Nonsurgical Treatment of Voice Disorders

7.1 Fundamental and Related Chapters

Please see Chaps. 2, 4, 5 and 8 for further information.

7.2 Introduction
Many voice problems do not require surgery if properly identified and treated. Though phonosurgical management of
certain vocal pathologies is critical, many voice disorders are treated effectively by non-surgical means. This chapter
gives a brief overview of several categories of voice disorders that are primarily treated without surgery.

7.3 Surgical Indications and Contraindications

Four to 10% of otolaryngologic visits are related to gastroesophageal reflux disease-related laryngeal complaints. Up to
50% of voice disorder patients may have coexisting laryngopharyngeal reflux (LPR). LPR manifests in many ways: sore
throat, globus, hoarseness, throat clearing, dysphagia, chronic cough, and postnasal drip. The diagnosis of LPR is based
on patient history and laryngeal signs noted during laryngoscopy. These include edema and erythema of the larynx,
pseudosulcus (infraglottic edema), Reinke’s edema, interarytenoid mucosal changes, contact ulcers, granulomas, and
posterior pharyngeal mucosal cobblestoning. It has been associated as well with paradoxical vocal fold motion disorder
and asthma. It has also been linked to the development of leukoplakia and potentially, laryngeal cancer. Studies have
alluded to the frequent association of LPR and/or gastroesophageal reflux disease (GERD) with subglottic stenosis in
adults and children. It is critical to treat LPR after any type of airway reconstruction. Symptoms can be quantified by
means of the Reflux Symptom Index and findings by the Reflux Finding Score. It is felt that both the acid and pepsin
contribute to the inflammation associated with LPR and/or GERD. The gold standard in diagnosis remains the 24-h
doubleprobe (esophageal and pharyngeal) pH study. With this study, a reflux event is defined as a 5 second drop in the
intraluminal pH below 4.0. The standard of care for the treatment of LPR is the proton pump inhibitor (PPI), which works
to irreversibly inhibit the proton pumps of the gastric parietal cell. Recent studies have shown that twice-a-day therapy
appears to result in the highest symptom resolution. Most clinicians and studies support duration of treatment of at
least 4–6 months. It takes several months for affects to be noted by the patient, so patients typically need
encouragement to remain compliant with their medication. Several controversies in the treatment of LPR include the
strength of association between cough and LPR and duration of treatment. An additional point of contention is the use
of histamine type 2 (H2RA) receptor antagonists in combination with PPIs. A few studies have confirmed that the H2RAs
do not add any additional efficacy to treatment; however, many clinicians have noted significant improvement in LPR
control with H2RAs, especially when given at night for the treatment of nocturnal acid breakthrough.

7.4 Vocal Fold Granuloma

Vocal fold granulomas (specifically nonintubation related) are notoriously recalcitrant to surgical therapy when
underlying causative factors (such as LPR) are not controlled. Most vocal fold granulomas are located in the posterior
third of the vocal fold either unilaterally or bilaterally. When granulomas occur postsurgically, they can occur anywhere
an operative site exists. LPR plays an important role in the development of granulomas as do phonotrauma and trauma
secondary to endotracheal intubation. Intubation granulomas are more common in women, presumably because their
smaller larynx is more prone to trauma from the endotracheal tube. One study found that of patients with LPR, up to
75% responded to clinical treatment with PPIs; however, 21% demonstrated recurrence. The other treatment options
for granulomas are voice therapy and botulinum toxin type A injection to the thyroarytenoid muscle. The latter causes a
temporary paresis of the vocal fold to reduce extensive interarytenoid contact. Vocal fold granulomas also often occur
(and recur) due to an underlying glottal insufficiency that may not be recognized by the treating physician. Excessive
vocal fold closure pressure is applied to the arytenoids in an attempt to compensate for the glottal insufficiency,
resulting in vocal fold granuloma formation or recurrence. Treatment for vocal fold granuloma due to glottal
insufficiency involves vocal fold augmentation and/or medialization (see Chaps. 31, ”Vocal Fold Augmentation via Direct
Laryngoscopy”; 38, “Silastic Medialization Laryngoplasty for Unilateral Vocal Fold Paralysis”; and 39, “GORE-TEX®
Medialization Laryngoplasty”).

