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76 The Voice and Voice Therapy
his chapter describes functional voice disorders. Most voice problems seen by the voice
clinician have no organic or neurological cause. Although the mechanisms of respira-
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they lack the proper functional balance. This results in a voice disorder classified by many as a
functional voice disorder. Sometimes an adult elects to habitually use a voice with hard glottal
attack (such as the “drill sergeant” voice). Many times, a child plays with their voice by making
odd sounds (such as truck noises, animal noises, etc.). Or the actor may elect to speak with
excessive loudness, or pitch that is excessively higher or lower than the modal register, or speak
with hoarseness or excessive nasality. When not playing a role, however, the actor’s voice is immediately normal. In other instances, an adult “puts too much effort” into their voice as a result of
physical or emotional stress or as compensation for the laryngeal and pharyngeal swelling that
accompanies laryngitis.
voice disorder” label: (a) excessive muscle tension or (b) psychogenic origin. In cases of excessive
muscle tension, benign vocal fold masses such as nodules, polyps, and Reinke’s edema may result.
To evaluate the effectiveness of a particular voice facilitating approach (see Chapter 7), a single
technique could produce different outcomes, depending on which of these two causes exist. For
example, the voice facilitating approach of change of loudness (see Chapter 7) in the patient with
psychogenic voice disorder might result in the rejection of the approach because the change might
be in direct conflict with the patient’s emotional needs. Conversely, for the patient with muscle
tension dysphonia, this same voice facilitating approach may be on target for reducing excessive
muscular tension.
tion, phonation, and resonance appear physically capable of normal voicing function,
To promote the study of therapy outcomes, we find two different causes under the “functional
Excessive Muscle Tension Disorders
Muscle Tension Dysphonia
Muscle tension dysphonia (MTD) is a persistent dysphonia that results from excessive laryngeal
and related musculoskeletal tension and associated hyperfunctional true and/or false vocal fold
vibratory patterns (Dabirmoghaddam et al., 2021; Dworkin et al., 2000). MTD is one of the most
common functional voice disorders (Khoddami et al., 2023). Morrison and colleagues (1983)
first described MTD as the occurrence of vocal dysfunction in the absence of laryngeal structural
abnormalities. In patients with MTD, the larynx is often noted to be elevated in the neck due to
increased extrinsic laryngeal muscle tension (Tomlinson & Archer, 2015; Van Houtte et al., 2011),
and pain is often reported in the neck, jaw, and shoulders (Dehqan & Scherer, 2019; Stemple
etal., 2000).
MTD can be categorized as primary or secondary based on whether organic pathological
conditions contribute to trigger the muscle tension behavior (Mansuri et al., 2019; Rosen, Murray
et al., 2000). Primary MTD occurs in the absence of current organic pathology, without obvious
psychogenic or neurological etiology. Patients with primary MTD represent up to 40% of the
dysphonias seen in voice clinics (Altman, Atkinson, et al., 2005; Dromey et al., 2008; Wenke
et al., 2023). Secondary MTD occurs in the presence of current or recent organic pathology, or
CHAPTER 3 Functional Voice Disorders 77
psychogenic or neurological etiology. Secondary MTD is believed to originate as a compensatory
response to primary etiology. MTD may be seen in both children and adults (Lee & Son, 2005).
Yang and Xu (2020) reported that over 7% of children referred for dysphonia presented with
functional aphonia.
Auditory-perceptual features of MTD can include strained or effortful voice quality, aberrant
pitch, breathiness, and vocal fatigue (Jafari et al., 2017; Roy et al., 2009). Reduced self-perceptions
of voice symptoms are also common in this population. Caldeira Martinez and colleagues (2021)
looked at two groups of women: one group presenting with MTD, one group without MTD.
Of those diagnosed with MTD, findings revealed worse results for the Voice Symptoms Scale
and the Vocal Fatigue Index. Physiological features considered core traits of MTD are generally
based on subjective measures and include laryngeal elevation and decreased space between the
hyoid bone and larynx, increased extrinsic laryngeal muscle tone, and the presence of one or
more patterns of excessive laryngeal or supralaryngeal constriction (Khoddami et al., 2015; Lowell
etal., 2012). Constriction patterns include anterior-posterior compression, medial compression,
and a sphincter-like combination of these two (Belafsky, Postma, Reulback et al., 2002). Excessive
vocal fold tension resulting in an underapproximation of the vocal folds may also be observed
(Hillman & Verdolini, 1999). In some patients, medial compression may be a normal configuration, however, and must be interpreted considering other laryngoscopic findings (Behrman
et al., 2003).
