergencies,’’ such events do
command 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 vocal
obligation. A politician who enters a debate with a weak voice or frequent
throat 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 physician
with the expectation that he/she will understand the predicament and pro-
vide last-minute, free advice. Not infrequently, the call comes from the
patient’s manager, who attempts to convey the patient’s symptoms with
limited information, making medical management difficult.
Ideally, the otolaryngologist can overcome this obstacle by seeing the
patient 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 traveled

out of the areadand treatment decisions may have to be made over the
phone. One must go back to the history and extract any available data
that may give a clue as to the likely diagnosis. Was the onset of the vocal
disorder an acute event that occurred during a show? Is it part of a pattern
that 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? Is
the patient sick?
Usually, an illness resulting in vocal difficulties is apparent. Patients com-
plaining of hoarseness associated with the symptoms of rhinosinusitis or an
acute upper respiratory tract infection will need over-the-counter or pre-
scription medications quickly in an attempt to lessen the effect on the voice
as soon as possible, followed by a reassessment. They occasionally request
their ‘‘usual’’ remedy, such as steroids, NSAIDS, or vitamin B12. The issues
surrounding 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 significant
pressures 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 professional
guidance. The otolaryngologist should have a low threshold to request
that 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 the
physician’s office, where the full diagnostic armamentarium is present.
This is particularly true for the patient with acute voice change in whom
high-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. Circumstances
may 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 the
patient risk performance when one should cancel.
On-site evaluation does allow the clinician to see the performance venue
and its acoustic and environmental features. One also can request to see the
transportation vehicle, if any, which is being used for long road trips. This
may reveal potential allergens, irritants, or other factors that can contribute
to voice disorders.
There are clearly significant limitations in the ability to diagnose and
treat optimally in on-site settings. The main limitation is the lack of easily
portable laryngeal videostroboscopy and high-resolution laryngeal imaging

equipment. Advancing technology is moderating this limitation, and one
should be equipped with appropriate instruments and therapeutics (see
‘‘Tools’’ section) if he/she is going to be able to provide adequate on-site
care.
Office evaluation
The office setting offers the best facilities to optimize patient care. This
separates the patient from one’s stressful setting to allow for a more focused
interview, and the otolaryngologist will have the full array of diagnostic in-
strumentation to make an accurate diagnosis and guide treatment. Outside
of 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 fold
mucosal pliability can be assessed clearly, and severe problems (eg, vocal
fold 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, curved
cannulas, injectable steroids and vitamin B12, ear curettes, various dental
mirrors, 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 to
handle most situations.
Limitations in equipment portability are being overcome by technologi-
cal advances. Flexible fiberoptic laryngoscopes are readily available, as
are the portable light sources that can optimize the assessment of a vocal
emergency on site; however, one should be armed with other equipment be-
cause many patients will refuse the topical anesthetic (out of fear that it will
affect one’s voice or swallowing) or simply will not tolerate the nasolaryngo-
scopy procedure. Rigid scopes also can be attached to portable light sources
and are equally equipped with an eyepiece to provide direct visualization of
the larynx. Historically, stroboscopy has not been an option, although por-
table stroboscopy units are becoming available, and handheld strobe lights
are under development. The key is to have rigid or flexible endoscopy with
quality illumination and, ideally, videostroboscopy to allow clear
1074 KLEIN & JOHNS
visualization of the larynx. Without this equipment, otolaryngologists are

discouraged from evaluating patients on site.
Office location
The optimal setting for the acute evaluation and management of a vocal
crisis 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, treat
the ailment. Some pathologic processes are obvious enough that a dental
mirror or flexible fiberoptic laryngoscope could reveal the pertinent findings;
however, it does not provide useful information regarding the effects of the
pathology on the laryngeal biomechanics and vocal fold oscillation. In
addition, the resolution and magnification may be inadequate to reveal
secondary pathologies or chronic fibrovascular changes.
Typically, the decision to purchase a videostroboscopy unit is driven by
finances; 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 an
alarming rate, many affordable, satisfactory units are available.
Aside from proper imaging equipment, one must be prepared to treat
patients acutely, because there may be only hours before a performance
or vocal commitment. Therefore, a stock of injectable steroids and other
commonly used medications is essential. Maintaining a supply of over-
the-counter remedies can help to postpone a trip to the pharmacy for the
performer or production staff until a more convenient time is available.
Evaluation and management of the acutely ill performer

Hours until show time
The pressure of performance is transferred from the patient to the physician
in these situations. A significant amount of time, money, and effort has been
invested 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 fold
hemorrhage, vocal fold tear, or other significant laryngeal injury has
occurred to warrant cancellation of the performance. Therefore, visualizing
the larynx in some way is imperative. In the absence of a show-stopping finding
and after the most accurate possible diagnosis has been made, a frank discus-
sion should occur between the patient and physician, involving the event/show
management only at the patient’s discretion. This discussion should focus on
whether the patient believes that he/she will be able to perform acceptably. If
the 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, in
which case supportive measures to facilitate vocal performance can be
pursued.
Days until show time

The benefit of having several days to manage a vocal emergency is simply
having the luxury of time. Patients can be seen in the office with optimum di-
agnostic equipment and the benefit of videostroboscopy. Precise diagnosis
plus 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 acute
phonotraumatic events resolve spontaneously. If a vocal fold hemorrhage
has occurred, serial observation for resolution can be performed, and show
cancellation may be avoided. The luxury of time also enables the otolaryngol-
ogist to administer a larger range of medications. Antibiotics, steroids (if indi-
cated), and supportive medications will have time to take effect. Oral steroids
can be used in lieu of intramuscular injection, and voice therapy can be enter-
tained. Working with a speech pathologist with singing expertise offers the
benefit 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 vocal
goals can be considered and weighed into the decision-making process.
The role of voice therapy to modify maladaptive vocal behaviors becomes
more important, and working with a skilled speech pathologist or singing
voice specialist should be encouraged. Disorders, such as LPR, allergic rhi-
nitis, and chronic sinusitis, can be managed more effectively. Acute changes
can be sorted out from chronic changes, allowing the performer to return to
baseline 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 edema
arising 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 is
available. Patients need to understand that steroids are a short-term solu-
tion, cannot be used frequently with hope for significant effects, and carry
risks 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 voice
is small. Fortunately, most performers who have acute laryngeal edema are
responsible individuals who have had the misfortune of acquiring a viral ill-
ness at an inopportune time. These patients are ideal candidates for acute
use 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 effect
within an hour and lasts approximately 24 hours. Depomedrol begins to
take effect within 24 hours and has effect for approximately 5 days. A short
burst and taper of oral methylprednisolone is the authors’ choice for oral
steroids. A corticosteroid dosing equivalency chart is given in Table 1.
Nonsteroidal anti-inflammatory drugs

Ibuprofen and other NSAIDs commonly are available over the counter
and are taken frequently by ill performers to relieve sore throat and facial
discomfort. Although the anti-inflammatory effect of these medications
may 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 in
over-the-counter cold remedies. These medications are effective in providing
nasal 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 and
phenylephrine) have minimal systemic side effects and are effective; how-
ever, they carry the risk for rhinitis medicamentosa and should only be
used 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 allergic
rhinitis, but also have a drying effect, although less severe than with oral de-
congestants. Patients should be counseled regarding these medications’ side
effects. Nonsedating antihistamines (eg, loratadine) are more appropriate to
use around performance times than are sedating antihistamines (eg,
diphenhydramine).
Mucolytics
Mucolytics, such as guaifenesin, offer symptomatic relief by thinning
secretions. Short- and long-acting formulations are available. Long-acting
Table 1
Corticosteroid comparison chart
Equivalent glucocorticoid Potency relative to hydrocortisone Half-life

Agent dose (mg) Anti- inflammatory Mineral-corticoid Plasma (min) Duration of action (h)
Short acting
VOCAL EMERGENCIES
Hydrocortisone (Cortef, Cortisol) 20 1 1 90 8–12
Cortisone acetate 25 0.8 0.8 30 8–12
Intermediate acting
Prednisone 5 4 0.8 60 12–36
Prednisolone 5 4 0.8 200 12–36
Triamcinolone 4 5 0 300 12–36
Methylprednisolone 4 5 0.5 180 12–36
Long acting
Dexamethasone 0.75 30 0 200 36–54
Betamethasone 0.6 30 0 300 36–54
Commonly prescribed replacement steroid equivalents: prednisone, 5 mg ¼ cortisone, 25 mg ¼ dexamethasone, 0.75 mg ¼ hydrocortisone (Cortef), 20 mg.
Data from Adrenal cortical steroids. In: Drug facts and comparisons. 5th edition. St. Louis (MO): Facts and Comparisons, Inc.; 1997. p. 122–8.
1077
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 the
known risk for dysphonia and fungal superinfection associated with these
medications [14]. Many performing artists report an improved sense of
well-being with a vitamin B12 injection intramuscularly when they are ill.
The efficacy of this is unknown. Patients should be counseled that herbal
remedies 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 not
been proven. In general, the authors recommend that performers avoid
any spray, lozenge, or liquid that gives a numb or tingling feeling in the
throat (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 effects
of 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 to
perform can be an extremely difficult decision. Pressure for these individuals
to perform can be extreme. The cost of canceling an event extends beyond
the large financial cost to the patient, crew, and venue. Artists and orators
are 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 for
the 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 voice
rest in these situations to avoid the potential of vocal fold scarring. Outside
of these situations, the decision to cancel a show is a judgment call between
physician and patient. The physician must decide whether the severity of the
Acutely ill vocal

performer
Phone
triage
Significant
change in voice
quality
No Yes
• Full performance • Evaluation by otolaryngologist in

• Medical evaluation and office or on-site (rarely)
therapy as appropriate • Laryngoscopy (with stroboscopy,
ideally):
rigid transoral, flexible transnasal
Vocal fold
hemorrhage or
tear?
Yes
No
• Non-performance
Risk of jeopardizing career?
Yes • Absolute voice rest
• By suboptimal performance • Medical therapy as
• By further laryngeal indicated
injury/severe laryngitis • Follow up in clinic
No
Severe
Laryngeal
edema?
No Mild/Moderate
• Full performance • Modified voice rest

• Medical therapy as • Consider modification of
indicated performance
• Follow up by phone or duration/intensity
in clinic • Consider corticosteroids;
oral or intramuscular
depending on time to
Note: Individual situations vary and care should be performance
tailored to the patient’s specific needs and • Medical therapy as indicated
circumstances • Follow up in clinic next day
following performance
Fig. 4. Management algorithm: less than 24 hours until performance.
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 acceptably
well. If the patient wishes to perform, full discussion of the potential adverse
consequences 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 patient
and recommend nonperformance. The decision to recommend nonperfor-
mance is rare; in a review of 40 singers with acute illness before show
1080 KLEIN & JOHNS
time, cancellation of performance was necessary in only two cases [4]. A

simple algorithm for management is outlined in Fig. 4.
Summary
Acute management of vocal emergencies can be a difficult and stressful
element of this specialty. A thoughtful history, coupled with appropriate di-
agnostic instrumentation, is the cornerstone of evaluating a patient with
a vocal emergency. Understanding the various causes of acute dysphonia
in the performing artist, as well as awareness of the additional pressures
placed upon performing artists, empowers the otolaryngologist to help
patients 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] Sataloff RT. Professional voice: the science and art of clinical care. San Diego (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, Hawkshaw M. 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,*
a
Department of Otolaryngology, University of Colorado School of Medicine,
Denver, CO 80262, USA
b
Philadelphia Ear, Nose and Throat Associates, 1721 Pine Street,
Philadelphia, PA 19103, USA
c
Department of Otolaryngology-Head and Neck Surgery, Drexel University College
Otolaryngologists should be familiar with the potential side effects and

interactions of medications that are prescribed commonly to professional
voice 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), perceptual
disturbances (eg, hallucinations and delusions), cognitive disturbances (eg,
delirium and confusion), behavioral disturbances (eg, insomnia), and drug
interactions are all important possibilities of which the prudent practitioner
should be aware. Drug-induced symptoms can occur even with standard
dosages and at any time during the course of treatment. An awareness of
the potential for side effects caused by adrenocorticoids, antihistamines,
decongestants, antisecretory drugs, and other medications will help the
clinician to avoid or detect and treat drug-induced disorders, as will an
awareness 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 or
preexisting psychiatric disorders, is important in preventing and detecting
drug-induced disorders. The drugs discussed in this article can have seriousd
and 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 or
the other. In addition to psychiatric side effects, other adverse reactions can
occur (eg, cardiac arrhythmias, hypertension, and local effects). Certainly, all
reactions, particularly psychiatric symptoms, are not caused by medication;
however, some can be a manifestation of a coexisting or preexisting psychiatric
or other disorder that has been aggravated by a combination of medications.
Drug-induced psychiatric disorders

The manifestations of drug-induced psychiatric disorders can be related
to 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, and mania. Associated behavioral signs
include increased physical activity, rapid speech, insomnia, and mood eleva-
tion. Psychiatric symptoms that occur during the course of treatment also
may be related to the medical or psychiatric condition being treated. For
example, anxiety disorders and panic attacks are known to occur in asso-
ciation with thyroid, parathyroid, and adrenocortical disorders; Langhan’s
cell endocrinopathies; collagen vascular disorders (eg, systemic lupus eryth-
ematosus, rheumatoid arthritis, temporal arteritis, and periarteritis no-
dosa); neurologic (eg, multiple sclerosis) and neurotologic (eg, Ménière’s
disease) [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 be
distorted) 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-induced
psychiatric disorders because they tend to be taking more medications
and, therefore, are more likely to experience drug interactions. Older
patients also tend to have other medical conditions that can prolong drug
metabolism and increase systemic drug levels.
Preexisting organic brain disease and drug abuse also can be risk factors
for the development of psychiatric side effects. Patients who have a history
EFFECTS OF MEDICATIONS ON THE VOICE 1083
of drug dependence or abuse often manifest delirium. The presence or

history of a mood disorderddepression or maniadalso is a risk factor
for psychiatric side effects to medications [2]. Adrenocorticoids can aggra-
vate or unmask depression or mania in these patients. Even a family history
of 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 in
a particular patient can be additive. The overall low incidence of psychiatric
side effects with a particular medication might increase in the presence of
other factors. An understanding of the risks in each individual patient is
essential in selecting medications. Physicians should routinely ask patients
to bring in or to make a list of all medications that they have taken during
the 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 upset
and 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, and
psychoses are not uncommon psychiatric effects. Symptoms tend to be pro-
portional in incidence to the dosage and duration of steroid use. Iatrogenic
Cushing’s syndrome, which can be caused by long-term steroid use, also can
manifest these signs [2,4]. A personal or family history of affective mental
illness can predispose a patient to the psychiatric side effects of steroids.
Some drugs, such as corticotropin, can cause an increase in endogenis
corticosteroids causing similar effects. The potential for steroid abuse in
professional voice users cannot be overemphasized, and the side effects
should not be dismissed as insignificant.
Treatment of side effects may need to be considered when steroid use is
required. A concomitant use of a histamine-2 receptor antagonist
(H2 blocker) or proton pump inhibitor (PPI) can assist with gastrointestinal
upset. A carefully titrated insulin sliding scale can help to control blood
sugar elevation in diabetics [3]. Severe depression might require antidepres-
sant treatment, and an antipsychotic medication or a mood stabilizer may
become necessary to treat steroid-induced mania. Insomniadas an isolated
side effect or as part of a manic episodedalso could require medical
intervention.
Inhaled steroids are used primarily for respiratory disorders and present
more local than systemic effects. Nasal steroids have had few documented
effects on the voice; however, orally inhaled steroids have demonstrated
oral candidiasis, dysphonia, pharyngitis, and cough and often are not rec-
ommended for use in professional voice users unless absolutely needed for
asthma control because of the common voice effects [3,5]. Ipratropium bro-
mide, a nasally or orally inhaled medication used primarily for pulmonary
symptoms, has shown side effects that include hoarseness and cough. Fluti-
casone, one of the more common medications used for asthma and used also
as a primary nasal steroid, lists a prevalence of 2% for hoarseness and sore
throat for the orally inhaled preparation. Salmeterol xinafoate and flutica-
sone propionate (Advair) lists the same incidence of hoarseness and throat
irritation, attributing it to either drug. It does not seem to be dose depen-
dent. Triamcinolone, pirbuterol acetate, and albuterol list voice changes
as part of their common side effects. Voice difficulties due to lack of respi-
ratory support in uncontrolled asthma need to be taken into consideration
when 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 without
physician supervision. Moreover, some patients do not realize that their
OTC 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 as

