Survey of Voice Disorders

It is apparent that most people, regardless of their degree of understanding of voice and voice disorders, are able to distinguish a typical voice from disordered voice. This statement is supported by the findings of a study by Anders et al who reported that recorded voice samples could be easily identified and ranked by trained and untrained groups alike—training did not necessarily enhance the accuracy of perceptual identification. 1 Though we may be able to perceive differences in voice, defining typical versus disordered voice is not so easy. What is it that the listener detects in the voice signal that allows for the discrimination between typical and disordered voice? It appears that there are a number of characteristics (age, gender, racial type, body size/type, etc.) that determine a range for typical voice type and quality. As we are exposed to the vast range of voice types throughout our lives, we learn that voices may be highly differentiated but still be considered within typical expectations. 2 We gain experience as to the limits of typical voice and, thereby, develop a mental scale by which typical voice is gauged. As long as a particular voice does not deviate substantially from this internal gauge in terms of parameters such as pitch, loudness, quality, and duration, it will be considered within the typical range. 3


In contrast, a voice disorder exists when a speaker’s voice quality, pitch, loudness, vocal flexibility, and/or stamina deviates from expectations related to age, sex, body type, speaking community, communication needs, and/or performance needs. 4 The clinical presentation of a voice disorder is often labeled as dysphonia, a word whose literal meaning can be understood as a condition (“-ia”) of bad (“dys”) sound (“phon”). Dysphonia is also a medical diagnosis used by healthcare professionals and the healthcare industry. The terms “voice disorder” and “dysphonia” are often used interchangeably, although one should keep in mind that a voice disorder does not require the presence of a “bad sounding” voice. For example, an individual who experiences pain and tightness when speaking may produce a perceptually normal voice and yet be diagnosed with a voice disorder due to deviations in vocal stamina and/or flexibility that limit their ability to use voice for communication or performance needs.


Voice disorders and accompanying perceived dysphonia exist along a continuum of severity, from an absence or minor degree of the observed deviant voice characteristic to an extreme amount. The lower end of this continuum may be best acknowledged as a “minimal” level, because even typical voice signals are not necessarily perfect. On the opposite end of the continuum, an extreme level of voice deviation is highly noticeable and, most probably, has a significant effect on patient and listener alike. It is important that voice therapists have parameters by which they not only designate the severity of the perceptual characteristics of the voice but also account for the impact the voice problem may have on the speaker’s ability to communicate and obtain employment. 5 The following severity terminologies attempt to incorporate several of the possible diverse effects of dysphonia 3:




  • Mild: While the listener experienced in the perceptual characteristics of the disordered voice may consider the voice disordered, the lay listener may consider the voice to be only unusual in nature and within typical expectations. The voice characteristics are not distracting, and the ability to effectively communicate is not affected. The dysphonia does not interfere in any substantial manner with phonation.



  • Moderate: Both trained and untrained listeners would consider the voice dysphonic. There may be intermittent periods in which the voice characteristics are highly distracting. The ability to effectively communicate is noticeably affected under certain conditions (e.g., noisy environments). The dysphonia may occasionally cause phonation to cease or become highly effortful.



  • Severe: Both trained and untrained listeners would consider the voice extremely dysphonic. The voice characteristics are highly distracting. The ability to effectively communicate is consistently affected. The dysphonia causes phonation to be mainly absent or extremely effortful.


The voice therapist is encouraged to closely compare the perceived abnormal voice characteristic(s) to all parts of these definitions. It may be that a disordered voice does not show all the characteristics mentioned under each definition, or it may show characteristics crossing definitions. In these cases, intermediate ratings (e.g., mild-to-moderate) may be appropriate. In addition, certain dysphonia types (e.g., inappropriately high pitch) may be considered abnormal but not necessarily disrupt the ability to phonate.


Voice disorders, whether chronic or transient, mild or severe, are experienced by a large percentage of the general population across all ages of the lifespan. Lifetime prevalence rates have been estimated at approximately 30% with point prevalence rates (number of cases at a single point in time) approaching 7% in the adult population. 6,​ 7,​ 8 Some groups are at a greater risk for the development of voice problems. Data from treatment-seeking populations consistently demonstrate that individuals who rely on voice production for their job-related duties, the so-called professional voice users, experience a greater frequency of voice problems than others. Among this group include teachers, singers, actors, clergy, lawyers, and others. 9 Nonprofessional voice users also experience voice problems with great frequency, which can be explained by the range of possible causes underlying dysphonia—as you will learn in this chapter.


Underlying the onset and maintenance of voice disorders is some impairment or inefficiency in body function. These impairments can relate to anatomical, physiological, behavioral, and/or psychological abnormalities which disrupt the efficiency and effectiveness of voice production and the perceptual impressions of the sound produced. For example, changes in vocal fold structure, neuromuscular control, and/or behavioral regulation of vocal subsystems are impairments which can often be identified in speakers with voice disorders. When the impairment results in the inability to produce adequate voice for the needs of a speaker, it creates a disability. A professor who experiences vocal fatigue and progressive dysphonia during lectures could be said to have a disability if it affects the teaching process.


When a disability leads to a restriction in life activities, such as that same professor having to take time off from teaching or not being able to find a job due to his or her restricted teaching abilities, the condition is known as a handicap. 10 Speech–language pathologists (SLPs) and otolaryngologists seek to determine the underlying impairment(s) causing a vocal disability. The underlying impairment becomes a primary target of voice treatment through voice therapy, medical management, or a combination of those two. As an example, disabilities and handicaps related to phonation can be improved by modifying a speaker’s vocal demands and/or environment. By rehabilitating or improving the anatomical, physiological, and/or behavioral impairments underlying the voice disorder, reductions in disability and handicap often naturally follow.


Any impairment has a point of origin or cause—this is known as the etiology of the problem. For example, a structural change in the margin(s) of the vocal fold(s) (e.g., the formation of a polyp or nodule) can be classified as an impairment, but their origin is related to excessive phonotrauma of the vocal fold tissue. The physical characteristics of the nodules, the cellular and proteomic activity leading to their development and maintenance, and the manner in which they negatively impact vocal fold oscillation are related to the pathology—the state, condition, or characteristics of the problem. To treat a voice disorder, it is typically necessary to identify not only the pathology but also the underlying etiology and address both as part of a treatment plan to affect a positive change in the pathological state of the voice mechanism.


