10
Management of the Patient with Laryngitis
Introduction
Dysphonia is a problem that afflicts millions of
people on an annual basis.1 Its impact on quality of
life varies from patient to patient depending upon
the underlying laryngeal abnormality and whether
the voice difficulties are episodic or chronic. The
literature base is replete with research on many
different benign and malignant causes of dysphonia.
However, the possible role of allergy in the
pathogenesis and expression of vocal pathologies
has not been extensively investigated, despite the
fact that allergic diseases of both the upper and
lower respiratory subsystems are among the most
prevalent illnesses regularly treated by physicians
throughout the world.
Inasmuch as the larynx is an integral component of
the unified airway,2,3 it is not unreasonable to
suggest that it is as susceptible as other juxtaposed
respiratory structures to the development of
adverse allergy manifestations. The sparse data base
on the potential causal relationship between allergy
and vocal pathologies provides a rich opportunity
for theoretical discussions and seminal research on
this subject. Prospective outcomes of these
endeavors may prove valuable to medical and
health science practitioners from various
james paul dworkin phd &
robert j. stachler md
subspecialties who frequently evaluate and manage
patients with allergies.
The overall objectives of this chapter are to: (1)
discuss the integrated or common airway concept,
(2) offer a brief overview of normal anatomy and
physiology of the phonation subsystem, (3) review
various clinical and laboratory laryngeal evaluation
methods that may facilitate differential diagnosis and
treatment of allergy-related signs and symptoms,
(4) specify the importance of cooperative roles of
physicians and other clinicians in the care of patients
with allergic laryngeal sequelae, (5) review types and
causes of benign laryngeal abnormalities, (6) offer a
synopsis of the current literature on laryngeal
allergy, (7) propose a model of allergic laryngeal
abnormalities that patients may present, and (8)
detail alternative pharmacologic, phonosurgical, and
behavioral therapeutic strategies that may be
employed with the allergic patient to improve
associated dysphonia and other possible phonation
subsystem signs and symptoms.
Unified Airway
Both Hurwitz2 and Grossman3 discussed the
frequent coexistence of upstream and downstream
respiratory tract inflammatory conditions, including
233
 Managing the Allergic Patient

transient and chronic laryngopharyngeal Phonation Subsystem Anatomy

involvement. More recently, deBenedictis and Bush and Physiology
demonstrated that these allergic manifestations
represent a continuum of inflammation throughout All mammals possess a larynx. Figure 10.1 illustrates
this integrated tract of respiratory organs.4 They that this complex organ is a component of the
further suggested that arbitrary separation of the upper airway and it is suspended in the anterior
airway into upper and lower subdivisions ignores neck by a sling of extrinsic muscles, ligaments, and
the inherent anatomic and physiological coupling of specialized joints in the approximate vicinity of the
this single integrated system. fourth, fifth, and sixth cervical vertebrae. It
functions as a biologic valve for: (1) breathing, (2)
A considerable amount of research has been
airway protection during swallowing, (3) coughing
conducted in the past couple of decades focusing
to help clear bodily secretions and any foreign
on the possible causal interrelationships between
particles from the tracheobronchial tree and
sinusitis, rhinitis, and lower respiratory tract
endolarynx, (4) bowel evacuation, (5) heavy lifting,
functional abnormalities.5–10 These investigators
and (6) childbirth. These functions occur
have reported that as much as 90% of all patients
involuntarily or reflexively. The vocal folds within
with asthma also suffer from rhinosinusitis; and that
the larynx, in concert with downstream expiratory
approximately 25% of those with allergic rhinitis
experience occasional hyperreactive lower
respiratory tract symptoms, such as pulmonary
congestion, shortness of breath, spasmodic
coughing, and throat clearing due to perceptions of
excessive endolaryngeal mucous accumulation.
These findings have bolstered support for the
model of a unified airway; one common system of Speech

organ linkages that is subject to widespread,

simultaneous, and reactive (i.e., delayed) allergic
manifestations. To date, debate continues within
the clinical and scientific communities regarding
how these allergy-induced interrelationships are Operative site
Vocal cords (larynx)
driven. Additionally, the specific role of the
phonation subsystem in this inflammatory loop
remains unclear, particularly with respect to Esophagus
whether it assumes a largely passive or reactive
Trachea
role, or whether its phylogenetic anatomic position
enforces a physiologically more active and
integrative role during times of allergic and
Figure 10.1 Sagittal view of the anatomic position of the
nonallergic common airway inflammation.11 larynx within the unified airway.

234

efforts, can also be voluntarily recruited to vibrate
and produce vocalizations known as voice. Over
the course of early childhood, humans learn how
to coordinate respiratory airflow dynamics,
biomechanical vocal fold activities, and upstream
articulatory adjustments for the purposes of
generating various speech sounds to communicate
their thoughts and wishes.
䊏 Laryngeal Skeleton
The larynx is composed of three pairs of small
cartilages (arytenoid, corniculate, cuneiform) and
three large unpaired cartilages (thyroid, cricoid,
epiglottis). Figure 10.2 illustrates these structures and
their interconnecting membranes and ligaments.
The trachea directly links the larynx with the lungs.
There are two synovial articulations or laryngeal
joints: cricothyroid and cricoarytenoid. Hinge-like
action of the former paired joints increases the
anteroposterior length of the vocal folds. This
adjustment results in increased tension and reduced
cross-sectional mass of these structures; most
notably influential during pitch variations in speech
and song. The primary action of the latter joints is
rocking motion of the arytenoids; anteromedial
action is of paramount importance for vocal fold
adduction, and posterolateral action is essential for
vocal fold abduction. There is little evidence in the
scientific literature to support classic textbook
descriptions of rotary and gliding motions of the
arytenoid cartilages during voice production or
other valving activities.
䊏 Laryngeal Muscles
Figures 10.3 and 10.4 illustrate the various intrinsic
and extrinsic muscles of the larynx, respectively.
Suffice it to say that the true vocal folds arise from
Patient with Laryngitis 10
or are components of the thyroarytenoid muscle
bundles. The intrinsic group of muscles work
harmoniously to open, close, tense, and relax the
vocal folds during breathing, swallowing, and
speaking. Although this entire group probably
works in a coordinated and collective manner to
achieve these movements; for ease of review,
specific functions can be attributed to individual
components. That is, contractions of the
thyroarytenoid, lateral cricoarytenoid, and
interarytenoid muscles generally contribute to vocal
fold adduction. As noted earlier, the cricothyroid
muscles chiefly lengthen and tense the vocal folds,
which decreases their cross-sectional mass.
Posterior cricoarytenoid muscle contractions are
critical for vocal fold abduction, associated with
deep breaths and cessation of vibrations during
running speech to accommodate the demands of
voiceless consonant production and to terminate
voicing at the completion of an utterance.
The extrinsic muscles can be divided into two
subgroups: suprahyoids and infrahyoids. In general,
these elongated, strap-like muscles help to stabilize
and alter the position of the larynx in the neck
through anatomic linkages with neighboring head,
neck, and chest structures. Contractions of the
former group tend to pull the larynx
anterosuperiorly, especially during swallowing and
upward pitch adjustments during singing.
Conversely, contractions of the infrahyoid muscles
act to lower the larynx, such as during descending
pitch production. It is important to note that
anatomic or physiological alterations involving these
extrinsic muscles, as may occur with head and neck
cancer surgery, can contribute to substantial
swallowing difficulties, and, to a lesser extent,
limited pitch range during singing.
235
 Managing the Allergic Patient

Corniculate cartilage

Muscular process of arytenoid

cartilage
Vocal process

Cricoid cartilage

Cricoid, arytenoid and corniculate

cartilages, viewed from in front
Epiglottis
Epiglottis

Hyoid bone Hyoid bone

Thyrohyoid membrane
Thyrohyoid membrane
Superior cornu of
Superior cornu of thyroid cartilage
thyroid cartilage
Thyroid cartilage lamina
Thyroid cartilage lamina
Corniculate cartilage
Cricothyroid ligament
Arytenoid cartilage
Inferior cornu Vocal ligament
of thyroid cartilage
Inferior cornu
Cricoid cartilage of thyroid cartilage
Cricoid cartilage
Trachea
Trachea
Anterior aspect Posterior aspect

Epiglottis Epiglottis

Hyoid bone Hyoid bone

Thyrohyoid membrane
Thyrohyoid membrane
Thyroid cartilage
Corniculate cartilage
Thyroid cartilage Arytenoid cartilage
Vocal process
Vocal ligament
Cricothyroid ligament
Muscular process
Cricoid cartilage Cricothyroid ligament
Cricoid cartilage
Trachea
Trachea
Right lateral aspect Sagittal section
Figure 10.2 Cartilaginous framework of the larynx, with associated ligaments and membranes.

236
 Patient with Laryngitis 10

Epiglottis
Foramen for superior
laryngeal vessels and
Aryepiglottic fold nerve (internal branch)
Cuneiform tubercle

Corniculate tubercle Oblique and transverse

arytenoid muscles
Aryepiglottic muscle

Oblique arytenoid
muscle Posterior crico-arytenoid
muscle
Transverse arytenoid
muscle Vertical
part Crico-thyroid
Posterior crico-arytenoid
Oblique muscle
muscle
part
Cricoid cartilage

Muscular
Cricoid Arytenoid process
Epiglottis cartilage cartilage Vocal
Posterior process

Aryepiglottic crico-arytenoid
muscle muscle
Lateral
Transverse crico-arytenoid
and oblique Thyro-epiglottis
muscle muscle
arytenoid
muscle Transverse and
oblique arytenoid
Thyro-arytenoid muscle
Posterior muscle
crico-arytenoid
muscle Lateral Cricothyroid
crico-arytenoid muscle
Crico-thyroid muscle Thyroid
muscle Thyro-arytenoid cartilage
(cut away) muscle Vocalis Vocal
muscle ligament

Figure 10.3 Intrinsic laryngeal muscles.

䊏 The Vocal Folds of mucosa and stratified, nonkeratinizing squamous

Figure 10.5 demonstrates the normally white and
glistening appearances of the true vocal folds within
the framework of the thyroid cartilage. The space
between the vocal folds is called the glottis, and it
varies in its anterior and posterior dimensions
during various biological and phonatory behaviors.
The vocal folds consist: of (1) an outermost layer
epithelium, known as the cover, and (2) deeper
layers, which contain the aforementioned
thyroarytenoid muscle fibers, as well as high density
fibroblasts and elastic and collagenous tissues.
Immediately deep to the cover there exists a
potential space known as Reinke’s area, which
consists mainly of amorphous material with few
fibroblasts or elastic tissue. Later in the chapter, we

237
 Managing the Allergic Patient

Digastric muscle
(anterior belly)
Mastoid process
Mylohyoid muscle
Hyoid bone
Stylohyoid muscle
Sternocleidomastoid
muscle (severed) Digastric muscle
(posterior belly)
Thyrohyoid muscle
Thyrohyoid muscle
Omohyoid muscle
Oblique line of
Thyroid cartilage thyroid cartilage

Cricoid cartilage Sternothyroid muscle

Sternohyoid muscle
Omoyhoid muscle
Thyroid gland (severed)

Sternothyroid Sternohyoid muscle

muscle (severed)

Mastoid process
Styloid process
Stylohyoid

Digastric
Digastric (posterior belly)
(anterior belly)
Stylopharyngeus
Geniohyoid
Thyrohyoid
Sternohyoid
Omohyoid Oblique line

Sternothyroid

Scapula
Sternum
Figure 10.4 Extrinsic laryngeal muscles.

will discuss the biomolecular make-up of the
endolarynx and true vocal folds, particularly as it
pertains to the presence or absence of mast cells
and eosinophils, which normally mediate allergic
inflammation in other components of the
respiratory subsystem.
Hirano described the cover-body concept of vocal
fold vibration.12 His elaborate explanations more
than 30 years ago have been instrumental in the
development of modern phonosurgical procedures
for benign vocal fold pathologies. Because Reinke’s
space possesses a gelatinous consistency, it enables