7.5 Infectious and Inflammatory Disorders

Fungal laryngitis is increasingly recognized as a cause of laryngitis. The widespread use of steroid based inhalers for the
treatment of obstructive pulmonary disease has been a major contributor to the increase in fungal laryngitis incidence.
Fungal laryngitis may be mistaken for leukoplakia. Clinical appearance of whitish plaques surrounded by erythematous
mucosa is characteristic. Predisposing factors apart from inhaler use include radiotherapy, prolonged antibiotic use,
smoking, and immunosuppression. Dysphonia may occur in 5–50% of patients using inhaled steroids. There appears to
be a dose-dependent dysphonia in 34% of patients treated with beclomethasone dipropionate or budesonide when
administered via pressured metered dose inhalers. The most common organism implicated is Candida, but the presence
of Aspergillus, Blastomyces, Histoplasma, and Coccidioides has also been documented in cases of fungal laryngitis.
Diagnosis is based on demonstration of fungal spores, hyphae, and/or pseudohyphae within upper epithelial layers of
the laryngeal mucosa by culture or biopsy, both of which are done via laryngoscopy or office endoscopy. However, often
the disease is treated clinically based on the characteristic findings. Inhalers used with a spacer decrease laryngeal
deposition of the medication and can help with reduction or complete elimination of the offending agent. Treatment of
fungal laryngitis rests on removal of the offending steroid when possible and antifungal medication. If the organism
persists, then treatment with an oral conazole agent for 3–4 weeks is commenced. Current standard of care, however, is
use of an oral conazole medication as initial treatment especially in the immunocompromised patient. Chemical
laryngitis—specifically steroid inhaler laryngitis—is another common cause of dysphonia in the inhalerusing patient.
Hoarseness is the most frequent local side effect of steroid inhalers. Several factors may contribute to this chemical
irritation: the steroid “its preparation, the drug carrier” the type of inhaler device, mechanical irritation due to cough,
inflammation of the upper airways and surrounding irritating triggers such as smoke. One study noted the following
mucosal changes in patients with inhaler-related dysphonia: vascular lesions such as dilated blood vessels, capillary
ectasias and varices, and “areas of thickening, irregularity, and leukoplakia.” These changes appear to improve after
cessation of the steroid inhaler. In addition, some have attributed dysphonia secondary to steroid inhaler use to steroid
myopathy, as both vocal folds appear atrophic and glottal closure is incomplete. Actual muscle bulk change due to
steroid inhalers is controversial and not supported by scientific evidence. Some findings can overlap with those of LPR;
therefore, LPR should be optimally controlled in conjunction with reduction or discontinuation, when possible, of the
inhaler. Autoimmune disorders are relatively rare but several of these have effects on the vocal folds and subglottis.
Rheumatoid arthritis (RA) affects 2–3% of the adult population, and 25–53% of patients have involvement of the larynx.
The main two manifestations of RA at the level of the vocal folds are cricoarytenoid arthritis and rheumatoid lesions of
the vocal fold. Systemic treatment of RA is favored to treat rheumatoid nodules; if they persist and cause a functional
voice problem, then surgery is indicated. Vocal fold hypomobility associated with cricoarytenoid (CA) arthritis has
resolved in some reports with systemic treatment and possibly steroid injection into or near the CA joint. Systemic lupus
erythematosus (SLE) infrequently manifests itself in the larynx but can be associated with laryngeal edema in up to 28%
of patients and vocal cord paralysis in 11% of patients with SLE. Wegener’s granulomatosis (WG) is a rare disease that
involves principally three anatomical areas: the head and neck, lower respiratory tract, and the renal system. The cause
of WG is unknown, but the disease is pathologically described by three findings: necrosis, granulomatous inflammation,
and vasculitis. Signs associated with laryngeal involvement include wheezing or stridor, dyspnea, and dysphonia.
Diagnosis is based on a blood test for the identification of antinuclear cytoplasmic antibody (ANCA) and specifically c-
ANCA, which is found in 90% or more of patients with active WG. Subglottic stenosis is a major concern; the vocal folds
proper are usually not involved. Systemic treatment incorporates use of corticosteroids and other immunosuppressive
drugs, especially cyclophosphamide. If the stenosis is critical however, patients go on to either endoscopic or open
surgical treatment, with or without tracheostomy depending on severity of the disease (see Chaps. 6, “Glottic and
Subglottic Stenosis: Evaluation of Upper Airway Disorders”; 29, “Subglottic Stenosis”; 45, “Glottic and Subglottic Stenosis:
Laryngotracheal Reconstruction with Grafting”; and 46, “Glottic and Subglottic Stenosis: Cricotracheal Resection with
Primary Anastomosis”). The disease state should be under good medical control before performing surgical procedures
for airway stenosis. Laryngeal amyloidosis is a rare and benign idiopathic disease, which presents as a primary disease or
secondary with other disease processes. It comprises 0.2–1.2% of all benign tumors. The disease is indolent and when
found in the larynx, can cause slowly progressive dysphonia and dyspnea; airway symptoms in general appear to
predominate. When present in a secondary form, it can be associated with multiple myeloma, medullary thyroid
carcinoma, and small cell carcinoma. Amyloid deposits or lesions are described typically as “firm, nonulcerating, orange-
yellow, to gray epithelial nodules.” Definitive diagnosis is based on histopathologic presence of amyloid fibrils in a
twisted β-pleated sheet patter with affinity for Congo red dye. The underlying condition in the secondary form requires
treatment; however, systemic treatment frequently may not eliminate the amyloid deposits. When the airway or voice
is compromised, surgical intervention is warranted. Serial laser laryngoscopy is often effective at controlling symptoms.
More advanced disease may require laryngofissure with partial or total laryngectomy. Primary (localized) and secondary
(systemic) amyloidosis are distinguished based on physical exam (for tender bones, heart failure, hepatosplenomegaly,
lymphadenopathy), blood/serum and urine testing, chest and bone radiography, abdominal subcutaneous fat aspiration,
CT exam of suspicious parts of the body, and rectal biopsy.