part 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, causing
significant drying and consequent voice changes and pathologies. Sedation
also 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 in
patients who are taking monoamine oxidase inhibitors (MAOIs) [2]. These
medications can produce dangerously high levels of norepinephrine because
the MAOIs impair the metabolism of sympathomimetic medications [2].
Sympathomimetic medications by themselves also can cause psychiatric
side effects. Young children and elderly patients who have organic brain
syndrome are the most vulnerable. It may become necessary to discontinue
the suspected culprit medication or to prescribe sedation or treatment with
a high-potency antipsychotic, such as haloperidol. Low-potency antipsy-
chotics, such as thioridazine or chlorpromazine, should not be taken with
phenylpropanolamine because the combination can cause hypotension.
The antihistamine and anticholinergic components of a combination
antihistamine 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’s
mental status following the administration of physostigmine confirms the
diagnosis 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 certain
cytochrome P-450 enzymes, and the antidepressants fluvoxamine and nefa-
zodone interfere with certain P-450 enzymes [6]. When these antidepressants
are prescribed with other medications that are metabolized by the same
P-450 enzymes, competition between the medications for the enzymes im-
pairs the liver’s ability to metabolize each as efficiently as usual. This can
cause blood levels of these medications to become dangerously high and
lead to significant side effects or even a fatal reaction [6]. These antidepressants
cannot be used in combination with astemizole for the same reason. Lorata-
dine, fexofenadine, and cetirizine can be used with these antidepressants
because 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 voice
complaints. Antisecretory medications, which decrease stomach acid
production, are commonly used in the treatment of reflux laryngitis. The
1086 ABAZA et al
two primary classes of drugs prescribed for this condition are the PPIs and
the 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 significant
side 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 recent
study from England indicated an increased risk for hip fractures with
long-term and high-dose PPIs and, to a lesser extent, H2 blockers, particu-
larly in men. The investigators recommended that in patients older than 50
years of age, an absorbable form of calcium should be taken with high-dose
or 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 is
less than 0.2%, it is significantly higher among hospitalized patients, the
elderly, 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 within
2 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 withdrawal
syndrome that includes anxiety, insomnia, and irritability [11]. Cimetidine
can increase the blood level and action of tricyclic antidepressants, such
as amitriptyline, doxepin, imipramine, and nortriptyline; blood levels of
these antidepressants can reach toxic levels, resulting in tachycardia and
other side effects. The inhibition of the cytochrome P-450 enzymes by rani-
tidine or cimetidine also can lead to potentially dangerous side effects with
certain other cytochrome P-450 metabolized medications. Cimetidine is the
more potent inhibitor of the two; ranitidine is one fifth to one tenth as
potent. 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 be
considered when they are prescribed for a patient who is taking cimetidine.
An alternative is to use a short-acting benzodiazepine, such as oxazepam or
lorazepam. The metabolism of these short-acting antianxiety medications is
not affected by ranitidine or cimetidine [2]. Cimetidine also can increase the
blood levels of serotonin reuptake inhibitors and antipsychotic medical
anticonvulsants [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 use

a 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 in
the treatment of endometriosis and postmenopausal sexual dysfunction [12].
High-dose progesterone birth control pills, generally not available in the
United States, can cause similar androgen-like changes in the voice [13].
Most low-dose contraceptives have a significantly lower chance of voice
changes, usually reversible when the medication is discontinued. Van Lierde
and colleagues [14] evaluated 24 professional voice users during the use of
oral 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 for
numerous health reasons. In professional voice users, estrogen replacement
may 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 cause
androgenic effects [3].
Hypothyroidism, with thyroid hormone replacement, is one of the more
common disorders found in women. Sometimes diagnosed in professional
voice users by voice changes alone, careful monitoring of supplemental thy-
roid hormone replacement can be particularly important in a professional
voice 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 the
medications cause side effects. Hoarseness, cough, pharyngitis, nervousness,
muscle spasm, and tremor have been reported with zidovudine; because
HIV 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 been
reported. Oseltamivir phosphate is not recommended in patients who have
airway disease, secondary to reports of bronchospasm and decreased lung
capacity. 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
1088 ABAZA et al
relief of minor pain and fever. Delay in clotting is a known complication of

aspirin and all NSAIDs, so avoidance of these medications is recommended
often for professional voice users. A low dosage of aspirin is used often for
cardiac prevention and is a situation where the minimal bleeding risk likely
is outweighed by the cardiac prevention benefit. Newer cyclooxygenase-t
inhibitors, now available by prescription, do not have the same bleeding is-
sues or gastrointestinal upset because of a different pathway, but they do
have other significant cardiac side effects [15].
Topical anesthesia and narcotic use in professional voice users, particularly
before a performance, should be discouraged. Narcotics can be associated
with signs of dysarthria, in addition to mental impairment [16]. Impairment
of physical feedback of the voice by these types of agents can predispose the
user to injury and more significant long-term voice disabilities and can be
more career-ending than a performance cancellation may be.
Diuretics
Diuretics are used to eliminate fluid in medical conditions such as cardiac
or renal failure. In premenstrual women, excess fluid can be found in Rein-
ke’s space and other tissues because of increased circulation of antidiuretic
hormone. 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 are
used in conjunction with other antihypertensive medications. Several angio-
tensin-converting enzyme inhibitors, such as captopril and enalapril, have
had case reports of hoarseness, cough, and aphonia [17]. Careful monitoring
of the voice is important when these medications are needed for other health
concerns.
Other medications
Numerous other medications have had hoarseness reported as a side
effect [17]. Antineoplastic agents (eg, vincristine), tricyclic antidepressants
(eg, amitriptyline and nortriptyline), clonazepam (Klonopin), and ropinirole
hydrochloride (Requip) are a few of the more common medications that list
hoarseness 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, as
well as dosage changes.
Homeopathic medications
The realm of homeopathic and herbal remedies is beyond the scope of this
article but it warrants a mention. Professional singers often use what they view
as natural solutions to medical problems. Often, patients are reluctant to
inform their physician about the use of these medications; therefore, it is
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
important for the otolaryngologist to stress the impact that these substances
may have on the body and on the efficacy of other medications. A few common
substances 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] Sataloff RT, Hawkshaw MJ, Anticaglia J. Medications and the voice. In: Sataloff RT, 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] Yang Y, 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. The H2-antagonist therapy withdrawal 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.
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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] MicromedexÒ healthcare series [Internet database]. Greenwood Village (CO): Thomson
Micromedex. Updated periodically.
40 (2007) 1091–1108
Vocal Fold Masses

Kenneth W. Altman, MD, PhD, FACS
Department of Otolaryngology, The Mount Sinai School of Medicine, One Gustave L.
Levy Place, Box 1189, New York, NY 10029, USA
Although many performers consider vocal fold masses, such as nodules, the
bane of their existence, it is rare that these lesions are true career-breakers. It is
essential, however, that the many issues contributing to the development of
these lesions be identified and a multidisciplinary approach instituted to
obtain the best possible and most consistent outcome. In the context of the
professional 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 increase
the risk for malignancies and the possibility of such cannot be overlooked.
Also, the title of this article, vocal fold masses, has been chosen to reinforce
the concept that these inflammatory conditions add weight to the vocal folds
and impair vocal closure. This article reviews the multifactorial contributions
to voice disorders with emphasis on the pathophysiology of vocal masses, de-
scribes the resulting effects on voice function, and elaborates on the types of
masses encountered in professional voice users.
Multifactorial contributions to developing vocal masses

Voice use demands (overuse) and vocal technique (misuse) are central to
the trauma and pathogenesis of vocal fold masses in professional voice
users. Common to performers and other professionals is a passion for com-
munication that often pushes the scope of voice use relating to amount of
time, intensity, frequency of use, vocal range, and more advanced tech-
niques. Young performers, in particular, usually use their voices in many
different roles that include self-management and day jobs also requiring
their voices. The blossoming use of cellular telephones, especially in loud
public environments, significantly adds to this sustained and repetitive vocal
trauma. Trauma and subsequent inflammation manifest as vocal limitations
E-mail address: kenneth.altman@mountsinai.org
1092 ALTMAN
that frustrate the professional voice user, and there is a tendency to try to
exceed these limitations.
Paying tribute to these personality factors in the pathogenesis of nodules
and polyps, Yano and colleagues 1982 [1] recognized significantly higher ex-
troversion scores on Maudsley Personality Inventory in these patients. More
recently, Roy and colleagues [2] used the Multidimensional Personality
Questionnaire to evaluate personality features distinct to functional dyspho-
nia and those who have vocal nodules. They determined that the functional
dysphonia 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 medical
conditions, medications, and the environment add to the synergy in pathogen-
esis of vocal fold masses. With the larynx at the epicenter, the significant inter-
relations of the respiratory and upper gastrointestinal tracts also predispose
the vocal folds to further damage. These contributing diseases include rhinitis,
allergy, sinusitis, asthma, bronchitis, laryngopharyngeal reflux, and others
discussed elsewhere in this issue. Environmental factors include allergens,
dust and other particulates, tobacco smoke, and a host of occupational
irritants.
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 nodules
using 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 (one
to two episodes). In a follow-up study by Ulualp and colleagues [4], 9 pa-
tients who had vocal nodules and posterior laryngitis underwent similar
evaluation, in which 78% were found to have pharyngeal acid reflux (signif-
icantly higher than controls). It is believed that the baseline inflammation
resulting from LPR episodes predisposes the vocal folds to the stresses
from vocal overuse and misuse.
In a series of allergy patients who had laryngeal disease, Hocevar-Boltezar
and colleagues [5] found that treatment of 70 patients who had laryngitis and
positive allergy skin tests resulted in an improved outcome compared with 5
patients who did not receive treatment, suggesting that hypersensitivity to in-
halatory and nutritional allergens makes laryngeal mucosa more susceptible
to 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 vocal
fold masses, it is important to understand how biomechanical factors work
VOCAL FOLD MASSES 1093
on the membranous vocal folds to produce such lesions. Jiang and col-
leagues [6] developed a mathematical computer-based model to describe
the vibratory response of the vocal folds during phonation using the finite
element method. They found that in normal phonation, mechanical stress
was the least at the midpoint of the membranous vocal fold and highest
at tendon attachments. In contrast, during hyperfunctional dysphonia there
was 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 was
increased 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 produced
a high mechanical stress at its base during vibration. The authors concluded
that intraepithelial stress plays an important role in the pathogenesis of nod-
ules and other masses, and that an abnormal vibratory mode may be more
damaging than a high intensity of vibration [6].
In a follow-up study using a self-oscillating model, mechanical stress was
noted to periodically undulate with the vibration of the vocal folds, and that
vocal impact caused a jump in the normal stress value [7]. The model was
also able to confirm that stress was significantly higher on the surface of
the 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 as
reactive 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 on
strobolaryngoscopy. There is a clinical decrease in phonatory pitch along
with 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 vocal
fold vibration and phase closure often leads to phase asymmetry (depending
on 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 qualities
contribute to the initial vocal trauma that leads to the development of
this 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 and
colleagues [8] reviewed 150 patients who had muscle tension dysphonia, in
which 34 had polyps, 20 had nodules, and 12 had vocal cysts. They found
a 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
1094 ALTMAN
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 seem
to 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-year
period. Some 66% of these patients were primary school teachers, and
55% of referrals were 51 to 60 years of age. Overall, vocal nodules were
found in 4.2%. In a Finnish study, Smolander and Huttunen [10] surveyed
181 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 laryngologist
initially evaluates patients after they have experienced voice limitations
over a period of time, it is uncommon to have an isolated lesion without
concomitant 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 it
may 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 1156
patients and found 372 who had nodules and 784 who had polyps. Sataloff
and colleagues [12] reviewed their experience with videostroboscopy on 377
patients 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 vocal
fold 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 the
anterior/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, and
pathology was found in two thirds overall, with pseudocysts or nodules in
one third overall.
De Bodt and colleagues [14] characterized evolution of these nodules
from 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. The
degree of dysphonia in childhood and the presence of allergy were also pre-
dictors of persisting voice complaints in adolescence. This study reinforces
multifactorial contributions to the development of these lesions, including
behavior. The female preponderance from childhood to adolescence, cou-
pled with adult female preponderance in other studies, further confirms
that females are at particular risk. Perhaps the softer intensity of female voi-
ces leads to more hyperfunction in adult professional environments with
louder background noise.
One additional note is made of preponderance of nodules in patients who
have congenital microweb. Ruiz and colleagues [15] reviewed a sample of
107 patients who had vocal nodules and recognized microweb in 9.4%, al-
though the presence of microweb did not affect nodule location. Although
this is a small portion of those patients who develop nodules, it does imply
that the clinician should have a heightened awareness of the presence of mi-
crowebs, which may have additional implications of treatment and
prognosis.
The pathophysiology of vocal nodules relies on the mid-membranous vo-
cal fold experiencing maximal shearing and collision forces. This location
corresponds to the junction of the anterior to middle vocal folds (because
the posterior third of the vocal folds is coupled to the vocal process of the
arytenoids). 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 epithelial
hyperplasia.
Consequently, the histology of nodules is distinct from polyps and other
vocal 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 and
organized collagen. Polyps also have a more pronounced epithelial reaction
and a more dense fibrous stroma than polyps. Immunohistochemical char-
acterization of nodules reveals a thickened basement membrane zone rich in
collagen type IV and more intense fibronectin staining [17].
Patients who have vocal nodules present with chronic hoarseness, often
with repeated episodes of more severe voice loss. Singers may complain of
a loss of ability to sing high notes softly, with frequent voice breaks, in-
creased breathiness, and vocal fatigue. Strobolaryngoscopy reveals bilateral
symmetric superficial swelling of the vocal folds at the striking zone junction
of the anterior to middle thirds (Fig. 1A). There is slightly decreased ampli-
tude of the mucosal wave, but the wave is generally symmetric. Because
there is hourglass-shaped glottal closure, there is consequently decreased
phase closure (Fig. 1B).
The mucus layer on the surface of the vocal folds is also important for
lubrication and reducing friction. Patients who have vocal nodules may
1096 ALTMAN
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.
subsequently have irregular vibration of the surface mucus layer, perhaps re-
sulting in drying, leading to impaired lubrication and an exacerbation of the
surface 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 the
passaggio (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 using
a hammer over a long period of time without gloves. As a result, calluses
form 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 treatment
of 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 other
vocal fold. Microsurgical technique is addressed elsewhere; it is imperative
to preserve normal anatomy, keeping the plane of dissection superficial,
and to minimize trauma to the lamina propria.
Polyps
Vocal polyps are unilateral, occasionally pedunculated masses encountered
on the true vocal fold. They occur more often in males, after intense intermit-
tent voice abuse, history of aspirin or anticoagulant use, or other vocal
trauma, such as endotracheal intubation. Kotby and colleagues [16] reviewed
19 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
(superficial lamina propria) with subsequent extravasation of blood, resultant

local 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 as
or called a pseudocyst.
Pathologically, polyps are acellular, with thickened epithelium over su-
perficial lamina propria and increased vascularity in an abundant delicate
fibrin 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 of
laminar 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 have
more prominent decreased mucosal wave amplitude. Thibeault and col-
leagues [21] characterized gene expression in vocal polyps compared with
Reinke edema. They found evidence of enhanced expression of extracellular
matrix proteins in vocal polyps corresponding to increased mucosal wave
stiffness observed on strobolaryngoscopy.
Both nodules and polyps result in excess air egress during phonation (with
a relatively breathy voice), and earlier vocal fatigue, frequent voice breaks in
Fig. 2. Vocal polyps. (A) Hemorrhagic. (B) Broad-based, nonhemorrhagic.

1098 ALTMAN
singers, and worsening hoarseness with high-pitched soft phonation. As such,

this decreased vocal efficiency with decreased mucosal wave phase closure has
been quantified with decreased subglottal and acoustic power [22]. Because
polyps are asymmetric masses of the vocal folds, they are more prone to result
in chaotic vibrations and aperiodic mucosal waves [23].
In the treatment of patients who have vocal polyps, all of the factors that
contribute to voice disorders should be addressed from a multidisciplinary
perspective, and polyps are usually addressed with microsurgery. An evolving
treatment modality for particularly hemorrhagic polyps is the use of office-
based technology using lasers. The wavelength of the lasers is well absorbed
by hemoglobin, and damage to the epithelium is minimal. In one recent pilot
study evaluating the use of the pulsed-dye laser (585 nm), small vascular
polyps showed greater potential for resolution over larger polyps [24].
There have also been reports (and anecdotal observation by the author of
this article and others) that small vocal polyps may completely resolve with
conservative nonsurgical treatment [25]. One would expect that smaller le-
sions and those that have been present for shorter periods of time may be
more prone to regression, especially in patients who are more compliant
with treatment.
Cysts
Cysts are subepidermal epithelial-lined sacs located within the lamina prop-
ria, and may be mucus retention or epidermoid in origin. Mucus retention
cysts form when a mucous gland duct becomes obstructed (usually during
an upper respiratory infection or with 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 in

a 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 patients
who have nodules and polyps, but with less vocal limitation than expected
from its size. The voice often sounds diplophonic (particularly with epider-
moid cysts), whereby there is great pitch instability and there is splitting of
the fundamental frequency overtones. As with nodules and polyps, this is
usually accompanied by vocal hyperfunction, which is often compensatory.
Bouchayer and colleagues [26] reviewed their experience with 157 cases of
cysts, sulci, and mucosal bridges over a 10-year period. Cysts were present in
78, and more commonly in females. Female professional singers may note
increasing vocal limitation and voice roughness when they are premenstrual
[27], and there is anecdotal evidence of varying cyst size with the female
monthly cycle. Consequently, many phonosurgeons exercise caution when
operating on premenstrual women.
On strobolaryngoscopy, the vocal folds appear asymmetric with occa-
sional evidence of the subepithelial mass (Fig. 3). Because of displacement
of lamina propria, there is significant decreased or absent mucosal wave
on the side of the cyst. Phase closure depends on the cyst size and whether
there is the development of a contralateral reactive callus.
Shohet and colleagues [28] compared stroboscopic findings between cysts
and polyps. They determined that the mucosal wave was the most important
parameter in differentiating cysts from polyps. They also found the mucosal
wave to be diminished or absent in 100% of vocal fold cysts, and the wave
to be present in 80% of polyps.
Treatment again requires a multidisciplinary approach addressing factors
that contribute to voice disorders. Although it is imperative to respect vocal
limitations, a true cyst does not resolve with conservative management. The
phonosurgical approach is discussed elsewhere in this issue, but requires
more extensive dissection because the cyst is in the submucosal plane. The
cyst may also be associated with intracordal scarring, requiring a more elab-
orate dissection. Consequently, recovery of the mucosal wave is prolonged
and may never return to being completely normal.
Furthermore, leaving behind a minute fragment of epithelium in the cyst
sac may result in recurrence of the cyst. Some vocal professionals have been
know to have cysts that do not cause substantial limitation to their singing
careers and have been observed without surgery. Consideration of surgery in
Fig. 3. Vocal cyst.