Numerous factors may contribute to the development of MTD, including deviant body
posture and misuse of neck and shoulder muscles, high stress levels, excessive voice use, persistently
loud voice use, and laryngopharyngeal reflux disease (Altman, Atkinson, et al., 2005; Faralli
etal., 2017; Van Houtte et al., 2011). Patients frequently demonstrate significant emotional
stress or conflict (Deary & Miller, 2011), suggesting an interaction between personality and
psycho-emotional status and the voice (Caputo Rosen et al., 2021; Dietrich et al., 2008; Kryshtopava etal., 2017; Mersbergen, 2011; Bainbridge et al., 2017; Seifert & Kollbrunner, 2005).
Understandably, voice-related quality of life is diminished in persons with MTD (Kooijman
et al., 2005).
For inexperienced and experienced voice clinicians alike, MTD can sometimes be difficult
to differentiate from other forms of dysphonia, such as adductor spasmodic dysphonia and vocal
tremor. This is because some patients with adductor spasmodic dysphonia, vocal tremor, or MTD
present with symptoms that overlap to such a degree that a correct diagnosis is not easy. Findings
from several studies examining diagnostic elements such as patient interview, visualization of the
larynx, acoustic and aerodynamic evaluation, electromyographic evaluation (Khoddami etal.,
2018), and perceptual judgments may help the clinician arrive at the correct diagnosis in a timely
manner (see Barkmeier & Case [2000], Dworkin et al. [2000], and Maryn et al. [2010] for
reviews). For example, comparison of laryngeal behaviors during quiet breathing, counting from
1 to 10 in usual voice compared with falsetto and whispered speech, comparison of all-voiced
versus all-voiceless utterances, variation of pitch and loudness during sustained phonation versus
connected speech, and singing or crying may elicit differing patterns between adductor spasmodic
dysphonia and MTD.
The key difference between laryngeal behaviors in individuals with adductor spasmodic
dysphonia versus MTD is the consistency of laryngeal postures across and within each of the
78 The Voice and Voice Therapy
examination tasks. Patients with MTD maintain hyperadduction of the involved laryngeal structures across all tasks, whereas those with adductor spasmodic dysphonia tend to demonstrate more
intermittent hyperadduction (Kodama et al., 2024; Leonard & Kendall, 1999). In patients with
adductor spasmodic dysphonia, voice severity is perceived to be worse for connected speech than
sustained vowels; this is not the case in patients with MTD, where no difference is usually heard
(Roy et al., 2005, 2014). In patients with MTD, voice severity is generally perceived to be the
same on connected speech regardless of whether the sentences are all voiced or all voiceless; this
is not the case for patients with adductor spasmodic dysphonia (Roy et al., 2007). In Chapter5,
comparisons are made between MTD and problems such as essential tremor and adductor spasmodic dysphonia.
Treatment for MTD typically focuses on relaxation of the head and neck muscles. In Chapter7,
we present the voice facilitating approaches of chant talk, chewing, digital manipulation, focus,
laryngeal massage, relaxation, and yawn-sigh, all of which can be effective in minimizing or
eliminating MTD. Studies investigating the effects of laryngeal massage have been appearing in
the literature since the early 1990s, but the evidence base remains extremely small. A review by
Mathieson (2011) indicates that there is evidence that laryngeal manual therapy, in various forms,
can be a useful primary intervention in cases of MTD (see also Craig et al., 2015; Khoddami etal.,
2023; Van Houtte et al., 2011). Khoddami and colleagues divided 30 elementary teachers with
MTD into three types of therapy groups: voice facilitating techniques (VFT), manual circumlaryngeal therapy (MCT), and a combination of these two approaches (VT). The results suggested
that all three approaches were effective for these teachers, with the combination of VFT and MCT
being the most effective.
Ventricular Dysphonia
Ventricular dysphonia, sometimes known as dysphonia plicae ventricularis, refers to the pathological interference of the false vocal folds during phonation. Sataloff (2005) describes ventricular
dysphonia as phonation using false vocal fold vibration rather than true vocal fold vibration, most
commonly associated with severe muscular tension.