2.3 Voice Disorder Classifications


Wide varieties of classification models exist which subdivide voice impairments based on one or more dimensions. 3 For the purposes of this book, we will use an etiological framework for classifying voice disorders broadly into functional and organic categories, 11,​ 12 and a third category of idiopathic to account for laryngeal conditions affecting the vocal folds for which the underlying cause has yet to be definitively identified. As you will learn in later chapters of this book, the category into which a voice disorder is assigned upon diagnosis, in addition to the subtype within a category, can substantially impact the treatment options recommended to the patient.


2.3.1 Functional Voice Disorders


A functional voice disorder is caused by vocal behaviors. These behaviors are tied to neuromuscular activity under the influence of conscious and subconscious mechanisms. Vocal behaviors can be a primary (e.g., the first, or original) etiology of a voice problem or a secondary etiology. A specific criterion for the diagnosis of a primary functional voice disorder is that no structural, neurological, or other systemic condition can be identified as an existing etiology of the current impairment. 13 In some cases, a primary functional voice disorder is precipitated by an acute systemic condition such as upper respiratory infection, but at the time of clinical presentation the precipitating organic condition has resided and no other illness or impairment could otherwise explain the voice problems. A synonym for this category is “nonorganic,” and some authorities have also used the labels “muscle misuse” and “psychogenic” voice disorders as the broad category label. The term “psychogenic” relates to the strong ties between psychological processes and voice production, and the belief by some that most subtypes of functional voice disorders are caused by emotional and psychological reactions 4 to life events. It is true that the cranial nerves controlling laryngeal muscles are intimately connected to the emotional centers of the brain, 14 and a detailed history often reveals major life events and/or stressors in the recent past of patients diagnosed with primary functional voice disorders. 15 A behavioral change in the activity of respiratory, laryngeal, and supralaryngeal muscles that are under the influence of the voluntary motor pathways is the common thread among functional voice disorders, a major reason we include these impairments within this category.


An important concept in understanding functional voice disorders is that, while structural, neurological, or systemic etiology is not necessary for diagnosis, structural changes to the vocal folds may develop as a result of the vocal behaviors. For example, vocal nodules are structural changes to vocal fold tissue. However, if a patient never used his or her voice, the nodules would not develop. In a majority of cases, the behavior underlying the functional voice disorder is imbalanced or dysregulated control of laryngeal, respiratory, and/or perilaryngeal muscles characterized by excessive muscular activation. 16 This excessive kinetic pattern of muscular contraction is sometimes referred to as vocal hyperfunction and voice problems resulting from these patterns are commonly labeled as hyperfunctional voice disorders. 4


The neuromotor imbalance characteristic of functional voice disorders can arise from habituated muscle tension and vocal inefficiency, compensatory behaviors to some other physiological impairment, and/or psychological stress. In effect, the patient’s use of the vocal mechanism has resulted in the dysphonia. Patients can present with more than one etiology underlying their current voice difficulties. It is not uncommon for functional voice disorders to develop in response to a primary organic etiology. In these cases, the functional component is labeled as a secondary etiology. One reason this can occur is that many patients attempt to compensate for a change in voice due to an organic etiology by adjusting the balance between respiration, phonation, and resonance when producing voice. This can lead to maladaptive hyperfunctional voicing patterns that cause an additional impairment. In such cases, the functional etiology would be secondary to the original organic cause.


2.3.2 Organic Voice Disorders


Organic voice disorders are caused by structural, systemic, or neurological changes to the respiratory and/or laryngeal mechanisms necessary for phonation. Organic voice disorders are not initially caused by vocal behaviors—conceptually, even in the absence of voice use, the organic changes would still develop. The onset of organic voice disorders can be due to endogenous factors (from within one’s own body—e.g., inflammatory cellular activity, neurodegenerative conditions) or exogenous factors (from outside one’s own body—e.g., surgery affecting respiratory or laryngeal structures). Organic voice disorders can also occur in conjunction with functional voice disorders. In most of those cases, the organic disorder is the primary etiology and the functional disorder is the secondary etiology, developing in response to the organic condition.


Certain structural changes to vocal fold tissue may be caused by organic and/or functional etiologies. For example, vocal process granulomas (see below) maybe due to phonotrauma via vocal behaviors (functional cause) or from reflux and/or intubation (organic causes). In these cases, it can be difficult to determine if the etiology is purely organic or if there is a functional component to the onset of the problem. Voice disorder subtypes which fall into both categories or which can be challenging to label into one specific category will be described below.


2.3.3 Idiopathic Voice Disorders


Idiopathic voice disorders have underlying etiologies which have not been conclusively identified. The impairment and disability can be understood in these conditions, and often successfully managed, but the origin of the problem has yet to be determined. This diagnosis should be used with great care and only after an exhaustive assessment has been completed.


2.4 Functional Voice Disorders


▶ Table 2.1 illustrates subtypes of commonly observed voice disorders along with associated clinical characteristics that tend to have a functional cause. It should be very obvious from this table that many clinical characteristics are similar across functional subtypes. It is also true that perceptual, acoustic, and aerodynamic characteristics can be similar when comparing functional with organic voice disorders. These similarities indicate the vital importance of laryngeal visualization and referral to an otolaryngologist for medical evaluation prior to any final diagnosis being made and treatment being implemented.









































Table 2.1 Clinical characteristics of functional voice disorder subtypes. Subtypes with * represent those with possible multifactorial etiologies in addition to functional voicing behaviors. Clinical characteristics listed are those most commonly associated with the subtypes, although there can be great variability in clinical presentation from speaker-to-speaker

Subtype


Clinical Characteristics


Muscle tension dysphonia


Endoscopic




  • Normal laryngeal structure (primary MTD)



  • Supraglottic compression of the false vocal folds in the medial (toward midline) dimension.



  • Supraglottic anterior-posterior compression (the petiolus of the epiglottis approximates the arytenoids).



  • Excessive medial compression at the glottis, often manifested by tight closure (“hyperadduction”) at voicing onsets.



  • Posterior glottal gap



  • Vocal fold bowing during contraction


Aerodynamic




  • Increased mean and peak subglottal pressure



  • Increased phonation threshold pressure



  • Decreased transglottal airflow


Acoustic




  • Decreased cepstral peak prominence



  • Increased perturbation (e.g., larger measures of jitter and/or shimmer)



  • Increased spectral noise (e.g., lower measures of harmonic-to-noise ratio)



  • Increased fundamental frequency



  • Decreased physiological frequency range


Auditory-Perceptual




  • Dysphonia often characterized by roughness associated with increased perturbation but sometimes breathiness resulting from glottal gaps secondary to the hyperfunction.