1100 ALTMAN
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-shaped
closure 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, that
may 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). When
comparing patients who had nodules to those who had UVFL/RL, they
found 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 of
reducing voice use, speech therapy, and treatment of LPR, Fig. 4B shows
significant improvement in the right reactive callus. As such, contralateral
reactive lesions are often not removed in microsurgery for the primary le-
sion, because the reactive lesion tends to resolve with conservative
management.
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 is
epidermoid in origin and has ruptured. Intracordal scarring may also be
found after vocal surgery involving the lamina propria, with the use of
the 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.)
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.
Discussion on vocal sulcus (epithelial scarring) goes beyond the scope of

this article, although it can certainly affect the professional voice [30].
Intracordal scarring is suspected on strobolaryngoscopy when there is
markedly reduced or absent mucosal wave (usually asymmetric), which often
affects phase closure. From a professional voice standpoint, it is crucial to dif-
ferentiate between an uncomplicated subepithelial cyst and an intracordal
scar, because the latter is a more complex problem with worse prognosis for
professional voice rehabilitation. A convex subepithelial fullness of the mem-
branous vocal fold may warrant exploratory microflap surgery to tease out re-
maining cyst sac and adynamic fibrous components. Because the extracellular
matrix components of the lamina propria largely determine the biomechanical
properties 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 true
masses, they develop as a result of the same multifactorial and shearing
forces that lead to masses, and they also predispose to the development of
polyps and vocal hemorrhage. Fig. 5A and B show strobolaryngoscopic
examples of a varix and hemorrhage.
Treatment options for these aberrant vessels have traditionally included
microdissection and the use of the CO2 laser, which lead to an increased risk
for postoperative scarring or sulcus. More recently, there has been renewed
interest in the use of pulsed angiolytic lasers that have a wavelength within
the 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
1102 ALTMAN
Fig. 5. (A) Vocal varix, and (B) vocal fold hemorrhage (both on the patient’s right; left of the
figure)
wavelength) on 12 patients who had microvascular and hemorrhagic lesions

and found no adverse scarring or reduction in the mucosal wave postopera-
tively. Zeitels and colleagues [33] also recognized the potential for the pulsed
KTP and the 585-nm pulsed-dye laser in a series of 39 patients.
Granulomas
Although vocal process granulomas are not on the membranous vocal fold
and often do not cause vocal symptoms, it is important for the clinician to un-
derstand differences with other vocal fold masses. Vocal process granulomas
occur in response to trauma, most commonly from LPR, exacerbating chronic
cough, or throat clearing. They may also occur after endotracheal intubation
resulting 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 contact
granuloma being male.
The granuloma may appear as solitary or bilobed (Fig. 6) and often does
not affect mucosal wave or phase closure on strobolaryngoscopy (unless
there 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, and

vocal process impact on cough or phonation. Botox to the thyroarytenoid
muscle has also been shown to be helpful in reducing the glottal impact in
cases refractory to LPR treatment and speech therapy. Because there is
a high recurrence rate after surgical excision, surgery is reserved for cases
in which the lesion is (1) enlarging; (2) compromising the voice, breathing,
or swallowing; or (3) suspicious for malignancy.
Fig. 6. Left vocal process granuloma.
Papilloma
Respiratory papillomatosis is an infection caused by human papillomavi-
rus (HPV), which is also known to more commonly cause cervical, vaginal, pe-
nile, and anal warts. Although relatively uncommon in the larynx, it is still
considered to be among the most common laryngeal neoplasms. There are
more than 50 strains of HPV, but HPV 6 and 11 are among the most common
in the larynx. As with genital warts, there is an approximately 2% likelihood of
malignant degeneration in laryngeal papilloma, most commonly found with
strains HPV 16 and 18. Once the wart is manifested, there is overall about
a 10% likelihood of spread to the trachea or 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 forms
may have a superficial spreading presentation, again with vascular stippling
seen 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 of
thickened diseased epithelium can present with a decreased mucosal wave.
There are many controversies related to papilloma and HPV, including
a high prevalence of greater than 40% with HPV-positive serology but still
relatively low overt infection rates, suggesting an important role of host im-
mune recognition [35]. The many treatments for papilloma go beyond the
scope of this discussion, although shaver excision and CO2 laser excision
are also used in select instances. The greater depth of penetration of the laser
1104 ALTMAN
Fig. 7. Vocal fold papilloma involving the left vocal fold.
than is visibly apparent increases the risk for scarring and implantation of
the virus (an epithelial disease) into deeper tissues of the vocal fold and
use of the CO2 laser is avoided in most centers. Pulsed-dye lasers are now
considered the mainstay. The emerging use of the HPV vaccine for the
most 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 refer
to a proliferation or redundancy of the superficial lamina propria (Reinke
space). 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 of
the mass effect of the edema, often with phase asymmetry because of
ball-valving and asymmetric edema. Treatment is aimed at reducing airway
obstruction while preserving voice quality. Surgically, it is paramount to
preserve some epithelium and remaining superficial lamina propria so that
patients may maintain some degree of mucosal wave postoperatively. It is
also imperative to stage procedures in patients who have bilateral disease
to 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 be
instituted before surgery to maximize the postoperative outcome.
Leukoplakia and dysplasia

Leukoplakia, or white plaque, refers to a spectrum of diseases affecting
the vocal fold epithelium, and includes hyperkeratosis, dysplasia, and early
Fig. 8. Bilateral polypoid corditis.
verrucous changes. Overall, when leukoplakia is present there is an 8% to

14% 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 initially
with subtle hyperkeratotic epithelium resulting in decreased or sluggish mu-
cosal wave on strobolaryngoscopy (Fig. 9A). Progression, particularly with
dysplastic or premalignant changes, may be exophytic in a surrounding bed
of erythema (Fig. 9B). Microflap excision, carbon-dioxide lasers, and
pulsed-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 and
mild dysplasia is centered on eradication of disease while preserving neigh-
boring normal anatomy and voice quality. Severe dysplasia and carcinoma
in situ must be treated more aggressively.
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
Fig. 10. Vocal fold squamous cell carcinoma.
Vocal fold carcinoma

Squamous call carcinoma is by far the most common form of laryngeal
malignancy. Those patients who have a history of tobacco smoking account
for about 90% of cases, and the likelihood is far greater with a concurrent
history of excess alcohol consumption. There are also anecdotal and indirect
data 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 of
suspicion.
Features of squamous carcinoma include exophytic, ulcerative, and infil-
trative. Consequently, one may see on strobolaryngoscopy an area of focally
decreased 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 in
papilloma 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 from
leukoplakia is more challenging because leukoplakia may form a continuum
from keratosis to severe dysplasia to microinvasive disease. Nevertheless,
the degree of clinical suspicion and evidence of microinvasion with focally
decreased mucosal wave should mandate further evaluation [38].
Summary
There are several vocal masses that can affect the professional voice. It is
important to understand the multifactorial contributions and pathogenesis
of each to determine prognosis. Strobolaryngoscopy plays a crucial role in
differentiating the spectrum of masses and in guiding optimal management.
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40 (2007) 1109–1131
Vocal Fold Paresis and Paralysis

Adam D. Rubin, MDa,b,
Robert T. Sataloff, MD, DMAc,*
a
Lakeshore Professional Voice Center, Lakeshore Ear Nose and Throat Center,
21000 East 12 Mile, Suite 111, St. Clair Shores, MI 48081, USA
b
University of Michigan, Department of Otolaryngology–Head and Neck Surgery,
Ann Arbor, MI 48109, USA
c
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 are
most important when evaluating vocal fold mobility disorders.
The nuclei of the recurrent laryngeal nerve (RLN) axons lie within the
nucleus ambiguus in the medulla of the brainstem. The RLN axons travel
with the vagus nerve down the neck until they branch off at the level of
the aortic arch on the left and the subclavian artery on the right. On the
left, the nerve passes inferior and posterior to the aortic arch and reverses
its course to continue ly into the visceral compartment of the neck. The right
RLN loops behind the right subclavian artery and ascends superomedially
toward the tracheoesophageal groove. Both RLNs travel just lateral to or
within the tracheoesophageal groove and enter the larynx posterior to the
cricothyroid joint. The positions of the nerves in the neck make them sus-
ceptible to iatrogenic injury during surgery. Low in the neck, the course
of the right recurrent nerve is more oblique, lateral, and probably more
prone to injury than the left RLN [2].
Approximately 5 out of 1000 people have a nonrecurrent laryngeal nerve
on 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 the
level of the cricoid cartilage and enters the larynx directly, without looping
around the subclavian artery. This anomaly occurs in conjunction with a
retroesophageal 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 denervation
of these muscles results in an inability to close the glottis with resulting
breathy voice and possible aspiration.
The PCA is the main vocal fold abductor. Paralysis of this muscle results
in an inability to abduct during inspiration. Denervation of the PCA usually
causes the arytenoid cartilage to subluxate anteromedially in unilateral vo-
cal fold paralysis. The denervatedPCAno longer counters the anterior pull
on the arytenoid cartilage by the vocal ligament [5]. If both PCA muscles
are denervated, as in the case of bilateralRLNparalysis, airway obstruction
may occur.
The IA muscle is actually three muscles: the transverse arytenoideus mus-
cle and two oblique arytenoideus muscles. The function of the IA muscle is
not completely understood; however, it may assist in vocal fold adduction
and provide medial compression to close the posterior glottis [5].
Superior laryngeal nerve

The laryngeal nerve (SLN) branches from the vagus nerve just inferior to
the nodose ganglion, which contains the sensory cell bodies of the SLN. The
nerve travels inferiorly along the side of the pharynx, medial to the carotid
artery, and splits into two branches at about the level of the hyoid bone. The
internal division of the SLN penetrates the thyrohyoid membrane with the
laryngeal artery and supplies sensory innervation to the larynx. The external
division 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, although
its 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 after
nerve injury without restoration of vocal fold movement. Vocal fold paresis
implies vocal fold hypomobility due to neurologic injury and may result
from weakness of the RLN, SLN, or both. Nerve injury may be unilateral
VOCAL FOLD PARESIS AND PARALYSIS 1111
or bilateral. Vocal fold paresis may present as dysphonia, loss of the upper
register of the voice, hoarseness, breathiness, throat pain, choking episodes,
or decreased vocal stamina. Laryngeal findings may be subtle and include
asymmetric vocal fold movement, bowing, and rotation of the larynx. Vocal
fold paresis may also present as muscle tension dysphonia or in conjunction
with benign vocal fold lesions, such as vocal nodules or cysts resulting from
compensatory 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 may
occur with or without concomitant SLN injury, depending on the cause
and site of the lesion. The RLN is at risk for injury during many surgical
procedures, such as thyroid, anterior cervical spine, and thoracic surgery.
The true incidence of vocal fold paralysis remains unknown. The incidence
of injury to the recurrent laryngeal nerve from thyroid surgery has been
reported as between 0.3% and 13.2%, and from anterior cervical spine
surgery as between 2% and 21.6% [6,7]. Mechanisms of iatrogenic injury
include 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-
Barré, and Parkinson disease [8–15]. Cerebrovascular accidents may result
in 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 unusual
cases include disorders such as Gerhard syndrome, laryngeal abductor
paralysis that may be familial (autosomal dominant, autosomal recessive
or 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 also
injure the nerve [21].
Idiopathic vocal fold paralysis is not well understood. Some suspect a
viral cause, because many patients report an upper respiratory infection
before the onset of vocal symptoms. There are several infectious causes
that have been reported to cause RLN paralysis, such as Lyme disease, ter-
tiary syphilis, Epstein-Barr virus, and herpes [22–25]. Other causes of RLN
injury 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 mechanism

and 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 injury
means that Wallerian degeneration has occurred distal to an injured site
(axonotmesis). Second-degree injury usually occurs after a crush injury
and also results in complete recovery. Because the endoneural sheaths
remain intact in a second-degree injury, synkinesis does not occur. Third-
degree injury includes endoneural scarring, which can cause misdirected
regeneration. 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, typically
it 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 transection
of the RLN there is atrophy of the TA and PCA muscles. After 3 months,
however, the muscle fiber diameters of the denervated muscle begin to
increase. By 9 months, the fiber diameters of the denervated muscles ap-
proach those of normal muscle. Spontaneous reinnervation may occur after
nerve transection and prevent muscle atrophy. The source of the reinnerva-
tion is not known, but may include regenerating fibers from the transected
RLN, the SLN, cervical autonomic nerves and nerve branches innervating
pharyngeal constrictors [40].
Although reinnervation after a complete RLN transection prevents mus-
cle wasting, typically it does not restore useful movement to the vocal fold
because of synkinesis. Synkinesis results from nonselective innervation of
adductor and abductor muscles. As a result, muscles that perform opposite
functions contract simultaneously, resulting in immobility or hypomobility
of the vocal fold [41]. The clinical picture depends on the proportion of
adductor and abductor fibers reinnervated.
Crumley [39] describes a classification system for laryngeal synkinesis. In
Type I synkinesis, or ‘‘favorable synkinesis,’’ there is little or no vocal fold
movement. The patient’s airway and voice are fairly normal, however.
Types II, III, and IV are considered ‘‘unfavorable synkinesis.’’ A spastic
vocal fold that may twitch without control characterizes type II. Voice qual-
ity is poor. In type III synkinesis there is tonic adduction of the vocal
fold. This adduction results in a reasonable voice, but the airway may be
compromised. Type IV synkinesis involves tonic abduction of the vocal fold

resulting in a breathy voice and greater risk for aspiration. Type III synki-
nesis probably results from greater reinnervation of the LCA in comparison
with 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 various
conditions. Iatrogenic trauma during thyroidectomy has been historically
accepted as the most frequent cause of SLN paralysis [42,43]. In 1980,
Adour and colleagues [44] reported that SLN palsy was part of a combined
cranial polyneuropathy attributable to viral infections. Similarly, Dursun
and colleagues [45] suggested that viral infections, such as herpetic cold
sores and upper respiratory infections, are commonly associated with this
condition. A likely explanation is that infections lead to viral neuritis, result-
ing in SLN damage. To the best of our knowledge, this retrospective review
included the largest population of confirmed SLN paresis and paralysis in
the 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 probably
contributed to vocal fold hemorrhage, which resulted in further voice dys-
function. Often, several months elapsed after the causative infection before
the patients sought medical attention. Before the diagnostic examination,
these patients attributed the symptoms of SLN damage to upper respiratory
infections. The development of compensatory mechanisms, such as muscle
tension dysphonia (MTD), which subjectively improved voice quality, some-
times resulted in further delays in seeking treatment. As expected, singers
were more aware of their symptoms than nonsingers, and delay in seeking
attention tended to be shorter in this population. This observation was con-
firmed in a study by Eckley and colleagues [46] that demonstrated that voice
range measurement is a useful parameter for analyzing the effects of SLN
paresis or paralysis on voice and may also be used for measuring outcome
following voice therapy. The effects of SLN paresis on vocal range help
explain the sensitivity of professional voice users (especially singers) to the
effects 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 other
common viruses. This evidence suggested infection at some undetermined
time 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 be
taken, particularly during thyroid surgery, to protect the external branch
of 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 who
had goiters had preoperative SLN paresis, which worsened postoperatively.
Some 58% of the SLN pareses were present at 1 year follow-up, although
most 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 suggest
identification of the external branch of the SLN to prevent injury [48]. Less
common 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. The
variability 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 monotone
voice, and poor vocal performance, especially at higher pitches [42,45]. SLN
paresis and paralysis may cause vocal fatigue, hoarseness, impairment of
volume, loss of upper range, loss of projection, and breathiness. Vocal fa-
tigue may be caused by the additional effort required to raise vocal pitch
and to project, by hyperfunctional compensatory gestures, or by pathologic
neuromuscular fatigue in cases of marked paresis. The clinical manifesta-
tions of SLN paresis or paralysis, particularly loss of upper range, are
more troublesome in singers and professional speakers. These patients often
develop MTD to generate a stronger voice. In Dursun’s [45] series, 23.8% of
the patients had MTD that seemed to be compensatory. It must be remem-
bered that SLN paresis may be the underlying cause of voice misuse and
consequent 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 upper
laryngeal 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 of
the 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 must
occur to cause laryngeal tilt toward the weak side, another sign of unilateral
SLN paresis [50]. Flaccidity of the affected vocal fold may cause irregular
vertical movements during respiration, which in turn causes various config-
urations of the glottis. A bowed vocal fold may be evident in SLN paresis or
paralysis. These vocal folds are slightly concave, and glottic closure is
usually incomplete. This finding may be associated with other coexisting

