Figure 9–1. A 40-year-old women with symptoms of throat clearing, dryness, and change in voice quality. Laryngeal examination showing evidence of laryngitis sicca.

Two: Direct Irritation of the Vocal Folds By Inhaled Particles and Pathogens

The nose carries a thin mucociliary blanket (McB) that is secreted by the nasal and paranasal mucosal lining. The McB acts as a filter to inhaled pollutants and traps undesired pathogens and particles. Loss of this blanket secondary to bacterial infection, inherited diseases such as cystic fibrosis, diseases of the immune system, allergy, or following extensive sinus surgery, can lead to direct inhalation and deposition of these particles or pathogens in the upper and lower respiratory tract. As a result, patients may suffer from change in voice quality, vocal fatigue, and throat symptoms. As review, phonatory changes following inhalation of air pollutants may be the result of three mechanisms: One is the direct deposition of these particles on the vocal folds with subsequent edema and inflammation that may result in alterations in voice quality and phonatory disturbances. The second possible mechanism for the phonatory changes secondary to inhalation of air pollutants is cough. Although this is elicited as a defensive behavior upon direct contact of the inhaled particles with the vocal folds, inadvertently it can lead to vocal fold surface damage, hemorrhage, and mucosal tears. See Figures 9–2 and 9–3. The third mechanism is through the effect of inhaled particles on the lower airway.⁹ The impact of lower airway diseases is discussed more thoroughly later in this chapter.

Three: Alteration in Resonance

The nose and, to a lesser extent, paranasal sinuses, in addition to the oral cavity, pharynx, and pyriform sinus, play a role as resonators. Resonance, defined as amplification of sound by reflection on various structures, is a component of voice production. In professional voice users, resonance is crucial in differentiating one’s vocal timbre. It is also of crucial audibility and a focus of attention in vocal pedagogy and therapy. By using resonance properly, singers embrace the audibility and quality of their voices and learn how to project with minimal glottal effort.¹⁰ The nasality of sound is often referred to as nasalance, an acoustic term that reflects “the ratio of nasal acoustic energy to nasal plus oral acoustic energy” in speech.¹¹ Patients may be stratified as being hyponasal as in cases of nasal polyposis and adenoid hypertrophy, or hypernasal as in cases of velopharyngeal incompetence. It is important to recognize that nasalance may vary with different languages, dialects, and with the ratio of vowels to consonants in a sentence.^12–14 Not surprisingly, nasal and paranasal sinus surgery can impact speech and vocal characteristics. In a study by Hosemann et al on the impact of endoscopic sinus surgery on voice, 6 out of the 21 patients with sinusitis who had surgery had noticeable change in voice quality. More so, there was a decrease in the bandwidth of the formants of vowel /a/ postoperatively. This effect was more pronounced in those who had total ethmoidectomy and bilateral surgery compared with those who had minor disease and had surgery on one side only.¹⁵ Similarly, the study by Chen et al on the effect of sinus surgery on speech using voice recording before and one month after surgery, reported significant effect on nasality and on the acoustic signal in operated patients. There was a decrease in the nasality for the high vowel /i/ and an increase for the non-high vowel /ae/, which were commensurate with the spectral changes observed.¹⁶

Four: By Affecting the Lower Airway

The coexistence of paranasal sinus disease and lower airway disease, often referred to as the “unified airway disease,” as in patients with allergy and or asthma, has been an issue of investigation for many decades. The pathogenic relationship has been based on many mechanisms, perhaps the most important of which is postnasal drip with subsequent seeding of inflammatory and infectious secretions into the lower airway. The continuous postnasal discharge, swept posteriorly by the ciliary action of the nasal mucosa, may itself act as an irritant and as a source of infection to the larynx and lower airway. Other suggested mechanisms include presence of paranasal cell mediators, the nasal-bronchial reflex, decreased responsiveness of ß-agonist receptors due to infection in the sinuses, and stimulation of extrathoracic airway receptors thus provoking lower airway irritability.^17–19