  • Strain and effort when speaking



  • Hard glottal attacks (voicing onset)


Visual & Tactile




  • Decreased thyrohyoid space



  • Pain when palpating anterior and lateral margins of neck in the vicinity of the larynx



  • Elevated larynx



  • Bulging sternocleidomastoid muscle


Psychogenic dysphonia/aphonia


Endoscopic




  • Similar to MTD


Aerodynamic




  • Similar to MTD, unless aphonia present


Acoustic




  • Similar to MTD, unless aphonia present


Auditory-Perceptual




  • Dysphonia on a continuum from mild dysphonia to aphonia



  • Characteristics of dysphonia typically more variable compared to MTD


Visual & Tactile




  • Similar to MTD


Mutational falsetto


Endoscopic




  • Elongated vocal folds associated with increased longitudinal tension; Otherwise normal.


Acoustic




  • Increased fundamental frequency


Aerodynamic




  • Possible increased phonation threshold pressure due to increased vocal fold tension


Auditory-Perceptual




  • Abnormally high pitch


Pitch breaks




  • Breathy voice



  • Hard glottal attacks



  • Normal sounds produced during vegetative voicing (cough, throat clear, etc.)



  • Often stimulable for lower pitch during diagnostic probes


Tactile & Visual




  • Elevated larynx


Nodules


Endoscopic




  • Bilateral symmetric or quasi-symmetric exophytic masses at mid-membranous vocal folds



  • Hourglass closure pattern



  • Normal or minimally reduced mucosal wave at site of mass – will be more affected with larger/stiffer nodules



  • Normal or minimally effected vibratory amplitude, symmetry, and periodicity – will be more affected by larger/stiffer nodules



  • Compensatory hyperfunction (medial & anterior-posterior compression)


Aerodynamic




  • Increased subglottal pressure



  • Increased phonation threshold pressure



  • Increased transglottal airflow


Acoustic




  • Variable effects on fundamental frequency



  • Decreased physiological frequency range



  • Increased perturbation



  • Decreased cepstral peak prominence



  • Decreased harmonics-to-noise ratio


Auditory-Perceptual




  • Breathy or hoarse voice quality



  • Pitch breaks



  • Excessive loudness in some speakers


Polyps


Endoscopic




  • Unilateral exophytic mass at mid-membranous vocal fold



  • Possible contralateral reactive mass



  • Hourglass closure pattern



  • Increased vascularity – often a prominent vessel feeding into the mass



  • Reduced mucosal wave at site of mass



  • Reduced amplitude and symmetry and periodicity of vibration



  • Compensatory hyperfunction (medial & anterior-posterior compression)


Aerodynamic




  • Increased subglottal pressure



  • Increased phonation threshold pressure



  • Increased transglottal airflow


Acoustic




  • Variable effects on fundamental frequency



  • Decreased physiological frequency range



  • Increased perturbation



  • Decreased cepstral peak prominence



  • Decreased harmonics-to-noise ratio


Auditory-Perceptual




  • Breathy or hoarse voice quality



  • Pitch breaks



  • Excessive loudness in some speakers


Pseudocysts*


Endoscopic




  • Unilateral exophytic mass at mid-membranous vocal fold, with translucent appearance



  • Reduced adduction of arytenoid on affected side may be visible.



  • Hourglass closure pattern



  • Mucosal wave, amplitude, symmetry, and periodicity may be unaffected or only minimally affected. Larger masses may exacerbate signs in this domains



  • Compensatory hyperfunction (medial & anterior-posterior compression) in more severe masses


Aerodynamic




  • Increased subglottal pressure



  • Increased phonation threshold pressure



  • Increased transglottal airflow


Acoustic




  • Variable effects on fundamental frequency



  • Decreased physiological frequency range



  • Increased perturbation



  • Decreased cepstral peak prominence



  • Decreased harmonics-to-noise ratio


Auditory-Perceptual




  • Breathy or hoarse voice quality



  • Pitch breaks



  • Excessive loudness in some speakers


Cysts*


Endoscopic




  • Unilateral mass at mid-membranous vocal folds, often appearing as a white subepithelial capsule



  • Hourglass closure pattern



  • Reduced mucosal wave—typically to a greater extent than other mid-membranous lesions



  • Reduced amplitude, symmetry, and periodicity—will be more affected by larger/stiffer cysts



  • Compensatory hyperfunction (medial & anterior-posterior compression)


Aerodynamic




  • Increased subglottal pressure



  • Increased phonation threshold pressure



  • Increased transglottal airflow


Acoustic




  • Variable effects on fundamental frequency



  • Decreased physiological frequency range



  • Increased perturbation



  • Decreased cepstral peak prominence



  • Decreased harmonics-to-noise ratio


Auditory-Perceptual




  • Breathy or hoarse voice quality



  • Pitch breaks


Granulomas*


Endoscopic




  • Unilateral or bilateral exophytic masses at vocal process of arytenoids



  • Possible groove in at one arytenoid caused by contralateral contact patterns.



  • Erythema (redness) and edema in posterior larynx may accompany lesions (suggestive of reflux)



  • Compensatory hyperfunction (medial & anterior-posterior compression)


Aerodynamic




  • May be within normal limits when no dysphonia present



  • Increased subglottal pressure and transglottal airflow expected if granulomas interfere with glottal closure



  • If compensatory hyperfunction is present without glottal incompetence decreased transglottal airflow could be expected


Acoustic




  • May be within normal limits when no dysphonia is present.



  • Characteristics of MTD when compensatory hyperfunction is present


Auditory-Perceptual




  • Often within normal limits



  • May be strain when compensatory hyperfunction is present.


Edema*


Endoscopic




  • Unilateral or bilateral translucent or pale white puffiness in vocal fold cover



  • In Reinke’s edema, large balloon-like enlargement of vocal folds often with prominent vasculature



  • Complete closure pattern



  • Reduced mucosal wave, amplitude, symmetry, and periodicity


Aerodynamic




  • Increased subglottal pressure



  • Increased phonation threshold pressure


Acoustic




  • Low fundamental frequency



  • Decreased physiological frequency range



  • Increased perturbation



  • Decreased cepstral peak prominence



  • Decreased harmonics-to-noise ratio


Auditory-Perceptual




  • Extremely low pitch



  • Rough voice quality



  • Strain


Vascular injury


Endoscopic




  • Unilateral or bilateral prominent vasculature.