238

R L
Figure 10.5 Videostroboscopic image of the right (R) and
left (L) vocal folds.
fluid vibratory motion of the cover over the vocal
fold body (thyroarytenoid muscle fibers) during
phonation. Detailed appraisal of such activity can
be achieved in the clinical setting using
laryngovideostroboscopy. This quasi-slow motion
imaging technique reveals traveling waves of
mucosa from the inferior to superior surface of the
vocal folds. Scarred or fibrotic vocal folds, as a
result of invasive benign or malignant pathologies,
do not produce normal mucosal waves.
䊏 Peripheral Laryngeal Innervation
Volitional voice production depends upon a
complex loop of neural interactions between the
central nervous system, peripheral nervous system,
and various respiratory and speech musculature.
13
Kotby et al described a six-level hierarchy of
laryngeal neuromuscular integration. Of these
interrelated segments, the higher levels generally
function to activate, inhibit, and modulate output of
the lower levels for purposeful voice production.
Some of the lower level activities are organized into
reflex pathways. Based on a top-down model of
control, conceptual programming of speech and
Patient with Laryngitis 10
voice occurs at the highest level. At the cerebellar
level below, movement adjustments are
coordinated, and errors are detected and corrected
for accurate performance. The pyramidal or upper
motor neuron system serves the next level of
function as the primary initiator of all muscular
contractions through synapses with motor nuclei of
all cranial and spinal nerves normally involved in
speech production. The extrapyramidal level
functions as an ongoing, automatic and subconscious
regulator of all sensorimotor outputs and underlying
muscle tone, via complex loop circuitry between the
central and peripheral nervous system. The
vestibular–reticular level helps to activate and
regulate motor inputs to and sensory outputs from
the cranial and spinal nerves (lower motor neurons)
and the muscles responsible for speech and voice
production. The lower motor neurons represent the
lowest level of this integrated system. They form
motor units within the muscle tissues they innervate
to stimulate muscle contractions for volitional
movement purposes.
The vagus or Xth cranial nerve pair arise from the
medulla on the brain stem. They descend into the
neck through the jugular foramen, and distribute
three primary branches that help control and
regulate voice and speech activities: (1) pharyngeal
nerve, (2) superior laryngeal nerve, and (3)
recurrent laryngeal nerve. The first of these
branches provides nerve fibers to the pharynx and
most of the soft palate. The second branch contains
an internal and external laryngeal nerve component.
The former one enters the larynx and divides into
two additional branches, both of which contain
sensory fibers from the mucous membranes that
line the endolarynx above the vocal folds, and from
neighboring muscles’ spindles and stretch receptors.
239
 Managing the Allergic Patient
The external branch is the chief motor nerve supply
of the cricothyroid (pitch changing) muscle and
inferior constrictor muscles of the pharynx. The
recurrent laryngeal nerve or third primary branch of
the vagus nerve, descends past the larynx and then
loops back up to provide motor innervation to all of
the other intrinsic laryngeal muscles. Whereas the
right recurrent nerve loops under the ipsilateral
subclavian artery en route to the larynx, the left one
descends more inferiorly in the chest, deep to and
winding under the arch of the aorta, before it
ascends in the tracheoesophageal groove to enter
the larynx behind the cricothyroid joint on either
side. In addition to its widespread motor inputs, it
supplies sensory filaments to the mucous
membranes within the lining of the subglottis,
immediately below the vocal folds. These fibers
transmit afferent output from these tissues as well
as stretch receptors in the surrounding musculature.
Mechanoreceptors mediated by the recurrent and
superior laryngeal nerves are abundantly located
within the mucosal lining, muscles, and joints of the
larynx. These sensory elements influence
respiratory and vegetative reflexes, and they
contribute to what may be termed the intrinsic
laryngeal monitoring system, as they relay oscillating
discharges to the lower brain stem in response to
air pressure fluctuations that occur during voice
production. Polysynaptic loops are then formed
with the motor neuron pools of the vagus nerve at
this level to establish the so-called tonic servo-
14
reflex system of the larynx. Figure 10.6 offers a
schematic representation of these hierarchical
neurologic pathways associated with voice
production. For more detailed reviews of the
neurologic substrates of phonation, the reader is
15,16
referred to other sources.
240
䊏 Voice Production
As shown in Figure 10.1, vocal fold vibrations during
speech efforts send a traveling wave of acoustic
energy upstream through the vocal tract. This
pathway, which includes the oral and nasal cavities,
acts as a resonating chamber to enhance, absorb,
and reflect the sounds generated into distinctive
voice qualities. The infraglottal tract consists of the
respiratory musculature, lungs, trachea, and
immediate subglottis. These structures function as a
collective power source for phonation by providing
ongoing airflow dynamics required to drive vocal
fold vibrations during speech efforts. The vibratory
activity itself is largely a passive act. That is to say,
at the start of a vibratory cycle the vocal folds are
volitionally preset in an adducted position at the
midline of the glottis. Assuming the lungs have
been supplied with a sufficient amount of inspired
air in preparation for speech, pressure increases
within the trachea with expiratory effort to
generate upstream airflow to induce vocal fold
vibrations and voice. When subglottic pressure
exceeds the level of resistance created by the
adducted vocal folds, a puff of air is emitted into
the vocal tract. This momentary break in the glottal
seal initiates the vacuumous Bernoulli effect. This
aerodynamic phenomenon results from increases in
the velocity of air molecules passing through the
narrow glottic inlet. As this occurs, air pressure
between the vocal folds decreases, which, in turn,
induces glottic closure to complete the vibratory
cycle (closed–open–closed). This wave is assisted
by intrinsic laryngeal myoelastic properties.
Sustained phonation depends upon adequate
intrinsic laryngeal muscle and elastic glottal closing
forces, and sufficient and continuous infraglottal
 Patient with Laryngitis 10

Speech area in temporal

cerebral cortex

Voice area in motor

strip of precentral gyrus

Corticobulbar tract
Nucleus ambiguus

Brain stem
10th cranial
(vagus) nerve

Spinal cord

Superior laryngeal
nerve
Hyoid bone
Vagus nerve

Thyroid cartilage
(Adam’s apple) Recurrent
laryngeal nerve
Cricoid cartilage

Figure 10.6 Central and peripheral nervous system interactive substrates of voice production.

airflow support to initiate and drive vocal fold
vibrations.
䊏 Parameters of Voice
Quality, loudness, and pitch are the primary
parameters of human voice. Quality represents the
overall timbre or pleasantness of voice. The rhythm
and symmetry of vocal fold vibrations, and the
adequacy of glottal closure, significantly influences
vocal quality. Irregular motion and glottal
incompetence during the closed phases of vibration
usually result in escapes of unphonated air, which
distorts the voice signal. Hoarse, harsh, raspy,
breathy, wet-gurgly, spasmodic, and tremorous, are

241
 Managing the Allergic Patient
common terms used to classify vocal quality
disorders. The speech diagnostic terms hyponasality
and hypernasality are sometimes used within this
context of vocal quality disturbances. However,
these disorders result from upstream
velopharyngeal and nasal cavity disturbances.
Vocal loudness, also referred to as intensity, is
measured in decibles (dB). This parameter largely
depends on the degree of subglottal pressure,
glottal resistance created by the adductory forces
of the intrinsic laryngeal muscles, transglottal airflow
rate, and amplitude or excursion of the vocal folds
from the midline of the glottis during the open
phases of vibration. Generally, increases in the
degree of these variables produce perceptually
louder voice, and vice versa. A voice that is
habitually either too loud, too soft, limited in range
(monoloud), or characterized by unusual volume
outbursts represents abnormal loudness control.
Vocal pitch is measured in cycles per second or
Hertz (Hz). It is directly related to the frequency of
vocal fold vibrations; the faster the cyclic speed the
higher the pitch, and vice versa. Intrinsic laryngeal
muscle contractions that alter the length, tension,
and cross-sectional mass of the vocal folds
significantly influence pitch adjustments during
speaking and singing. When the vocal folds are
lengthened, they are concurrently under more
tension and their cross-sectional mass is reduced.
These biomechanical alterations promote faster
vibratory speed, and thus higher pitched voice.
Conversely, when the vocal folds are shortened,
intrinsic tension is reduced and cross-sectional mass
is increased. These biomechanical alterations retard
the speed of vocal fold vibrations, and thus
contribute to the production of lower pitched
voice. These opposing physiological phenomena
242
can be envisioned by stretching and relaxing a
rubber band, and alternately plucking it to
appreciate the differences in the speed of vibration
and the perceived pitch under each associated
condition. Adult females normally generate an
habitual pitch of 256 Hz; equivalent to the middle
“C” note on the piano keyboard. Male
counterparts habitually vocalize at approximately
one half this speed, one full octave below middle
C. Abnormalities in pitch control are usually
categorized as either too high or too low for the
individual’s age and sex. Limited pitch range
(monotone) and unusual pitch outbreaks (shrill) are
also problems of concern.
It is important to note that in addition to the
aforementioned biomechanical vocal fold and
respiratory activities, voice output is also
significantly influenced by the dynamic adjustments
in the shape of the supraglottic larynx, pharynx,
and oral and nasal cavities during speaking and
singing. These vocal tract components variably
enhance and attenuate sound energy levels at
various frequencies of production. Because each of
us possesses a unique anatomic configuration of
this complex system, we accordingly exhibit voice
attributes that are easy to identify perceptually and
distinguish us from all other speakers.
Evaluating the Allergic Patient
with Voice Complaints
䊏 Team Approach
A team approach to the evaluation and treatment
of patients with suspected laryngeal allergic
sequelae is usually most successful. Members in this
effort should minimally include an allergy physician

with a background in otolaryngology or
immunology, a speech-language pathologist with
expertise in the area of vocal pathologies, and a
nurse practitioner. The diagnosis of chronic allergic
laryngitis should be considered for patients who
present with histories of upper respiratory allergies
and co-occurring phonation subsystem disturbances,
such as globus sensations, excessive laryngeal
mucus and reactive throat clearing and coughing
behaviors, dry-itchy throat, and voice difficulties.
With this clinical population, the history component
of the examination usually produces the most
indispensable diagnostic data. In this vein, the
exploration of antecedent events or triggers of
allergy symptoms almost always proves to be of
paramount importance to accurate diagnoses, as
does the time course or seasonality of such
complaints. Whether the patient suffers from any
co-occurring diseases, such as asthma, otitis media,
sinusitis, and chronic acid reflux, should be
evaluated because these conditions can exacerbate
the underlying allergy. Prior or current use of
medical or complementary therapies to treat these
problems should be factored into the differential
diagnostic and subsequent management equations.
After a thorough review of the patient’s
background history, the physician should conduct a
comprehensive physical examination, with special
attention paid to the tympanic membranes and
middle ears for signs of effusion. Next, the nose
should be examined to determine the presence of
edema, mucosal paleness or hyperemia, mucoid or
mucopurulent rhinorrhea, or nasal polyps. Such
findings may be sequelae to allergic rhinitis. The
status of the pharynx should be evaluated next for
signs of lymphoid hypertrophy or prominent lateral
pharyngeal bands. The head and neck exam is
Patient with Laryngitis 10
usually completed with mirror or fiberoptic
examination of the larynx to rule out significant
laryngeal pathology, which may require closer
analysis via videolaryngostroboscopy. The latter
instrumentation technique is often performed by a
speech-language pathologist, in consultation with
the referring physician. During this examination,
vocal fold biomechanics and glottal, supraglottal,
and perilaryngeal tissue appearances are appraised
for significant variations from normal characteristics.
Oftentimes, for patients with notable dysphonia at
presentation, additional voice laboratory studies are
indicated, including acoustic and speech
aerodynamic analyses, and voice sampling using a
high quality (e.g., digital) audiotape format. If allergy
is suspected following analyses by team members
of all examination results, serum (in vitro) or skin
testing should be conducted to confirm the
presence and types of allergies.
In general, dysphonia can develop acutely or
gradually. In some cases, voice difficulties are
intermittent. In others, the problem is more
persistent. The severity of the disturbance is not
necessarily correlated with the frequency of
symptoms. Patients with transient dysphonia may
present with severely abnormal voice
characteristics; those with more chronic conditions
may exhibit only mild difficulty, and vice versa. In all
cases, the degree of dysphonia may worsen,
improve, or remain stable over the course of the
problem. The underlying causes, coupled to any
ongoing treatments, usually dictate these potentially
variable clinical presentations.
In the following segment of the chapter commonly
employed qualitative and quantitative phonation
subsystem evaluation techniques are described in
detail. Most of the procedures discussed are not
243
 Managing the Allergic Patient