7.6 Neurologic Disorders

7.6.1 Spasmodic Dysphonia
Spasmodic dysphonia (SD) is a focal dystonia characterized by vocal task specific action or intention induced spasms.
Dystonias in general are disorders of central motor processing, and SD can be found in conjunction with other disorders,
such as Meige’s syndrome, although typically it is isolated to the larynx. There are three classic types of SD. Adductor SD
(1) comprises 80% of patients with the disorder. Abductor SD (2) and patients with both adductor and abductor activity,
mixed SD (3), comprise the rest of disease population. Adductor SD is marked by a “strained-strangled” speech pattern
caused by premature and excessive glottal closure, whereas abductor SD is marked by breathy speech breaks and an
overall hypophonia due to inappropriate glottal opening during speech. SD typically presents in a female patient in her
mid-30s, and if it has been present for some time, many patients develop compensatory changes, which may mask the
true diagnosis. Patients may not demonstrate speech breaks during singing or laughing tasks, and patients find
worsening of symptoms when under psychological stress. Diagnosis rests primarily on auditory-perceptual evaluation of
connected speech supplemented by flexible nasopharyngolaryngeal examination. Diagnosis can be difficult, as patients
may have associated essential tremor or actually have muscle-tension dysphonia; both disorders can cause voice breaks.
Few if any medications have been successful in ameliorating symptoms of SD. Some patients find that alcohol or
benzodiazepines are helpful to reduce the stress that may be the trigger for SD. The standard of care in the treatment of
SD is injection of the affected muscle(s) with botulinum toxin (BTX), which causes a temporary chemical denervation of
the thyroarytenoid–lateral cricoarytenoid muscle complex in adductor SD and the posterior cricoarytenoid muscle in
abductor SD (see Chap. 35, “Botulinum Toxin Injection”). Prior to this, recurrent laryngeal nerve section was performed;
however, recurrence of symptoms was typical (despite complete nerve section) and the overall voice quality worsened.
Voice therapy can be used as adjunctive therapy to treat compensatory behaviors or assist in differentiating SD from
muscle-tension dysphonia. Some newer surgical techniques have been developed but no long term data is available and
thus are presently experimental and not validated.

7.6.2 Essential Tremor

Essential tremor is the most common movement disorder, affecting 0.4–5.6% of those over age 40. However, the
disease also appears to have a bimodal age distribution, with 4.6–5.3% of cases occurring in the first two decades of life.
There appears to be a familial association in 17–100% of individuals transmitted in an autosomal-dominant inheritance
pattern with variable penetrance. Three areas of the body may be involved to varying degrees: head, hands, and vocal
tract. Essential tremor of the voice is seen in 12–30% of patients with essential tremor, and a head tremor in 50%.
Essential tremor of the voice is marked by a regular 4- to 12-kHz frequency oscillation of the affected muscles. Several
drugs have also been associated with tremor production, and Parkinson’s disease is also considered in the differential
diagnosis. Pharmacotherapy, specifically with primidone and propranolol, is employed as first-line treatment but is more
effective for limb-based tremor than voice. Recently, some work has emerged concerning botulinum toxin A injections
for treatment of voice tremor. The difficulty with local treatment, however, is that multiple muscles are involved in voice
tremor (both intrinsic and extrinsic laryngeal musculature), so the benefit of simple thyroarytenoid–lateral
cricoarytenoid muscle complex injection is not nearly comparable to benefit of botulinum toxin A seen in SD treatment.
Medically refractory cases are treated with thalamotomy or deep brain stimulation (DBS); bilateral thalamotomy is
associated with significant vocal side effects such as hypophonia and significant data for DBS in treatment of voice
tremor is pending.