The pathogenic relationship between sinusitis and asthma has been underscored by the improvement in breathing following endoscopic sinus surgery. The long-term effect of functional endoscopic sinus surgery on asthma was evaluated by Senior et al using a questionnaire that was answered by 72 patients who underwent surgery.²⁰ The follow-up time ranged from 6 to 10.6 years. Of 30 patients who had asthma as a comorbid disease, 27 reported improvement in their asthma, and 74.1% reported a decline in the number of asthma attacks.²⁰ Similarly, a study by Ikeda et al in 15 patients who had endonasal endoscopic sinus surgery, both peak expiratory flow and total intake of glucocorticoid were compared 6 months prior to surgery and 6 months after surgery. There was a marked improvement in the peak expiratory flow in all patients and a reduced need for intake of glucocorticoid in almost half the patients.²¹

Oral Cavity, Oropharyngeal Cavity, and Voice

The oral and oropharyngeal cavities are integral parts of the vocal tract, the shape of which can markedly impact voice quality. Anatomical and pathologic variations in these cavities carry important sequalae on the resonant characteristics of the vocal signal. A review of the literature supports the link between voice and variations in the dimensions of the oral and oropharyngeal cavities.^22–26 In a normal physiologic state, through the position and manipulation of the articulators such as lips, tongue, and jaw, one can tune his or her voice. Protruding the lips for instance can lower all the formants whereas lifting the larynx does the opposite. Similarly, moving the mandible affects mostly the position of the first formant whereas movement of the tongue affects mostly the position of the second formant. Modulating the shape of the laryngopharyngeal complex may also cluster the formants’ energy for a better performance.²² Today with the applicability of real time and dynamic magnetic resonance imaging (MRI) as emerging speech research tools, the interplay between the structures of the laryngopharyngeal complex and voice is better understood. There are more and more reports on the usage of radiologic imaging in the configuration of vocal tract dimensions at various registers. Recently high temporal fidelity with high spatiotemporal resolution in capturing the shape of the vocal tract during speech has been reported.²⁷ Another report by Echternach et al using dynamic MRI on 12 professional singers who were asked to sing the vowel /a/ using an ascending scale and at three different degrees of loudness, articulatory differences such as lip opening, pharyngeal width, and position of the larynx in the vertical dimension, were shown to vary with loudness and pitch. The pharyngeal width varied more with sound pressure rather than with vocal pitch.²⁸

In addition to the length and configuration of the oropharyngeal complex as being determinants of formants’ position and dispersion, the dimensions of the palate are also strongly linked to vocal classification. The study by Marunick et al on nine female singers demonstrated that palatal dimensions, in particular the depth and volume, can assist in stratifying a singer’s voice as soprano, mezzo and alto.²³ Similarly, Macari et al reported that rapid maxillary expansion impacts the first two formants, F1 and F2 for the vowel /a/. The study was conducted on 14 patients who had maxillary constriction and underwent treatment.²⁴ See Figure 9–4. Along the same line of investigation, facial measurements, namely, length and projection of the upper and lower jaw, related to the fundamental frequency and habitual pitch. A significant negative moderate correlation between maxillary and mandibular width and F0 has been reported in a study on 50 subjects. Similarly there is a significant association between F3, F4, and the length of the mandible and maxilla for the vowels /a/, /i/, /o/, and /u/.²³

That strong interplay between the oral cavity, pharyngeal dimensions, and voice is also clearly displayed in numerous reports that relate obesity to dysphonia in the context of variations in the oropharyngeal morphology. Da Cunha et al reported in their investigation of 45 obese patients, a higher prevalence of phonatory symptoms, namely, hoarseness and vocal strangulation compared to non-obese subjects.²⁹ Busetto et al demonstrated an inverse relationship between measurements of the upper airway and several obesity parameters. The cross-sectional area of the pharynx and oropharyngeal cavity correlated negatively with body mass index, waist, hip, and sagittal abdominal diameter.³⁰ Considering the intimate relationship between obesity and pharyngeal morphology, and given the role of this latter in voice production, it stands to reason that obesity as a morbid condition impacts significantly voice, at least at the oropharyngeal level.