Perceptual voice examination BOX 10.1

Place of exam:
Patient’s name: Sex: DOB:
ID #: Date of exam:
Examiner:
Vocal parameters
[Note: Circle the applicable impressions]
1. Quality: normal
a. Hoarse [mild, moderate, severe] b. Breathy [mild, moderate, severe]
c. Raspy [mild, moderate, severe] d. Strained [mild, moderate, severe]
e. Gurgly [mild, moderate, severe] f. Tremorous [mild, moderate, severe]
g. Hyponasal [mild, moderate, severe] h. Hypernasal [mild, moderate, severe]
2. Pitch: normal
a. Too high [mild, moderate, severe] b. Too low [mild, moderate, severe]
c. Monotone [mild, moderate, severe] d. Pitch breaks [mild, moderate, severe]
3. Loudness: normal
a. Too loud [mild, moderate, severe] b. Too soft [mild, moderate, severe]
c. Monoloud [mild, moderate, severe] d. Outbursts [mild, moderate, severe]
4. Maximum phonation time: [ 1 3 5 7 9 11 14 + seconds]

routinely performed by physicians, unless they have 䊏 History of the Dysphonia and Initial
undergone training in the area of otolaryngology, Examiner Impressions
or they have worked closely with medical
The origin and course of abnormal voice signs and
colleagues or speech-language pathologists with
symptoms are of vital importance to differential
such expertise. Notwithstanding this limitation, it is
diagnosis and management. Initially, the examiner
not unfeasible to suggest that virtually all of the
should render a perceptual impression of the
techniques below can be easily learned by the
overall severity of dysphonia that the patient
inquiring and determined physician, regardless of his
exhibits during the history-taking process. The
or her medical subspecialty background. Those
types of underlying disturbances in vocal quality,
clinicians who prefer to send the dysphonic patient
pitch, and loudness should be noted, and each
to a laryngologist should, at the very least, achieve
perceived difficulty should be behaviorally defined
a working knowledge of the rationale for and
and rated with respect to degree of impairment.
diagnostic benefits of all of these testing
Box 10.1 provides a rating form that may prove
procedures. Acquiring this understanding will foster
helpful for such purposes.
communication with the practitioners to whom the
patient is referred, and such information will The examiner should employ a logical sequence of
facilitate comprehensive diagnostic and treatment questions to evaluate the background of the
discussions. problem. First, questions regarding how long the

244

dysphonia has existed, and whether it varies in
degree from day to day, should be asked. If there
is a previous history of dysphonia, ascertain what
types of treatments may have been rendered in
the past to improve the problem. Second, the
examiner should note whether the dysphonia
characteristics vary during the interview. Third,
whether the patient has determined the possible
cause, or can link the voice difficulties to specific
times or events, are important factors that must be
explored. For example, has there been a recent
exacerbation of allergic symptomatology that might
account for the voice difficulty, owing to
significantly associated coughing or throat clearing
behaviors, which may have resulted in vocal fold
trauma. Fourth, the patient should be asked
whether the difficulty has improved at all since the
onset. If so, it would be important to inquire as to
what such improvement might be attributed. Fifth,
if the patient reports that there are times in the
day when the voice is better or worse, these
fluctuating abilities should be discussed to try to
determine possible causal conditions. Sixth, the
astute examiner should always ask whether there
have been days since the onset of dysphonia when
the voice was completely normal for long periods
of time. Seventh, it is essential to rule out
significant comorbid medical problems for which
the allergic patient may have been treated, and to
which the dysphonia may be fully or partially
attributed. For example, recent intubation
anesthesia, laryngeal trauma, thyroid or neurologic
disease, illness, or injury, and severe
laryngopharyngeal reflux should be considered as
possible causes, either acting alone or in
combination with the allergy history. Eighth,
determine if the patient abuses the vocal folds;
Patient with Laryngitis 10
excessive throat clearing, coughing, yelling, smoking,
limited water intake and substantial consumption of
diuretic beverages, regular use of inhaled
corticosteroids, and routine use of decongestant
medications are prime examples of behaviors that
can provoke vocal fold swellings and generalized
signs and symptoms of laryngitis. Ninth, inquire as
to whether the patient is suffering from any type of
swallowing difficulty. A significant degree of
laryngitis can cause odynophagia and glottal
incompetence, which can result in aspiration
symptoms. Aspiration usually elicits coughing
reactions. Coughing can exacerbate existing
laryngeal swellings, which increase the swallowing
difficulties. This vicious cycle is not uncommon, and
it needs to be broken to restore nutritional balance
and relieve the patient of potentially deleterious
pulmonary side effects. Tenth, if the patient sounds
stridorous at rest, during exertion, or both,
auscultation of the upper airway with a
stethoscope on the larynx to confirm the possible
presence of laryngeal airflow difficulty can be
diagnostically valuable. Stridor is usually associated
with anatomic or physiological glottal obstruction,
as may occur with severe vocal fold swellings, large
ball-valving glottic or subglottic lesions or stenosis,
or bilateral abductor vocal fold paralysis. Stridor
may act alone to cause dyspnea, or it may occur in
combination with downstream (e.g., asthma;
COPD) or upstream (e.g., allergic rhinitis;
rhinosinusitis) airway diseases. Table 10.1 provides
a synopsis of these steps for easy reference.
The initial impressions rendered by the examiner,
and answers to the various questions posed to the
patient, provide indispensable data ultimately
required to formulate a differential diagnosis of the
245
 Managing the Allergic Patient
Exploring the history of dysphonia
Examination steps
1. Impression of dysphonia severity
2. Perception of specific voice difficulties
3. Inquire into onset and previous history of dysphonia
4. Discuss any daily variability
5. Explore patient’s self-impression of problem and
possible cause
6. Review whether problem has improved, worsened,
or remained stable since onset
7. Establish whether voice is ever completely normal
8. Explore possible etiologies
9. Review vocal/abuse history
10. Discuss swallowing and/or breathing difficulties
dysphonia and a possible treatment plan for this
specific problem. Acute onset dysphonia can usually
be tracked to a specific recent event, injury, or
illness. Profound yelling at a ballgame, prolonged
intubation during a surgical procedure, direct
laryngeal trauma in an accident, laryngeal
anaphylaxis or non-IgE-mediated allergic laryngitis
secondary to substantial antigen exposure, neck or
thoracic surgery that normally places the recurrent
laryngeal nerve at risk for either stretch neurapraxia
or resection injury, repetitive intubation-extubation
abrasion of the vocal folds, stroke, Guillain–Barré
syndrome, and closed head injury are some of the
most common potential etiologies of sudden voice
difficulties. Not infrequently, if the resultant
laryngeal abnormality causes significant glottal
incompetency, the patient may also suffer from
aspiration symptoms and a more complicated
clinical course. The prognosis for spontaneous
recovery of normal voice within a relatively short
246
TABLE 10.1
Objectives
1. Determine extent of voice disability
2. Ratings of vocal quality, pitch, loudness abnormalities
3. Establish origin & background of problem
4. Determine whether dysphonia is acute or chronic
5. Establish correlations between patient and examiner’s
perceptions
6. Determine overall history of the problem
7. Rule out significant vocal pathology
8. Rule out iatrogenic, trauma, illness, reflux, asthma, cancer, etc.
9. Determine incidence of throat clearing, yelling, smoking,
coughing
10. Determine coexisting problems or causal interrelationships
period of time without phonation subsystem
medical intervention largely depends upon the
underlying etiology of the acute dysphonia.
The cause of clinically significant dysphonia that
develops gradually is not usually clear-cut. It is not
uncommon for a patient to complain that the
dysphonia began with very mild (subclinical)
characteristics, and then converted over time into a
more severe impairment. Such progression is often
due to correlated worsening of the causal
condition.
Summarily, whether the dysphonia is mild,
moderate, or severe in degree, acute or slowly
progressive, intermittent or chronic, the examiner
must be fully aware of the developing history of
the problem, and the inherent probability of self-
improvement to ensure an accurate differential
diagnosis and appropriate treatment
recommendations.

䊏 Voice Sampling
Contextual speech and voice characteristics will be
automatically obtained during the history-taking
process. In addition to the collection of these
important data, the examiner should request the
patient to perform specific tasks. First, instruct the
patient to take a deep breath and then prolong the
vowel /a/ for as long and steady as possible. This
maximum phonation time (MPT) task is usually
measured in seconds, and the patient’s mean
performance over two trials should be calculated
and encircled on the aforementioned rating form
(Box 10.1). Normally, adults should be able to
generate at least 14 seconds of MPT; children can
usually normally sustain voice for at least 10
seconds. Abnormal performance is often
attributable to glottal incompetence and
consequential air wastage during the phonatory
effort. Downstream pulmonary system limitations
may also cause reduced MPT, owing to insufficient
vital capacity or forced expiratory volume, as may
occur in the asthmatic patient. Second, ask the
patient to sing up and down a musical scale at his
or her most comfortable pitch level. Assess the
number of notes that can be sung, as well as the
associated voice features throughout the task.
Patients with dysphonia often exhibit difficulty
raising or lowering pitch from their habitual level,
because this activity requires finite vocal fold
stretching and relaxing adjustments, respectively.
Swellings or lesions involving these structures
typically restrict their flexibility and cause pitch
production limitations, along with disturbed quality
and volume parameters. Third, ask the patient to
cough sharply to assess the force of glottal closure
during this abrupt vocal fold behavior. Significantly
Patient with Laryngitis 10
Allergy and voice symptom
questionnaire BOX 10.2
Subject’s ID #: Date:
Scoring format: 0 = never; 1 = sometimes; 2 = often;
3 = always
Directions: place a 0, 1, 2, or 3 score at the end of
each statement below, following the above listed
score format definitions.
Score
1. I clear my throat
2. I suffer from coughing
3. I yell and scream at work, home, and play
4. I suffer from nasal drainage into my throat
5. I suffer from a stuffy nose
6. I suffer from a runny nose
7. I suffer from itchy/watery eyes
8. I suffer from sneezing
9. I suffer from swallowing difficulty
10. I suffer from a feeling like something is stuck in
my throat
weak or breathy coughing often signifies glottal
incompetence, and usually strongly correlates with
the dysphonia characteristics. Patients who cannot
generate volitionally adequate coughing activity,
regardless of the cause, may be at risk for
aspiration and pulmonary infection because
physiological integrity of the glottal valve is of
paramount biologic importance during swallowing
and tracheobronchial mucus clearing.
䊏 Voice Symptom Questionnaire
Box 10.2 is a questionnaire that can be used to
determine the extent to which a patient exhibits
and experiences specific signs and symptoms that
collectively may be manifestations of allergy and
causally related to vocal fold abuses and voice
difficulties.
247
 Managing the Allergic Patient

䊏 Examination of the Larynx visually robust; use of a three-chip camera and

video monitor interface can improve these inherent
Mirror limitations. The well-equipped clinical facility may
include an examination cart containing a
The larynx interior can be viewed using several
laryngovideostroboscopy system, which affords
different instruments and methods. The oldest,
quasi-slow motion images of vocal fold vibrations,
simplest, and least expensive approach is the
mucosal wave dynamics, and overall laryngeal
mirror examination. Whereas this exam does not
anatomy. This unit usually includes a rigid
enable video or photographic documentation of
laryngoscope, strobe light source, and a single or
the findings, it is generally quick and easy to
multiple chip camera. Some advanced systems
perform. Physicians initially may utilize this method
include powerful digital computer connections that
for screening purposes to determine whether
materially enhance data analyses, storage, and
additional appraisal is required using fiberoptic
retrieval. All of these endoscopic approaches to the
endoscopes, special light sources, and video
laryngeal examination are expensive to conduct.
recording devices. Unlike fiberoptic scopes, the
Even without the video (stroboscopy) interface, the
mirror uniquely provides a quasi-three-dimensional
flexible or rigid scopes and light source can cost as
view of the larynx and it offers realistic depth of
much as US$5000.00 If a camera, video monitor,
field and coloration images of the vocal folds and
video recorder, and color printer are added for
surrounding soft tissue boundaries. If this exam
more comprehensive evaluation options, the price
reveals clinically significant laryngeal pathology, or if
tag can easily exceed US$10 000.00 The low-end
an adequate view could not be obtained with the
videostroboscopy systems may cost more than
mirror, the examiner should proceed with or refer
US$25 000.00 The advanced systems are priced at
the patient to another practitioner for endoscopic
US$60 000.00 and up. Such costs often prove
evaluation for more detailed analyses.
prohibitive for many practitioners, particularly those
Flexible or Rigid Fiberoptic Endoscope whose practices do not include patients with
(Stroboscopy) nonallergy-related vocal pathologies. The value of
such technology in the differential diagnosis of
If examination of the larynx is the primary
voice disorders has been discussed by several
objective, use of a rigid endoscope is
clinical researchers.17,18
recommended. This instrument usually affords
more enhanced pixel resolution and optical
amplification for visual appraisal and video 䊏 Acoustic Analysis
recording purposes than its flexible endoscope Whereas perceptual impressions of dysphonia are
counterpart. However, if the exam focus is on the vital to the differential diagnosis and treatment
entire vocal tract, and possibly the immediate plan, computerized measures of the voice
subglottis, then use of a flexible scope will be abnormality provide the means to quantify the
necessary. Images obtained with this type of levels of impairment of each voice parameter, using
instrument are narrow field and usually are not normal voice referents for baseline comparisons.