7.6.3 Parkinson’s Disease

Parkinson’s disease (PD) affects nearly 1 million persons in the United States, and in severe forms, leads to considerable
disability. The disease is caused by neurodegeneration within the nigrostriatal tracts of the basal ganglia, a neural center
for motor control, which leads to decreased dopamine release. The hallmark clinical findings are bradykinesia, tremor,
postural instability, and muscle rigidity. Phonatory effects include hypophonia, breathy dysphonia, and vocal tremor. The
voice takes a monotonic quality. Many patients experience dysphagia and dysarthria. One study reported that 87% of PD
patients demonstrated vocal fold bowing. The treatment of the voice component of PD involves a specialized voice
therapy program, Lee Silverman Voice Treatment (LSVT), with or without vocal fold augmentation to improve glottic
configuration and closure. Typically, LSVT is sufficient alone and vocal fold augmentation is not required. Treatment of
PD is pharmacologic using dopamine agonists and medically refractory cases may undergo DBS or pallidotomy. No data
are available currently regarding the effect of DBS on the voice in PD.

7.6.4 Muscle Tension Dysphonia

Muscle tension dysphonia (MTD) is a term used to describe voice disorders that are related to excessive and poorly
regulated laryngeal muscle activity during speech. Many synonyms are used in clinical practice and these include
hyperfunctional dysphonia, muscle misuse, and tension-fatigue syndrome to name a few. The “muscletension”
descriptor has been applied to muscle contraction patterns seen on flexible laryngoscopy of the endolarynx; these are
classified from types I–IV, with type I being very mild constriction with an excessive posterior glottic chink, to type IV, a
concentric closure pattern of the supraglottis. Some of these patterns are seen in other disorders as well such as
adductor SD or even in normal voices and these are not pathognomonic. MTD can present as a primary problem often
associated with post-URI onset, inappropriate pitch use, reflux, or significant voice demands. It can also present in a
secondary form as excessive compensation for glottal insufficiency. Circumlaryngeal massage has been used in
conjunction with voice therapy to assist in reducing laryngeal height, as these patients frequently hold their larynges in
an abnormally elevated position secondary to increased muscular tension. In the most severe or refractory patients,
topical anesthetization of the endolarynx has assisted in decreasing laryngeal tension because of altered sensation and
proprioception. Functional dysphonia or aphonia is a separate term that should be used for psychogenic dysphonia or
conversion disorder. Those with conversion disorder have experienced significant psychological trauma from an event
that causes the aphonia; as such, these patients require intense psychiatric treatment in addition to voice therapy.
“Malingering” or “factitious dysphonia” would be included under this term.

7.6.5 Paradoxical Vocal Fold Motion Disorder

Paradoxical vocal fold motion disorder (PVFMD) is a disorder marked by desynchronized or paradoxical adduction of the
vocal folds during inspiration and/or expiration. As a result, the patient exhibits inspiratory stridor and/or experiences a
sensation of airway restriction. This is often confused with the wheezing of asthma that, in contrast, occurs in the
expiratory phase. Symptoms also include choking, aphonia or dysphonia, and chronic cough. Many terms have been
used in the past to describe this condition, including vocal cord dysfunction, factitious asthma, psychogenic asthma,
irritable larynx syndrome, and episodic paroxysmal laryngospasm. The differential diagnosis is bilateral vocal cord
paralysis, hereditary abductor paralysis, posterior glottic stenosis, or cricoarytenoid joint fixation. PVFMD has many
causes and has been classified into five organic and two nonorganic categories, based on etiology. These include
brainstem compression, severe cortical or upper motor neuron injury, nuclear or lower motor neuron injury, movement
disorder, gastroesophageal reflux, factitious or malingering PVFMD, and conversion disorder PVFMD. When associated
with a conversion disorder, it is seen in primarily high-achieving, perfectionistic adolescents who are usually athletes, as
well as in young female professionals. Patients complain of exercise-induced episodes of airway restriction, irritant-
exposure triggers, or symptoms after a meal. Flow-volume loops have been used to assist in diagnosis; however, both
false positives and false negatives are generated, and there is no consistent pattern. The gold standard in diagnosis is
demonstration of PVFMD during flexible laryngoscopy, which may be seen at rest of after administration of a trigger
(exercise, perfumes, etc). Treatment consists of elimination or avoidance of triggers, including reflux and allergy
treatment, and respiratory retraining therapy administered by the speech pathologist. Any coexisting asthma/reactive
airway disease must also be aggressively treated. Occasionally, psychiatric treatment may also be required. Some have
attempted use of heliox (80% helium, 20% oxygen) to decrease work of breathing, but results have been mixed.