  • May take form of varix, ectasia, telangiectasias, and/or hemorrhage


Aerodynamic




  • May be within normal limits



  • With compensatory hyperfunction, may be similar to MTD


Acoustic




  • May be within normal limits



  • With compensatory hyperfunction, may be similar to MTD


Auditory-Perceptual




  • May be within normal limits



  • With compensatory hyperfunction, may be similar to MTD


2.4.1 Muscle Tension Dysphonia


Description


Muscle tension dysphonia (MTD) can be of two types, primary MTD and secondary MTD. Primary MTD is a change in voice quality, pitch, loudness, flexibility, and/or stamina which occurs in the absence of any current structural, systemic, or neurological changes to the subsystems of voice. Secondary MTD results in similar voice changes but occurs in response to a primary organic etiology. MTD also goes by the broader label of functional dysphonia, although that term has also been used to refer to functional voice disorders primarily resulting from psychological factors. 4,​ 13


MTD is a common voice disorder, accounting for 8 to 45% of all diagnoses among treatment-seeking populations. 7,​ 17,​ 18,​ 19 As with most functional voice disorder subtypes, MTD is diagnosed more frequently in females than in males and can occur in patients across the lifespan. 7,​ 19 MTD presents along a continuum of perceived severity, both from the patient’s perspective and the clinician’s perspective. The dysphonia resulting from MTD can manifest as a wide range of changes in quality, pitch, and/or loudness. Symptoms and signs of MTD form a cluster of dimensions which can vary from patient to patient. Typical symptoms of MTD include some combination of the following:




  • Tension, soreness, and/or pain in neck and/or shoulder region.



  • Vocal fatigue.



  • Variable or consistent changes in voice quality, pitch, or loudness (dysphonia).



  • Loss of frequency range.



  • Globus sensation in throat.



  • Increased effort needed to produce voice.


2.4.2 Etiological Characteristics


A number of theories have attempted to explain the genesis of primary MTD, and thorough assessment will often lead the identification of one or more of the following:




  • Technical misuse of the vocal mechanism, often related to heavy vocal demands or unique vocal requirements associated with a professional or social activity. The frequency and/or type of voice use can lead to musculoskeletal tension in a similar manner as one might experience in the limbs after heavy or sustained exercise. Muscular tension in the subsystems of voice can limit vocal flexibility, stamina, and phonation physiology, the third causing dysphonia. As the speaker begins to subconsciously compensate for these changes, the poor technical control can develop into a habituated (e.g., chronic) incoordination of respiratory, laryngeal, and articulatory musculature; excessive contraction of intrinsic and extrinsic laryngeal muscles; inappropriate resonant focus; and/or improper control of vocal frequency and intensity. 13,​ 20,​ 21



  • Musculoskeletal tension may be a learned adaptation (compensation) from an acute (transient) organic condition, such as an upper respiratory infection, allergic reaction, or laryngopharyngeal reflux (LPR). As the organic precipitator fades or heals, the speaker’s muscular adaptation is so habituated that they are unable to independently restore an efficient physiological balance in the subsystems of voice. 3,​ 20,​ 21



  • Excessive musculoskeletal tension can be induced by psychological and/or trait characteristics of the individual. Factors such as personality, emotion, and stress have long been linked with musculoskeletal tension in the subsystems of voice. 22 Mental illness has also been associated with behavioral changes in vocal function, although we will identify this cause as a separate subtype of functional voice disorder below. 4 In the case of emotion and stress, it is believed that hyperfunctional voicing behaviors arise subsequent to disinhibition of subcortical pathways in response to environmental triggers. The subcortical emotional release may result in poor control over respiratory and phonatory subsystems. Psychological distress has also been associated with a “pressor” response that results in hyperfunctional muscular reactions in the laryngeal and respiratory muscle. 4,​ 12,​ 13,​ 20


The excessive musculoskeletal tension of secondary MTD is thought to develop as a compensatory adaption for an existing organic condition. MTD occurs in varied populations of speakers, including professional and nonprofessional voice users, singers and nonsingers, in addition to adults and children. Both primary and secondary MTDs are characterized by similar clinical signs which are detailed in ▶ Table 2.1. 23


Clinical Characteristics


Visual inspection of the larynx with endoscopy in patients with primary or secondary MTD will often reveal signs of muscular hyperfunction. Hyperfunction can be visualized in at least three ways: (1) medial compression of the supraglottic false vocal folds (▶ Fig. 2.1), (2) anterior-posterior supraglottic squeezing which often obscures views of the anterior vocal fold regions (▶ Fig. 2.2), and (3) tightly compressed vocal folds and arytenoid cartilages at the onset of phonation. When stroboscopy is added to the endoscopic exams, it is not uncommon to observe a posterior glottal gap and shortened open phase of the vibratory cycle. Voices which are perceptually rough might include visual signs of reduced periodicity, mucosal wave, and symmetry of vibration. In patients who manifest increased activity in the posterior cricoarytenoid, a clinical sign might include bowing either unilaterally or bilaterally while the vocal folds are adducted.



Hyperfunctional signs in muscle tension dysphonia (MTD). Endoscopic view of larynx demonstrating medial compression of the false vocal folds in a case of primary MTD, obscuring the lateral portions of


Fig. 2.1 Hyperfunctional signs in muscle tension dysphonia (MTD). Endoscopic view of larynx demonstrating medial compression of the false vocal folds in a case of primary MTD, obscuring the lateral portions of the true vocal folds.


(From Bhattacharyya A. Laryngology: Otorhinolaryngology—Head and Neck Surgery Series. 1st edition. New York: Thieme Publishers, 2014.)



Hyperfunctional signs in muscle tension dysphonia (MTD). Endoscopic view of larynx demonstrating anterior-posterior compression of the larynx in a case of secondary MTD subsequent to glottal insuffici


Fig. 2.2 Hyperfunctional signs in muscle tension dysphonia (MTD). Endoscopic view of larynx demonstrating anterior-posterior compression of the larynx in a case of secondary MTD subsequent to glottal insufficiency. Notice the petiolus of the epiglottis (the bump just above the most anterior part of the vocal folds) bulges posteriorly and approximates the arytenoid cartilages, obscuring the anterior vocal folds.


(From Kendall K, Leonard R. Laryngeal Evaluation, 1st edition. New York: Thieme Publishers, 2010.)


The physiological changes observed during laryngeal endoscopy and videostroboscopy influence the aerodynamic and acoustic measurements obtained during the comprehensive voice evaluation. Aerodynamic characteristics of MTD include increases in subglottal air pressure and decreases in transglottal airflow. Acoustic characteristics reflect the reduced periodicity and stability of phonation. These are manifested in elevated measures of frequency and amplitude perturbation (jitter and shimmer, respectively) and decreased cepstral peak prominence. Phonation instability can introduce additive noise in the acoustic signal, which is reflected in decreased values of harmonic-to-noise ratio. Because of the excessive muscular tension underlying MTD, reduced flexibility of laryngeal function can be measured in a compressed physiological frequency range.