Maryn and colleagues (2003) describe four types of ventricular phonation under two broad
headings: compensatory and noncompensatory. The first type, compensatory, is a reaction to true
vocal fold disease (paralysis, true vocal cord surgery, etc.). In the three noncompensatory types,
the vocal folds are capable of normal vibration. Of these, the first type, habitual, is caused by
excessive vocal use; the second type, psycho-emotional, is provoked by physical and psychogenic
tension and distress; and the third type has no known origin and is classified as idiopathic.
Although the first anatomical illustrations of the ventricular (also known as false) vocal folds
were done in 1775 by Santorini (Nasri et al., 1996), their role in phonation was not completely
understood (Arnold & Pinto, 1960). In 1860, Czermak was the first to recognize that involvement
of the false folds in phonation is a pathological phenomenon (Saunders, 1956). Although the
ventricular folds physiologically move with the arytenoid cartilages and are brought together to
assist in glottic airway closure, they do not approximate the median line (covering the true vocal
folds) during normal voice production, and they normally do not participate in vocal vibration
(Nasri et al., 1996). While ventricular dysphonia is most commonly produced by the vibration
CHAPTER 3 Functional Voice Disorders 79
of the approximating ventricular folds, it is often heard when the true vocal folds vibrate in an
abnormal fashion due to the false folds riding or loading them.
Sometimes the ventricular voice becomes the substitute voice of patients who have had resection due to severe disease of the true folds (such as cancer, severe recurrent respiratory papilloma,
or large polyps). The ventricular voice is usually low pitched because of the large mass of vibrating
tissue of the ventricular bands (as compared to the smaller mass of vibrating tissue of the true
folds) or from the combined mass of the true and false vocal folds. In addition, the voice has
little pitch variability and is therefore monotonous. Finally, because the ventricular folds have
difficulty in making a good, firm approximation for their entire length, the voice is usually quite
hoarse and may also be breathy. This combination of low pitch, monopitch, and hoarseness makes
most ventricular voices sound very unpleasant. If no persistent true cord pathology continues to
force patients to use their ventricular voices, this disorder usually responds well to voice therapy.
Sometimes, however, hypertrophy (enlargement) of the ventricular folds is present, which makes
their normal full retraction somewhat difficult. Ventricular phonation is impossible to diagnose
by the sound of the voice alone (Maryn et al., 2003). Laryngoscopic examination during phonation shows the ventricular folds moving laterally toward one another, covering (partially or
completely) from view the true folds that lie below (Alipour et al., 2013; Bailly et al., 2014; Nemetz
et al., 2005).
In some cases of ventricular dysphonia, a special form of diplophonia (double voice) can be
heard, which results when the true and false vocal folds vibrate because the false vocal folds are
sitting atop the true folds (loading the true folds with the ventricular folds) (Aichinger et al.,
2017). That is, the ventricular folds often do not vibrate as a sole source of sound but load the true
vocal folds and alter the sound they produce. Identification and confirmation of which vibrating
structures the patient is using for phonation can be made by flexible or rigid laryngostroboscopy
(McFarlane et al., 1990). In ventricular phonation, the true vocal folds are slightly abducted, with
the ventricular folds in relative approximation and very possibly resting on the true vocal folds. In
normal phonation, the opposite relationship between the true and ventricular vocal folds occurs;
that is, the true vocal folds are adducted, and the ventricular folds are abducted. Once ventricular
phonation is confirmed by laryngoscopy, any physical problem of the true vocal folds that might
make normal phonation impossible should be eliminated. For example, when one true fold is
paralyzed or is too stiff (due to postsurgical scarring) to vibrate, the false fold is brought into the
phonatory act. Figures 3–1 and 3–2 show ventricular fold vibration secondary to a prolapsed right
ventricle (protrusion of ventricular tissue into the laryngeal lumen between the true and false vocal
folds). Note how the voice facilitating approach of inhalation phonation (see Chapter 7) decreases
the impingement.
We have known ventricular phonation to become habituated after a bout of flu when the true
vocal folds were too swollen to vibrate. Ventricular fold phonation in such cases is a compensation technique used by the patient to generate a form of phonation. It is usually not the best
compensation for the problem and is generally responsive to voice therapy, such as inhalation
phonation, pitch elevation, or breathy voice onset (see Chapter 7). In those rare cases where voice
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therapy alone is not effective in eliminating ventricular phonation, treatment options include
pharmacological therapy (injection of anesthetics or botulinum toxin) (Kendall & Leonard, 1997;
Theodoros et al., 2007) and surgery (Friedrich et al., 2010).