conditions, 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 glottic
configuration in SLN paresis and paralysis. The studies reflect different
opinions [50,52–54]. Contraction of a normal CT muscle rotates the poste-
rior commissure toward the inactive side, which causes the paralyzed vocal
fold to shorten and form an obliquely shaped glottis [49,50,55–57]. A
thinned, shortened, and bowed vocal fold and an oblique glottis deviating
to 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 not
rule out paralysis or paresis. Moreover, these findings may be observed if
CT contractions are weak or if the patients have MTD, which involves
not 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 and
physical examination. The history should define the main complaints and
symptoms of the patient and likely cause of the hypomobility. One should
inquire about previous surgeries, prolonged intubations, and trauma. A
complete medical history should be taken, including a thorough neurologic
review of systems, smoking and alcohol history, and other questions to eval-
uate for possible malignancy. Questions pertaining to possible infectious
causes should be asked, and a thorough vocal history should be taken to
define 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 high
lesion of the vagus nerve, the palate deviates to the intact side. The physician
should 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 should
be evaluated during various phonatory tasks at several frequencies and in-
tensities, as discussed elsewhere [60]. The laryngologist should look for
asymmetric movement, vocal fold bowing, horizontal and vertical position
of the vocal folds, and tilting of the posterior larynx. The presence of struc-
tural lesions and signs of laryngopharyngeal reflux disease can be observed
also. 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 extremely
helpful 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 in
other 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 less
obvious than usual. Such information is important in designing optimal
therapy, 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. These
muscles permit adduction, abduction, and longitudinal tension of the vocal
folds. The laryngeal nerves supply the cricothyroid muscle, which is the pri-
mary structure responsible for increasing longitudinal tension. Maintaining
stretch of the vocal fold is extremely important for pitch control, volume,
and stability during soft singing, especially from the upper mid-range and
higher. The recurrent laryngeal nerves innervate all of the other intrinsic
muscles of the larynx. Paralysis or paresis may involve one or both vocal
folds, although only one vocal fold is involved in the vast majority of cases
[64]. When the recurrent laryngeal nerve is paralyzed, the vocal fold appears
to stand still, except for slight respiratory motion. The ability to alter longi-
tudinal tension is maintained, however. The vocal processes are therefore
usually at the same level, and even the paralyzed side lengthens as pitch is
increased. Consequently, if the normal vocal fold can cross the midline far
enough 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 cannot
move ly or inferiorly to meet the injured side if laryngeal nerve paralysis
is 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 is
especially true if both recurrent and laryngeal nerves are paralyzed, but
problems occur even with isolated laryngeal nerve paralysis in the presence
of abduction and adduction. Bilateral laryngeal nerve paralysis is often
more difficult to diagnose and is probably missed frequently. Patients who
have this condition have a ‘‘floppy’’ epiglottis, rendering their larynges dif-
ficult to see. Their vocal quality, volume, and pitch range are impaired. It is
often 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 made
reliably 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, central
disease (especially multiple sclerosis) can produce unexpected neurologic
signs, and if no cause is found after a paralyzed recurrent laryngeal nerve
has been thoroughly evaluated, addition of a MRI of the brain and other
studies should be considered. Because of the seriousness of missing intra-
cranial lesions, many physicians obtain MRI of the brain and 10th cranial
nerve with enhancement in all cases and this practice certainly is not
unreasonable.
A few clinical maneuvers are useful for making paresis more apparent.
Repeated maneuvers alternating a sniff with the sound /i/ are particularly
helpful in unmasking mild PCA paresis. Repeated rapid phonation on /i/
with a complete stop between each phonation frequently causes increased
vocal fold lag as the pathologic side fatigues more rapidly than the normal
side. 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 vocal
fold lag is sometimes easier to see during whistling. Laryngeal posture dur-
ing this maneuver provides particularly good visibility of rapid vocal fold
motions. A glissando maneuver, asking the patient to slide slowly from
his or her lowest to highest note and then slide back down, is invaluable
for assessing SLN function. The vocal process should be observed under
continuous 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 vocal
folds 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 specific

causes of vocal fold paresis and paralysis. These may include tests for syphilis,
Lyme disease, diabetes, thyroid dysfunction, collagen vascular disease, myas-
thenia gravis, thyroid neoplasm, and other conditions. In addition to testing
gag 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 is
well recognized that recovery of laryngeal nerve function is common if the
injury was not caused by transection of the nerve. Even when the nerve is
transected, some innervation may occur. Consequently, it is best to delay
surgical intervention for approximately 1 year, if possible, unless the nerve
is known to have been divided or resected. This plan does not mean that
treatment should be delayed, however, but only irreversible surgery. The
collaboration 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 have
dysphonia. Voice therapy is invaluable in the management of vocal fold pa-
resis and paralysis. In all cases, the speech-language pathologist can provide
detailed preoperative and postoperative assessment. Such assessment is of-
ten of diagnostic value. It is also of great help to the surgeon in objectively
evaluating the efficacy of treatments. In addition, voice therapy sometimes
avoids the need for surgery, saving the patient from exposure to unneces-
sary surgical risks. Heuer and colleagues [65] studied 19 female patients
and 22 male patients who had unilateral recurrent nerve paralysis and
found that after excellent voice therapy, 68% of the female patients and
64% of the male patients considered their voices satisfactory and elected
not 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 are
pending, 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 understanding
through educated participation in the voice restoration process. The impor-
tance of this factor should not be overlooked in the art of medicine and
medicolegal prudence.
In people who have unilateral vocal fold paralysis, initial assessment not
only quantitates and documents vocal dysfunction but also explores a wide
range of potentially useful compensatory strategies. In addition, the speech-
language pathologist identifies spontaneous compensatory behaviors that
may 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 in
these 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 and
trial therapy session, increasing vocal ease and endurance. Moreover, if the as-
sessment reveals improved voice with a different pitch, training in safe pitch
modification in combination with other techniques may also provide rapid im-
provement. Indeed, under good guidance, therapy sometimes produces
astonishingly rapid improvements in voice quality despite persistence of the

neurologic deficit. In any case, initial assessment is worthwhile to document
vocal condition before surgery is considered and to get an estimate of how
much 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 and
endurance. Generally, several therapy sessions are needed to optimize vocal
function. 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 for
therapy 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 and
agility. Training includes head and neck muscle relaxation exercises, aerobic
conditioning, abdominal and thoracic muscle strength and control exercises,
attention to respiration, and various voice exercises that build limb strength
through multiple repetitions with light weights. Forced adduction exercises,
often recommended in speech pathology texts, such as pushing or pulling on
chairs, 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. When
available, 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 limb
strength for walking.
Like surgery, therapy is least successful in combined paralysis. In most
patients 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 have
reached 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 been
successful, the postoperative voice therapy course should be short. Never-
theless, the patient is working with a ‘‘new voice.’’ At least a few sessions
with a speech-language pathologist generally help the patient apply effective
principles learned in preoperative therapy. It is particularly important for
the 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 measures
should be repeated.
If the patient is interested in optimizing voice quality, it is reasonable to
continue therapy as long as it continues to produce voice improvement. This
judgment 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 after

surgery.
Bilateral vocal fold paralysis creates much greater problems; this is true for
bilateral recurrent, bilateral , or bilateral combined nerve paralysis, or combi-
nations thereof. There is still no satisfactory treatment of bilateral recurrent
nerve 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 is
rarely definitive. It is hoped that laryngeal pacing can provide a solution to
these problems, as discussed later in this article. If so, there is an important
role of the voice therapist following pacemaker implantation.
Surgical therapy
The two main surgical options for patients who have unilateral vocal fold
paralysis are medialization and reinnervation. The most common and im-
portant techniques for surgical management of patients who have vocal
fold 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 have
highlighted 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 and
laryngeal 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 and
Company, 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, it
has few (if any) indications today. The senior author (RTS) has not used
Teflon since 1988. Teflon is permanent and leads to a chronic granuloma-
tous inflammatory response [69]. Teflon can also migrate and may even
spread 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 of
vocal fold function is possible but the patient needs or wants immediate
symptomatic improvement. Gelfoam is absorbed within 3 months. If vocal
fold 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 may
be 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 medialize
paralyzed vocal folds [69,71]. Collagen incorporates into host tissue [69].
Some report collagen lasting as long as 3 years. Collagen may be injected

into the vocal ligament. It softens scar tissue and can improve the vibratory
qualities 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 to
improve closure of the posterior glottis. Some laryngologists believe that af-
ter a long duration of vocal fold paralysis, the cricoarytenoid joint scars and
becomes 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 years
after RLN injury, however [75,76].
Reinnervation
Several reinnervation procedures for the paralyzed vocal fold have been
described using the ansa cervicalis [74], phrenic nerve [77,78], preganglionic
sympathetic neurons [79], hypoglossal nerve [80], and nerve–muscle pedicles
[74,77–82]. The main purpose of reinnervation procedures is to prevent
denervation atrophy of laryngeal muscles. Crumley [74] reports improved
vocal quality and restoration of the mucosal wave after reinnervation using
the ansa cervicalis. The ansa cervicalis provides weak tonic innervation to
the intrinsic laryngeal muscles. Reinnervation of the TA muscle restores ten-
sion resulting in a more normal mucosal wave. Reinnervation of the PCA
and LA muscles stabilizes the arytenoids and prevents inferior displacement
of the vocal process, which may occur in some patients. Crumley [74] reports
additionally that the ansa cervicalis–RLN anastomosis is particularly useful
in cases of synkinesis after nerve injury resulting in jerky movements of the
vocal folds. Although there is still synkinesis after ansa–RLN anastomosis,
the weak tonic innervation supplied by the ansa produces a vocal fold that is
less spastic.
Attempts to design reinnervation techniques that might avoid synkinesis
and 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 muscle
is 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 reinnervation
pathway 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 fold
paralysis.
Tucker [81] has reported improvement in voice quality and restoration of

adduction of the unilateral paralyzed vocal fold after nerve–muscle pedicle
transfer. This technique involves implanting a piece of strap muscle inner-
vated by nerve terminals from the ansa cervicalis into one of the denervated
laryngeal muscles, usually the LCA or TA [82,86]. Tucker [86] also reports
better vocal quality in patients who have unilateral vocal fold paralysis when
they are treated with nerve–muscle pedicle and medialization, than when
treated with medialization alone.
Bilateral vocal fold paralysis

Although voice quality is typically good in the presence of bilateral vocal
fold paralysis (BVFP), airway patency is jeopardized by the paramedian
position of the vocal folds. Tracheotomy may be required acutely, followed
by surgery to improve the size of the glottic airway. Surgical techniques are
designed to lateralize one or both vocal folds to improve airway patency and
assist with decannulation. Voice quality is impaired when the paralyzed vo-
cal fold is lateralized. The most important of these techniques are reviewed
elsewhere [68].
Cordotomy and arytenoidectomy with or without suture lateralization of
the vocal fold are the most commonly performed lateralization procedures
to treat bilateral vocal fold paralysis [87]. These procedures are typically per-
formed endoscopically with use of the CO2 laser. The advantages of using
the 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 antireflux
medication 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 engages
and lateralizes the vocal fold. The authors have reported in animals, prom-
ising potential advantages of this new device including more control of the
lateralization 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 no
reported clinical success with such a technique [91]. Tucker [81] has reported
airway improvement and return of abductor function after nerve–muscle
pedicle 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 the
cricothyroid 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) for
bilateral severe paresis to eliminate synkinesis and permit unopposed action
of the PCA to abduct the vocal folds.
When both vocal folds are paralyzed in the cadaveric position, as from
a high vagal lesion, the airway may be fine, but voice and swallowing may
be impaired. In this setting, unilateral or bilateral medialization procedures
may 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 and
bilateral paralysis [91,94–102]. FES systems have been used to restore motor
function to patients who have spinal cord injury, to control heart rhythms in
cardiac disease, and to restore sensory function (cochlear implant, for exam-
ple) [91].
Unlike cardiac pacemakers, laryngeal pacers require an efferent and an
afferent limb. An afferent limb is needed to provide information to enable
effective timing of muscle contracture [95]. For example, in the setting of
unilateral vocal fold paralysis (UVFP), if the paralyzed side is stimulated
to adduct when the innervated side is abducted, this does not result in im-
provement of glottic competence or voice. In the setting of BVFP, firing
of the phrenic nerve, a change in intrathoracic pressure, or chest wall expan-
sion can provide the afferent input signaling inspiration [91,96]. This activity
results in stimulation of the PCA muscles to abduct the vocal folds. In the
setting 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 the
vagus 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 muscles
themselves, 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 depending
on 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 model
of canine UVFP, maximal adduction was achieved with stimulation intensi-
ties from 3 to 7 V, pulse duration of 0.5 milliseconds, and frequencies from
84 to 100 Hz [97]. In human patients who had vagal nerve stimulators placed
for intractable seizures, abduction was noted at 20 Hz, whereas 40 Hz was
required for adduction. Pulse duration of 3 milliseconds and stimulation
intensities of 3 mA were used for all patients [101]. Some implantations of

laryngeal pacers have been done in patients who have bilateral vocal fold
paralysis. 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 be
added to stimulate abduction with inspiration [102].
Gene therapy
Gene therapy may offer future treatment options for recurrent laryngeal
nerve injury. Several growth factors have been identified that promote neu-
ronal survival and sprouting. Delivery of genes encoding such growth
factors into host tissue may protect against neuronal degeneration and stim-
ulate regeneration after nerve injury. Shiotani and colleagues [103] delivered
the gene for IGF-I in a nonviral vector to the rat thyroarytenoid muscle
after RLN transection. Rats who received the gene demonstrated greater
reinnervation and less muscle atrophy than rats who did not receive the
treatment.
Viral vectors carrying gene products can be delivered to the CNS by ret-
rograde transport after peripheral injection into nerve or muscle. Rubin and
colleagues [104] demonstrated that delivery of viral vectors to the CNS is
possible 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 most
common 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 because
of 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 or
pressure on the vagus nerve exerted by the herniating central nervous system
tissue [105,109]. Other causes of vocal fold paralysis in children include birth
trauma, 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 also
may 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, careful
listening to the airway and child’s cry, full head and neck examination with
particular attention to the neurologic exam, fiberoptic examination of the
airway, direct laryngoscopy and bronchoscopy to assess cricoarytenoid joint
function and to look for other anomalies, and MRI from the brain and skull
base through the mediastinum. EMG is used at some centers [111].
Recovery rates for pediatric vocal fold paralysis have been reported from
16% to 64%. Function may return after 6 weeks to 5 years [105]. Children
who have UVFP can be observed in most cases, although occasionally a tra-
cheostomy may be warranted. Positioning maneuvers can be performed to
try to prevent aspiration. Type I thyroplasty has been performed in some
cases [112]. BVFP typically requires urgent airway management and tracheot-
omy. Lateralization procedures, such as arytenoidectomy or cordotomy, may
be performed if bilateral paralysis does not recover [105,107]. Many otolaryn-
gologists recommend waiting at least 12 months before surgery, but this too is
controversial [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 vocal
fold paralysis. It is extremely important for the otolaryngologist to be aware
of this condition, because it can usually be treated successfully if diagnosed
promptly. 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 the
arytenoid helps clarify the condition [119].
Traditionally, arytenoid dislocation has been suspected by history and
absence of the jostle phenomenon present in many cases of unilateral vocal
fold paralysis. Often it is not diagnosed until direct laryngoscopy reveals
impaired passive mobility of the vocal fold. Preoperative differentiation
between vocal fold paralysis and arytenoid dislocation should be possible
in virtually all cases. If not considered specifically, however, it is often
missed. Disparity in height between the vocal processes is much easier to
see in slow motion under stroboscopic light at various pitches. In posterior
dislocations, the vocal process is higher on the abnormal side. In anterior
dislocations, 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 appearance
can prove particularly helpful in cases of arytenoid dislocation, because
many 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 joint

space; and laryngeal EMG to differentiate an immobile dislocated arytenoid
joint 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 before
treatment with vocal fold injection, adduction/rotation, or other surgery.
Even many months after injury it has been possible to move the arytenoid
enough to bring the vocal process back to normal height and allow good
approximation 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 enable
us to improve voice, swallowing, and airway, we have not been able to
restore useful movement consistently to the paralyzed vocal fold. With the
development of new diagnostic and surgical techniques, we will continue
to improve our understanding and treatment of the paralyzed or paretic
vocal 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*
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, and
enhancement of communication [1]. The American Speech-Language-
Hearing Association (ASHA) states that the speech-language pathologist
should 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 with
diagnosis 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 is
being produced in a reasonably efficient, nonabusive manner, then interven-
tion by a speech-language pathologist need not be conducted. It is not
within the speech-language pathologist’s scope of practice to provide special
training 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. In
the case of the professional voice user, increased demand and expectations
for voice quality may be present and should be considered when judging
normalcy 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.
E-mail address: RTSataloff@phillyent.com (R.T. Sataloff).
1134 SCHNEIDER & SATALOFF
include: analyzing vocal behaviors perceptually and objectively; analyzing