Auditory-perceptual, tactile (via laryngeal palpation), and external visual signs can also inform clinical hypotheses of the presence of MTD. Voice quality is often perceived as rough and strained, although some speakers can manifest breathiness. During voicing, onsets at the initiation of a breath group might also display hard glottal attacks—a sharp burst of loudness during the initial sound of a word. When the larynx of patients with MTD is palpated, there is often a reduced thyrohyoid space and many patients report pain or soreness when pressure is applied centrally and laterally around the laryngeal region. In some patients, the sternocleidomastoid muscle bulges during speaking, and the larynx can be extremely elevated even at rest.


As previously mentioned the severity of MTD varies widely from patient to patient, although the reported symptoms are generally a consistent problem either throughout the day or during periods of heavy voice use. In severe cases of primary and secondary MTD, the hyperfunction of the intrinsic laryngeal muscles may be so great that the false vocal folds compress medially and closely approximate each other. This may result in vibration of the false vocal folds along with or instead of the true vocal folds, a condition known as ventricular phonation. The voice quality of ventricular phonation is characterized by severe roughness, low pitch, and strain.


In some cases of MTD, the hyperfunction can manifest as incomplete glottal closure, believed to occur when the vocal fold adductor muscles co-contract with the antagonistic abductor muscle, the posterior cricoarytenoid. The voice quality in these cases of MTD is characterized by breathiness, which can be subtle or extreme depending on the degree of hyperfunction. An alternative theory for breathiness associated with MTD is that glottal insufficiency results from severe fatigue in the laryngeal adductor muscles after chronic hypercontraction. 11 It is important to understand that this same voice quality can be caused by clinical psychiatric or psychological disorders, as discussed below; therefore, it is of utmost clinical importance to determine if mental illness is a possibility. If suspected, referral to a mental health professional is warranted. This referral can also be appropriate for those diagnosed with MTD where psychological processes associated with personality, emotional responses, and stress reactions are so great that the knowledge and skills of the SLP are inadequate to address them as part of a treatment plan.


Treatment


Research evidence and clinical experience support voice therapy as an effective intervention for MTD, given the presence of certain prognostic variables. Among the positive prognostic indicators include a compliant and motivated patient, recent onset as opposed to a long history of dysphonia, positive physiological health, and a lack of secondary gain associated with the voice problem. Secondary gain is an extraneous benefit that is independent of beneficial voice therapy; secondary gain may perpetuate and reinforce the disorder. Behavioral treatments targeting a physiological balance in the vocal subsystems are often effective for improving vocal outcomes within six to twelve treatments sessions, sometimes longer, when delivered by a skilled and knowledgeable clinician. As described in Chapter 8, resonant approaches, flow phonation, vocal function exercises, semioccluded vocal tract exercises, and manual circumlaryngeal massage/reposturing are some of the strategies that can be effective for treating primary or secondary MTD. 24,​ 25,​ 26,​ 27,​ 28,​ 29


Psychological Processes and MTD


In addition to serving as a phonemic and linguistic marker during speech production, human phonation is influenced by psychological processes in the mind of the speaker (i.e., those mental processes which include reasoning, judging, analyzing, perceiving, feeling, etc.) and causes psychological reactions in the mind of the listener. A speaker will use phonation to convey emotion, personality, and intent among other paralinguistic features. A listener will make judgments about a speaker based on their perception of voice, judgments which include decisions about a speaker’s sincerity, character, motivation, sociocultural background, and also likeability. 12 Speakers are cognizant of these listener reactions, and use information from listener responses to inform subsequent use of voice. In both normal and dysphonic speakers, these psychological processes are intimately linked to and constantly influence phonation. 4


It is logical to consider that psychological responses to life activities and the environment, including emotional and stress reactions, can influence phonation physiology in such a way that those reactions become a facilitator of dysphonia. For example, many nervous speakers have experienced acute examples of dysphonia when giving a speech to a public audience. When associated with chronic dysphonia, these psychological responses typically manifest as increased muscular tension and are linked to broader physiological impairments associated with MTD—a physiological imbalance between the subsystems of voice. The Trait Theory explains the development of functional voice disorders as a behavioral response to environmental stimuli which is then manifested in excessive muscle tension. 22 This can be further understood as heightened sensitivity to specific stimuli causes some speakers to respond physiologically in the form of dysregulated motor control in the subsystems of voice. According to this theory, individuals with personality dimensions of elevated neuroticism and low extraversion are most at risk for the development of functional voice disorders. 22,​ 25,​ 30


It is also logical to consider that an existing dysphonia can result in subsequent psychological reactions that further influence phonation physiology. These reactions may cause dysphonia to be maintained over time or progress in severity and form. However, these are often natural, intensified psychological reactions by speakers to environmental stress and/or the sound of their own dysphonic voice. While these reactions and the stressors that trigger them can often be identified with skillful evaluation techniques, their presence does not necessarily indicate a psychological disorder. Thus, MTD in both primary and secondary forms is often associated with psychological reactions to the environment and/or a speaker’s perception of their own dysphonic voice, but this should not be automatically interpreted as a speaker suffering from a mental illness.


The onset and maintenance of voice disorders have been linked to psychological factors such as reactions to interpersonal relationships, social communication, and other life-related activities. 4,​ 31,​ 32,​ 33 To investigate possible psychological sources of muscular tension, it is important to utilize a screening tool as part of a comprehensive voice evaluation. An individual’s personality type has also been associated with an increased risk of functional voice disorders. 25,​ 30,​ 34 In such cases, it can be useful to incorporate a personality profile or questions which probe more deeply into personality characteristics (e.g., introversion/extroversion). The information gained from these tools will help the clinician to better understand how a patient’s psychological processing, physiological reactions to that processing, and personality relate to the voice impairment. This information can then be used to develop an effective and comprehensive treatment plan that may include counseling by the clinician and/or referral to appropriate mental health professionals.


2.4.3 Psychogenic Dysphonia


Description


It is important to realize that voice production can be influenced by mental illness—psychiatric or psychological disorders with specific diagnostic criteria defined by the Diagnostic and Statistical Manual of Mental Disorders. 35 In our classification model, we categorize psychogenic dysphonia as a subtype of functional voice disorders caused by some form of mental illness. The auditory-perceptual characteristics of psychogenic dysphonia can range from mild to severe dysphonia, and in some cases complete aphonia presenting as a whisper. Our narrow definition of psychogenic dysphonia differs from a number of previous sources; some have used this term as a categorical label for all functional voice disorders, while others have referred to psychogenic voice problems specifically as “functional dysphonia” or “functional aphonia” depending on the auditory-perceptual characteristics of the voice. 4,​ 12,​ 13,​ 36


Etiological Characteristics


Voice impairments resulting from psychogenic dysphonia have been associated with a number of psychiatric conditions, including conversion disorders, somatization disorders, and mood disorders among others. 4,​ 35 These diagnoses are made by psychiatrists and psychologists, not the SLP, indicating the necessity for referral whenever a mental health issue is suspected. It can be difficult to differentiate MTD from psychogenic dysphonia because the clinical presentation is similar and, as noted earlier, MTD can be exacerbated by personality and reactions to life stress. It is best practice to refer patients to mental health professionals whenever psychological dysfunction is suspected.