FI GUR E 31 . Ventricular fold
phonation. Prolapsed right
ventricle in a 75-year-old trumpet
player. Voice is low in pitch,
hoarse, and breathy due to the
ventricular (false) vocal fold
impinging on the true vocal fold.
80
FIG URE 3 2. Intervention using
inhalation phonation. With the
voice facilitating approach of inhalation phonation, the ventricular
(false) vocal fold impinges less on
the true vocal fold.
CHAPTER 3 Functional Voice Disorders 81
Benign Pathologies Resulting From Excessive Muscle Tension Disorders
Vocal Fold Nodules
Vocal fold nodules are the most common benign lesions of the vocal folds in both children and
adults (Almero et al., 2021; Lee et al., 2022; Birchall & Carding, 2019; Zhukhovitskaya et al.,
2015). They are caused by continuous abuse of the larynx and misuse of the voice. Nodules are
generally bilateral, whitish protuberances on the glottal margin of each vocal fold, located at the
anterior-middle third junction. However, McFarlane and Watterson (1990) demonstrate in their
study of 44 cases of vocal nodules that there can be considerable variation in the size, number, and
location of vocal nodules in both children and adults. Of the variations that can be observed and
documented in vocal nodules, perhaps the most striking is that nodules can range from singular
to two, three, and even four (quad nodules) in number. While these variations are interesting,
two important facts remain. First, nodules are responsive to voice therapy, and second, the classic
description of number and location (juncture of anterior and middle third) is generally accurate
(see Video 3–1). Vocal nodules are typically characterized as bilateral, midmembranous vocal fold
lesions of the basement membrane zone and the superficial layer of the lamina propria (Martins
et al., 2010; McFarlane & Von Berg, 1998; Rosen, Lombard et al., 2000). In the early stages of
development, the nodule is soft and pliable. With continuous phonotrauma, the nodule becomes
more fibrotic and may be slightly larger, or it may become more focused, smaller, and harder.
Video 3–1. This video shows a comprehen-
sive approach to vocal nodules in a young
male patient. The clinician supplements
intervention by using visual examples of
different loudness levels; demonstrates good
vocal production and then directs the patient
to imitate; and finally, asks the patient to
reflect on the level of vocal loudness that
would be appropriate for various scenarios
in his life. Again, appreciate how the patient
becomes a full partner in his own voice
intervention. Grand Rounds: How do vocal
nodules develop?
As the bilateral nodules approximate one another on phonation, there is usually an open
glottal chink anterior and posterior to the nodule contact point, which results in a glottal hourglass
figure. This open glottal chink (produced by the nodules coming together in exact opposition to
one another) results in a lack of complete vocal fold adduction.
This faulty approximation leads to breathiness in the voice and air wastage, the perception
of which increases as nodule size increases (Shah et al., 2005, p. 93). Also, the increased mass
of the vocal folds as a result of the nodules contributes to the perception of a lower habitual
speaking pitch and hoarseness, which again is positively correlated with nodule size (Shah etal.,
82 The Voice and Voice Therapy
2008, p. 23). This leads to a breathy, flat kind of voice that often seems to lack appropriate
resonance. Patients complain that they need to clear their throat continually and often perceive
that they have excessive mucus or something on the vocal folds (Bonilha et al., 2012; Levendoski
et al., 2014). Excessive throat clearing often becomes an identified vocal abuse, which may lead
to further enlargement or further organization and consolidation of the nodules (Leydon et al.,
2009). Typical patients with vocal nodules complain that their voices seem to deteriorate with
continuous voicing; they may start the day with good voices that become increasingly dysphonic
with continuous vocal usage. With prolonged speaking and singing, perhaps coupled with vocal
abuse and misuse, phonation rapidly deteriorates. The findings that nodules are associated with
reduced vocal amplitudes due to air wastage may also be associated with hyperfunctional attempts
to generate a louder voice (Conserva et al., 2022).
Vocal nodules in children before puberty are more common in boys. In their review of 254
cases of children with vocal nodules, Shah and colleagues (2005) reported that nodules were
most commonly observed in males between the ages of 3 and 10 years. This is consistent with
findings by Aoki and colleagues (2021), who reported nodules primarily in boys ages 7 to 12 years.