7.6.6 Postviral Vagal Neuropathy

Postviral vagal neuropathy (PVVN) is marked by chronic cough, with or without laryngospasm or PVFMD. The cough is
thought to be a result of altered laryngeal sensitivity such as in post viral neuralgias of other cranial nerves. The trigger
may be an irritant or even palpation of the larynx. Laryngeal electromyography (EMG) is used to confirm subtle
neuropathic findings of paresis. These patients are frequently treated for allergies, LPR, and PVFMD and may be
refractory to treatment. When faced with this situation, treatment with the anticonvulsive agent gabapentin should be
considered, which decreases neural sensitivity. Treatment success ranges from 37.5 to 80%, depending on level of motor
involvement of the neuropathy. A starting dose of 100mg three times a day is recommended, increasing to 300mg three
times a day for symptom control.

7.7 Allergy and Voice Disorders

Allergic diseases can manifest in the larynx in several ways. The classic description is that of laryngeal angioedema, an
acute life-threatening process initiated by exposure to a specific allergen. This process is associated with
immunoglobulin IgE-mediated anaphylaxis, but it is also seen in a non-IgE-mediated anaphylactoid response. Treatment
of this disorder involves immediate airway control and injection of epinephrine with use of steroids and H2 blockers
after the initial episode. Food allergy may lead to milder swelling of the vocal tract with dysphonia and may actually
stimulate or worsen LPR. Avoidance of the triggering allergen and antihistamines are the recommended treatment.
Many patients also suffer from chronic postnasal drip secondary to allergic rhinitis. These patients tend to frequently
clear their throats, which leads to maladaptive laryngeal muscle usage and can lead to the development of vocal fold
lesions. Exposure and allergy to aerosolized irritants can also lead to muscle-tension dysphonia. Mold and volatile
organic compounds (VOC) are the usual suspects. VOCs include alcohols, aldehydes, and ketones. Again, avoidance
and/or removal of the source of the irritant are the mainstay of treatment. Immunotherapy is an important
consideration for treatment of allergy in the professional voice user, as it avoids drying effects of antihistamines in the
endolarynx.