vocational, educational, and psychologic factors that may interact with
vocal behaviors and precipitate, maintain, or exacerbate vocal difficulty;
and designing and implementing an individual program for modifying vocal
behaviors [2].
Similar to physicians and their subspecialites, speech-language patholo-
gists vary in their backgrounds and experience in the treatment of voice
disorders. Furthermore, the curricula that speech-language pathologists
complete during education and training vary widely and typically only ad-
dress normal and disordered voice production at a general level. Curricula
rarely provide education or knowledge about the professional voice. Before
making 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 of
voice disorders with special emphasis on the treatment of professional voice
users. There are many factors to consider when working with professional
voice users. The following is not meant to be an inclusive list but is intended
merely 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 typically
has increased awareness of minute changes in the voice production and
quality. A speech-language pathologist must therefore be ‘‘super sensitive
to super speaking.’’ The goals of the professional voice user or performer
are typically different from those of a nonperformer and must be considered
as such. With that in mind, it is important to learn the patient’s expectations
and provide a realistic perspective on the possible outcome of therapy based
on the diagnosis and response to trial therapy techniques during the initial
assessment.
Further consideration must be given to body and self-awareness issues in
performers 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 to
make changes as instructed. Professional voice users may have increased
awareness of vocal behaviors, depending on their previous depth of training.
Body and self-awareness are important skills to develop or maximize in the
voice user. They aid the patient in developing, recognizing, and maintaining
techniques for efficient voice use.
Environmental contributions also should be noted. As a professional
voice user, the patient may be in detrimental performance situations that
may not be obvious to a treating clinician. These may include poor acoustics
while performing, interference of costumes and clothing, positional factors,
and so forth, which can be significant contributing factors to suboptimal
voice performance. The clinician must therefore ask specific questions
or even attend a rehearsal or performance to make a complete assessment
of conditions.
VOICE THERAPY FOR THE PROFESSIONAL VOICE 1135
Psychologic factors also commonly contribute to voice problems. The

voice 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 to
10 different emotions. This finding indicates an emotional/psychologic con-
nection to the voice. Psychologic factors may be related to the patient’s
response to the voice disorder and its effect on his or her life. Or, the voice
disorder may be the manifestation of a larger psychological issue that is
causing a voice disorder, as in psychogenic voice disorders. In either case,
treatment should be tailored to the needs of each patient with careful history
taking and thorough examination. The speech-language pathologist may act
as a patient advocate speaking with the physician and acting as a catalyst for
a referral to the appropriate psychologic professional as deemed necessary
by the physician.
Emotional factors also can affect the patient’s overall response to the
voice disorder. Is the patient able to cope with the voice disorder? How
will it affect his or her current life, voice demand and expectations, and ca-
reer? Are past vocal experiences, the diagnosis, or other people’s responses
affecting therapy sessions or outcomes [4]? These basic questions should be
addressed 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’s
care. Treatment by an interdisciplinary team is important when treating
anyone who has a voice disorder and crucial when treating the professional
voice user. The members of the team may include a laryngologist, speech-
language pathologist, singing voice specialist or singing teacher, acting voice
specialist, voice researcher or scientist, singing coach, or psychologist (Table 1).
Relationships with other arts medicine specialists are also important, including
neurologists, pulmonologists, gastroenterologists, endocrinologists, physiat-
rists, psychiatrists, and others.
In some centers the interdisciplinary team may be in one facility, but not
always. Whenever possible, it is beneficial for voice therapy and singing
voice therapy to be completed by two different professionals. When this oc-
curs adequate time is spent on both areas of the voice, the clinicians can
work together to target areas in the speaking and singing voice, and each
clinician can advise the patient within the area in which they are working,
regardless of the individual background. If team members are not within
the same facility it is important to build relationships within the community
to maximize patient care.
In specific cases other specialists may be included in the interdisciplinary
team. The voice researcher or scientist can provide valuable insight and per-
spective regarding the care of a voice patient because of his or her specific
knowledge and skill set in acoustic measurement and voice production. Re-
ferral to a singing voice coach may also be useful following rehabilitation
work with the speech-language pathologist and singing voice specialist.
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
The singing voice coach is a valuable aid in the development of artistic style
and repertoire for the voice user. A psychologist or psychiatrist may prove
valuable in a team setting, providing the patient with counseling for the
management 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 or
other injury throughout the body.
Regarding the interdisciplinary team, singing and acting voice specialists,
in addition to the singing coach, have no formal licensing or certification
board. It is therefore important to understand that resources from commu-
nity to community can vary widely, as can the backgrounds and knowledge
of various voice professionals. For example, singing and acting voice
teachers and coaches are not trained to work with the injured voice and
therefore may not have experience in this area. Singing voice specialists
and acting voice specialists are experienced teachers who have acquired
such training, usually through apprenticeships.
The interdisciplinary approach to the treatment of voice disorders is
increasingly 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 and
Speech Trainers Association to present a joint statement, ‘‘The role of the
speech language pathologists, the teacher of singing, and the speaking voice
trainer in voice habilitation’’ [5]. This statement is intended to encourage
interdisciplinary treatment of voice disorders and to encourage professionals

working with voice patients to work within the scope of practice and laws
regarding treatment. It is important for professionals to stay within the
bounds 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 the
treatment of dysphonia’’ [6]. This statement recognizes the importance of
voice therapy in conjunction with medical and surgical management in
treating voice disorders as supported by clinical research and expert experi-
ence. These statements should be used to advocate for speech pathology
services 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, and
assembling initial impressions and recommendations. This evaluation pro-
vides the clinician with baseline information about vocal function, patient
stimulability and possible therapy techniques and approaches, expectations
of 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 beginning
with the onset and development of the voice problem and the circumstances
under which it ensued. The patient’s previous or current medical diagnoses
and treatments should be reviewed. The duration of the voice disorder and
its constancy are also important factors. In some cases, voice problems can
be intermittent over many years with the patient not having pursued treat-
ment until the problem worsened significantly. Knowing this information
can give the clinician perspective on the patient’s overall voice disorder.
Whether or not the patient had received voice therapy previously should
be 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 therapy
techniques.
A complete inventory should be taken regarding vocal hygiene, including
hydration and intake of drying agents; engagement in phonotraumatic
behaviors, including yelling, shouting, loud talking, coughing, and throat
clearing; exposure to other irritants, including smoking, exposure to second-
hand smoke, and stage smoke; and behavioral factors that may include sleep
patterns, overall rest, and environmental factors. In addition, vocal
demands should be reviewed and the patient should provide examples of

voice use during a typical day. Throughout this inventory, the patient
should explain the primary vocal complaints so as to provide the clinician
with a possible starting point for intervention. The patient’s initial concerns
are addressed immediately and this may increase his or her motivation to
continue 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 history
of professional voice use, whether it be singing, acting, public speaking, or
a combination thereof. The clinician should also ask about the genre of mu-
sic the patient is singing, voice classification, performance venues, and the
size 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 how
long he or she has studied, the specific school of training, and whether he or
she is studying currently. This process provides information about the types
of vocal techniques the patient may already use or be aware of, or those that
may need to be developed or reworked further.
The clinician should request that the patient share his or her professional
goals and expectations for voice. Ideally, voice therapy should be tailored to
accommodate the patient’s professional and career goals concurrently with
satisfying the clinician’s therapeutic objectives. Even though the singing
voice specialist typically performs a more thorough evaluation of the com-
plaints of a singer, the speech-language pathologist can play an important
role in singing voice rehabilitation and development. The clinician can use
knowledge of a patient’s background, education, and experience to assist
in development of efficient daily speaking voice and in articulating the
relationship between daily speaking routines and singing or stage voice.
Objective evaluation
Gathering and analyzing objective voice data is a crucial part of the
complete voice evaluation. Completing pre- and posttherapy voice measures
can supply objective data to assist in predicting therapy outcomes, to use in
research, and to provide tangible voice statistics for use by insurance
companies. The objective voice evaluation is discussed further in the article
about laboratory and strobovideolaryngoscopy evaluation elsewhere in this
issue.
Subjective voice evaluation

Respiration
The respiratory system is the source of power for voice production. Many
voice problems can be related to poorly coordinated breathing. The clinician
should pay special attention to the manner in which the voice user inhales
and then exhales air to produce voice during the evaluation. Observation
of the patient’s breathing pattern should be completed during reading and

conversational speech. Breathing patterns that may be inefficient for voice
production include clavicular breathing, upper thoracic breathing, or a com-
bination of the two. So-called ‘‘diaphragmatic breathing’’ can be the most
efficient breathing pattern because it tends to provide optimal balance of
inspiratory and expiratory muscle use. Speaking on residual air, shortness
of breath while speaking, gasping for air during inhalation, forced exhala-
tion, or decreased airflow during phonation are also common indicators
of vocal misuse.
Phonation
Phonation is defined as the production of sound at the level of the vocal
folds. A perceptual evaluation of phonation (vocal quality, loudness and
pitch) during reading and conversation should be completed. Vocal quality
characteristics 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 for
the particular setting. The pitch of the patient’s voice should be judged as
appropriate, high, or low for the age and gender. In addition, the frequency
of hard glottal attacks should be assessed.
Resonance
Vocal resonance refers to the way sound is shaped acoustically as it
travels through the vocal tract. Phonation begins at the level of the vocal
folds and moves up through the pharynx, oral cavity, and nasal cavity.
Frontal resonance or forward focus of sound is ideal for most efficient voice
production. It optimizes acoustics of the vocal tract while balancing oro-
nasal resonance. The use of resonant voice therapy, which places emphasis
on frontal tone focus, can increase perceived vocal loudness levels, which
then may allow the voice to be heard better in noisy situations without ex-
cessive strain. Various resonance patterns may be observed while making
a perceptual judgment of the voice, including oral, oropharyngeal, nasal, na-
sopharyngeal, and hypopharyngeal.
Posture
Body posture, how the body is held up against gravity, can have a direct
effect on respiration, phonation, and resonance. Posture is a complicated
interaction 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 be
assessed paying attention to placement of the hips, spine, shoulders, neck,
head, jaw, and even tongue while at rest and in movement. Posture may be
assessed statically in the sitting or standing position and in movement while
walking, running, dancing, teaching, and so forth. Considerations should be
made to observe the patient during activities in which they engage daily.
A brief explanation may be given to the patient so that posture can be

better understood. While sitting, posture can be described as the feet resting
flat on the ground, knees at a 90 angle, hips at a 90 angle, shoulders above
the hips, and ears above the shoulders. The chin should be in a neutral
position with the crown of the head as the uppermost point. At rest, the
tongue maybe resting on the alveolar ridge or behind the bottom incisors
and the jaw should be released. Postural adjustments should not produce stiff
movement but should allow for relaxation within a position. Abnormal pos-
tures that negatively influence efficient voice production may include, but are
not 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 adjustments
made in posture may allow the larynx to relax in the anterior neck, permit eas-
ier breathing, and subsequently result in more coordinated voice production.
Articulation
A global assessment of articulation should be completed judging clarity
and accuracy of articulatory movement for intelligible speech production.
Prosody
Prosody 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 tension
Muscle 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 and
retraining efficient muscle patterns. Box 1 provides examples of general
and specific areas where tension may occur.
Laryngeal palpation provides valuable information regarding specific
areas of tension that may include the suprahyoid area, the strap muscles,
and other related structures. The base of tongue should also be palpated
to assess the presence and degree of tension. Digital manipulation and laryn-
geal massage of the extrinsic laryngeal musculature can provide the clinician
with valuable information regarding tension. As demonstrated by Nelson
Roy, manual laryngeal musculoskeletal tension reduction may yield imme-
diate improvement in vocal quality or an identifiable release in laryngeal
tension [7]. These changes are useful in providing the patient with an
identifiable vocal change or release of tension and may indicate the patient’s
responsiveness to therapeutic intervention.
Oral mechanism examination

A general assessment of oral and facial structure and function should be
completed to rule out abnormalities or asymmetries in strength, range of
Box 1. Identifying areas of tension

Tongue
Anterior
Base of tongue
Jaw
Masseter
Temporomandibular joint
Laryngeal tension
Intrinsic laryngeal muscles
Anterior/posterior neck
Strap muscles
Suboccipital area, posterior cervical muscles
Sternocleidomastoid muscle
Shoulders
High shoulder posture
Tightness/stiffness
Winged scapulae
Upper chest
Anterior/posterior chest muscles
Clavicular area
motion, and coordination that may impact functional communication.

Structures include the face, mouth, dentition, tongue, and hard and soft
palate. Abnormalities may indicate neurologic problems that warrant
further evaluation.
Trial therapy
During 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 clinician
attempts 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 the
clinician should gain information about the patient’s self-awareness of exist-
ing habits and of changes in voice production that may occur. Judgments
can also be made by the clinician about the patient’s ability to learn new
techniques, their willingness to comply with voice therapy, and the overall
appropriateness for therapy. A statement of prognosis for outcomes
through voice therapy should also be made.
Impressions/recommendations
A 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 develop
an impression of the cause or contributing factors in the cause of the voice
disorder. The review of vocal hygiene, vocal demand, and overall voice use
provides the clinician with a place to begin educating the patient about his
or her voice. Although the trial therapy portion identifies facilitators for
improved 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 should
be discussed with the patient. The clinician should indicate to the patient
whether a course of voice therapy is recommended and what the expecta-
tions for follow-up sessions should be. The goals of therapy should then
be discussed with the patient and consideration should be given at that
time to the patient’s personal goals. Once the goals are delineated, other
referrals 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 approximate
length of the therapy in months, weeks, or sessions; and how often the ses-
sions should be scheduled (weekly, biweekly, monthly). The patient also
should be aware that home practice is a crucial part to success in therapy.
The clinician teaches the patient tools and provides support to improve
vocal efficiency and carryover of efficient voice use. It is the patients’ respon-
sibility to attend sessions, complete home practice, and work to carry over
efficient voice use in their everyday lives, with the clinician’s guidance so that
therapy goals can be met and independence in efficient voice use can be
achieved.
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 excellent
speaking voice. The means to reach this goal is to increase vocal efficiency
during speaking. The therapy techniques that are presented can be used to
address behavioral voice problems that may include organic or structural
changes that have taken place on the vocal folds.
Currently, in the speech pathology literature, therapy outcomes data are
limited. The therapy techniques discussed in this section are effective based
on clinical experience. Research has been referenced throughout this chapter
as 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 discussed
with the patient; including coordinating breathing, phonation, and
balancing oronasal resonance. This explanation should provide the patient

with a foundation for understanding voice production and the primary
focus of voice therapy. Vocal hygiene should be addressed and improved
to eliminate vocal stressors and promote an optimal environment for im-
proving vocal ease and quality. Furthermore, the voice user must be made
aware of vocal habits that promote abuse or misuse of the vocal mechanism
and 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 then
be introduced and practiced to begin retraining muscle patterns for voice
production. The vocal exercises work to maximize efficiency of the vocal
mechanism and promote carryover of targeted voice use into daily activities.
Body and self-awareness should be targeted from the onset of therapy to
promote carryover of the efficient voice learned during therapy.
Areas of tension and postural misalignment can have an adverse effect on
efficient voice production. Areas of muscle tension were identified during the
initial evaluation and should be addressed throughout therapy. The patient
should be taught a daily routine for stretches and massage. Table 2 provides
examples 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 head
placement. Slight misalignments in posture can cause increased muscle ten-
sion. For example, elevated chin placement tightens laryngeal and neck
muscles or an arched lower back makes relaxing the abdomen for lower
abdominal breathing difficult.
Facilitators for breath control and support