Laryngopharyngeal reflux disease was present in one-fourth of the cases reviewed by Shah and
colleagues, and in three-fourths of the cases there was evidence of vocal hyperfunction (p. 903).
As boys get older, there is less evidence of nodules, with adolescent and adult females showing
the highest prevalence of nodules (Herrington-Hall et al., 1988; Nagata et al., 1983). However,
in discussing the fact that vocal fold lesions are more common in women than men, Koufman
and Belafsky (2001) suggest that differences in incidence may be multifactorial and related to
hormonal, anatomical, inflammatory, and aerodynamic (Gramuglia et al., 2014) factors. Shah
and colleagues (2007) and Nuss and colleagues (2012) have developed reliable scales for grading
the size of vocal nodules in children, which should facilitate objective analysis of outcomes when
studying and following pediatric patients with vocal nodules.
Small nodules and recently acquired ones can be successfully treated with voice therapy
(Alegria et al., 2020; Leonard, 2009; Ruotsalainen et al., 2007), which is usually the first choice
of treatment by SLPs (Signorelli et al., 2011). Holmberg and colleagues (2001), reporting on
voice therapy success with 11 adult females with vocal nodules, found a significant decrease in
severity of dysphonia following behavioral voice therapy. In addition, videolaryngostroboscopy
at the end of therapy showed that the nodules had decreased in size and that edema was reduced
for nearly all clients. Alegria and colleagues employed three acoustic parameters to assess vocal
improvement after voice therapy for vocal nodules. Their meta-analysis included 147 patients with
vocal nodules. The authors found statistically significant improvements in fundamental frequency
and jitter and a nonstatistically significant effect on shimmer (Alegria et al., 2020). McFarlane
and Watterson (1990) reported success in 44 cases presenting both large and small nodules in
children and adults, and in both singers and nonsingers. They also document with pictures the
before-and-after therapy conditions of the larynx of a child and an adult singer. The nodules were
completely resolved via voice therapy.
Boone (1982) developed a four-point program for adults with vocal nodules that focuses on
identifying abuse-misuse; reducing the occurrence of such abuse-misuse; searching with the patient
for various voice facilitating approaches that seem to produce an easy, optimal vocal production
(see Chapter 7); and using the voice facilitating approach that works best as a practice method.
Although we strongly recommend voice therapy as the primary treatment for nodules, we also
CHAPTER 3 Functional Voice Disorders 83
acknowledge that larger nodules and long-established ones may be treated by surgery, followed
by a brief period of complete voice rest and then voice therapy (Pedersen & McGlashan, 2001).
However, a trial period of voice therapy is an appropriate conservative course of treatment prior
to surgery for nodules in nearly all cases (Mansuri et al., 2018; Pedersen et al., 2004). Because
voice therapy must follow if surgery is the treatment, then one might ask, “Why not begin with
a period of voice therapy?” It is not unusual for new nodules to reappear after surgical removal
of nodules or injection of steroids into the nodules (Lee et al., 2011; Wang et al., 2015, 2017).
Unless the underlying hyperfunctional vocal behavior is identified and reduced, vocal nodules have
a stubborn way of reappearing (Ferrand, 2012).
It is generally accepted that nodules result from continuous and prolonged traumatic use of
the voice (phonotrauma). In addition, a growing body of literature suggests that certain personality traits may predispose some children to engage in phonotraumatic voice use. Green (1989)
found that children with vocal nodules demonstrated more aggressive behaviors, acting out, and
disturbed relationships with peers compared to children with normal voices. This finding was
not supported, though, in a study by Roy (2011), who reported no evidence of amplified aggressiveness or immature behavior in children with vocal nodules compared to children with normal
voices. Roy did report, however, that children with nodules use their voice for socializing more so
than those children with normal voices. Yet, Krohling and colleagues (2016) gathered data from
reports of parents of children with voice disorders and found a slight increase in potential risk for
the development of emotional and/or behavioral issues. More recently, Lee, Roy, and colleagues
(2022) found that personality traits such as extraversion, impulsivity, and emotional reactivity
(among others), may predispose some children toward phonotrauma. This predisposition may
hinder positive and/or sustained response to voice therapy; thus, it is important that voice clinicians recognize a child’s personality type, including any psycho-behavioral characteristics, early
in the assessment, because these may very well contribute to ongoing phonotrauma and vocal
nodules. For a full investigation into personality in children with vocal nodules, see Lee, Roy, and
colleagues (2022).