7.8 Medications and Their Effects on Voice

Both allergy and post-URI patients can experience dysphonia related to persistent postnasal drip. Patients also
experience cough due to direct irritation from mucus or because of altered sensitivity of the endolarynx. Severe
coughing can result in phonotrauma, leading to vocal fold hemorrhage and vocal fold lesion formation. As a result, many
over the counter preparations are used for their antitussive and mucolytic properties. Guaifenesin is the most widely
used mucolytic and works best when the patient is well hydrated. Codeine and dextromethorphan are added to many
cold medicine preparations. Tramadol, which is a weak opiate, may have enhanced antitussive properties, without the
significant opioid side effects associated with codeine. Antihistamines again should be used with caution in the
professional voice user with allergy, as the drying effects on the vocal folds can be detrimental. Leukotriene inhibitors,
such as montelukast, and nasal corticosteroids can be used in allergic patients, with less drying. Despite widespread
clinical use of oral corticosteroids for acute dysphonia in the professional voice user, there is minimal scientific literature
concerning this subject. The corticosteroid mechanism of action is to prevent capillary dilation and decrease capillary
permeability, which consequently decreases edema. Typically, oral steroids are used in short bursts, with a tapering
dosage to avoid adrenocortical insufficiency and minimize long-term side effects. Intramuscular use is also reported for
the acute situation. A few studies have shown improvement in objective acoustic measures with use of steroids.
However, if used for a more extended period, corticosteroids can lead to fluid imbalance, systemic muscle weakness and
atrophy, gastrointestinal and neurologic problems, glaucoma, and electrolyte and metabolic disorders, and can lead to
fungal infection. Corticosteroids have been linked to peptic ulcer development; therefore, any patient on long-term oral
corticosteroids should be placed on at least an H2 blocker, preferably a PPI. Many medications have virilizing properties
and should be used with great caution in the professional voice user, or any patient for that matter. These medications,
such as Danazol, have been used for treatment of fibrocystic breast disease and endometriosis. Testosterone injections
have been administered to women complaining of loss of libido or energy and have been reported in female athletes for
enhanced performance. Nonphonatory side effects include acne, hirsutism, weight gain, and hairline recession. Voice
effects including lowering of fundamental frequency, vocal instability with pitch breaks, loss of high frequency vocal
range, and generalized dysphonia. For Danazol, the incidence may be as high as 10% in patients on the medication.
Histologically, water retention in the muscle and fiber hypertrophy are seen. Although some reports have stated that
effects are temporary and cease with discontinuation of the medication, there is potential for permanent voice change
as can be seen in histological studies. This can be particularly damaging to the voice professional, so great caution must
be used when considering prescribing these medications. During the premenstrual period of the menstrual cycle, many
women exhibit pitch lowering secondary to presumed venous dilatation and edema of the vocal folds. Low-dose oral
monophasic contraceptives have been shown to reduce this pitch variability and exhibit less androgenic side effects.
One group of medications that should not be overlooked is herbal remedies. Many have anticoagulant properties and
can predispose a person to vocal fold hemorrhage. These include dong quai (which actually contains coumadin), willow
bark, primrose, garlic in high doses, vitamin E in high doses, gingko biloba, ginger, feverfew, and red root. Some may
have crossreactivity to ragweed: goldenseal, chamomile after long-term use, echinacea, St. John’s wort, yarrow, dong
quai. Some herbal medications also may have hormonal effects, e. g., dong quai may increase effects of ovarian and
testicular hormones. Yam has progesterone-like properties, and licorice root also has progesteronic in addition to
estrogenic effects and can change vocal pitch. Primrose is a natural estrogen promoter, and melatonin acts as a
contraceptive in high doses.
7.9 Vocal Hygiene
A discussion of medical treatment of voice disorders would not be complete without discussing the importance of vocal
hygiene. Elements of vocal hygiene include understanding that medical problems affect the voice, understanding effects
of smoking, alcohol, drugs, hydration and nutrition, vocal stress and vocal exercise, and general vocal hygiene. Vocal
hygiene involves knowledge, avoidance, or reduction of irritants such as gastric juices or tobacco smoke, dehydration
and control of postnasal drip of any cause. The patient should be made keenly aware of the danger of “singing sick,” as
vocal injuries are more likely to occur in the sick singer than in a healthy one. The sick singer should take adequate vocal
rest, fluids, and medical care as needed. Vocal fold hemorrhage and vocal fold lesions are the most significant concerns,
and changing bad habits early in younger performers is critical to long-term vocal health.

7.10 Role of the Speech–Language Pathologist in Voice Therapy

The speech–language pathologist is instrumental in teaching the voice disorder patient about laryngeal anatomy and
vocal biomechanics, which are central to the voice therapy process for many disorders. The speech–language
pathologist with special training in voice disorders is an essential member of the diagnostic and therapeutic team
required for high-quality voice care. The speech–language pathologist specializes in assessing and treating behavioral
issues of the speaking and singing voice. Many patients with dysphonia struggle from a variety of poor behaviors and/or
speaking techniques or inappropriate use of the voice and these problems are all easily treated with the intervention of
the speech–language pathologist, using the overall global term of voice therapy. A detailed description of voice therapy
treatment methods for a variety of dysphonias is outside the focus of this book, but it is essential component of the
treatment of a wide variety of voice disorders is a nonsurgical approach to voice rehabilitation with voice therapy. Thus,
the speech–language pathologist plays a crucial role in all phases of modern voice care (diagnostic, therapeutic, and
rehabilitative).
Key Points
■ Up to 50% of voice disorder patients may have coexisting LPR.
■ Twice-a-day therapy with a proton pump inhibitor results in the highest symptom resolution.
■ Muscletension patterns I–IV seen in MTD are not pathognomonic for this disorder and can be seen in other voice
disorders such as spasmodic dysphonia, and even some normal voices.
■ PVFMD is treated best with multimodality treatment that includes respiratory retraining (voice therapy) and proton
pump inhibitors, as LPR is a common trigger for PVFMD episodes.