Because respiration is the power source for phonation, the patient must
be taught to balance inspiratory and expiratory muscles for efficient breath-
ing. Exercises for breath management may start with a simple explanation of
the respiratory system. This explanation may include a description of the
expansion of the lungs and diaphragm with subsequent expansion of the
rib cage and abdominal area during inhalation. As exhalation takes place
these areas begin to slowly deflate. Expiratory muscles may be engaged
but should not be hyperfunctioning. The patient must understand that it
is possible to coordinate breathing and vocalization without hyperfunc-
tional muscle use.
Appropriate terminology should be used when teaching a new breathing
pattern secondary to learned responses that many adults have to phrases
such 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 her
breathe. Phrases such as ‘‘expand for inhalation’’ versus ‘‘take a deep
breath’’ and ‘‘release/deflate for exhalation’’ or ‘‘engage the abdomen during
exhalation’’ rather than pushing or pulling in may be used. In addition, the
image of a newborn baby during quiet breathing with the belly rising on
inhalation and falling on exhalation may elicit understanding of the target
breathing pattern.
While establishing a more efficient breathing pattern, the patient may be
placed in multiple positions to experience the targeted feeling of expansion
during inhalation and active deflation during exhalation. Positions may in-
clude lying on the floor in the supine or prone position and concentrating on
expansion of the lower rib cage and abdomen during inhalation and then
slowly releasing air during exhalation. These two positions, with the help
of gravity, provide tactile feedback during expansion and deflation. They
also aid in decreasing shoulder and upper thoracic movement while breath-
ing. These strategies alter respiratory function, however, and should be used
cautiously and with knowledge of their purposes and limitations. Another
useful technique is instructing the patient to bend over at the waist with
arms extended to a chair or table so that his or her back is parallel with
the floor. The patient is instructed to expand the abdomen during inhalation
and feel the abdomen actively deflate during exhalation. These breathing
techniques and positions are not meant to be sustained but to increase
body awareness of an efficient pattern of breathing that can be applied
during daily activities. As the patient and clinician work through the
therapeutic hierarchy and gradually introduce simple to complex exercises

the patient should be instructed to use the new breathing patterns for short
periods multiple times throughout the day while breathing quietly and also
while 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 during
exhalation. It is important that the patient understand that inhalation
before phonation is as important as releasing air during exhalation to pro-
duce phonation. To achieve appropriate airflow during phonation, muscle
hyperfunction must be eliminated from the vocal tract by various exercises.
The yawn-sigh may be used to promote active inhalation while decreasing
muscular tension in the throat. It also creates increased oral space by lifting
the soft palate. The increased oral space and sensation of open throat should
be maintained during exhalation while producing a sigh. The patient may be
cued to place the tongue in a relaxed position behind the bottom incisors to
maintain oral space. When the targeted yawn-sigh can be replicated consis-
tently, the yawn can then be down-sized to an open-mouthed inhalation and
voicing 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 tissue
draped over his or her finger to provide a visual cue for airflow. The patient
is instructed to blow a passive airstream onto the tissue, which should feel
easy. Confirm this feeling with the patient. Once a consistent, passive
airstream is achieved, the patient is instructed to add his or her voice on
a /u/ vowel while maintaining the airstream. The patient should produce
a smooth, air-filled, easy voice. This voice may sound slightly more air-filled
than normal. The initial goal is to slightly overexaggerate the airflow during
the exercise, so ultimately the ease of voice production is maintained and
airflow can be normalized. Each trial should be modified until the targeted
voice is achieved. The air-filled, easy /u/ is then used as a facilitator into
words, 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 be
produced consistently independent of the facilitator.
Lip trills or tongue-out trills are other facilitators to coordinate airflow
and phonation. For lip trills, which are made using airflow to vibrate the
lips, the patient is instructed to expand during inhalation and produce
a lip trill with only airflow while exhaling. If this is difficult the patient
may place his or her index finger on each cheek and slightly press forward
releasing any lip tension. The patient may also be cued not to clench his
or 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 of
pitches. Once this is completed, the lip trill may be used as a facilitator in
initial /br/ words, phrases, and so forth. Similarly, with the tongue-out trill
the patient should relax the tongue over the bottom lip, expand during
inhalation, and produce a tongue-out trill without voicing during exhala-
tion. This facilitator requires that the tongue and jaw be relaxed and airflow
coordinated to produce the targeted tongue-out trill. When consistency is
achieved, voicing should be added and developed at one pitch and through
a range of pitches. The tongue-out trill can then be used as a facilitator into
open vowels, words, phrases, etc. When the targeted voicing is achieved the
use of the facilitator should be faded out.
When evaluating coordination of airflow and phonation, hard glottal
attacks (abrupt adductions of the vocal folds on words with an initial vowel)
should be addressed. Voicing should be initiated with airflow rather than
abrupt adduction of the vocal folds. This issue can be addressed by targeting
coordination of airflow and phonation. Easy onset exercises should be com-
pleted beginning with discrimination tasks so the patient is able to identify
hard 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 during
an /h/ and their closure during the voiced cognate. Cueing may be required
to ensure inhalation before each trial for optimal air supply throughout
voicing. The patient is then instructed to maintain the open feeling during
the /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 be
said using one breath. When a vowel-initiated word is found within a breath
group, linking should be used. Linking is used to connect the last sound of
the word previous to the vowel-initiated word. For singers or musicians it
may be described as tying the words together, just as notes on the staff
may be tied in legato.
Facilitators for oral resonance

To achieve an optimal balance of oronasal resonance, a relaxed vocal
tract must be maintained in addition to maintaining breath support and
appropriate airflow during phonation. In many hyperfunctional voice users,
it is difficult to achieve forward tone focus secondary to reduced space in the
oral 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, address
jaw tension through stretches and massage, and decrease tongue retraction
through stretches and tongue-relaxation exercises.
Resonance exercises may include the use of a hum to achieve improved
balance of oronasal resonance. The patient should be cued to maintain
oral space, which may be achieved by creating space in between the back
molars to release jaw tension and maintaining relaxed tongue placement

behind the lower front incisors and away from the roof of the mouth. The
patient 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 the
lips. This buzz can provide tactile feedback for the patient in working to
maintain frontal focus while increasing complexity of trials. If the patient
has difficulty achieving a hum without pressing, he or she may be cued to
release air through the nose and maintain a consistent airstream. When
the targeted hum is achieved consistently, it should be used as a facilitator
into vowels, words, phrases, and so forth. Eventually use of the facilitator
should be minimized and then eliminated.
Honking is used as an effective facilitator for developing awareness and
maintenance of balanced oronasal resonance. Honking is completed by
pinching 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 the
mouth. Tactile feedback should be provided with vibration or buzz at the
nasal bridge. When the patient is able to achieve consistent voicing and
awareness 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 the
nose and then repeated after releasing the nose maintaining airflow and
frontal 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 establish
a consistent stream of air coming past the lips. The patient is instructed
to expand and make an /f/ with the back molars parted and the top teeth
barely touching the bottom lip. Following the trial, confirm the feeling of
air past the lips. The patient is then instructed to use the same airflow
and breath support and produce a /v/ sound. A buzz should be felt on
the lower lip during this trial and should be confirmed with the patient. If
the patient has difficulty achieving the buzz, recheck jaw tension and oral
space. Production of a /v/ sound should become consistent and then may
be 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 begin
with /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 each
element. Choosing an appropriate therapeutic facilitator can be challenging.
Clinical judgment should be applied when choosing therapeutic techniques
and modifications should be made for patients as needed. When choosing
a facilitator, consider the patient’s primary complaints, the perceptual and
acoustic evaluation of his or her voice, and the physiology of the patient’s
current voice production versus the targeted efficient voice production. The
clinician should be aware of the benefits and limitations of each facilitator
and 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 evaluating
and treating professional voice users who have voice disorders, these factors
must be taken into careful consideration. Expert listening and management
skills must be used while staying within the scope of practice as a speech-lan-
guage pathologist. A multidisciplinary approach to the care of professional
voice users is crucial to care for this population. Professional relationships
should 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 developing
a therapy plan, the voice user’s previous experience should be taken into
consideration and addressed in therapy, as appropriate.
Further readings
Benniger MS, Jacobson BH, Johnson AF. Vocal arts medicine. New York: Thieme Medical
Publishers, Inc.; 1994.
Boone DR. Is your voice telling on you? How to find and use your natural voice. San Diego (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. San Diego (CA): Singular Publishing
Group, Inc.; 1997.
Rubin JS, Sataloff RT, Korovin GS. 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.
Zemlin WR. Speech and hearing science: anatomy and physiology. Englewood Cliffs (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
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, USA
There have been many advances in microsurgery for voice professionals

over the last three decades. Driven by a greater understanding of the anat-
omy and physiology of phonation, most of the advances provide greater
surgical precision through improved exposure and more delicate ins-
trumentation. Laryngologists who perform laryngoscopic surgery should
be familiar with the current state-of-the-art and should use the latest tech-
niques and technology for all voice patients and particularly for voice
professionals.
Laryngeal surgery may be performed endoscopically or through an exter-
nal approach. To provide optimal care, laryngologists must be familiar with
the latest techniques in both approaches. Modern microsurgery of the voice
is referred to widely as ‘‘phonosurgery,’’ although von Leden introduced
that term originally in 1963 for procedures designed to alter vocal quality
or pitch [1]. ‘‘Voice surgery’’ is a better term for delicate, precise laryngeal
surgery in general, although the term ‘‘phonomicrosurgery’’ has become
widely used. It is usually performed using the microscope, with small, mod-
ern instruments, and with great respect for the induplicatable anatomic
complexity 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 amount
of tissue disruption. Although endoscopic microsurgery seems intuitively
more 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.
1152 SATALOFF et al
provides good exposure of the surgical site and the abnormality can be
treated meticulously and thoroughly with endoscopic instruments. When en-
doscopic visualization is not adequate because of patient anatomy, disease
extent, or other factors, the surgeon should not compromise the results of
treatment or risk patient injury by attempting to complete an endoscopic
procedure. In such patients, it may be safer to leave selected benign lesions
untreated or to treat the pathology through an external approach.
Patient selection and consent

Before performing voice surgery, it is essential to be certain that patient
selection is appropriate and that the patient understands the limits and
potential complications of voice surgery. Appropriate patients for voice
surgery not only have voice abnormalities but also want to change their
voice quality, effort, or endurance. For example, not all people who have
‘‘pathologic’’ voices are unhappy with them. Sports announcers; female trial
attorneys 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 be
a disservice and even jeopardize a career. Similarly, it is essential to distin-
guish accurately between organic and psychogenic voice disorders before
embarking upon laryngeal surgery. Although a breathy voice may be caused
by numerous organic conditions, it is also commonly found in people who
have psychogenic dysphonia. The differentiation may require a skilled voice
team.
Although all reasonable efforts should be made to avoid operative inter-
vention in professional voice users (particularly singers), there are times
when surgery is appropriate and necessary. The decision depends on
a risk–benefit analysis. If a professional is unable to continue his or her
career, and if surgery may restore vocal function, surgery should not be
withheld. Making such judgments can be challenging. A rock or pop singer
who has a vocal fold mass may have satisfactory voice quality with only
minimal 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 ‘‘work
around’’ pathology safely for many years. In some classical singers, even
minor pathology may be disabling. For example, if a high soprano special-
izing in Baroque music develops a mild to moderate superior laryngeal nerve
paresis, she may experience breathiness and instability. If she gives in to the
temptation to compensate by slightly retracting her tongue and lowering her
larynx, the breathiness will be controlled because of increased adductory
forces, 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
VOICE SURGERY 1153
may be served better by surgical correction of the underlying problem than

by long-term use of hyperfunctional compensation (ie, bad technique) that
can 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 may
make the voice worse permanently and must consider this risk acceptable in
light 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 that
the voice may be worse after surgery. Other complications must also be dis-
cussed, including complications of anesthesia, dental fracture, recurrence of
laryngeal lesions, airway compromise, and vocal fold webbing. In addition
to the hospital’s standard surgical consent, we provide patients with addi-
tional written information before surgery. The patient keeps one copy of
the ‘‘Risks and Complications of Surgery’’ document, and one signed
copy remains in the chart. Specialized informed consent documents are
used for other treatments, such as injection of cidofovir, topical application
of mitomycin-C, injection of collagen, and injection of botulinum toxin,
even though such documents are not required. If medications are used for
treatment (rather than research) and are off-label uses of medicines
approved by the FDA for other purposes, their use does not require institu-
tional review board approval. We believe it is helpful and prudent to provide
patients with as much information as possible and to document that they
have been so informed.
It is often helpful for the laryngologist, speech-language pathologist,
singing voice specialist, and patient to involve the patient’s singing teacher
in 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 career
and concerns of each individual patient to help the voice professional make
the best choice.
Documentation
Preoperative objective voice assessment and documentation are essential in
addition to routine documentation of informed consent discussions. A high-
quality recording of the patient’s voice must be done before surgery. Auditory
memories of physicians and patients are not good in general, and the doctor
and postoperative professional voice user are often surprised when they com-
pare postoperative and preoperative recordings. Frequently, the preoperative
voice is worse than either person remembers. In addition, such documentation
is invaluable for medical–legal purposes. Photographs or videotapes of the
larynx obtained during strobovideolaryngoscopy are helpful. Complete
1154 SATALOFF et al
objective laboratory voice assessment and evaluation by a voice team should

be performed. Proper documentation is essential for assessing outcomes, even
for 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 be
taken into account, including the menstrual cycle, pre- and postoperative
voice therapy, concurrent medical conditions, psychologic state, and profes-
sional voice commitments.
Hormonal considerations may be important, especially in female patients
who have symptomatic laryngopathia premenstrualis. In patients who have
obvious vocal fold vascular engorgement or who have a history of premen-
strual vocal fold hemorrhages, it may be better to avoid elective surgery
during the premenstrual period. Except in patients in whom surgery is
intended to treat vessels that have hemorrhaged repeatedly and that are
only prominent before menses, it may be best to perform surgery between
approximately 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 been
fully 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 pressures
dictate inappropriate surgery or surgical timing that is not in the patient’s
best interest. For example, some professional voice users push for early sur-
gery for vocal nodules and promise to appear for voice therapy after a busy
concert season ends. This is not appropriate because therapy may cure the
nodules and avoid surgical risks altogether. Professional commitments often
require that appropriate surgery be delayed until a series of concerts or the
run of a play is completed. In treating vocal fold cysts, polyps, and other
conditions, such delays are often reasonable. They are made safer through
ongoing voice therapy and close laryngologic supervision. Sometimes
individualized treatments may help temporize. For example, aspiration of
a 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 when
therapy cannot cure a lesion, it ameliorates the abuses caused by compensa-
tory hyperfunction, and good preoperative therapy is the best postoperative
voice 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 informed
about surgery and other options. After surgery, voice therapy is medically
necessary for many conditions. It is important to long-term surgical out-
come to time surgery so that the patient is able to comply with postoperative
voice rest and postoperative rehabilitation.
VOICE SURGERY 1155
Many other conditions must be taken into account when deciding upon
the timing of voice surgery. Concurrent medical conditions, such as allergies
that produce extensive coughing or sneezing (which may injure vocal folds
after surgery), a coagulopathy (even temporary coagulopathy from aspirin
use), 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 psychologically
prepared as possible to accept them and to commit the therapeutic and re-
habilitation process. Sometimes psychologic preparation requires a delay in
surgical scheduling to allow time for the patient to work with the voice team.
There are few indications for benign voice surgery that contraindicate a
delay of several weeks. It is generally worth taking the time to optimize
the patient’s comfort and preparedness. Realistic, committed collaboration
by 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 not
received enough attention from the medical profession or from the general
public. 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 that
is 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 improved
and have become practical for many more people.
Vocal weakness, breathiness, instability, impaired quality, and other
characteristics can interfere with social and professional success. Many
problems (eg, breathiness, softness, instability, tremor, and change in habit-
ual pitch) are commonly associated with aging. For most people, these vocal
characteristics, 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 comprehensive
voice evaluation. Often, voice problems that one may ascribe to aging or to
genetic 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 serious
medical problem, so comprehensive medical evaluation is essential before
treating the voice complaints.
Once medical problems have been ruled out or treated, the next step for
vocal habilitation or restoration is a program of therapy or exercise
provided by a multidisciplinary team that incorporates the skills of a laryng-
ologist, a speech-language pathologist, and an acting-voice specialist. The
training involves aerobic conditioning to strengthen the power source of
1156 SATALOFF et al
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 and
other 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 makes
professional communication and social interaction difficult, especially in
noisy surroundings, such as cars and restaurants. When one has to work
too hard to communicate, it is often related to vocal deficiencies. When ex-
ercises and medications alone do not provide sufficient improvement, many
patients elect voice surgery in an attempt to strengthen their vocal quality
and endurance and to improve their quality of life.
Several procedures can be used to strengthen weak or injured voices. The
selection 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 must
be taken to ensure that patient expectations are realistic. In most cases, surgery
is directed toward bringing the vocal folds closer together so that they close
more firmly. This eliminates the air leak between the vocal folds that occurs
as a consequence of vocal atrophy from aging (atrophy or wasting of vocal
nodules or other tissues) or as a result of paresis or paralysis (partial injury
to a nerve from a viral infection or other causes). In some cases, the operation
is done by injecting a material through the mouth or neck into the tissues
adjacent to the vocal folds to ‘‘bulk up’’ the vocal tissues and bring the vocal
folds closer together. This is called ‘‘injection laryngoplasty’’ and is performed
usually using fat, collagen, or hydroxyapatite. This operation is sometimes
done in the operating room under local anesthesia and, in selected patients,
in the office with only local anesthesia. Alternatively, the problem can be
corrected by performing a thyroplasty. This operation involves making a small
incision in the neck. The skeleton of the voice box is entered, and the laryngeal
tissues are compressed slightly using Gore-Tex or silastic implants. This
procedure is generally done under local anesthesia with sedation. All of these
procedures usually are performed on an outpatient basis.
Recovery usually takes days to weeks, depending on the procedure. Any
operation can be associated with complications. Rarely, the voice can be
made worse. The most likely complication is that voice improvement is
not sufficient or that it does not last over time. When this problem occurs,
it can be corrected by ‘‘fine tuning’’ through additional injections or surgical
adjustment of the implant. Usually, satisfactory results are achieved the first
time.
Voice rehabilitation through medical intervention and therapy/exercise
training 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 does
not have major, serious medical problems (eg, end-stage heart disease) and is
VOICE SURGERY 1157
not on blood thinner medication that cannot be stopped safely for surgery, so
long as that person has realistic vocal goals and expectations. ‘‘Voice lift’’
surgery should be thought of as a comprehensive program stressing medical
diagnosis and physical rehabilitation, not as surgery alone.
Thyroplasty
Another excellent approach to medialization is type I thyroplasty. This
procedure was popularized by Isshiki and colleagues [2] in 1975, although
the concept had been introduced early in the century by Payr [3]. Thyro-
plasty is performed under local anesthesia. In classical thyroplasty, with
the neck extended, a 4- to 5-cm incision is made horizontally at the midpoint
between 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 to
5 mm by 3 to 10 mm. The inferior border is located approximately 3 mm
above the inferior margin of the thyroid cartilage. Care must be taken not
to 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 in
proper position. Since Isshiki’s original description, many surgeons have
preferred to remove the cartilage. Most preserve the inner perichondrium,
although techniques that involve incisions through the inner perichondrium
have 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 this
technique has become more popular, and several varieties of preformed
thyroplasty implant devices have been introduced commercially. Many of
these modifications have proven helpful, especially techniques that obviate
the need to carve individualized silicone block implants, a technique that
is often challenging for inexperienced thyroplasty surgeons. The silicone
block modifications described by Tucker [11] are also useful, particularly
the technique of cutting out a portion of the prosthesis to allow for the
placement of a nerve-muscle pedicle. We have generally abandoned all of
these techniques except during revision cases in favor of Gore-Tex in the
larynx 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 compensate
for vocal fold bowing and a variety of irregular laryngeal configurations.
Our preferred technique is slightly different from procedures published
previously.
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 through