Although symptomatic voice therapy has been effective in reducing or eliminating vocal
nodules, young patients with vocal nodules often require strong counseling psychological support
by the voice clinician (Andrews & Summers, 2002). Merati and colleagues (2008) studied
voice-related quality of life of children with voice disorders and reported that it is significantly
impaired in those with vocal nodules, particularly in the social-emotional and physical-functional
domains. The effect of vocal nodules on children may depend on the age of the child. Verduyckt
and colleagues note that parents and children themselves may understand, qualify, and report
symptoms of a voice disorder differently (2011). Connor and colleagues (2008) assessed the
attitudes of children with dysphonia across four age groups (toddler: ages 2 to 4 years; preschool:
ages 5 to 7 years; school age: ages 8 to 12 years; and adolescent: ages 13 to 18 years) and found that
as the children got older, the social and emotional handicap became greater as a result of having
vocal nodules and other forms of dysphonia. Providing therapy to children with vocal nodules is
important because children do not simply “outgrow” the problem. De Bodt and colleagues (2007)
questioned 91 adolescents who were diagnosed with nodules in childhood and found that 21%
had voice complaints persisting into postpubescence, with a statistically significant difference
between boys and girls. Nodules were still present in 47% of the girls and 7% of the boys, with
significantly higher long-term risks for dysphonic girls with allergy.
84 The Voice and Voice Therapy
Vocal Fold Polyps
Vocal fold polyps are one of the most common subtypes of benign vocal fold lesions (Kenny etal.,
2023). A vocal fold polyp is a focal abnormality of the superficial lamina propria, usually at the
same site where vocal fold nodules occur. This lesion, however, is thought to be slightly deeper
within the superficial lamina propria. Vocal fold polyps are usually unilateral, but a reactive lesion
is often found on the vocal fold immediately across from the polyp. Unlike vocal nodules, which
result from continuous or chronic vocal fold irritation, polyps are often precipitated by a single
vocal event. For example, a patient may have indulged in excessive vocalization, such as screaming
for much of an evening, which produced some hemorrhaging on the membrane at the point of
maximum glottal contact. Such hemorrhagic irritation eventually results in formation of either a
translucent, fibrotic, hyaline, hemorrhagic, or mixed polyp that adds mass to the vocal fold. Once a
small polyp begins, any continued phonotrauma will irritate the area, contributing to its continued
growth (Jeong et al., 2014; Nakagawa et al., 2012; Petrovic-Lazić et al., 2009).
Kleinsasser (1982) reviewed 900 cases of polyps and developed a description of vocal fold
polyps, their formation, and their treatment. Three-fourths of patients were male and one-fourth
female, with the mean age of both being around 40 years. In 90% of the cases, polyps were
unilateral; in 5%, they were bilateral; and in 5%, they were both multiple and unilateral. Over
80% of patients smoked; other contributing factors included inhaled allergens and irritants. Kenny
and colleagues identified laryngopharyngeal reflux as an additional contributing factor (2023). As
described by Rubin and Yanigisawa (2014), the gross appearance of vocal fold polyps varies: they
may be reddish or white, large or small, and sessile (broad-based) or pedunculated (narrow-necked
on a stem). Most are small and sessile, however. As polyps become more advanced, they become
increasingly more pedunculated. Polyps are associated with other vocal fold pathologies in 15%
of cases (Bouchayer & Cornut, 1991).
Kleinsasser (1982) further described vocal fold polyps as being responsive to surgery. Surgery
can sometimes be performed in the office as opposed to the hospital (Woo, 2006) and has been
found to be most effective when followed by vocal rest (Kaneko et al., 2017). The goal of vocal
fold surgery is to preserve as much superficial lamina propria as possible and to disrupt the glottal
margin as little as possible. Thus, microflap surgery designed to raise a flap of mucosa, remove a
benign lesion via suction, and then lay the flap back down on the vocal fold is common (Courey
et al., 1997; Hirano et al., 2008). Another technique, epithelial cordotomy, involves microdissection between the polyp and the residual normal superior lamina propria while disturbing as little
of the epithelium as possible (Benninger, 2000; Hochman & Zeitels, 2000). For a full review of
clinical trials including various phonosurgical approaches to VFPs conducted between 1999 and
2022, see Latoszek and colleagues (2023). These phonosurgeries include cold steel, pulsed dye
laser, CO
laser using microlaryngoscopy, KTP2 (potassium-titanyl-phosphate) laser and diode
2
laser, among others.