Clinical Characteristics


Endoscopic, auditory-perceptual, and acoustic clinical signs of psychogenic aphonia can be very similar to those of MTD, making it challenging to differentiate these two voice disorder subtypes in some patients. According to Verdolini et al, features of vocal impairment associated with psychiatric or psychological voice disorders include the following 35:




  • Variable (from speaker-to-speaker) voice quality ranging from perceptually mild dysphonia to complete aphonia.



  • Variable (from speaker-to-speaker) glottal adduction ranging from hyperadduction to hypoadduction.



  • Odynophonia (pain during phonation—also associated with a variety of other disorders).



  • Laryngeal pain (also associated with a variety of other disorders).



  • In the presence of aphonia, vegetative voicing behaviors (e.g., cough, throat clear) remain intact.



  • Decreased fundamental frequency (associated specifically with depression).


Treatment


A psychological screening is an important tool to consider as part of a routine voice evaluation protocol, but especially in cases where possible disordered psychological processes are suspected. Because these processes drive the physiological impairments underlying psychogenic dysphonia, referral to a mental health professional is the appropriate next step when evidence leads to the clinical hypothesis that psychogenic dysphonia is a possibility. This does not prohibit the use of clinical probes during the diagnostic process to determine if the patient is stimulable for improved voice, or even trial voice therapy to reestablish more functional voice production.


When appropriate referrals are made and the patient chooses a trial of voice therapy, the authors’ collective clinical experiences have found that aphonia is easier to treat than the irregular dysphonia that is typical in patients with underlying psychological disturbances. For aphonia, an initial goal is to establish vocal fold oscillation. Vegetative voicing behaviors (cough, throat clear, vocal fry, lip trills) often succeed in eliciting phonation. Once voicing is consistently established, the goal is to shape this into sustained phonation, usually following a hierarchy of vowel prolongation to syllables to words and then phrases. Psychogenic dysphonia can be highly variable in its characteristics, which can differentiate it from MTD. An initial goal in these cases is to establish a more consistent phonation pattern while unloading the hyperfunctional laryngeal behaviors that are underlying the dysphonia. Similar techniques as those used with MTD can be successful, although patients with psychogenic dysphonia might require more treatment sessions than those with aphonia to establish carryover. In both psychogenic aphonia and dysphonia, our experience suggests that any secondary gain from the voice problem will make treatment prognosis less favorable.


2.4.4 Mutational Falsetto


Description


Mutational falsetto is a functional voice disorder characterized by abnormally elevated speaking fundamental frequency. It is associated with failure to naturally lower vocal pitch during puberty, which can persist through adolescence and adulthood. 37 Because of its onset around the time of puberty, it has also been called “puberphonia.” Mutational falsetto is most commonly seen in males, although it can also affect females. 3,​ 37 The dysphonia of mutational falsetto occurs in the context of a normal laryngeal structure and neurological innervation.


Etiological Characteristics


The precipitating cause of mutational falsetto is not known and likely multifactorial. Various theories have been suggested, which include




  • Previous experience of an embarrassing pitch break (due to natural maturation processes), resulting in the maintenance of the “childlike” pitch because the speaker believes they have greater control of this higher fundamental frequency.



  • Embarrassment related to a sudden low pitch voice that is different from one’s peers.



  • Psychological immaturity.



  • A stronger feminine self-identification in a male.



  • Rewards of a higher-pitched voice related to singing.


These psychological factors are not the only possible cause of an elevated pitch in a teenage/adult male or female, reinforcing the need for a comprehensive voice evaluation and otolaryngologic evaluation prior to final diagnosis. Other causes of this voice type, which would not be mutational falsetto and not classified as a primary functional voice disorder, can include




  • Endocrine disorders affecting laryngeal development.



  • Hearing loss.



  • Underlying weakness/dysarthria in the laryngeal muscles resulting in atrophy and/or vocal strain.


Clinical Characteristics


Clinical characteristics associated with mutational falsetto are illustrated in ▶ Table 2.1. The most common and dominant symptom reported by the patient and/or their caregivers is an abnormally high pitch. Patients might also relate negative social reactions from peers and strangers when communicating, and gender confusion by listeners when speaking on the phone. The increased vocal fold tension causing elevated fundamental frequency can be observed on endoscopy and is represented by elongated vocal folds (due to excessive cricothyroid contraction). Other features of laryngeal structure, color, and movement fall within normal limits.


Acoustic signs of mutational falsetto are typically increased fundamental frequency, which will be present during sustained vowels and connected speech. This validates the clinician’s (and patient’s) perception of elevated pitch. In addition, auditory-perceptual features may include pitch breaks during connected speech, mild breathiness, and hard glottal attacks. These features reflect the patient’s lack of refinement in laryngeal and respiratory motor control. Interestingly, vegetative sounds such as coughing and throat clear, and sometimes humming, may be produced with normal voice quality. These behaviors can also be used during trial diagnostic probes intended to facilitate a reduction in pitch.


Treatment


The elevated fundamental frequency and subsequent high pitch in the context of a teenage or adult body is the most salient clinical characteristic of mutational falsetto. Once an accurate diagnosis is made, treatment for mutational falsetto can be efficient and highly successful. As with all voice treatments, a laryngeal exam performed by an otolaryngologist is a requirement prior to the initiation of voice therapy in order to rule in or out associated medical diagnoses. Voice therapy for mutational falsetto can often utilize a symptomatic approach focusing on the singular pitch abnormality. 31 Incorporation of circumlaryngeal massage and reposturing, shaping of low pitch vegetative voicing (e.g., grunts, growls), and humming are commonly utilized therapeutic strategies to establish a naturally lower pitch. Many patients quickly adapt their motor behaviors to accommodate the more natural pitch and are able to establish consistency in production within one treatment session. Some cases may need multiple treatment sessions, although in general cases of mutational falsetto do not require prolonged voice therapy.