a minithyrotomy, obviating the need to traumatize or transect strap mus-
cles. A 2-cm horizontal incision is made centered in the midline in a skin
crease near the lower third of the vertical dimension of the thyroid cartilage.
The cartilage is exposed in the midline, and the perichondrium is incised and
elevated. A 4-mm diamond bur is used to drill a 4-mm minithyrotomy. Its
anterior border is located approximately 7 mm from the midline in female
patients and 9 mm from the midline in male patients, and its inferior margin
is 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 is
important that minimal elevation be performed. A small pocket, only 2 to
3 mm in width, parallel to the inferior border of the thyroid cartilage is suf-
ficient. This is substantially different from the extensive elevation performed
during 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 vocal
fold position can be monitored by flexible laryngoscopy during the opera-
tion continuously during medialization or by checking the final position
visually at the conclusion of the operation. Once Gore-Tex has been
positioned optimally, it is cut a few millimeters outside the thyrotomy.
For closure, some surgeons use perichondrial flaps that are repositioned
and sutured. Alternatively, the thyrotomy can be filled with a few drops
of 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 the
cyanoacrylate the cyanoacrylate block. This prevents extrusion of the Gore-
Tex, and the cyanoacrylate ‘‘button’’ and Gore-Tex are removed easily
when revision surgery is necessary by pulling on the end of the Gore-Tex
that extends a few millimeters beyond the cyanoacrylate. Gore-Tex thyro-
plasty is so expeditious and atraumatic that it can be performed bilaterally
at the same sitting. This is done commonly to treat vocal fold bowing from
bilateral 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 the
conclusion of the procedure and removed on the first postoperative day. In
many cases, the procedure is performed as outpatient surgery, although
overnight 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 of
steroids or antibiotics in thyroplasty surgery. Many surgeons use both rou-
tinely. Sixty milligrams of prednisone taken the night before surgery can
help to minimize intraoperative edema, improving the accuracy of implant
VOICE SURGERY 1159
placement and vocal fold medialization, and thus, the final voice outcome.
In our practice, we have encountered only one infection after thyroplasty
in over 20 years, and that was believed to be due to contaminated sutures
recalled by the manufacturer shortly after that operation. Because a foreign
body is implanted during thyroplasty, many surgeons prefer to give antibi-
otics prophylactically.
Revision thyroplasty is a more complex matter. Most thyroplasties that
have required revision have been performed originally using a silastic block
or one of the preformed, commercially available implants. During these ini-
tial operations, a large thyroplasty window was created, and perichondrium
was elevated. Removing the silastic block and replacing it with Gore-Tex
generally 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 prosthesis
that had been placed originally. If revision is being performed because of in-
sufficient medialization, it is sometimes possible to elevate the anterior
aspect of the prosthesis and layer Gore-Tex medial to it. Such cases are
uncommon. More often, it is necessary to incise the fibrotic capsule in the
region 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 medialization
resulting 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 discussed
previously or endoscopically by injecting fat or collagen. Excessive anterior
medialization is corrected by reshaping the prosthesis. In such cases, the
original 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 of
the thyroid cartilage. When additional cartilage is removed to place the
prosthesis at the desired height, cartilage deficiency from the original oper-
ation often leaves the prosthesis unstable. In such cases, the implanted
device should be secured to the thyroid cartilage by sutures. In fact, when
using an implant other than Gore-Tex for primary or revision surgery, we
secure the prosthesis to cartilage with Prolene sutures to prevent migration
or extrusion.
Another common reason for revision is inappropriate patient selection. If
there is a large, symptomatic posterior glottal gap, thyroplasty alone is often
insufficient. Procedures to alter arytenoid cartilage position are necessary in
many 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 the
implant, 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 hematoma

along the vibratory margin or by infection vocal fold stiffness with perma-
nent dysphonia can result. Hemorrhage and edema also can produce airway
obstruction. Weinman and Maragos [16] reported on 630 thyroplasty proce-
dures. Seven of their patients required tracheotomy. Five of 143 patients
who 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 of
the 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 pitch
in specially selected patients, such as those undergoing gender reassignment
surgery. These operations do not provide consistently good enough voice
quality to be performed on a professional voice user for elective pitch
change. 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 not
modified by laryngeal surgery.
Indirect laryngoscopic surgery

Laryngoscopic surgery is generally performed through direct laryngos-
copy. Indirect laryngoscopic surgery has been performed for many years
and 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 pathology
whose 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 flexible
fiberoptic laryngoscope. When surgery is performed solely for injection (eg,
fat or collagen), an external or transoral technique may be used. External
injection may be performed by passing the needle through the cricothyroid
membrane and into the desired position lateral to the vocal fold or through
the thyroid lamina usually near the midpoint of the musculomembranous
vocal 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 the
transoral 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 tongue
themselves. Angled instruments designed specifically for indirect
VOICE SURGERY 1161
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.)
laryngoscopic surgery are passed through the mouth and guided visually.
Only a surgeon who is skilled in the necessary maneuvers should perform
the procedure. The advantages of this technique include relatively easy ac-
cess in anyone whose larynx can be visualized with a mirror, avoidance of
the need for an operating room procedure, and ready availability when de-
lays in getting to a hospital and waiting for an operating room might cause
serious problems. The procedure also has disadvantages. Precise control is
not as good as that accomplished with microlaryngoscopy under sedation
or general anesthesia, intraoperative loss of patient cooperation may result
in injury, and the ability to handle complications such as bleeding and
edema is limited. Nevertheless, at times the procedure is invaluable, and it
should be in the armamentarium of the laryngologic surgeon.
Direct laryngoscopy
Suspension microlaryngoscopy is the standard technique for endoscopic
laryngeal surgery. The concept of direct laryngoscopy was introduced by
Green [18] in 1852 using sunlight and supported later by Brünings [19]. The
history of phonomicrosurgery is reviewed in greater detail elsewhere
[1,20,21]. Many laryngoscopes are available. An instrument should be selected
for each patient that provides excellent exposure of the vocal folds, internal
laryngeal distension, and minimal distortion of the area of surgical interest.
In addition to choosing an appropriate laryngoscope, it is important to
understand principles of suspension and of internal distention and external
counterpressure. In most cases, the laryngoscope should provide visualiza-
tion of only the entire vocal fold and should distend the false vocal folds
and larynx in a way that optimizes visualization. Rarely, distension of the
false vocal folds is not desirable, and a laryngoscope positioned in the val-
lecula (eg, the Lindholm; Karl Storz, Culver City, CA) provides an
1162 SATALOFF et al
alternative. This is the exception rather than the rule. In addition to internal
distention, external counterpressure is important. Gentle pressure over the
cricoid 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 use
1 inch tape that extends from one side of the headrest of the bed to the other
and holds steady pressure on the larynx, maintaining the desired position.
There can be a disadvantage to counterpressure. Although it improves
visibility (especially anteriorly), it introduces laxity in the vocal folds that
may distort slightly the relationships between pathology and normal tissue.
Hence, an appropriate compromise must be achieved in each case to
optimize 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 other
literature [22,23].
Anesthesia
Local anesthesia
Local anesthesia with sedation is desirable in some cases for endoscopic
laryngeal surgery, especially if fine adjustments of vocal quality are to be
made, as during injection for vocal fold paralysis or reduction of a dislocated
arytenoid cartilage. Many techniques of local anesthesia are used. They in-
volve a variety of systemic, topical, and regional medications. The technique
described below has proven most effective in our experience but should be
considered only one of many options. In rare instances, direct laryngoscopy
may 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 anesthetic
application. We prefer a sedative that produces amnesia, such as propofol or
midazolam. 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 regional
blocks and local infiltration. Bilateral superior laryngeal nerve blocks are
achieved using 1% Xylocaine with epinephrine 1:100,000. Superior laryn-
geal nerve block is accomplished by injecting 1 to 2 mL of 1% Xylocaine
into the region where the nerve penetrates the thyrohyoid membrane, ante-
rior to a line between the greater cornu of the thyroid cartilage and the
greater cornu of the hyoid bone. Glossopharyngeal nerve blocks are placed
using 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 posterior
tonsillar pillar on each side. The tongue base is then infiltrated with 2 to
4 mL, using a curved tonsil needle and metal tongue depressor. Anesthesia
VOICE SURGERY 1163
is concluded with intratracheal topical application of 4 mL of 4% topical

Xylocaine administered through a midline injection in the cricothyroid
membrane (after anesthetizing the skin with 1% Xylocaine with epinephrine
1:100,000 or by spraying topical anesthetic between the vocal folds if they
can 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 metal
tongue 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 should
not 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 oxygen
saturation. If adequate topical and regional anesthesia cannot be established
or if adequate sedation cannot be achieved safely, the procedure should be
discontinued or general anesthesia should be induced. The patient and the
anesthesia team should be prepared for possible use of general anesthetic
in all cases.
Most laryngeal procedures can be performed safely under local anesthesia.
This choice provides the opportunity to monitor voice during the procedure
and protection from the risks of endotracheal intubation. There are disadvan-
tages. When maximal precision is necessary, the motion present during local
anesthesia may be troublesome. Greater accuracy is enhanced by general
anesthesia with paralysis. The safety of local anesthesia during some cases
of endolaryngeal surgery is questionable. In addition to mechanical surgical
problems, in some patients who have cardiac or pulmonary problems, the re-
spiratory suppression caused by sedation may be more hazardous than general
anesthesia. In addition, local anesthetics may produce side-effects. These may
include mucosal irritation and inflammation (contact dermatitis) that may
cause erythema and pruritus, vesiculation and oozing, dehydration of mucosal
surfaces 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 most
topical anesthetics used commonly in laryngology, and they should be used
only 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) and
ferrihemoglobin because the iron in methemoglobin is trivalent (or ferric) in-
stead of divalent (ferrous). Methemoglobinemia produces cyanosis, although
skin discoloration is usually the only symptom of acquired methemoglobine-
mia. Arterial blood gas analysis confirms the presence of methemoglobin. This
condition can be induced by any amine-type local anesthetic. Prilocaine and
benzocaine 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 not
found in the plasma. Methemoglobincythemia would be more accurate, but
methemoglobinemia is used commonly. Methemoglobinemia is treated by in-
travenous administration of methylene blue, although the condition is not life
threatening and resolves spontaneously. The notion that local anesthesia is
preferable to general anesthesia should be viewed with skepticism. The choice
depends on the patient, the lesion, the surgeon, and the anesthesiologist.
General anesthesia
Probably the most important consideration in general anesthesia for
voice 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 voice
patients. 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, well
informed anesthesiologist and laryngologist collaborate, the choice of anes-
thetic depends solely on the patient and lesion, and safe effective surgery can
be 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 agent
to avoid patient motion or swallowing. Intubation and extubation should be
accomplished atraumatically, using the smallest possible endotracheal tube.
Most laryngeal endoscopic procedures are short in duration, and a 5.0 mm
inner diameter endotracheal tube is generally sufficient, even for most mod-
erately obese patients. The laser may be used during many procedures, and
it is best to use a laser-resistant endotracheal tube in such cases.
Antireflux medications are prudent, especially in patients who have
symptoms and signs of reflux. Reflux may occur under anesthesia even in
patients who do not have significant clinical reflux. The combination of
acid 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 protecting
against cellular injury. Intravenous steroids should be used at the surgeon’s
discretion if there is no contraindication.
Endotracheal intubation provides the safest, most stable ventilation
under general anesthesia, and it generally provides adequate visibility. In
some 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
VOICE SURGERY 1165
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 oxygen
can 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 through
a Carden tube [26]. We use the Hunsicker catheter because of its easy place-
ment, security, and laser resistance and because the jet ventilation initiates
below the vocal folds. This seems to cause less mechanical interference at
the vibratory margin during surgery. The catheter must be placed between
the vocal folds carefully by an expert anesthesiologist or the laryngologist
and removed carefully to avoid intubation and extubation trauma as might
be caused by placement of any endotracheal tube. During any surgery that
uses jet ventilation, it is essential that the surgeon be a knowledgeable, co-
operative part of the anesthesia team. The airway must remain unobstructed
for expiration. If the laryngoscope moves or is removed and obstructs the
airway without a warning to the anesthesia team, pneumothorax may result.
Intermittent apnea is another alternative to intubation when the presence
of the endotracheal tube would otherwise obstruct the surgical field. In such
a case, the anesthesiologist ventilates the patient with a mask or with a small
endotracheal tube to reach an O2 saturation of 100%. Once 100% O2
saturation is reached, the endotracheal tube or mask is withdrawn, and
the surgeon operates on the larynx while the patient is apneic. The O2
saturation is monitored carefully, and when the O2 saturation drops to
95%, the surgeon stops operating, and the patient is ventilated via mask
replacement of the endotracheal tube. It is preferable to use an endotracheal
tube for ventilation because the patient does not have to be taken out of
laryngeal suspension to resume ventilation. Instead, the endotracheal tube
is placed over a 0 laryngeal telescope and introduced into the larynx under
direct visual guidance through the rigid suspended laryngoscope. This
allows maximal time for performing surgery during the apneic periods,
which, depending on the pulmonary health of the patient, can last for
5 to 7 minutes each. Additionally, time is not lost in resuspension and
reobtaining exposure, which can be a frustrating consequence of choosing
mask ventilation with intermittent apnea.
All the care exercised in gentle intubation may be for naught unless
similar caution is exercised during extubation. The most common error
during 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. The
surgeon should be present and attentive during intubation and extubation
to help minimize the incidence of such occurrences.
1166 SATALOFF et al
Anesthesia is a prime concern during nonotolaryngologic surgery involv-

ing general surgeons and other surgical subspecialists. Laryngologists are
frequently called on for guidance by professional voice users, surgeons,
and anesthesiologists. The anesthesiologist must appreciate that the patient
is 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. There
are few procedures that cannot be performed safely through a 6.5-mm inner
diameter or smaller endotracheal tube, and many can be performed with
mask anesthesia or a Brain laryngeal mask without intubating the larynx.
Alternatives to general anesthesia should be considered, such as spinal
blocks, regional blocks, and acupuncture. Many procedures commonly
done under general anesthesia with intubation can be performed equally
well using another technique. After surgery, postoperative voice assessment
by the anesthesiologist, patient, and operating surgeon is essential. If voice
abnormalities are present (other than very mild hoarseness that resolves
within 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 fold
pathology and mapping lesions for surgery. Four-millimeter and 10-mm
0 and 70 telescopes (Karl Storz, Culver City, California) and 30 and
120 telescopes are useful in some circumstances. Laryngeal telescopes allow
the surgeon to visualize lesions in great detail to appreciate the limits of
lesions 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.
VOICE SURGERY 1167
When laryngeal telescopes are not available, urologic rigid cystoscopes are
equivalent alternatives.
A technique known as ‘‘contact endoscopy’’ has been used by gynecologic
surgeons for many years. Its value in microlaryngeal surgery was recognized
by Andrea [28]. This technique uses a vital staining agent, such as methylene
blue. Contact endoscopy permits visualization of the cellular nature and the
integrity 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 surgical
intervention. Although this technique is relatively new and requires additional
study and experience, it seems to be valuable in selected cases.
Delicate microsurgery requires sharp, precise, small instruments. The few
heavy cupped forceps and scissors that constituted a laryngoscopy tray
through the early 1980s are no longer sufficient. It is now possible to obtain
microlaryngeal 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 should
include scissors (straight, up-biting, curved left, and curved right), small
grasping cupped forceps (straight, up-biting, right, and left), larger cupped
forceps (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 instruments
should be sharp at all times. Suctions should be thumb controlled, of several
sizes, and should include open tip and velvet eye designs. A suction/cautery
tip may be valuable occasionally and should be available, as should cotton
carriers. Nonreflective instruments with laser-resistant coating may be
advantageous in some situations. In addition, there have been important
advances not only in cold instrumentation, but also in powered instrumen-
tation and surgical laser technology (eg, CO2, Yag, pulsed-dye) with which
all microlaryngoscopic surgeons should be familiar [29].
Powered laryngeal surgery is a relatively new concept, although powered
surgery for other areas of the body has been used for many years [30].
Acoustic neuroma surgeons have used powered instruments such as the
House-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, but
powered laryngeal surgery is useful in the treatment of conditions such as
selected 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 powered
instruments safely, it is important to understand the blades and instrument
settings. 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 vacuum
setting. To remove papilloma near the vibratory margin or anterior
1168 SATALOFF et al
commissure in a controlled fashion, it is more appropriate to use a 3.5-mm