248

Coupled to perceptual speech ratings, quantitative
voice analyses, obtained prior to and following
specific treatments, can provide objective evidence
of notable improvement. Certainly, from an
academic point of view, such data are considered
indispensable to discussions of the suggested
benefits of alternative treatments for different types
of vocal pathologies.
There are many commercially available systems for
acoustic analysis. These computer interfaced units
contain software designed to perform complex
manipulations of voice signals via microphone
connections. In general, values derived from all of
these programs include: (1) fundamental frequency
of voice (i.e., the patient’s habitual pitch), (2) jitter
(i.e., the degree of pitch instability or perturbations
in the speed of vocal fold vibrations), (3) shimmer
(i.e., the degree of loudness instability or
perturbations in the amplitude of vocal fold
vibrations), and (4) harmonic-to-noise ratio (i.e.,
the overall amount of noise in the voice signal). It
is important to note that all normal voices contain
certain levels of perturbation and noise. If a
patient’s acoustic analysis results reveal wide
variations from the norms (jitter ≤1%; shimmer
≤0.5 dB or 5%; H/N ≥ 11 dB) for these values, the
presence of clinically significant dysphonia may be
demonstrated and quantified. Acting either alone
or in any combination, generalized vocal fold
swellings, load bearing vocal fold growths or
lesions, weak vocal fold motion, and poor
respiratory support can cause abnormalities in the
speed, stability, and completeness of glottal closure
during the cycles of vocal fold vibrations. Such
disturbances often translate into notable deviations
from these acoustic benchmarks. There is almost
always a very high correlation between these types
Patient with Laryngitis 10
of data and perceptual judgements of dysphonia
made by skilled listeners. For this reason, many
physicians and speech-language pathologists do not
believe that performing acoustic analyses with
expensive computer platforms is indispensable to
definitive descriptions, diagnoses, or treatments of
various voice disorders.
䊏 Speech Aerodynamic Testing
Commercially available systems enable
comprehensive evaluations of subglottal pressure,
glottal resistance, and transglottal airflow rate
during speech activities, using indirect or
noninvasive instrumentation methodologies. Most
systems include an anesthesia-like face mask that is
coupled to differential airflow and intraoral air
pressure transducers. This hardware unit is
interfaced with a computer platform and
specialized software so that detailed quantitative
analyses of the aerodynamic properties underlying
voice and speech production can be achieved.
Speech scientists and voice therapists might argue
that the study of phonation would be incomplete
without in-depth examination of this energy source
or power supply for vocal fold vibrations. The
minimal level of subglottal pressure required to
drive voice is 5 cmH2O/5 s. In the speaker with
normal voice, transglottal airflow rate averages
100 ml/s through the length of an utterance, and
the compression force between the vocal folds at
the onset of and during voice production (i.e.,
glottal resistance) averages between 35 and
50 cmH2O/lps. Patients with vocal fold pathologies
that cause glottal incompetence and air wastage
during phonation often exhibit higher than normal
subglottal pressure and airflow rate values, owing
to increased respiratory efforts to compensate for
249
 Managing the Allergic Patient
such difficulties. Limited MPT levels are also
common in these individuals. Patients with
obstructive glottal or subglottal lesions, and those
who suffer from downstream pulmonary subsystem
disease (e.g., asthma, COPD, neuromuscular illness/
injury, lung cancer), struggle with abnormally low
subglottal pressure levels, reduced transglottal
airflow rates, and high levels of glottal resistance;
those with adductor spasmodic dysphonia or
severely strained-tense voice production habits
exhibit similar speech aerodynamic disturbances.
The cost factor associated with this technology,
and the time involved in collecting these types of
data, prove prohibitive and unjustifiable for most
clinical practitioners. The most prevalent application
of such instrumentation occurs in speech
physiology laboratories in academic and specialized
clinical settings for the purposes of advancing the
knowledge base on this subject via scientific
research investigations.
䊏 Fiberoptic Endoscopic Examination
of Swallowing (FEES)
Patients who present with allergy-related dysphonia
may also complain of occasional, but usually mild
odynophagia, globus sensations, and general
swallowing difficulties. The possible role of
gastroesophageal and laryngopharyngeal reflux
disease must be considered in the differential
diagnosis of such patients, as these conditions have
been linked to the pathogenesis of certain types of
19
dysphonia. Additionally, laryngopharyngeal edema
secondary to oral allergy syndrome may be of
20–22
etiologic significance. This condition occurs
23–25
frequently in patients with food sensitivities,
which can, albeit rarely, cause anaphylactic shock
because the upper aerodigestive tract contains a
250
widespread population of mast cells. These
mediators of inflammation can contribute to cross-
reactivity between certain pollen inhalant antigens
to which a patient may be allergic, and specific
fruits or vegetables with structurally similar
antibodies. When the patient ingests such foods an
allergic reaction is elicited that may resemble the
signs and symptoms that occur secondary to pollen
exposure. Even if the response is mild in degree,
threshold swelling and associated pharyngeal and
laryngeal hypersensitivity may cause the
aforementioned dysphagia signs and symptoms.
Comprehensive history taking and physical
examination are essential procedures in the
diagnosis of oral allergy syndrome. In particular,
clinical investigation of dysphagia can be facilitated
using a simple in-office technique, such as FEES. A
flexible endoscope with camera attachment,
compatible light source, video monitor, and video
recorder are required equipment for this
procedure. Once the tip of the scope is positioned
for simultaneous viewing of the valleculae, posterior
pharyngeal wall, perilaryngeal folds and boundaries,
endolarynx, and piriform sinuses the patient can be
administered various foods (with green food
coloring for easy identification) for swallowing
analyses. Whereas this technique does not enable
evaluation of the oral phase of swallowing or
possible distal spread of aspirated material, it
provides excellent images of: (1) abnormal levels of
standing secretions in the valleculae, endolarynx,
and/or piriform sinuses, (2) abnormal degrees of
pharyngeal edema/erythema, laryngeal edema/
erythema, or both, (3) premature bolus spillage
into and abnormal retention within the valleculae,
(4) bolus penetration into the endolaryngeal cavity,
and frank and delayed violation of the glottis,
 Patient with Laryngitis 10

Sequential evaluation of dysphonia with suspected allergy TABLE 10.2

Clinical evaluation technique Purpose

1. History taking Background information on possible allergy related dysphonia

2. Voice sampling and ratings Perceptual impressions of vocal quality, pitch, and/or loudness difficulties

3. Maximum phonation time Determine total length of a continuous utterance. Measures glottal competence and
underlying integrity of respiratory support

4. Coughing assessment Evaluate power of volitional vocal fold compression force necessary to eject
tracheobronchial mucus accumulation or aspirated material

5. Allergy-related vocal abuse Elicit patient’s self-impressions of allergy-related behaviors that may abuse the vocal folds
questionnaire

6. Mirror exam of larynx Inexpensive appraisal of the anatomy and physiology of the larynx

7. Fiberoptic laryngoscopy Use of high tech flexible or rigid endoscope for detailed examination of laryngeal
anatomy and physiology

8. Videolaryngostroboscopy Coupling rigid or flexible fiberoptic scope with strobe light and computer platform for
digital, quasi-slow motion photography of laryngeal anatomy and physiology

9. Acoustic analysis Objective appraisal of Fo, Jitter, shimmer, and harmonic/noise ratio

10. Speech aerodynamic testing Qualitative appraisal of x– flow (transglottal airflow), Ps (subglottal pressure), and Rg
(glottal resistance)

11. FEES Fiberoptic scope analyses of pharyngolaryngeal anatomy, swallowing physiology and
dysphagia signs

(5) reflexive coughing (or lack thereof) in response
to observed penetration and suspected aspiration,
(6) abnormal retention of bolus in the postcricoid
area or piriform sinuses with possible delayed
spillage anteriorly into the endolarynx (aspiration),
and (7) esophageal reflux. Clinically significant
findings, which strongly correlate with the patient’s
chief swallowing complaints, often help to explain
the difficulties and may provide clues for effective
management strategies. Additionally, if aspiration is
suspected with FEES, referral to radiology for a
modified barium swallow (i.e., cookie swallow)
study (+/− esophagram) is indicated to verify the
problem and help regulate oral feeding decisions.
Table 10.2 offers a synopsis of the various clinical
examination techniques discussed in this section.
Benign Laryngeal Pathologies
The most common cause of dysphonia is self-
induced, hyperfunctional vocal fold misuse or
abuse. Common types of misuse include: (1) yelling
or screaming, (2) unusually excessive speaking,
especially at loud levels, (3) frequent singing,
(4) chronic throat clearing, coughing, or both, and
(5) tense, strained, and hard attack vocalizations.
Salespeople, coaches, preachers, teachers, trial
lawyers, professional speakers and singers, choir
participants, factory workers, emotionally unstable
individuals, and those with chronic allergies and
associated postnasal drainage and sticky-thick
endolaryngeal mucus accumulation are all prone to
habitual expression of one or more of these

251
 Managing the Allergic Patient
maladaptive behaviors. The end result of such
aggressive vocalizations and associated strong
collision forces of the vocal folds is diffuse
inflammation of these structures. This condition
may be transient or persistent, its onset may be
acute or gradual, and the severity of the resultant
dysphonia may vary from mild to severe both
within and between patients. The most common
laryngeal pathologies secondary to misuse factors
include bilateral vocal fold polyposis or Reinke’s
edema, discrete vocal fold polyps (hemorrhagic),
edematous or fibrotic vocal fold nodules,
submucosal vocal fold cysts, and contact ulcers on
the medial aspects of the vocal processes. Some
patients also exhibit signs of ventricular phonation,
often caused by subconscious recruitment of the
false vocal folds to compensate for the ill-effects of
true vocal fold lesions. This behavior, known as
plica ventricularis, is usually counterproductive
because the voice produced is rather cacophonous.
In general, misuse vocal pathologies result in
variable degrees of hoarse, breathy, raspy, harsh,
strained, low pitch, monopitch, soft volume, and
monoloud dysphonia characteristics.
Common types of laryngeal abuses include: (1)
smoking, (2) regular use of inhaled corticosteroids
for asthma, (3) frequent use of antihistamine
(decongestant) medications for allergies, (4) excess
caffeine consumption, and (5) limited H2O intake.
Various systemic, neurologic, and traumatic
conditions may also inadvertently result in laryngeal
abuse. These include: (1) laryngopharyngeal reflux,
(2) asthma, (3) allergies, (4) severe upper
respiratory infection, (5) thyroid disease, (6)
presbylaryngis, (7) sarcoidosis, (8) lupus, (9)
laryngeal trauma, (10) laryngeal joint arthritis, and
(11) various neurologic diseases or injuries, including
252
focal laryngeal dystonia (spasmodic dysphonia),
essential tremor, stroke, cerebral palsy, Parkinson’s
disease, amyotrophic lateral sclerosis, multiple
sclerosis, and recurrent laryngeal nerve paralysis.
The most common laryngeal pathologies secondary
to abuse factors include diffuse infectious laryngitis,
interarytenoid granuloma or pachydermia formation,
Reinke’s edema, vocal fold bowing or atrophy, vocal
fold paresis or paralysis, tremors, and paroxysmal/
episodic vocal fold dysfunction or laryngospasms,
also known as irritable larynx syndrome.
The latter condition has received considerable
attention in the last two decades.26–29 It is generally
characterized by interruptive, paradoxical,
paroxysmal, or episodic vocal fold movement
behaviors at rest and during phonatory efforts.
Many patients with these signs and symptoms suffer
from psychogenic or emotional disorders, including
Münchausen’s syndrome and conversion reactions.
Others exhibit these adventitious laryngeal
musculature contractions, in the absence of
growths or lesions, as a result of severe upper
respiratory viral infections, asthma, reflux disease,
allergies, and certain neurologic pathophysiological
mechanisms.30 Dependent use of systemic and
inhaled corticosteroids and bronchodilators for
asthma has been linked to episodic paroxysmal
laryngospasms and transient dysphonia. In some
patients, a large majority of whom also use
medications to treat co-occurring allergies, mild
vocal fold edema and erythema occur as a result of
mucosal inflammatory reactions to the steroid. In
others, moderate degrees of vocal fold mucosa
thickening and bowing are observed. Fortunately,
few patients exhibit dramatic laryngeal pathologies,
such as vocal fold leukoplakia, granuloma
formations, and endolaryngeal candidiasis.31 Because
 Patient with Laryngitis 10

laryngopharyngeal reflux has also been causally

linked to many of these pathologies, differentiating
the pathogenesis of these signs in patients suffering
from asthma and reflux disease can be very
difficult, especially if the examiner is unfamiliar with
A
steroid inhaler laryngitis.The patient who also
struggles with co-occurring allergies presents an
even more challenging clinical portrait. The extent
to which each condition and treatment modality
contributes, either alone or synergistically, to these
irritable larynx phenomena remains unclear to date.
In general, abuse vocal pathologies, regardless of
etiology, result in variable degrees of hoarse,
breathy, strained-strangled, spasmodic, tremorous,
pitch and loudness outburst, and reduced range of
pitch and loudness voice disturbances.
Figures 10.7–10.12 were obtained with a high
resolution camera and videolaryngostroboscopy B
system. They represent examples of some of the
benign vocal pathologies mentioned above. Type
specific allergy-related laryngeal abnormalities will
be illustrated in the next section of the chapter.
Because of space limitations, malignant laryngeal
Figure 10.7 Videostroboscopy images of two different
neoplasms will not be presented here. Table 10.3 patients with Reinke’s edema. Note the mild glottal
summarizes the most common benign causes of incompetence in each case during phonation. Each patient
was female, and complained of lower than normal pitch,
dysphonia and their consequential abnormal owing to the vocal fold swellings and associated reduced
anatomic and pathophysiological laryngeal effects. speed of vibration. Each patient had allergies, and each
admitted to: (1) chronic throat clearing behaviors due to
perceptions of sticky endolaryngeal mucus; and (2)
intermittent coughing, secondary to allergic reaction
bronchospasms.
Allergic Laryngitis: Scientific
Evidence Versus Clinical
Observations the larynx. Ostensibly, such discussions center on
whether laryngeal disturbances noted in some
allergic individuals represent: (1) local end-organ
䊏 Scientific Background responses, or (2) manifestations of systemic and
There has been a great deal of debate over the multiple end-organ sequelae.2,32,33 The scientific
past forty years regarding the effects of allergy on literature on this subject is not replete with