Cohen and Garrett (2007) examined the utility of voice therapy alone for patients with vocal
fold polyps and cysts. In their study of 57 patients, almost half experienced an improved voice.
Factors such as length of dysphonia, smoking status, allergy, and gastroesophageal reflux treatment
were not associated with treatment outcome. They also found that the type of polyp was associated
with voice improvement. Specifically, patients with translucent polyps were more likely to experience an improved voice than were those with fibrotic, hyaline, or hemorrhagic polyps. Klein and
CHAPTER 3 Functional Voice Disorders 85
colleagues (2009) followed 13 patients with polyps of varying sizes who underwent voice therapy
only while waiting for an optimal time for surgical polyp removal. They reported that slightly
more than half the patients experienced spontaneous resolution of their polyps, in all cases within
4 to 7 months. Patients who were more likely to experience resolution of the polyp were women
with small polyps. Nakagawa and colleagues (2012) compared the outcomes of voice therapy only
versus surgery for polyp removal. Of the 13, two patients were treated with voice therapy only,
nearly half experienced complete polyp disappearance at a 5-month follow-up visit, and nearly
one-fourth showed polyp shrinkage at a 4-month follow-up visit; all were satisfied with the outcome
in terms of their voice. Patients who were more likely to experience resolution of the polyp were
women with small polyps and a shorter duration of voice symptoms (3 weeks versus 14 weeks for
those who did not experience polyp resolution or shrinkage). More recently, Latoszek and colleagues
(2023) investigated the efficacy of three different treatments to address vocal polyps: voice therapy
only, phonosurgery, and a combination of both. Results revealed that all three treatments were
effective in eliminating the vocal fold polyps, with the combined treatment of voice therapy and
phonosurgery providing the greatest improvements in hoarseness, jitter, shimmer MPT, and the
physical subscale of the VHI 30. The VHI is discussed in detail in Chapter 6.
Taken together, these findings suggest that conservative treatment (that is, voice therapy only)
may be warranted as a first course of treatment for those patients who are willing to “wait it out” in
hopes of avoiding surgery. Nevertheless, a combination of conservative therapy and phonosurgery
has yielded positive results. Jeong and colleagues (2014) suggest that successful management
of vocal fold lesions depends on prudent patient selection and counseling, ultraprecise surgical
techniques, and vocal rehabilitation using various voice facilitating approaches (see Chapter 7).
Reinke’s Edema
Chronic diffuse swelling of the superficial lamina propria of the vocal fold is known as Reinke’s
edema (Thibeault, 2005). This edema is also referred to as polypoid degeneration of the vocal
fold (Martins et al., 2009). Within the lamina propria (see Figure 2–16), the collagen architecture
is disrupted, and a thick, gelatinous, fluid-like material develops in Reinke’s space (Sakae et al.,
2008). There may also be an altered number and size of microvessels within the subepithelial
space (Sugumaran et al., 2011). Reinke’s edema is usually bilateral but can be more pronounced
on one side. It is associated strongly with smoking, frequently with chronic vocal hyperfunction,
and occasionally with laryngopharyngeal reflux (Kamargiannis et al., 2011; Koszewski et al., 2015;
Marcotullio et al., 2002). Branski and colleagues (2006) suggest that Reinke’s edema may result
from prolonged exposure to inflammatory stimuli, accompanied by abnormal healing.
Reinke’s edema and related forms of vocal fold thickening are conditions often affecting the
anterior two-thirds of the glottal margin (the vibrating portion of the vocal folds) or the membrane
covering the muscular portion of the vocal fold. This is in contrast to vocal nodules and polyps,
which usually affect a localized area of the vocal fold. The more extensive the condition, the more
likely it is that the voice will be affected, and related symptoms will persist (Martins et al., 2017).
Dysphonia resulting from Reinke’s edema and related conditions is often responsive to voice
therapy. Success from voice therapy is highly dependent on eliminating the cause of the problem,
such as smoking. A behavioral program that promotes easy and proper use of the vocal mechanism
(vocal reeducation), along with reducing the source of the irritation (such as eliminating an allergy,