Oropharyngeal variations may also cause phonatory changes thru their predisposition to snoring and/or obstructive sleep apnea. In a report on 30 patients who snore versus 30 controls, the prevalence of hoarseness was significantly higher in the snoring group.⁶ This can be attributed to narrowing of the oropharyngeal lumen, thickening of the pharyngeal wall, and/or elongation of the epiglottis.^31,32 Shelton et al reported a direct relationship between the amount of adipose tissue in the vicinity of the pharyngeal airway and the severity of apnea. There was a direct correlation between the volume of adipose tissue and the apnea/hypopnea index.³³ In another study using magnetic resonance imaging, Mortimore et al demonstrated that even nonobese subjects with sleep apnea/hypopnea syndrome have more fat in the upper airway in comparison to subjects of same weight and no history of apnea.³⁴

Similarly, masses of the oral cavity and oropharynx have an effect on voice quality. Affected patients may complain of change in their vocal characteristics, loss of vocal power and range, in addition to impairment in swallowing and breathing. Examples would include patients with enlarged tonsils, vallecular cysts, or hypertrophic lingual thyroid. See Figure 9–5. Orbelo et al reported the case of a 10-year-old boy who presented with dysphonia secondary a congenital lingual thyroid gland. Although the patient had concomitant vocal folds pathology, his voice quality improved following lingual thyroidectomy.³⁵ Similarly Erylimaz and Basal reported a 22-year-old man who presented with dysphonia and dysphagia secondary to a lingual thyroid. Using both the transoral and transhyoid approach, the gland was removed successfully and the patient’s symptoms improved markedly.³⁶

Surgeries that alter the shape and position of the mandible, maxilla, and hyoid bone have also been shown to impact voice and speech. This has been attributed to the subsequent changes in the resonance characteristics of these structures.^37–40 To name a few is the effect of tonsillectomy, or adenoidectomy on voice, exemplified by an increase in F2 /i/ and /a/. Similarly, extirpation of soft tissues such as partial glossectomy can result in a significant increase in F2 and F3.³⁹

Laryngeal Pathology and Voice

The configuration of the vocal tract has a strong impact on voice quality. By mechanism of reflection on its various walls, the vocal signal that originates at the level of the vocal folds is amplified carrying distinctive acoustic features, characterizing one’s vocal identity. By altering the outline and thickness of the vocal tract wall, the position and dispersion of the formants, often referred to as preferred harmonics, are modulated. As a result, any change in the shape of the vocal tract can result in change in voice quality. Roers et al examined the vocal tract morphological changes or differences and their relation to voice classification. In their study on 132 radiologic images, they demonstrated that the length of the vocal tract significantly varied with different voice classification.²⁶

Not only functional variations in the vocal tract configuration are causes of voice disorders, but also systemic and local diseases as well. This has been clearly demonstrated in the literature through the numerous reports on the change in voice quality in patients with inflammatory, benign, and neoplastic laryngeal lesions. The laryngeal manifestations of autoimmune diseases on voice have been thoroughly discussed in Chapter 12 of this book. Another example of laryngeal mass is false vocal fold bulk seen in a patient with laryngocele who may present with change in voice quality and possible airway symptoms. See Figure 9–6.

Laryngoceles are abnormal dilatation of the Morgani ventricle. Etiologies such as congenital malformation, increased intralaryngeal pressure, and/or laryngeal tissue laxity have been suggested.⁴¹ Other causes such as neck surgeries and trauma must be ruled out. Affected patients may be asymptomatic; however, symptoms such as dysphagia, or shortness of breath, in addition to change in voice quality may prevail. In a review by Luzzago et al of 18 cases, hoarseness, airway symptoms, and neck masses were the most common symptoms present in 44% of the cases.⁴² The laryngopharyngeal symptoms are varied due to the extension of the laryngocele internally within the endolaryngeal lumen. Laryngoceles have also been seen in patients with chronic ventricular phonation as reported by Dray et al.⁴³