253
 Managing the Allergic Patient

A A

Figure 10.9 Videostroboscopy images of two different

patients with vocal fold nodules. (A) Derived from a
female with vocal abuse behaviors. She is a young mother
Figure 10.8 Videostroboscopy images of two different
of two pre-school-age children. She admits to chronic
patients. (A) A male patient with dust mite allergy and a
yelling and screaming activities. Additionally, she has
history of coughing spells, and hard glottal attack phonation
struggled with hay fever allergy since early childhood. Note
habits. Note the contact ulcerations on the posteromedial
that her nodules are bilateral and appear relatively mature
surfaces of the vocal folds. (B) A female with muscle
or fibrotic. (B) Obtained from a male adult with a history
tension dysphonia characteristics. She has several food and
of chronic throat clearing. He tested positive for dust mite
inhalant allergies. Note the strong contraction of the
allergy. Note the glottal incompetence caused by
ventricular vocal folds (plica ventricularis), which obscures
edematous nodules or polyps. In both cases, the voice was
observation of the true vocal folds.
hoarse-breathy in quality, low pitched, and volume was
reduced.

extensive and well-controlled investigations. The

empirical data base to date has not demonstrated
an unequivocal cause effect relationship between
antigen exposure and pathophysiological laryngeal
reactions in patients with either seasonal or
perennial allergies. However, several clinical
researchers have suggested a high correlation
between allergy and laryngeal symptoms, such as
chronic throat irritation and soreness and laryngitis.
The immunological mechanisms responsible for
upper airway inflammation in allergic patients have

254

A A
B B
Figure 10.10 Videostroboscopy images of two different
patients; both with vocal fold polyps. (A) Obtained from a
male with aggressive voice behaviors and chronic throat
clearing associated with both food and inhalant allergies.
Note the large hemorrhagic polyp on the right vocal fold,
which causes glottal incompetence and hoarse-breathy
voice quality, lower than normal pitch, and limited volume
output. (B) Obtained from a female with a discreet polyp
on the right vocal fold, with reactive edema of the
opposing fold. Voice was less impaired than the patient in
A above, but nonetheless hoarse and low pitched.
been well documented. However, those cellular
processes that may also induce chronic laryngeal
inflammation, edema, and associated dysphonia in
these same individuals after antigen provocation are
poorly understood. Despite clinical observations
Patient with Laryngitis 10
Figure 10.11 Videostroboscopy images obtained from two
different patients, each with a left vocal fold cyst. Note that
the cyst inhibits complete glottal closure during the closed
phases of vocal fold vibration associated with voice
production. The voice in each case was hoarse-harsh in
quality.
and anecdotes by many physicians and speech-
language pathologists suggesting a possible causal
relationship between allergic disease and various
types of benign vocal pathologies, there have been
few human investigations in this area, and animal
models of chronic laryngeal inflammation have
produced limited data.
Chadwick suggested that both upper and lower
airway allergic inflammation can induce varying
255
 Managing the Allergic Patient

Figure 10.12 Videostroboscopy images obtained from two

different patients with laryngopharyngeal reflux (LPR) and
allergy histories. (A) Derived from a patient with severe
interarytenoid granulation tissue (pachydermia), often a side
effect of LPR. Note the mild edema of the vocal folds as
well. This may be due to the coughing and throat clearing
behaviors, which the patient admits he exhibits frequently.
A (B) and (C) were obtained from the same patient, prior to
and following an 8-week program of pharmacologic
(proton pump inhibitor medication twice daily)
intervention. Note the significant improvement in the
appearance of the granuloma formations, shown in C.

degrees of primary and secondary biomolecular and

biomechanical laryngeal disturbances.34 Corey et al
described two primary forms of allergic laryngitis: (1)
acute, IgE-mediated, inflammation (anaphylactic),
and (2) chronic, cyclic (delayed), non-IgE-mediated
inflammation.35 In the former category, there is
B
rapidly developing and generally severe edema of
the loose areolar tissue matrix of the laryngeal
vestibule or inlet. In addition to airway compromise,
inspiratory stridor, globus sensations, lingual and
uvula swellings, nasal congestion, hoarseness, and
dysphagia may occur concurrently and exacerbate
breathing difficulty symptoms. Certain venoms, food
items such as peanuts and shellfish, drugs, and insect
bites have been causally linked to acute allergic
sequelae. Fortunately, these pronounced respiratory

C and phonatory subsystem reactions do not

commonly occur in the general population of
allergic individuals.
Chronic or delayed symptoms and signs of possible
allergic laryngeal reactions have been reported to
include odynophagia, episodic straining to produce
voice, transient throat clearing, coughing,
hoarseness, and vocal fold edema.36–38 It is
important to note that these symptoms are also
commonly seen in laryngopharyngeal reflux, and
current findings linking eosinophils to

256
 Patient with Laryngitis 10

Common causes of dysphonia TABLE 10.3

Common causes Resultant pathology Dysphonia features

Misuse
1. Yelling, screaming Reinke’s edema Hoarseness

2. Loud and excessive talking Discrete VF polys Breathiness

3. Frequent singing VF nodules Raspiness

4. Chronic throat clearing Submucosal VF cysts Strained-harsh-shrill

5. Chronic coughing Vocal process contact ulcers Low pitch/monopitch

6. Hard attack phonation Plica venticularis Soft volume/monoloud

Abuse
1. Smoking 1. Diffuse laryngitis, leukoplakia, cancer 1. Hoarseness, low pitch

2. Inhalers 2. ILS, paroxysmal VF motion, thick 2. Intermittent hoarseness, strained,

endolaryngeal secretions spasmodic

3. Antihistamines 3–6. Friable mucosa, sticky thick 3–6. Hoarse-raspy, low

4. Decongestants endolaryngeal secretions, sticky thick pitch, reduced volume
5. Excess caffeine perilaryngeal secretions
6. Limited H2O

7. Neurologic illness, injury, disease 7. VF paralysis/paresis, VF tremors, 7. Breathy-hoarse, strained-strangled,

VF spasmodic contractions tremorous, pitch/volume fluctuations

8. Laryngeal trauma 8. VF paresis/paralysis, joint 8. Hoarse-breathy, reduced pitch

subluxation and volume range

9. Systemic diseases 9 9
a. LPR a. Granulomas, pachydermia a. Hoarse-breathy
b. Asthma b/c. VF edema, sticky thick b/c. Intermittent hoarseness
c. Allergies endolaryngeal secretions d. Harsh, raspy, shrill with breathy
d. URI d. Diffuse laryngitis (+/− infectious signs) interludes
e. Thyroid disease e. VF paresis, myedema e. Hoarse-breathy, low pitch
f. Presbylaryngis f. VF bowing/atrophy f–i. Hoarse-breathy, reduced
g. Sarcoidosis g. VF paresis, edema, erythema pitch/volume range
h. Lupus h. VF submucosal nodules erythema,
i. Arthritis edema
i. CT/CA joint fixation/VF immobility

CA = cricoarytenoid; CT = cricothyroid; VF = vocal fold; LPR = laryngopharyngeal reflux; URI = upper respiratory infection.

gastroesophageal reflux may suggest commonality
in mechanisms between reflux and allergic
37,39
rhinitis. Whether these two conditions share a
common, chronic inflammatory relationship has yet
to be determined.
At a cellular level the primary two leukocyte
populations involved in allergic inflammation are
mast cells and the eosinophil.40 Mast cells are
basophilic and contain coarse cytoplasmic granules.
The primary substance contained in these granules
is histamine, a potent proinflammatory vasoactive
amine. In addition to histamine, mast cell granules
contain the anticoagulant heparin. These large cells
are located throughout the sinonasal tract mucosa,

257
 Managing the Allergic Patient
within most loose connective tissue of the body,
and along the path of blood vessels. Mast cells act
as primary mediators of the acute-phase allergic
response, and may be activated by inhaled,
ingested, and topical allergens. On exposure to a
previously sensitized antigen, mast cells degranulate,
releasing their contents into the tissues locally. In
addition to the effects of histamine, inhaled irritants
often cause swelling of the nasal and bronchial
mucosa secondary to release of reactive
39
neuropeptides such as substance P. Acute allergic
reactions are a function of the inflammatory
changes that occur in response to these mediators.
The phase of acute allergic response usually
declines rapidly postexposure. However, late-phase
responses are often delayed for as many as 6 hours
after initial allergen contact. The primary cellular
mediator of this latter response is the eosinophil,
which is a type of granulated leukocyte that is
recruited to the area of inflammatory reaction.
These granules possess toxic proteins that are
released during the late response phase and cause
mucosal injury, which can persist for many hours.
Light and electron microscopic studies of the
human larynx have revealed an abundance of mast
cells and substance P within the epiglottis and
immediate subglottis; neither the squamous
epithelium nor the associated neurons of the vocal
folds contain such cells or neuropeptide
39,40
properties. Two different mast cell phenotypes
have been recently demonstrated in human
laryngeal mucosa: (1) mast cells containing tryptase
alone, and (2) mast cells containing tryptase and
41
chymase. Similar phenotypes have been
documented to exist in abundance in the nasal and
42–44
bronchial mucosa. From a pathophysiological
point of view, these mast cell populations are most
258
evident in anatomic regions of the larynx where
edematous conditions most commonly occur.
Consistent with the lack of mast cells at the level
of the glottis, no known primary allergenic
reactions or eosinophilic infiltrates have been
documented within the vocal folds that would help
explain transient swellings of these structures in
some individuals with allergic rhinitis. Several
investigators have hypothesized the presence of
alternative causative mechanisms in this clinical
population, such as chronic throat clearing or
coughing to evacuate perceived postnasal drainage
or viscous mucus accumulation within the
hypopharynx or larynx.11,33,36–38 If and when these
secondary behaviors occur, they may result in vocal
fold trauma, edema, excessive intrinsic laryngeal
muscle tension levels, and variable degrees of
intermittent or persistent dysphonia.
Notwithstanding these theoretical considerations,
the true incidence of so-called allergic laryngitis is
unknown, and the actual pathogenesis of abnormal
laryngeal signs and symptoms in individuals with
known allergies remains elusive to date. However,
several recent investigations have reinforced earlier
research findings and have begun to shed additional
revealing light on this controversial subject.
Up until about 10 years ago, the scientific literature
data base on allergy-related dysphonia was rather
sparse, speculative, and inconclusive. With the
recent advent of high technology laryngeal and
respiratory subsystem examination equipment, the
possible causal relationship between allergy and
voice difficulties has been more comprehensively
studied. Earlier investigators suggested that inhalant
and food allergens occasionally provoke pale
edema of the vocal folds and associated chronic
laryngitis and dysphonia, which subside with