2.4.5 Functional Voice Disorders Related to Phonotrauma


Phonotrauma is a physical injury that occurs to the tissue of the vocal folds secondary to vocal behaviors (phonation + trauma = phonotrauma). The vocal behaviors which lead to phonotrauma have often been labeled as vocal abuse and misuse. Phonotrauma can result in abnormal tissue changes to the vocal fold structure. The development of these changes can be conceptualized in this way: As the vocal folds oscillate, they continually contact each other during the closing and closed phases of vibration. These collisions create mechanical stresses on the vocal fold tissue, which include impact stress and shear stress. 38 As a result of these stresses, the vocal folds continually experience cellular activity associated with wound healing, a normal process that maintains the health and integrity of the tissue.


Wound healing progresses in three phases: (1) inflammation, (2) proteomic deposition within the extracellular matrix (ECM) and cellular deposition in the vocal fold epithelium (epithelialization), and (3) tissue remodeling. 39 When mechanical stresses are too great or too frequent, they can overburden this wound healing process, injure the vascular supply of the vocal folds, disrupt the integrity of tissue remodeling, and lead to phonotrauma. 40 The products of this disrupted wound healing process can be a combination of edema, epithelial hyperplasia, and disorganization of the ECM leading to the development of abnormal masses in the vocal fold cover.


Certain regions of the layered vocal folds appear more susceptible to phonotrauma, including the basement membrane zone (BMZ), mid-membranous region of the vocal fold, and tissue in the cartilaginous glottis. As described in Chapter 1 and illustrated in ▶ Fig. 2.3, the BMZ is the region between the vocal fold epithelium and superficial layer of the lamina propria (SLLP) which bonds these two layers together. The BMZ itself is layered, consisting of a superficial lamina lucida and a deep lamina densa. The lamina lucida contains collagen and fibronectin proteins running vertically which connect this layer to the epithelium above and lamina densa below. The lamina densa also contains collagen fibers which anchor it to the SLLP below. It has been suggested that the BMZ proteomic composition and structure is crucial for maintaining tissue integrity of the vocal fold cover and its links to the vocal ligament. 41 Injury to the BMZ secondary to phonotrauma is a leading theory explaining the development of many benign masses which develop on the medial edges of the vocal folds secondary to acute or chronic phonotrauma. 39,​ 42,​ 43



Basement membrane zone (BMZ) of vocal folds.


Fig. 2.3 Basement membrane zone (BMZ) of vocal folds.


2.4.6 Vocal Fold Nodules


Description


Vocal fold nodules (VFN) are bilateral exophytic (growing outward; raised above the surface of the epithelium) masses located at the mid-membranous medial edges of the vocal folds (▶ Fig. 2.4; ▶ Fig. 2.5). Along with vocal fold polyps, cysts, and pseudocysts, they have been labeled a type of benign mid-membranous lesion. When a functional voicing behavior leads to phonotrauma and tissue change, the mid-membranous region is the most common area affected. Because the exophytic mass will restrict vocal fold closure on either side of the “bumps,” closure pattern in mid-membranous lesions is often exemplified by an hourglass configuration, as illustrated in ▶ Fig. 2.6. VFN are symmetrical or quasi-symmetrical and can vary in size and shape depending on their stage of development and the patient’s voice use patterns.



Vocal fold nodules. Vocal fold nodules are exophytic masses at the medial edges in the middle of the membranous vocal fold (or the juncture of the anterior 1/3 and posterior 2/3 of total vocal fold ti


Fig. 2.4 Vocal fold nodules. Vocal fold nodules are exophytic masses at the medial edges in the middle of the membranous vocal fold (or the juncture of the anterior 1/3 and posterior 2/3 of total vocal fold tissue). They appear symmetric or quasi-symmetric calluses or bumps in the vocal fold epithelium.


(From Kendall K, Leonard R. Laryngeal Evaluation, 1st edition. New York: Thieme Publishers, 2010.)



Vocal fold nodules.


Fig. 2.5 Vocal fold nodules.


(From Bhattacharyya A. Laryngology: Otorhinolaryngology—Head and Neck Surgery Series. 1st edition. New York: Thieme Publishers, 2014.)



Example of hourglass closure pattern typically seen in mid-membranous lesions.


Fig. 2.6 Example of hourglass closure pattern typically seen in mid-membranous lesions.


(From Fried M, Tan M. Clinical Laryngology. 1st edition. New York: Thieme Publishers, 2014.)


Etiological Characteristics


VFN are caused by phonotrauma and develop at the mid-membranous region (often referred to as the “nodal point”) because this area absorbs the greatest impact stress from collision forces during vocal fold vibration. 38 VFN develop in stages, starting out as a soft, small edematous excrescence (an abnormal outgrowth) which over time develops into a more fibrous, larger, and stiffer mass. At a microscopic level, VFN are characterized by epithelial hyperplasia (it becomes thicker), increased density of the BMZ with increased deposition of fibronectin, and possible separation from the epithelium above, along with increased levels of hyaluronic acid and disorganized elastin fibers in the SLLP. 42,​ 43,​ 44,​ 45 These changes are brought on by disruptions in the normal wound healing process secondary to phonotrauma, and it is likely that some individuals are genetically more susceptible to this type of physical injury than others. For example, VFN occur with much greater frequency in adult females than in adult males, and the same degree of vocal use can induce the formation of nodules in one individual but not in another.


VFN are common in speakers or singers who habitually use their voice for long periods of time each day or who frequently push their voice to extremes (e.g., loud, forceful speaking or singing). Because VFN develop over time, it is thought that sustained phonotrauma over many weeks and months promotes their development rather than an acute instance of severe phonotrauma. It is not surprising that many professional voice users experience VFN, including teachers, professional and recreational singers, actors, and clergy to name just a few. VFN are seen much more frequently in females than in males. Different theories have been proposed to explain this phenomenon including the greater frequency of collisions experienced by female vocal folds (they have a naturally higher rate of vibration) and the lower amounts of hyaluronic acid (which acts as shock absorber) in female vocal folds compared to males. 46


Clinical Characteristics


Glottal closure pattern associated with VFN is usually an hourglass configuration with nodules in contact with each other. This glottal configuration results in aerodynamic, acoustic, and auditory-perceptual consequences. In speakers with VFN, subglottal pressure and transglottal airflow are often found to be increased. Acoustically there is increased perturbation (e.g., jitter, shimmer) and decreased cepstral peak prominence along with lower harmonic-to-noise ratio (indicating elevated noise in the acoustic signal). Perceptually the voice often has a breathy quality, or hoarse quality when a rough component (due to irregular vocal fold vibration) is also present (hoarseness is a combination of breathy and rough voice qualities). Depending on the patient’s compensatory reactions to the altered tissue structure, vocal strain might also be present. Some speakers with VFN also speak with elevated vocal intensity, which can be a clinical sign of the vocal behaviors which led to the development of the nodules.