Laryngeal surgery that results in soft tissue resection can also markedly affect voice quality. The impact of supraglottic laryngectomy on voice in 33 male patients revealed a reduction in the maximum phonation time and fundamental frequency with an increase in the perturbation parameters and noise to harmonics ratio.⁴⁴ Similarly following vertical hemilaryngectomy, there is also worsening of most of the acoustic parameters. In a study by Kim et al on 13 patients treated with vertical laryngectomy, there was a significant difference in the mean flow rate and perturbation parameters in comparison to controls. These phonatory changes were attributed to changes in the supraglottic and glottic configuration, namely, supraglottic voicing, incomplete closure, abnormalities in arytenoid adduction, and blunting of the anterior commissure.⁴⁵ When combined with radiation therapy, laryngeal surgery results generally in worse phonatory results. In a review of the voice and swallowing condition following laser endoscopic laryngeal excision, Jepsen et al has reported poorer outcome in patients who were irradiated.⁴⁶ Nevertheless with the introduction of robotic surgery, vocal dysfunction has been markedly reduced. In a prospective study by Roh et al on 21 patients with early glottic cancer who underwent partial supraglottic resection, the functional voice outcome was not affected.⁴⁷

Obstructive Airway Diseases

Asthma and Voice

Asthma is a worldwide disease with a prevalence of around 8% in adults in the United States.⁴⁸ It is defined as “reversible obstructive airway disease in the absence of an alternative explanation such as heart failure.”⁴⁹ It is characterized by narrowing of the airway with varying degrees of obstruction as a result of bronchial smooth muscle contractions in addition to mucosal inflammation and thickening of the airway secretions. Airflow measurements, namely, reduction in the peak expiratory flow, that is the maximum airflow in the beginning of a forced expiration, is commonly used to make the diagnosis and to follow up on the effect of therapy. An obstructive pattern is invariably observed and can be provoked with the administration of methacholine and reversed with bronchodilators. See Figure 9–7.

The reversible airway obstruction characteristic of asthma lead to a constellation of clinical symptoms of cough, paroxysms of dyspnea, chest tightness, and wheezing. As a result of this impairment in breathing, patients may complain of phonatory symptoms that can be ill defined and prevalent only after vocal loading. Professional voice users in particular, in view of their highly demanding vocal careers, are more susceptible than others to disturbances in their respiratory system. The phonatory symptoms may be more accentuated following prolonged performance, very similar to exercise-induced airway symptoms. This airway hyperreactivity often described as “airway reactivity–induced asthma “is being more and more diagnosed as a cause of vocal fatigue, shortness of breath, and abnormal laryngeal muscle tension patterns observed in singers. The cascade of events starts by hyperventilation while singing, followed by decreased airflow that leads to a compensatory hyperfunctional behavior, that manifests as excessive tension all along the vocal tract starting from the tongue and jaw to the level of the vocal folds.⁵⁰ In addition to the excessive vocal loading, singers are also exposed to occupational hazards such as stage smoke and allergens that may worsen their airway hyperreactivity and promote further the prevalence of phonatory symptoms.

There are quite a few reports in the literature on the phonatory changes and symptoms in patients with asthma. A large population study of 19,330 participants (which included asthmatics and non-asthmatics) were evaluated for subjective dysphonia and the presence of 12 types of organic vocal fold pathologies; out of 616 patients with asthma 7.8% had organic laryngeal lesions versus 7% in the control group. Moreover, 11.3% of those without vocal fold lesions had subjective dysphonia in the asthmatic group compared to 5.5% in the control group.⁵¹ Similarly, in a prospective cross-sectional study by Bhalla et al on 46 asthmatic patients, they found that patients on inhaled corticosteroids had a higher prevalence of pharyngeal inflammation and worse vocal performance compared to those not on inhaled corticosteroids. They were also more likely to experience hoarseness, vocal weakness in addition to cough and throat irritation compared to controls.⁵² Likewise in the study by Dogan et al on 40 patients with mild to moderate asthma, there were both subjective as well as objective phonatory changes compared to age- and sex-matched controls. There was a significant difference in the self-assessment component using the VHI with 40% of asthmatic patients having above normal VHI scores.⁵³ Based on the retrospective study by Mirza et al, all patients who had started on inhaled corticosteroids and bronchodilators developed dysphonia 2 to 12 weeks following the initiation of treatment. The change in voice quality was described as rough with drop in vocal pitch.⁵⁴ In another study by Sellars et al using self-administered voice symptom score and perceptual evaluation in 43 patients with asthma, the median voice score was 26, and in 30% of the cases the (GRBAS) score was above one. It is worth noting that there was a significant association between the dose of inhaled corticosteroids and the GRBAS overall grading score.⁵⁵ In a cross-sectional controlled study by Hamdan et al on 50 subjects (31 asthmatic and 19 controls), the prevalence of dysphonia was significantly higher in asthmatic patients compared to controls. On perceptual evaluation, the overall grade of dysphonia, asthenia, and straining were also significantly higher.⁵⁶