removal of the inciting agents along with topical or
45–49
oral corticosteroids and immunotherapy. Some
of these researchers described the differential vocal
fold anatomy secondary to acute (anaphylactic)
reactions versus chronic allergic laryngeal
symptoms. In acute cases, diffuse edema and
erythema of the entire larynx was observed,
involving the epiglottis, true and ventricular vocal
folds, and the immediate subglottis. In chronic
cases, inflammation was confined to the true folds
without significant erythema. None of these
authors included both subjective and objective
laryngeal imaging, perceptual, acoustic, and speech
aerodynamic measurements to substantiate their
suggestions that patients exhibit a parallel
correlation between allergy symptom exacerbation
with antigen exposure and increasing voice
difficulties.
Corey et al acknowledged the paucity of
epidemiologic data on the existence and
prevalence of allergic diseases that affect the larynx,
other than evidence on laryngeal anaphylaxis and
edema secondary to IgE-mediated antigen
exposure.33 These authors reviewed over 200
videostroboscopic examinations of the larynx
obtained from patients with voice complaints.
Symptoms described by those individuals with
histories of nasal allergies in addition to dysphonia
included limited pitch range, frequent throat
clearing, postnasal drip, chronic cough, and globus
sensations. Mild vocal fold edema, sticky-thick
endolaryngeal secretion accumulation, mildly
erythematous arytenoids, and hyperactive laryngeal
reflexes were among the most notable
observations. Although many of these
pathophysiological conditions have also been
1,40
causally linked to laryngopharyngeal reflux, thick,
Patient with Laryngitis 10
viscid mucous strands within the larynx that bridge
the vocal folds have not been shown to be
common side effects of acid reflux disease in the
absence of allergies.
Naito et al studied 30 individuals diagnosed with
chronic laryngeal allergy on the basis of skin testing
for inhalant allergens and laryngeal examinations.50
The primary complaints of these patients were
persistent globus sensations and nonproductive
coughing spells. Laryngeal examinations
demonstrated abnormally pale, glistening, and
edematous arytenoid mucosa. Approximately 90%
of these individuals experienced significant
symptomatic improvement with oral H1
antihistamines. The authors suggested several
criteria for the diagnosis of laryngeal allergy,
including: (1) history of allergic disease, supported
by positive skin or in vitro allergy testing, (2)
foreign body sensation, itching of the larynx, and/or
persistent dry, nonproductive cough, (3) glistening,
pale edema, primarily involving the arytenoid
mucosa, and (4) normal findings on chest and sinus
X-rays and pulmonary function testing.
Within the past decade several researchers have
combined the technology of videostroboscopy,
speech aerodynamic, and acoustic analysis for
quantitative evaluations of the phonation subsystem
in patients with perennial and food allergies.51,52
These authors identified the coexistence of
irregular glottic edema, excessive and sticky
endolaryngeal mucous secretions, and dysphonia in
allergic subjects. Whether the sticky-thick mucous
accumulation clinging to the vocal folds originated
from the membranes of the nasal cavity, larynx,
tracheobronchial tree, or combinations thereof, was
not clarified by these authors. Reflux disease and
associated vocal abuses were also examined.
259
 Managing the Allergic Patient
Whereas many of the allergic subjects showed
laryngeal signs of laryngopharyngeal reflux, a very
small subset actually reported underlying symptoms
of reflux. A complex interrelationship between
allergy, reflux disease, vocal abuse, and dysphonia
was suggested by these authors. Additionally,
pulmonary function studies were performed on a
small subset of allergic patients, and approximately
25% of these individuals exhibited abnormal
spirometry findings, which were considered
possible manifestations of previously diagnosed
asthma or mild lower respiratory system allergy-
related hyperreactivity.
Lack53 and Cohn et al54 reviewed the importance
of considering allergic factors in the etiology
equation of all chronic inflammatory processes of
the unified airway. These researchers suggested
that allergic rhinitis and associated postnasal
drainage can specifically result in pharyngitis and
laryngitis; and that these allergic inflammatory
reactions can be amplified if acute viral/bacterial
sinusitis develops. That laryngeal inflammation
causes dryness, which in turn provokes itching or
tickling sensations and reactive throat clearing and
coughing, was discussed by these investigators. As
mentioned earlier, these abusive behaviors
mechanically traumatize the vocal folds, and they
can lead to mucosal tears, hemorrhaging, and
Reinke’s edema. Persistent abuse can also result in
widespread supraglottal swelling and erythema. To
overcome any associated voice difficulty, patients
may inadvertently bear down on phonation to
drive more proficient speech production.55 This
compensatory strategy may cause the development
of habitual muscle tension dysphonia, which can
aggravate the underlying vocal pathology and
trigger a vicious cycle of interrelated, abnormal
260
laryngeal biomechanical and biomolecular activities
and changes. Chadwick acknowledged that
distinguishing the direct laryngeal effects of allergic
disease from the adverse influences of nonallergic
conditions, such as vocal misuse and vocal fold
abuses in the same patient, can be very difficult.34
He suggested that studies focused on
demonstrating a possible causal relationship
between allergy and laryngeal pathology must ferret
out and evaluate all collateral medical and
behavioral factors via careful subject selection
methods. This approach would enable researchers
to specify the individual or synergistic
pathophysiological sequelae of the many different
conditions that may adversely affect laryngeal form
and function.
Other clinical researchers addressed these concerns
and experimental recommendations, by conducting
three separate prospective studies of patients who
tested positive for allergies to the perennial dust
mite antigen Dermatophagoides pteronyssinus. In the
first two investigations,56,57 placebo-controlled
research protocols were employed, in which one
group of subjects was challenged with an active
antigen for D. pteronyssinus, and the other group
was exposed to a placebo suspension. At the
outset of the first study, the researchers
hypothesized that because the mucosa throughout
the respiratory tract is contiguous, oral inhalation of
a dust mite antigenic suspension in allergic
individuals would elicit type I, IgE-mediated
responses within the larynx. Results demonstrated
that low dose antigen challenge was inadequate to
stimulate clinically significant laryngeal responses.
The second experiment utilized higher doses of the
antigen. Moderate to severe signs of respiratory
dysfunction (i.e., shortness of breath, chest tightness,

1 2
Figure 10.13 Videostroboscopy image obtained from a
dust allergic male patient prior to (1) and following (2)
direct provocation of the larynx with a high dose of a dust
mite antigen. Note the significant amount of sticky-thick
endolaryngeal mucus accumulation post-exposure.
bronchospasms, wheezing, coughing, throat clearing,
and reduced FEV1 levels) were experienced by the
first two subjects who received the antigen
solutions. These unexpected pulmonary side effects
forced the researchers to terminate the experiment
prematurely, with accrual of only three subjects.
Figure 10.13 is a representative example of one of
the most salient laryngeal reactions to the high
dose antigen challenge in the experimental subjects.
Note from this videostroboscopy photograph the
production of a significant amount of sticky-viscous
endolaryngeal secretions immediately following such
direct exposure, as compared to the corollary
baseline image. Vicious throat clearing reactions
were prominent and likely contributed to the mild
vocal fold edema noted and exacerbating dyspnea
symptoms. What could not be explained with
certainty was whether these secretions originated
in the larynx, or if they were coughed upstream
from the lower airway as a consequence of
concomitant bronchospasms.
Patient with Laryngitis 10
The third investigation addressed the frequent co-
occurrence of reflux disease in allergic patients, and
the extent to which this comorbid problem might
potentially influence or camouflage any laryngeal
abnormalities that may be observed in these
individuals.58 To control for this anticipated
complication, all prospective control (nonallergic)
and experimental (dust-allergic) subjects with
histories of gastroesophageal or extraesophageal
(i.e., laryngopharyngeal) reflux diagnoses and
treatments were disqualified from study
participation. Results revealed that on more than
15 different comparative phonation and respiration
subsystem analyses, there were no significant
differences between the two groups of subjects.
That is, all subjects exhibited normal phonation and
respiration subsystem characteristics.
Several Japanese researchers demonstrated type 1
hypersensitivity reactions in the larynx using animal
models. In one study, guinea pigs were sensitized
with ovalbumin, and laryngeal inflammation was
stimulated with passive cutaneous anaphylaxis.59
Significant populations of eosinophilic and
basophilic cells were observed in the sensitized
laryngeal mucosa of these animals. In addition,
ovalbumin-specific hyposensitization decreased with
extent of this cellular infiltration of the larynx. In a
separate study, Brown Norway rats that were
sensitized to Japanese cedar pollen, a major
seasonal antigen in Japan, were examined.60 Results
revealed a significant increase in esoinophilic
infiltrate in the laryngeal mucosa of these sensitized
rats when compared with a control population.
These animal studies supported the concept that
certain forms of laryngeal edema in humans may
result from inhalant antigen exposure in allergic
individuals.
261
 Managing the Allergic Patient
䊏 Clinical Observations
Physicians frequently encounter patients who
complain of respiration and phonation subsystem
allergy side effects. In most cases, these reactions
are delayed. That is, they are causally related more
too late phase release by eosinophilic cells of toxic
proteins into the affected mucosa than to acute
mast cell degranulation and proliferation. When
patients present with clinically significant signs and
symptoms of suspected laryngeal allergy, they almost
always report having recently experienced repetitive
exposure at work or play to inciting allergens to
which they are sensitive. The direct laryngeal
provocation studies that were reviewed earlier lend
support to these clinical observations. That is, when
dust mite allergic patients were challenged with
sufficiently high doses of this antigen, they exhibited
the aforementioned widespread respiration and
phonation subsystem pathological reactions. These
combined sequelae are excellent examples of the
functional and pathophysiological relationship
between and co-occurring vulnerability of the
various components of the unified airway. Earlier
research investigations demonstrated many similar
findings, but to lesser degrees of severity, owing to
less controlled methodologies and the absence of
challenge protocols.
Figure 10.14 summarizes a proposed symptomatic
train of interrelated unified airway responses to
substantial inhalant antigen exposure in the allergic
patient. These abnormal signs and symptoms may
occur acutely or as late phase reactions, depending
upon the intensity of the inciting antigen and the
severity of the patient’s allergy. Note from this
figure that initially the patient may simultaneously
experience nasal and pulmonary congestion. A
262
Inhalant antigen exposure
Nasal congestion
Runny nose
Postnasal drainage
Pharyngitis/Laryngitis
Throat clearing
Coughing
Vocal fold edema
Dysphonia
Upstream mucous migration
Pulmonary congestion
Bronchospasms, coughing
Figure 10.14 Flow diagram illustrating the parallel and
sequential train of inhalant antigen-related symptoms
and signs. Note that both downstream and upstream
pathophysiological allergic reactions may induce
inflammatory laryngeal responses. Laryngeal reactions may
be acute or delayed, and they may be primary or
secondary in origin.
common side effect of the former reaction is a
runny nose, which often leads to postnasal drainage
into the pharyngeal and laryngeal cavities. This
downstream mucous discharge may result in
localized mild inflammation, itchy and tickling throat
sensations, and a globus feeling. Concurrently,
underlying pulmonary congestion induces
bronchospasms, which cause shortness of breath,
vigorous coughing activities, and decreased
respiratory support for speech production.
Clearance of the tracheobronchial tree of excessive