laryngeal skimmer blade at 500 rpm in the ‘‘oscillate’’ mode with the suction
set at a low vacuum setting. Although some surgeons prefer using powered
instruments under endoscopic control rather than using a microscope, we
generally prefer using a microscope to permit binocular vision and bimanual
manipulation. Surgeons should have endoscopes available and be comfort-
able with their use. In some cases, difficult anatomy precludes visualization
of certain regions of the larynx, especially at and above the anterior commis-
sure with the operating microscope. In such cases, the best way to remove
pathology may be with the use of a 70 telescope for visualization and a pow-
ered skimmer blade for resection. Delicate microdissection is the most
controlled 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 helpful
especially for selected papillomas and neoplasms.
Laryngeal microsurgery
Submucosal infusion, hemorrhage control, steroid injection
The concept of laryngeal infusion was introduced in the 1890s for the
purpose of anatomic studies [31,32]. The technique has been used for a vari-
ety of purposes, including infusion of steroids to disrupt adhesions in vocal
fold scar, placement of collagen along the vibratory margin, and separating
benign and malignant lesions from underlying structures. The technique has
been become more popular among clinicians since the 1990s [33,34].
Submucosal infusion may be appropriate for a variety of vocal fold
masses, but it has disadvantages as well as advantages. Infusion usually is
performed using a solution made by combining 9 mL of sterile saline with
1 mL of epinephrine 1:1000 (a 1:10,000 dilution). A small amount of this
mixture is infused submucosally using a 30-gauge needle to increase the fluid
content 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 define
the vocal ligament more clearly. In lesions such as sulcus vocalis, vocal fold
scar, and papilloma, this technique is extremely helpful. In other lesions
such as small vocal fold cysts, it may obscure the pathology, making surgery
more difficult. When used in appropriate cases, the epinephrine causes vaso-
constriction and helps minimize bleeding. When bleeding occurs, it can be
controlled in most cases with topical application of epinephrine 1:1000 on
a small cottonoid. Rarely, cauterization with a laser or cautery is required.
Infusion of saline and epinephrine does not have to be limited to the vocal
fold. 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 into
the surgical field, providing direct access to lesions that involve the deep re-
cesses of the laryngeal ventricle.
VOICE SURGERY 1169
In some cases, submucosal infusion may be performed with a substance

other 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 for
infusion initially. It is as effective as saline and epinephrine in defining the
lesion 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 may
result in muscle atrophy. If steroid injection is used, it is important for
the surgeon to use an aqueous solution, not an oil-based preparation. One
of the authors (RTS) recommends against using steroid suspensions that
are ‘‘milky-colored,’’ such as Kenalog (Westwood Squibb, Buffalo, New
York). Occasionally, the white suspended particles can precipitate and
form a plaque that takes months to resolve. Precipitation and the formation
of plaques have not been encountered with steroid solutions, which are
typically clear liquids such as dexamethasone. Cidofovir can also be used
sparingly 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, it
is 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 vocal
fold cysts provides a good window into the evolution of voice surgery.
Vast improvements in surgical care of vocal fold abnormalities occurred
in the 1980s and 1990s. These changes have resulted largely because of
advances in knowledge of the anatomy and physiology of the vocal tract,
technologic developments that have improved our ability to examine and
quantify voice function, and the availability of better surgical instruments
[35–37]. Because the human is the only species with our layered lamina
propria structure, there is no experimental animal for vocal fold surgery.
Therefore, surgical advances have been based largely on anecdote and
common sense. Consequently, it is essential to reevaluate results continually
and 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 choice
for benign vocal fold pathology was ‘‘vocal cord stripping,’’ an operation
abandoned except perhaps in selected cases of laryngeal cancer. Until the
mid 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 diseased
mucosa with new, healthy mucosa. Mucosal healing in the oral cavity and
elsewhere in the upper respiratory tract was rarely a problem; so, why should
there be a problem on the vocal folds? We had no explanation for the
1170 SATALOFF et al
patients who seemed to have normal vocal folds but terrible voices after this
operation, and we tended to diagnose their persistent dysphonia as psycho-
genic. In retrospect, knowing what we do now about vocal fold anatomy and
physiology, we have no explanation for the fact that so many of those pa-
tients were not permanently hoarse. Nevertheless, the beginning of the end
of vocal fold stripping came in 1975 when Hirano [35] described the anatomy
of 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 scar
were numerous, primarily in the intermediate and deep layers of the lamina
propria and the muscle. Most benign vocal fold pathology is superficial.
Moreover, research from numerous centers highlighted the importance of
the complex mucosal wave created during phonation [37–43]. Consequently,
although delicate microsurgery had been advocated by a small number of
far-sighted laryngologists in the past, the need for this approach to voice
surgery quickly became generally accepted [44]. Eventually, surgeons began
to think of the anatomy and function of the vocal fold and of pathology in
layers and to conceptualize surgery in layers. This paradigm resulted in the
current concepts and techniques of phonomicrosurgery, which are designed
to remove the pathology without disturbing adjacent normal tissue.
Vocal fold microsurgery developed rapidly in the 1980s and became the
new standard of care. It was based on the notion that surgery should be de-
signed to remove pathology without promoting scar formation (ie, without
stimulating fibroblasts in the intermediate layer of the lamina propria or
deeper). 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 propria
would be traumatized directly by contact with the contralateral vocal fold
during 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 and
illustrated in 1986 [44]. It has been recommended by numerous other au-
thors since that time [44–49]. This technique was attractive because the vocal
folds looked ‘‘healed’’ almost immediately. This surgical concept was based
on reasoning, not on research. Although this is unfortunate, in many ways it
is unavoidable. In the absence of an animal model with a layered lamina
propria, 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 at
our results to see whether our common sense is producing consistently fa-
vorable outcomes in our patients. Laryngeal microflap surgery was a great
improvement over vocal fold stripping. Since laryngologists began operating
with delicate, small instruments and handling tissues gently, we have seen
VOICE SURGERY 1171
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.)
far fewer cases of permanent dysphonia from extensive vibratory margin

scar. Nevertheless, the results of microflap surgery were not uniformly pleas-
ing. Many were excellent (as were the results of some vocal fold strippings
years ago), but careful strobovideolaryngoscopic analysis and voice assess-
ment showed too many cases in which the final outcome was inexplicably
not perfect. Despite what seemed to be technically flawless operations,
a small number of patients had severe, prolonged stiffness for many months
after vocal fold surgery, and critical analysis revealed permanent stiffness
even in some patients who were happy with their voice results. Moreover,
some of this stiffness was located anterior and posterior to the region of
the mass in areas that had been normal preoperatively. This critical assess-
ment of surgical results led to the uneasy feeling that we were still doing
something wrong. The problem became clear immediately with the base-
ment membrane research of Gray [50].
1172 SATALOFF et al
Before Gray’s landmark discovery, microflap surgery made sense. Now,

it usually does not. Gray demonstrated a complex basement membrane
structure between the epithelium and superficial layer of the lamina propria.
Moreover, he illustrated that the epithelium and basement membrane are
attached to the superficial layer of the lamina propria through an intricate
series of type VII collagen loops. These loops emanate from and return to
basement membrane cells. Type III collagen fibers of the superficial layer
of the lamina propria pass through them. This highly sophisticated architec-
tural arrangement is probably variable from person to person and perhaps
from family to family. Basement membrane structures and the integrity of
their 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 not
simply manipulating structurally insignificant tissue. Rather, we are ripping
apart delicate, functionally important anatomic structures.
Armed with this new anatomic knowledge and evidence that previous
surgical 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 technique
counterproductive. 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 with
the smallest possible amount of their overlying mucosa, or a mini-microflap
is 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 dissection
is 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 generally
easy to do once the mass has been reflected medially because the mucosa
is stretched because of the lesion. The micro-miniflap is a small, medially
based pedicled flap. It should not be confused with Dedo and Sooy’s [52]
much larger ‘‘micro-trap-door flap’’ for use in supraglottic stenosis or
with Ossoff and colleague’s larger ‘‘serial micro-trap-door flaps’’ used for
subglottic stenosis [53,54].
Good, prospective scientific data comparing vocal fold stripping and
microflap and mini-microflap surgery are not available. Initial anecdotal
impressions and the data presented on excision of 96 vocal fold masses in
60 patients (49 of them singers) [51] provide convincing evidence that
VOICE SURGERY 1173
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 as much adjacent mucosa 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.)
mini-microflap surgery and limited mass excision with overlying mucosa

(without disturbing any adjacent tissue) (Fig. 5) provide substantially better
results than the microflap surgery advocated originally by us. There is less
extensive and prolonged postoperative stiffness with this procedure than
was encountered after some cases of microflap surgery. Mini-microflap sur-
gery is recommended for excision of vocal fold submucosal and epithelial
cysts, polyps, and similar lesions. When a mini-microflap cannot be created,
resection of the mass with the smallest possible amount of overlying mucosa
should be performed.
Vocal fold polyps and nodules

Like the vocal fold masses discussed previously, vocal fold polyps and
nodules should be removed conservatively to preserve normal mucosa and
should remain superficial to the intermediate layer of the lamina propria.
1174 SATALOFF et al
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.)
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 the
mucosa using cupped forceps. Nodules rarely require surgery. If they are
diagnosed correctly, more than 90% resolve or become asymptomatic
through 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 are
accompanied by an obvious central blood vessel that extends from the su-
perior surface of the vocal fold. Occasionally, feeding vessels may course
along the vibratory margin or originate below the vocal fold edge. Promi-
nent feeding vessels should be cauterized with a carbon dioxide laser (at 1
W, 0.1 single pulse second, 30 mj, defocused) or resected to help prevent re-
current hemorrhage and polyp formation (Fig. 6). We prefer resection in
most cases. The polyp can then be removed from the vibratory margin
VOICE SURGERY 1175
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.)
with traditional instruments (Fig. 7) or laser. We use cold instruments, but

the 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 submucosal
hemorrhage emanating from the enlarged, weakened blood vessel. More
rarely, 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 after
exercise) and that change the mass of the vocal fold. This is a proven but
uncommon 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 be
indicated 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 soaked
in 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 beam
tangentially 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 some
cases, the mucosa may be gently retracted using alligator forceps with a cot-
tonoid along the superior surface, stretching blood vessels onto the superior
1176 SATALOFF et al
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.
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 such
that laser vaporization cannot be performed safely, delicate resection of the
vessel 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 by
Hochman and colleagues [55] in 1999. Thirty-four of the 42 patients re-
ported were women, 84% of the patients who had documented hemorrhages
were women, and 39 of 42 of the patients were singers.
Most ectasias and varices are located in the middle of the musculomembra-
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
VOICE SURGERY 1177
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.)
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 in
the superficial layer of the lamina propria because the mucosal wave reaches
its 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 of
hemorrhages, 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 is
referred to as the striking zone [55]. It is believed that chronic mechanical
trauma to the microvasculature is responsible for the development varicosities
and ectasias and that direct collision forces are responsible for most of the vas-
cular abnormalities that occur on the medial surface of the vocal fold. The fact
that so many such abnormalities are on the superior surface rather than on the
vibratory margin probably is due to the fact that the maximum sheering
stresses during oscillation are on the superior surface. Because of the whip-
lash-like mechanism of injury, superficial vessels are more likely to be injured
than 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 remained
the same or improved in all patients who underwent excision of ectasias or
varices using cold instruments [55].
This had not been the experience with laser management of similar
lesions in earlier years before this technique was developed. Although the
resection of vessels is preferred in most cases, laser cauterization should
be considered, particularly for lesions far lateral to the vibratory margin.
1178 SATALOFF et al
Regardless of location, the importance of avoiding trauma to adjacent

tissues cannot be overstated.
In patients who have extensive hemorrhage distorting a vocal fold, an
incision along the superior surface with evacuation of the hematoma may
expedite healing. In general, this is not necessary. If the bulging vocal fold
has not flattened satisfactorily through resorption of the hematoma within
a few days after the hemorrhage, evacuation may be considered. Surgery in-
volves suction evacuation of the hematoma through a small incision on the
superior 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 superior
surface, 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 fold
has healed. The voice improvement that follows unilateral evacuation of
Reinke’s edema is often surprisingly good, and patients frequently elect
to 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 vocal
fold, sometimes even adynamic, even though this complication theoretically
should 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.)
VOICE SURGERY 1179
when surgery has been performed well. If it occurs on one side and there is
Reinke’s edema on the other side, the polypoid side usually compensates.
Voice quality is generally satisfactory, and (most importantly) phonation
is not effortful. If stiffness occurs bilaterally, the voice is hoarse and requires
high phonation pressures. Patients are unhappy not only with voice quality,
but especially with the fatigue that accompanies increased effort required to
initiate and sustain phonation. Under these circumstances, they often feel
that 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 before
surgery is performed on the second vocal fold, this situation can be avoided
in nearly all cases.
Granulomas and vocal process ulcers

Vocal fold granulomas may occur anywhere within the larynx, but most
commonly they occur in the region of the vocal processes or elsewhere on
the 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 associated
with laryngopharyngeal reflux, but voice abuse, premature vocal process
contact caused by lateral cricoarytenoid muscle dominance, and other fac-
tors may play a role. These lesions should be differentiated from neoplasms
and true granulomas, which are caused by conditions such as tuberculosis
and sarcoid.
Treatment begins with excellent control of laryngopharyngeal reflux and
voice therapy. Botulinum toxin injections into the lateral cricoarytenoid
muscles may be helpful. The pulse dye laser is effective in some patients.
When surgical excision is required, injury to the perichondrium should be
avoided.
Sulcus vocalis and vocal fold scar

Sulcus vocalis is seen as a longitudinal groove along the vibratory margin
of the vocal fold. In sulcus vocalis, the superficial layer of lamina propria is
absent, although it may be relatively thin, and the epithelium is adherent to
the 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 is
not 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 I
sulcus 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 slight
impairment of mucosal wave may cause dysphonia, particularly in high-
pitched voices. Type III sulcus is a true sulcus vocalis, with complete absence
of the superficial lamina propria.
Type I sulcus requires no treatment. Type II sulcus may respond to voice
therapy. When therapy is insufficient, vocal fold medialization is often ade-
quate. Relieving glottic insufficiency and permitting firm vocal fold contact
often allows the focal folds to compensate and produce good voice, without
surgery on the vibratory margin. Type III sulcus is also treated with voice
therapy to eliminate compensatory hyperfunction, but therapy alone is
rarely adequate. Surgery is generally necessary to restore the mucosal
wave and eliminate glottic insufficiency.
The principles of surgery for sulcus vocalis and vocal fold scar are the
same and are discussed in greater detail in other literature [60,61]. These
conditions present with two problems: glottic insufficiency and impaired
mucosal wave. Glottic insufficiency can be improved by medialization sur-
gery (injection or thyroplasty). Restoration of the mucosal wave is more
challenging. It may be accomplished by resecting the sulcus, approximating
the mucosal edges and implanting fat; elevating the sulcus and implanting
fat or another substance; or through multiple incisions (essentially multiple
Z-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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2007, Vol.40, Issues 5, The Professional Voice

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Otolaryngol Clin N Am

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

Clinical Anatomy and Physiology

pathologic conditions. Contrary to popular practice, however, surgeons

Larynx: the intrinsic muscles

branch. The external branch supplies the cricothyroid muscle. An extension

vocalis contraction is active, particularly in the membranous segment of the

Larynx: extrinsic muscles

Training of the intrinsic musculature results in vibratory symmetry of the

The supraglottic vocal tract

hyponasal speech characteristic of severe adenoid hypertrophy is obvious.

The tracheobronchial tree, lungs, and thorax

The musculoskeletal system

voice dysfunction. Stance deviation, such as from standing to supine, pro-

The psychoneurologic system

Overview of phonatory physiology

variation because of changes in the distance between the fundamental fre-

progressively larger components of the bronchial tree and eventually to the

Although inspiration is extremely important, this discussion concen-

Active expiration is created by forces that decrease thoracic volume. Ac-

Medical History in Voice Professionals

A comprehensive history and physical examination usually reveals the

essential to proper treatment selection and patient counseling in singers and

How old are you?

What is your voice problem?

abnormalities of the leading edge of the vocal folds, such as laryngitis or

Fatigue is often caused by misuse of abdominal and neck musculature,

Do you have any pressing voice commitments?

How much voice training have you had?

patient’s current voice teacher in such circumstances. It often takes years of

Under what kinds of conditions do you use your voice?

How much do you practice and exercise your voice?

or contact irritation, altering voice function. Activities such as cheerleading,

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

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

Do you have pain when you talk or sing?

subject. A detailed review of odynophonia is beyond the scope of this pub-

What kind of physical condition are you in?

Have you noted voice or bodily weakness, tremor, fatigue, or loss

Do you have allergy or cold symptoms?

Do you have breathing problems, especially after exercise?

Have you been exposed to environmental irritants?

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

Do any foods seem to aﬀect your voice?

Do you have morning hoarseness, bad breath, excessive phlegm, a lump

Do you have trouble with your bowels or belly?

Are you under particular stress or in therapy?

Do you have problems controlling your weight? Are you excessively

Do you have menstrual irregularity, cyclical voice changes associated

Do you have jaw joint or other dental problems?

Do you or your blood relatives have hearing loss?

Have you suﬀered whiplash or other bodily injury?

changes in technique, with consequent voice fatigue, loss of range, diﬃculty

of recurrent or superior laryngeal nerve injury may explain a hoarse,

What medications and other substances do you use?

Physical Examination of Voice

Complete ear, nose, and throat examination

Thinning of the enamel of the central incisors in a normal or underweight

vibration. It is generally performed with the tongue in a ﬁxed position, how-

Other techniques to examine vocal fold vibration

analog) [22]. Ultrahigh-speed photography provides images that are in true

Measures of phonatory ability

range. It is measured in sound pressure level (SPL) in reference to 0.0002 mi-

superiorly and laterally 30 to 45 . The TA muscle is encountered approxi-