The aforementioned subjective as well as self-perceived phonatory changes in asthmatic patients are invariably substantiated by abnormal findings on acoustic analysis. Dogan et al in his evaluation of voice quality in asthmatic patients, reported a significant difference in the acoustic parameters compared to controls. Asthmatic women had significantly higher perturbation parameters, namely, jitter and shimmer, and asthmatic men had significantly higher shimmer compared to controls of the same gender. There was also a significant difference in the noise-to-harmonic ratio value between female asthmatic patients and controls.⁵³ This increase in the intensity perturbation parameter has been corroborated in numerous other studies.^52,56,57 In a study by Lavy et al on 22 asthmatic patients using inhaled steroids, cycle-to-cycle irregularities were reported in almost 40% of the cases and maximum phonation time was reduced in more than two-thirds of the patients. In another prospective cross-sectional study by Bhalla on 46 patients with asthma, those on inhaled corticosteroids had significantly higher values for the acoustic perturbation parameters and higher closed-phase quotient scores.^52,57

In addition to the phonatory and acoustic changes described above laryngeal abnormalities are seen as well. The prevalence of laryngeal movement disorders and vocal fold abnormalities is higher in patients with asthma compared to controls. In the study by Sellars et al on 43 asthmatic patients, 26 had either a functional or organic laryngeal abnormality. Mild and moderate laryngitis, defined as diffuse edema and redness of the glottis region, were the most common laryngeal findings. The most common functional laryngeal abnormalities observed were the presence of a glottic chink and false vocal fold phonation.⁵⁵ The laryngeal pathologies were mostly present in asthmatic patients receiving corticoid steroid inhalers. Based on a retrospective study by Mirza et al on 10 patients who were started on corticosteroids inhalers and bronchodilator therapy, vocal fold changes in the form of mucosal plaques, mucosal thickening, hyperemia, dilated vessels, capillary ectasias, and free vocal fold edge irregularities were reported.⁵⁴ In the study by Dogan et al, posterior laryngitis was present in 33 patients out of 40 asthmatic patients, a finding that was attributed to excessive throat clearing, cough, and possible irritation from refluxate material.⁵³ Similarly, in the study by Bhalla on 46 asthmatic patients, the pharyngitis scores were higher in the asthmatic group compared to controls, more often those on inhaled corticosteroids.⁵²

The use of laryngeal video stroboscopic examination provided greater information on the vocal fold vibratory behavior in asthmatic patients. Based on the study by Dogan et al, abnormal laryngeal videostroboscopic findings were present in 97.5% of the 40 asthmatic patients enrolled in their study. The most common abnormalities were the degree of glottic closure (60%), irregularities in vibration (67.5%), phase, and amplitude asymmetry (30% and 40%, respectively). Additional findings included mucosal wave abnormalities and hyperadduction of the ventricular bands.⁵³ More so, one out of 4 patients had vocal fold bowing during phonation, a finding that was corroborated by the study of Lavy et al which showed apposition abnormalities in 43% of the cases, and mucosal changes and supraglottic muscle tension were present in 58% and 40% of the cases, respectively.⁵⁷ In the study by Mirza et al, eight out of nine patients receiving a combination of inhalers in the form of dry powder, had a decrease in vocal fold vibration, amplitude, and the extent that mucosal waves’ propagation were attributed to various vocal fold pathologies.⁵⁴

The phonatory symptoms experienced by asthmatic patients and the associated laryngeal findings seen on laryngeal examination may be the result of the inherent breathing impairment associated with asthma, the presence of allergy, the intake of corticosteroid inhalers, and last the presence of co-morbidities such as sinonasal pathologies and gastroesophageal or laryngopharyngeal reflux disease. These four pathogenic mechanisms are briefly discussed below:

1. Impaired breathing: Respiration is an important component in voice production. As a power supply, the lungs energize the oscillator and set the vocal folds into vibration. Diseases of the respiratory system may alter the strength and consistency of subglottic pressure, and thus markedly affect vibratory behavior resulting in change in voice.⁵⁸ A recent study has shown the routine pulmonary function testing reveals unexpected pulmonary disease in many voice patients in whom pulmonary dysfunction is not suspected.⁵⁹

In asthmatic patients, breathing is impaired secondary to constriction of the bronchi smooth muscles, mucosal inflammation, and thickened secretions. The episodic airway obstruction leads to increased airway resistance manifested aerodynamically by a decrease in the expiratory peak flow and by reduction in maximum phonation time. Given the vital importance of breathing in phonation, voice is subsequently affected.⁵⁸ In addition to the aforementioned obstructive pattern, the increase in the amount and viscosity of the respiratory secretions exacerbates throat clearing and cough with subsequent irritation to the vocal folds. As a result, asthmatic patients may develop vocal fold pathologies such as exudative lesions of the lamina propria.^53,60,61

2. The high prevalence of allergy in patients with asthma: Asthma can be triggered either by infectious diseases or by allergy. When allergy is the culprit, patients may also complain of dysphonia. Randhawa et al have investigated the impact of airborne allergies on voice and have demonstrated an increase in Voice Handicap Index in patients who were allergic to more than 4 allergens. The conclusion was that vocal dysfunction may be underdiagnosed in patients with allergy.⁶² Brook et al in their investigation on the utility of allergy testing in patients with persistent laryngeal symptoms, of 998 patients tested for allergy, 27 had primary complaints in the larynx and 51.8% percent of those were positive for one inhalant allergen at least. More so, based on these findings, the odds of having a positive allergy testing was similar in patients with laryngeal and nasal complaints.⁶³ Similarly, the study conducted by Turley et al on 134 patients revealed a higher prevalence of dysphonia in patients with allergic and non-allergic rhinitis compared to controls.⁶⁴ Other studies have demonstrated a prevalence of allergy in up to 76% of patients with dysphonia or laryngeal complaints.^{63, 65} In a study by Randhawa et al on 15 patients with primary dysphonia, two-thirds had positive allergy testing. The authors alluded to the high prevalence of allergy in patients with atypical symptoms related to undiagnosed laryngopharyngeal diseases.⁶⁶ In another study conducted on singers using an allergy questionnaire, those with two or more vocal complaints were 25% more likely to have allergy compared to those with no vocal complaints.⁶⁷ Similarly, in the study by Simberg et al, subjects with allergy tended to have a higher prevalence of dysphonia compared to those with no allergy. The authors have used a questionnaire to solicit information on vocal symptoms in a group of 49 students with known allergy compared to another group of 54 students with no allergy.⁶⁸ In another study conducted on 30 subjects with known seasonal pollen allergy, Millqvist et al reported a higher prevalence of respiratory and phonatory symptoms in this group of patients compared to controls. This was also evident by the higher VHI scores in the functional and physical domains and in the overall score.⁶⁹ Krouse et al in another study examining the laryngeal manifestation of perennial allergy in 21 subjects with positive skin testing, again the VHI score was significantly higher in the allergic group compared to controls.⁷⁰

Patients with allergy present with nonspecific laryngopharyngeal symptoms such as cough, globus, throat clearing, and dysphagia, in addition to change in voice quality. Pathogenic mechanisms for these phonatory complaints include postnasal discharge reaching the glottis,⁶⁷ increased muscular activity of the posterior cricoarytenoid muscle via activation of negative pressure receptors in the nasal cavity, and the activation of the rhinolaryngeal reflex.⁶⁵ The phonatory symptoms when present are often substantiated by acoustic changes such as an increase in the perturbation parameters. In a study by Niedzielska et al the mean values of shimmer and Jitter were higher in patients with allergic rhinitis compared to controls.⁷¹ Along the same line of investigation, Koc et al in his study on perennial allergic rhinitis, the mean VHI score and the mean s/z ratio were higher in patients with allergy compared to controls. The authors concluded that allergy may result in laryngeal dysfunction, the impact of which may be significant on quality of life.⁷²