mucous production occurs with coughing, which
induces upward migration of the sticky mucus
secretions into the larynx. Volitional and reflexive
throat clearing and coughing occurs in response to
these accumulated secretions in the upper airway.
These behaviors result in vocal fold edema, which
exacerbates the mild laryngeal swelling caused by
postnasal drainage. Vocal fold edema contributes to
voice difficulties and vocal fatigue. If exposure
continues to a sufficient degree, the cycle repeats
itself, and becomes vicious until broken by
elimination of the inciting antigen, bodily adaptation,
and/or pharmacologic intervention.
䊏 Treatment Caveats
The most effective treatment for laryngeal
inflammation in allergic patients is presently unclear.
This is true largely because the precipitating cause
is not consistent from patient to patient. There are
many other medical conditions that are known to
induce phonation and respiration subsystem
abnormalities that are very similar to those that
may be causally related to allergy. The treating
physician must therefore differentiate which
laryngeal signs and symptoms are likely attributable
to the patient’s allergy problem, which are
probable manifestations of coexisting ailments, and
which could be due to the synergistic adverse
effects of two or more conditions.
Managing Laryngeal Symptoms
in the Allergic Patient
This section addresses treatment strategies for the
allergic patient who may present with abnormal
laryngeal signs and symptoms. Here, the term
Patient with Laryngitis 10
laryngitis will be used to represent any type of
glottal or supraglottal inflammation, whether
generalized or focal in appearance or acute,
chronic, or anaphylactic in origin. It will be assumed
that the physician has considered conditions other
than, or in addition to, allergy that may be causally
related to the patient’s laryngitis. Common misuse
and abuse factors, neurologic disorders, and
malignant neoplasms should all be reviewed in the
differential work-up of the patient prior to
construction of the treatment plan. It is important
to realize that co-occurring etiologies of laryngitis
are more likely the rule rather than the exception
in the allergic patient. Thus, a combination of
different therapeutic approaches may be necessary
to ensure the most successful outcomes. Because
of space limitations, only a sample of such
treatment strategies can be discussed in this
chapter.
䊏 Acute Laryngitis
Acute laryngitis may occur in different forms,
depending upon whether the inflammation is
secondary to anaphylaxis or infections. These two
primary types will be discussed separately.
Anaphylaxis
Acute, fulminant, life-threatening edema of the
larynx can be IgE- and non-IgE-mediated. Certain
foods, inhalants, plants, and insect or animal bites
are allergenic; responses by sensitive patients are
usually severe and IgE mediated. It is important to
note, however, that less severe non-IgE-mediated
acute reactions to these allergens can also occur.34
In either case, following exposure the patient may
initially present with lip swelling and decreased
sensation; associated drooling may be evident as the
263
 Managing the Allergic Patient
reaction progresses. Moderate to severe responses
include tongue swelling, dysphagia, and difficulty
breathing. Initial airway distress may be
characterized by progressive pulmonary congestion,
labored and rapid respiration, significant shortness of
breath, and inhalatory stridor. Laryngeal examination
typically demonstrates generalized supraglottal
edema and muffled voice quality. Severe signs and
symptoms almost always require emergent
management to stabilize the airway. Treatment
consists of oxygen per mask and epinephrine
(adrenaline) injection of 0.3 ml of 1 : 1000 solution
subcutaneously. IV steroid injections, consisting of
hydrocortisone 80–100 mg, or dexametasone
(10 mg) should be administered as soon as IV
access is obtained. Topical epinephrine can be given
via inhalation, if needed. For supplemental support,
IV or IM antihistamines and H1 and H2 blockers may
be rendered to counteract any additional allergic
responses. Special attention should be given to
those individuals with acute laryngeal edema that
may be due to abnormal metabolic-mediated
allergenic drug reactions (e.g., patients on ACE
11
inhibitor or blocker medication). Unlike patients
with IgE-mediated reactions, these types of patients
do not respond as well to epinephrine; they may,
instead, require aggressive airway management if
significant airway obstruction occurs before the
steroids, H1 and H2 blocker treatments have had a
chance to be effective.
Infectious Laryngitis
Viral infections are clearly the most common
causes of acute laryngeal inflammation. The most
common forms include parainfluenza virus,
rhinovirus, adenovirus, and general influenza
61
viruses. Prior to full symptom onset, the patient
264
may experience mild postnasal drainage, subtle
dysphonia, and frequent throat clearing in response
to perceived peri- and endolaryngeal mucous
accumulation. As the viral infection progresses,
these symptoms worsen; voice becomes barely
audible, and fever usually ensues within 24 hours.
Patients with an associated productive cough and
discolored sputum should be treated appropriately
with antibiotics. For patients who present with
clear sputum, the treatment of choice is
expectorant medication, use of a humidifier, and
total voice rest. Nonproductive, dry-hacking
coughing can be treated with over-the-counter
cough syrups or prescription-strength cough
suppressants, such as dextromethorphan, codeine
hydrocodone, or benzozoate. Topical nasal steroid
sprays or nasal antihistamines are generally helpful
for postnasal drainage symptoms. Decongestants
should be used sparingly in patients with substantial
nasal congestion and recalcitrant nasal drainage.
This cautionary note is especially applicable to
patients with histories of high blood pressure, as
decongestants can exacerbate this condition.
Additionally, the use of antihistamine and
decongestant medication by any patient can result
in significant drying of the mucous membranes of
the entire vocal tract, which can adversely affect
underlying laryngeal inflammation. This predictable
anticholinergic sequela is usually counterproductive,
and most often associated with first generation
antihistamines. Significant sedative effects are also
experienced by those who use these drugs. Even
topical decongestants should be recommended
with extreme caution (i.e., maximum of 48–72
hours of prescribed use) to prevent rebound
rhinitis medicamentosum. Antibiotics are prescribed
when patients exhibit one or more of the following
 Patient with Laryngitis 10

bacterial infection signs and symptoms: fever, chills, However, when treatments fail to resolve the
yellow and purulent sputum, and exudative problem and symptoms worsen, it is usually wise
appearing tonsils, posterior pharyngeal wall, to establish an airway proactively via fiberoptic
epiglottis, or vocal folds. In such cases, augmented intubation or tracheostomy.
penicillin or a second generation macrolides is
usually quite effective. For patients with penicillin
allergy, telithromycin or clarithromycin serve as
䊏 Chronic Laryngitis
As the term implies, patients with this condition
excellent substitutes. Antibiotic therapy should be
suffer with persistent symptoms for at least 10 days
continued for a sufficient period to eradicate the
to 2 weeks. These often include, sore throat,
infection.
odynophagia, globus sensation, and variable hoarse-
breathy vocal quality. Intermittent shrill vocalizations
Infectious Epiglottitis
are not uncommon in those individuals who try to
Acute inflammation of the epiglottis is usually
compensate for the inherent dysphonia by bearing
caused by invasive Haemophilus influenzae type b.
down on the larynx during speech efforts. The
Because of the previously described abundance of
level of severity of these symptoms may vary from
mast cells within the supraglottic tissues, the
mild to profound, depending upon the underlying
epiglottis is susceptible to prominent swelling
etiology. Because there are numerous possible
secondary to viral pathogens as well as inciting
interrelated causes of chronic laryngitis, the
antigens to which the patient may be allergic. The
examining physician may be initially perplexed with
condition can be life-threatening if this side effect is
respect to discovering the actual cause in any given
severe and encroaches the glottis. In a stable
patient. It is most important to rule out a malignant
airway, especially in an adult, first line defense is
laryngeal neoplasm during the primary work-up of
antibiotic therapy. Clavulanate, cefoxitin, and
patients with these clinical presentations; especially
clarithromycin have all been shown to be effective.
those with long histories of heavy tobacco abuse
If associated inflammation of the subglottis and
who are at high risk for developing head and neck
trachea occur, because these sites also possess an
cancers. It is beyond the scope of this chapter to
abundance of mast cells, irritable coughing and
delve into this subject matter.
biphasic stridor may result. These combined
sequelae are indications for hospital admission and
close observation. ER treatment in such cases Vocal Misuse
usually involves inhaled aerosolized epinephrine, Coaches, preachers, teachers, factory workers,
followed by injections of corticosteroids along with singers, sports enthusiasts, and others who
Heliox (a combination of 70% helium and 30% frequently exhibit excessively loud voice behaviors
oxygen), if available. Because these emergency are prone to chronic inflammation of the vocal
measures of management are often quite successful folds. In many cases, the unusually hard vocal fold
in gradually reversing the inflammatory conditions, collision forces associated with yelling or aggressive
tracheostomy tube placements are rarely required. speech activities can convert from general swelling

265
 Managing the Allergic Patient
into discrete lesions, such as nodules or
hemorrhagic polyps. Hoarse-harsh vocal quality and
reduced pitch range are the most salient
abnormalities. Occasionally, patients complain of
co-occurring extrinsic laryngeal and
temporomandibular joint muscle tension and
tenderness. These symptoms may vary in severity
from day to day, but they often persist in some
form for many months. First line treatment in most
cases is complete cessation of the inciting patterns
of voice abuse. In severe cases, strict voice rest
may be indicated for a period of 10 days to 2
weeks. Use of microphones, whistles, sign language,
and other compensatory communication strategies
are all effective methods of reducing vocal fold
stress when the patient is permitted to begin using
voice again. A formal voice therapy program is
typically recommended at this time, focusing on:
(1) the specific cause of the chronic laryngitis, (2)
rationale for voice conservation, (3) importance of
adequate daily hydration, (4) steam inhalation, and
(5) specific voice production exercises. This
program usually consists of between six and ten
1-hour sessions over the course of 2 months.
Patients who continue to struggle with the
aforementioned symptoms, despite these
conservative treatment methods, may require
phonosurgical intervention for persistent vocal
fold lesions, followed by a short stint of additional
voice therapy. Patients with co-occurring allergies
will also continue with their pharmacologic and
medical therapies throughout this treatment
program.
Laryngopharyngeal Reflux
This condition is very common in the general
population, and it often co-occurs in patients with
266
allergies. Acting alone or in combination with
allergy, reflux disease can cause substantial
laryngitis. When acid material chronically enters the
hypopharynx it can ultimately induce locoregional
tissue ulcerations, erythema, and inflammation, as
previously described.19 Unlike patients with
gastroesophageal reflux, those with
laryngopharyngeal reflux do not typically complain
of heartburn and indigestion, which are
symptomatic of esophagitis. Rather, they experience
variable degrees of sore throat, coughing,
odynophagia, and dysphonia symptoms. Although
reflux events can only be definitively identified
using multiple probe pH monitoring systems, in
most cases the diagnosis is made empirically during
the clinical examination on the basis of history,
presenting signs and symptoms, and previously
positive responses to nonprescription antacids.
Initial treatments may include educational materials
regarding the disease entity, and proper eating
habits. Neither food nor drink is permitted within 2
hours of bedtime; girdles and tight fitting clothes
are discouraged, as are smoking and alcohol use.
Excessive use of caffeine and spicy food are
similarly prohibited. Throat clearing in response to
acid or sour taste sensations is also discouraged.
Instead, patients should be instructed to take a
drink of water and swallow several times for relief.
Additionally, they should be encouraged to stifle or
suppress all vigorous coughing activities to reduce
vocal fold stress and general laryngeal inflammatory
reactions. All other forms of vocal abuse or misuse
should be discouraged as well. The previously
mentioned cough suppressant medications may
prove helpful. Patients with persistent reflux
symptoms, irrespective of having employed
significant behavioral modifications, are good

candidates for pharmacologic intervention.
Depending upon the severity of the laryngeal signs
and symptoms, either once or twice daily proton
pump inhibitor therapy is prescribed (e.g.,
esomeprazole magnesium, rabeprazole sodium,
lansoprazole); in severe cases, an H2 blocker (e.g.,
ranitidine) can be added prior to bedtime. Surgical
intervention for laryngopharyngeal reflux is
preserved for rare instances of obstructive
granuloma formation on the vocal processes of the
arytenoid cartilages, the interarytenoid tissue bridge,
or both. Even in these cases, an 8- to 12-week trial
program of the aforementioned behavioral and
pharmacologic therapies is recommended first,
whenever possible. Patients with co-occurring
allergies should continue on their allergy
medications in the usual way.
Allergies
The recognition that chronic laryngeal inflammation
and dysphonia can be related to allergy is a recent
development. As such, the most appropriate
treatment for allergic laryngeal inflammation is
presently unknown. Empirical management includes
environmental control of the inciting allergens. At
first, patients should be encouraged to avoid the
food or inhalants known to induce allergic
reactions. Behavioral modification strategies should
be introduced next. Patients will benefit from
discussions about the adverse laryngeal effects of
constantly clearing their throats of perceived
standing secretions. They should be encouraged to
swallow these accumulations; using a drink of water
to help flush down the sticky-thick mucus is usually
helpful. Cough suppressant medication may also be
of value in patients with intractable coughing spells.
A vigilant daily routine of adequate hydration (i.e.,
Patient with Laryngitis 10
8–10 glasses of water) must be reinforced;
caffeinated beverages should be completely
discouraged, as they induce the opposite tissue
effects. Habitual vocal misuse behaviors and
laryngeal abuse conditions, as described earlier,
must also be eliminated to maximize potential
reduction of laryngeal inflammation. Voice therapy,
as noted above for reflux laryngitis, may be
required. Significant laryngeal pathologies, such as
reactive nodules, polyps, submucosal cysts, and
pronounced Reinke’s edema, ultimately may require
phonosurgical intervention plus voice therapy for
optimal treatment outcomes.
From a pharmacologic management approach, the
use of antihistamines theoretically makes sense for
allergic patients with chronic symptoms that do not
significantly improve with behavioral modifications
alone. As mentioned earlier, first generation
antihistamine drugs (e.g., chloropheniramine,
diphenhydramine) produce substantial
anticholinergic effects. Consequently, these
medications are generally contraindicated, owing to
their potential drying effects on the laryngeal
mucosa; friable vocal fold covers secondary to local
dehydration are at risk for injurious side effects
during voice activities. If antihistamine therapy is
necessary to relieve overall significant allergy
symptoms, second generation alternatives (e.g.,
loratidine, fexofenadine, desloratidine) are
recommended because they may produce fewer
adverse laryngeal and sedative side effects.
Decongestants may improve nasal congestion
symptoms, but their sympathomimetic sequelae
may prove counterproductive to the professional
voice user. It is also tempting to treat chronic
laryngeal inflammation with topical corticosteroid
medications. However, as discussed earlier, inhaled
267
 Managing the Allergic Patient
corticosteroids have been shown to cause adverse
or irritable vocal fold phonatory biomechanical
disturbances. Whereas allergy immunotherapy
may hold promise as an effective laryngeal
allergy treatment method, substantial clinical
research in this area of investigation is required
to confirm this hypothesis. Additionally, further
studies are indicated relative to the
pathophysiological mechanisms that may be
involved in individuals with allergies who
present with signs and symptoms of laryngeal
inflammation.
Ultimately, the development of unequivocal
treatment algorithms for patients with acute or
chronic laryngitis secondary to allergy and related
disorders will depend upon numerous prospective,
randomized clinical treatment trials from several
cooperative groups of researchers, in order to
accrue a sufficient number of patients. Figure 10.15
illustrates a synopsis of the possible treatment
alternatives for acute and chronic laryngitis in the
allergic patient.
Summary and Conclusions
The primary objective of this chapter was to sensitize
readers about the potential adverse effects of allergy
on laryngeal form and function. To achieve this goal
several subsections were included in order to: (1)
review the possible causal interrelationships between
allergy and various benign vocal pathologies, (2)
describe the anatomic and physiological roles of the
larynx in the unified airway, (3) detail voice
laboratory laryngeal examination techniques, (4)
compare and contrast acute and chronic forms of
laryngitis, secondary to various types of allergic
268
reactions, (5) provide an overview of the scientific
literature base on the role of the larynx in allergy,
and (6) discuss behavioral, pharmacologic, and
surgical intervention alternatives for allergic patients
who complain of occasional but significant voice
difficulties. To facilitate these discussions, numerous
algorithms, figures, and tables were incorporated into
the respective subsections of the chapter. The
information presented in each topic area was by no
means all inclusive. Rather, the brief overview of each
subject was designed to stimulate physicians to
consider that for any given patient with allergic
disease, the larynx is as susceptible to inflammatory
reactions as all other components of the unified
airway.
For completeness, discussions were rendered
regarding the pathophysiological phonation subsystem
effects of other conditions that frequently co-occur in
patients with allergies, such as reflux disease, asthma,
irritable larynx syndrome, and chronic voice abuse
behaviors. This information was included to
emphasize that during the evaluation work-up of the
patient with allergic disease, the probable complex
coexistence of several aerodigestive and airway
disorders must be explored and, when necessary,
factored into the differential diagnosis and ultimate
treatment plan. The central theme of the chapter
focused on the importance of cooperative
interactions of physicians and allied health clinicians
from different subspecialties in order to ensure
comprehensive and successful treatment outcomes
with this multivaried clinical population. With such
objectives in focus, these practitioners were
cautioned that when patients with allergic diseases
present with complaints of intermittent or chronic
voice difficulties, these problems should not be
dismissed as completely unrelated to the allergy.
 Patient with Laryngitis 10