On examination, laryngopharyngeal signs of inflammation such as erythema and edema of the vocal folds and posterior glottis are commonly seen. Although these are non-specific, especially in the context of confounding diseases such as laryngopharyngeal reflux disease, when present, the diagnosis of allergy should be thoroughly investigated. In a large study by Hah et al looking at the prevalence of laryngeal diseases and associated factors in 19,000 patients, the authors reported a positive association between allergic rhinitis and vocal nodules, laryngitis, and epiglottic cyst. It is worth noting that laryngitis and vocal fold nodules were among the most common five laryngeal pathologies observed with a prevalence of 3.5% and 1.5%, respectively. The authors speculated that chronic throat clearing may precipitate laryngeal inflammation and thus lead to laryngitis.⁷³ These clinical observations were further substantiated by both human and animal studies supporting the causal relationship between allergen and vocal dysfunction. The study by Roth et al on five subjects challenged with an active allergic suspension revealed an increase in the phonatory threshold pressure after the allergen challenge. The authors concluded that vocal dysfunction can be secondary to the direct effect of the inhalant allergen on the vocal folds, and thus a causal relationship between the two is highly plausible.⁷⁴ More so, the animal study of Belafsky et al demonstrated a significant eosinophilic infiltration in the subglottis and trachea following sensitization to dust mite antigen and exposure to the same antigen and iron soot for 4 weeks.⁷⁵

3. Use of corticosteroid inhalers: A third and probably most common cause of dysphonia in asthmatic patients is the use of inhalers as a treatment modality. Despite the usefulness and established role of steroid inhalers in controlling patients with chronic asthma, there are undesired side effects to these medications such as throat clearing and dysphonia.⁷⁶ Numerous studies have shown that the prevalence of change in voice quality in patients treated with inhaled corticosteroids can be as high as 58% of the cases studied.^77–83 The meta-analysis by Rachelefsky et al on the adverse reactions to inhaled corticosteroids has shown that the potential to develop dysphonia, pharyngitis and or oropharyngeal fungal infection increases markedly with the use of any inhaled corticosteroid and depends heavily on the dosage and mode of usage.⁸⁴ In a study by Ihre et al looking at the prevalence of voice disturbances in asthmatic patients on steroid inhalers, a positive correlation between the use of inhaled cortisone and vocal symptoms was found. Based on the results of a questionnaire that consisted of 25 questions, some of which were related to voice, hoarseness was the most commonly reported symptom (52%) 2 weeks after the intake of the inhaled steroids. Other symptoms included lump sensation and excessive throat clearing.⁶⁰ Elderly subjects and those with voice-demanding professions had a higher prevalence of vocal disturbances compared to young subjects. More so there was a positive correlation between voice problems and the dosage of inhaled steroids, citing that those with more severe asthma had more voice problems compared to those with mild asthma. These results concur with the report by Kriz et al in 1977 on 23 asthmatic patients using triamcinolone acetonide aerosol. In his study, the most common side effects that occurred one to two weeks after initiation of the aerosol were hoarseness in 52% of the cases, followed by a coated tongue in 35% and sore throat in 26%.⁸⁵

There are many reasons why phonatory symptoms in asthmatic patients may occur. These mechanisms include fungal infection (candidiasis), steroid-induced mucosal irritation and microtrauma, muscle-induced atrophy, and last is mucosal and mucous secreting glands atrophy. Based on a report by Vogt, the prevalence of oropharyngeal candidiasis in patients using corticosteroids inhalers can reach up to 77%.⁷⁹ See Figure 9–8. Several proposed mechanisms for the development of infection have been suggested. One is the development of the infection due to reduced immunity of the mucosal surface at the interface with the inhaled particles.⁸⁶ Fidel suggests that both local and systemic cell-mediated immunity are needed to protect against oropharyngeal candidiasis. Another suggested mechanism is elevated salivary glucose level.⁸⁶ In a study by Knight and Fletcher, the concentration of glucose within saliva withdrawn from three patients on steroids was elevated (mean of 32.8 mg/100 mL). The authors concluded that high glucose level in a bacterial flora medium allows fungi to grow and multiply.⁸⁷

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