Acute

Anaphylaxis Severe epiglottitis Infectious

ER visit Antibiotic RX Expectorant/Humidifier

O2 Epinephine Voice rest

Cough suppressant

IV/IM Antihistamines
Topical epinephrine IV Steroids
H1/H2 Blockers Nasal steroids
Antihistamines
Intubation/Tracheostomy Decongestants

Chronic

Vocal misuse LPR Allergy

Allergy meds Voice rest Voice rest Diet Allergy meds Avoidance Voice rest

No clearing Cough Nasal steroids

Eliminate voice abuses
No coughing suppressants Antihistamines
Decongestants
Immunotherapy
Voice RX PPI (+/–H2 blockers)
Hydration

Phonosurgery Voice RX
No clearing Cough
No coughing suppressants

Phonosurgery
Voice RX

Figure 10.15 Tree diagram illustrating unilateral, sequential, or concurrent treatment alternatives for various types of acute
or chronic laryngitis.

Diagnostic conclusions that the two conditions are
not causally interrelated may prove premature in
many cases; a causative association may be more
likely in these individuals than a simple relationship of
coexistence. Finally, the need for carefully controlled
research investigations of the primary and secondary
laryngeal effects of allergy and commonly associated
disorders was demonstrated, with hopes of
stimulating additional scientific inquiry in this area of
interest.

269
 Managing the Allergic Patient
REFERENCES
1. Koufman J. The otolaryngologic manifestations of
gastroesophageal reflux disease (GERD): a clinical
investigation of 225 patients using ambulatory 24-hour pH
monitoring and an experimental investigation of the role of
acid and pepsin in the development of laryngeal injury.
Laryngoscope 1991;101(suppl 53):1–78.
2. Hurwitz B. Nasal pathophysiology impacts bronchial
reactivity in asthmatic patients with allergic rhinitis.
J Asthma 1997;34:427–431.
3. Grossman J. One airway, one disease. Chest
1997;11(suppl):11S–16S.
4. de Benedictis F, Bush A. Rhinosinusitis and asthma:
epiphenomenon or causal association? Chest
1999;115:550–556.
5. Smith JM. Epidemiology and natural history of asthma,
allergic rhinitis, and atopic dermatitis (eczema). In:
Middleton JE, Reed CE, Ellis EF, et al, eds. Allergy principles
and practice, 2nd ed. St Louis: Mosby; 1983:771–803.
6. Braman SS, et al. Airway hyperresponsiveness in allergic
rhinitis:a rsik factor for asthma. Chest 1987;91:671–674.
7. Slavin RG, et al. Sinusitis and bronchial asthma. J Allergy
Clin Immunol 1980;66:250–257.
8. Fokkens W, et al. The interactions between upper and
lower airways and allergic rhinitis. The nose 2000 and
beyond: International Rhinologic Society programs and
abstracts. Biennial meeting of the International Rhinologic
Society, Washington, DC; Sep. 21–25, 2000. Washington,
DC:A-158(abs.).
9. Irvin CG. Sinusitis and asthma: an animal model. J Allergy
Clin Immunol 1992;90:521–533.
10. Voegels R, et al. Can endoscopic nasal surgery improve
asthma symptoms? The nose 2000 and beyond:
International Rhinologic Society programs and abstracts.
Biennial meeting of the International Rhinologic Society.
Washington, DC; Sep. 21–25, 2000. Washington, DC:
A-30(abs.).
11. Chadwick SJ. The pharynx and larynx. In: Krouse JH,
et al, eds. Allergy and immunology: an otolaryngic approach.
Philadelphia: Lippincott Williams & Wilkins; 2002:249–270.
270
12. Hirano M. Phonosurgery. Basic and clinical
investigations. Otologia (fukuoka) 1975;21:239–442.
13. Kotby MN, et al. Electromyography and neurography
in neurolaryngology. J Voice 1992;6:159–187.
14. Dworkin JP, et al. Use of topical lidocaine in the
treatment of muscle tension dysphonia. J Voice
2000;14:567–574.
15. Titze I. Principles of voice production. New Jersey:
Prentice-Hall; 1994.
16. Blitzer A, et al. Neurologic disorders of the larynx.
New York: Thieme; 1992.
17. Dworkin JP, et al. Videostroboscopy, mirror, and
fiberoptic laryngoscopy: objective comparisons. J Med
Speech-Lang Path 2004;12:99–107.
18. Sataloff RT, Spiegel JR, Hawkshaw MJ.
Strobovideolaryngoscopy: results and clinical value. Ann
Otol Rhinol Laryngol 1991;100:725–727.
19. Koufman JA. Laryngopharyngeal reflux 2002: a new
paradigm of airway disease. ENT J 2002;81:2–7.
20. Patorello EA, et al. Mechanisms in adverse reactions to
food: the mouth and pharynx. Allergy 1995;50:41–44.
21. Amlot PL, et al. Oral allergy syndrome: symptoms of
IgE mediated hypersensitivity to foods. Clin Allergy
1987;17:33–42.
22. Ortolani C, et al. The oral allergy syndrome. Ann
Allergy 1988;61:47.
23. Bircher AJ, et al. IgE to food allergens are highly
prevalent in patients allergic to pollens, with and without
symptoms of food allergy. Clin Exp Allergy 1994;24:367.
24. Ebner C, et al. Common epitopes of birch, pollen, and
apples: studies by Western and Northern blot. J Allergy
Clin Immunol 1991;88:588.
25. Eriksson NE. Clustering of foodstuffs in food
hypersensitivity and inquiry study in pollen-allergic patients.
J Allergol Immunol Pathol 1984;12:28.
26. Andrianopoulos MV, Gallivan GJ, Gallivan KH. PVCM,
PVCD, EPL, and irritable larynx syndrome: What are we

talking about and how do we treat it? J Voice
2000;14:607–619.
27. Gallivan GJ, Hoffman L, Gallivan KH. Episodic
paroxysmal laryngospasm: voice and pulmonary assessment
and management. J Voice 1996;10:93–105.
28. Koufman JA. The differential diagnosis of paradoxical
vocal cord movement. Visible Voice 1994;3:3.
29. Morrison M, Rammage L, Emami AJ. The irritable
larynx syndrome. J Voice 1999;13;447–455.
30. Martin RJ, et al. Paradoxical vocal cord motion in
presumed asthmatics. Semin Resp Med 1987;8:332–338.
31. DelGaudio JM. Steroid inhaler laryngitis. Arch
Otolaryngol Head Neck Surg 2002;128:677–681.
32. Cohn JR, Spiegel JR, Sataloff RT. Vocal disorders in the
professional voice user: the allergist’s role. Ann Allergy
Asthma Immunol 1995;74:363–376.
33. Corey JP. Allergy for the laryngologist. Otol Clin North
Am 1998;31:422–426.
34. Chadwick SJ. Allergy and the contemporary
laryngologist. Otol Clin North Am 2003;36:957–988.
35. Corey JP, Gungor A, Karnell M. Allergy for the
laryngologist. Otol Clin North Am 1998;31:189–205.
36. Alimov AL. The clinical symptomatology in the
diagnosis of allergy in acute and chronic laryngitis. Otol
Rhinol Laryngol 1968;30:71–75.
37. Hogan SP, Rothenberg ME. Review article: the
eosinophil as a therapeutic target in gastrointestinal disease.
Alimen Pharmacol Ther 2004;20:1231–1240.
38. Baroody FM. Allergic rhinitis: broader disease effects
and implications for management. Otolaryngol Head Neck
Surg 2003;128:616–631.
39. Domeji S, et al. Similar distribution of mast cells and
substance P and calcitonin gene-related peptide-
immunoreactive nerve fibers in the adult human larynx.
Ann Otol Rhinol Laryngol 1996;105:825–831.
40. Ishi J, et al. Local eosinophilia of the nose, the larynx,
and the trachea in rats sensitized with Japanese cedar
pollen. Arerugi 1997;46:1251–1257.
41. Ishida H, et al. Immunohistochemical study on
distribution of mast cell phenotypes in human laryngeal
Patient with Laryngitis 10
mucosa: evidence for laryngeal type I allergy. Ann Otol
Rhinol Laryngol 2005;114:139–143.
42. Shanahan F, et al. Human lung mast cells: distribution
and abundance of histochemically distinct subpopulations.
Int Arch Allergy Appl Immunol 1987;83:329–331.
43. Irani AM, Schwartz LB. Mast cell heterogeneity. Clin
Exp Allergy 1989;19:143–155.
44. Okuda M, Ohtsuka H, Kawabori S. Basophil leukocytes
and mast cells in the nose. Eur J Respir Dis Suppl
1983;64:7–15.
45. Pang LQ. Allergy of the larynx, trachea, and bronchial
tree: Symposium on Allergy and Otolaryngology. Otol Clin
North Am 1974;7:719–734.
46. Williams RI. Allergic laryngitis. Ann Otol Rhinol
Laryngol 1972;81:558–564.
47. Sala E, et al. Occupational laryngitis with immediate
allergic or immediate-type specific chemical hypersensitivity.
Clin Otolaryngol 1996;21:42–48.
48. Rea WJ. Elimination of oral food challenge reaction by
ingestion of food extracts: a double blind study. Arch
Otolaryngol 1984;110:248.
49. Rea WJ. Environmental aspects of ear, nose and throat
disease. Part 1. J Clin Ecol Otorhinol. Allergy 1979;41:41.
50. Naito K, et al. Laryngeal allergy: a commentary. Eur
Arch Otorhinolaryngol 1999;256:455–457.
51. Dixon HS. Allergy in laryngeal disease. Otol Clin North
Am 1992;25:239–249.
52. Jackson-Menaldi CA, et al. Allergies and vocal fold
edema:a preliminary report. J Voice 1999;13:113–122.
53. Lack G. New perspectives in pediatric allergic rhinitis
and comorbid disorders. J Allergy Clin Immunol 2001;108:
S9–15.
54. Cohn JR, Sataloff RT, Branton C. Responsive asthma-
related voice dysfunction to allergen immunotherapy: a
case report of confirmation by methacholine challenge.
J Voice 2001;15:558–560.
55. Cohn JR, et al. Airway reactivity-induced asthma in
singers (arias). J Voice 1991;5:332–337.
56. Reidy PM, Dworkin JP, Krouse JH. Laryngeal effects of
antigen stimulation challenge with perennial allergen
271
 Managing the Allergic Patient
Dermatophagoides pteronyssinus. Otol Head Neck Surg
2003;128:455–462.
57. Dworkin JP, et al. Effects of sequential
Dermatophagoides pteronyssinus antigen stimulation on the
anatomy and physiology of the larynx. ENT J (in press).
58. Carron M, et al, The effect of dust mite allergies on
the phonation subsystem. Paper at COSM 2007, San
Diego.
272
59. Iwae S, Ishida H, Amatsu M. Laryngeal type I allergy in
sensitized guinea pig. Larynx Jpn 1995;7:1–6.
60. Lidegram M, et al. Mast cells in the laryngeal mucosa of
the rat: a quantitative and immunohistochemical study at
the light and electron microscopic levels. Acta Anat (Basel)
1996;157:135–143.
61. Turnidge J. Responsible prescribing for upper
respiratory tract infections. Drugs 2001;61:2065–2077.