Treatment


The recommended first-line treatment for VFN is almost always voice therapy, which can directly address the etiology of the impairment (vocal behaviors). When VFN are diagnosed in their early formative stages, the prognosis for voice therapy to facilitate a return to normal tissue remodeling and improved vocal function is very good, given a skilled clinician and a motivated patient. Even with small chronic nodules that are resistant to complete resolution, voice therapy can rehabilitate vocal function by restoring an appropriate physiological balance in the vocal subsystems to produce a voice that is acceptable in quality and function for the speaker.


As nodules mature over time, the tissue changes become more resistant to complete resolution secondary to voice therapy. Some long-standing vocal nodules will require surgical excision when voice therapy does not achieve adequate improvement to serve the speaker’s needs. There are some patients who undergo surgery, for various reasons, before receiving an appropriate dose of voice therapy. In such cases, voice therapy should always be recommended after surgery to facilitate restoration of a physiological balance in the subsystems of voice, promote healthier and more sustainable voice use patterns, and prevent a return of the VFN.


2.4.7 Vocal Fold Polyps


Description


The word “polyp” is a general term referring to a growth that protrudes from epithelium. Polyps can occur in many different parts of the body other than the vocal folds. Vocal fold polyps (VFP) are usually unilateral exophytic masses located at the mid-membranous medial edge of the vocal fold. Although VFP can occur bilaterally, a more common finding is the presence of contralateral reactionary swelling on the opposite vocal fold. These contralateral masses are often characterized by edema and are thought to form in response to repeated trauma from collisions with the stiff polyp. A period of voice rest (1–2 weeks) often reveals significant reduction in size of the contralateral swelling and illuminates the prominence of the primary exophytic polyp.


Etiological Characteristics


VFP are caused by phonotrauma and their development may be exacerbated by stimuli such as reflux, smoking, allergies, and infections. 47 One theory suggests that polyps develop secondary to phonotrauma-induced rupture of small blood vessels within the vocal folds. 47,​ 48 On endoscopy, it is not uncommon to visualize enlarged blood vessels leading into VFP, suggesting prior injury to the vasculature. At a microscopic level, VFP are characterized by epithelial hyperplasia and sometimes atrophy, increased fibronectin clustered around abnormal vascularity along with decreased collagen deposition in the region of the BMZ, and other vascular abnormalities in the vocal fold cover. 42,​ 43,​ 47 It has been suggested that vocal folds experiencing the formation of VFP are characterized by reduced collagen type IV deposition in the BMZ compared to other benign mid-membranous lesions, a condition which might put a speaker at risk for polyp development over some other benign mass. 42 Although histologically they are somewhat similar, VFP appear to result in greater changes below the epithelium (submucosal), while VFN result in greater changes to the epithelium itself. 49


VFP occur in similar clinical populations as nodules, although there is an increased frequency of polyps seen in males and VFP are uncommon in children. In addition to predominantly unilateral development, a difference between VFP and VFN is the belief that polyps can develop after an acute event, such as screaming or high intensity phonation throughout a day or multiple days. This contrasts with nodules, which develop over a longer period of time. VFP have a predilection to create stiff segments within the vocal folds which impact vibratory amplitude and mucosal wave to a greater extent than VFN. 49 This may result from VFP affecting the submucosal region to a greater extent. VFP can be characterized by a broad-based attachment at the mid-membranous region (referred to as sessile polyps) or be attached to this region by a thin stalk that allows the bulk of the polyp to move within the glottis during phonation (referred to as a pedunculated polyp).


Clinical Characteristics


Visually VFP can take on different forms including a smooth, bright red mass indicative of recent hemorrhage or dull reddish mass suggesting prior bleeding (▶ Fig. 2.7; ▶ Fig. 2.8). Some VFP take on a more fibrotic appearance as a dull opaque or dull white and smooth excrescence. The morphological qualities of polyps may depend on the age of the mass and how recent vascular injury was associated with their development. Other than specific visual characteristics, the clinical signs of VFP are very similar to those of VFN. Glottal configuration typically assumes an hourglass configuration with the polyp preventing anterior and posterior segments of the vocal folds from touching. Subglottal pressure and transglottal airflow are typically increased. Increased perturbation, decreased cepstral peak prominence, and decreased harmonic-to-noise ratio are also characteristic of VFP. The voice is often perceived as breathy or hoarse with strain present in some individuals due to functional compensation for the impairment.



Vocal fold polyp; This hemorrhagic polyp is filled with blood. A reactive contralateral lesion may also be present, hidden beneath the bright white mucous.


Fig. 2.7 Vocal fold polyp; This hemorrhagic polyp is filled with blood. A reactive contralateral lesion may also be present, hidden beneath the bright white mucous.


(From Kendall K, Leonard R. Laryngeal Evaluation, 1st edition. New York: Thieme Publishers, 2010.)



Vocal fold polyp; This fibrous polyp has a broad base along the mid-membranous vocal fold.


Fig. 2.8 Vocal fold polyp; This fibrous polyp has a broad base along the mid-membranous vocal fold.


(From Kendall K, Leonard R. Laryngeal Evaluation, 1st edition. New York: Thieme Publishers, 2010.)


Treatment


The recommended front-line treatment for VFP is often voice therapy, although prognosis for complete resolution of the mass and return to normal tissue remodeling is not as good compared to nodules. There is also debate as to whether voice therapy or surgery is the most effective first option. Factors that might influence voice therapy prognosis include the size and age of the lesion, the vocal demands of the patient, history of past lesions, and motivation of the patient. Whether or not surgical excision comes first, it is crucial that the patient receives voice therapy to target the underlying primary etiology. This will typically require a focus on vocal hygiene to identify and reduce phonotraumatic behaviors, in addition to techniques which restore a physiological balance in the vocal subsystems during speech production.


2.4.8 Vocal Fold Pseudocysts*


Description


Vocal fold pseudocysts are exophytic polyp-like edematous masses located most commonly at the mid-membranous region of the vocal fold. This subtype is a more recent label and has been classically described as an edematous polyp. As with the subsequent discussion of vocal fold cysts, we qualify this diagnosis with an asterisk because, in this case, current theory suggests that pseudocysts develop secondary to phonotrauma in the context of an underlying glottal incompetence due to scar or vocal fold paresis (i.e., an associated organic etiology). 50,​ 51,​ 52,​ 53


Etiological Characteristics


Pseudocysts develop in the subepithelial space very close to the BMZ. As illustrated in ▶ Fig. 2.9, these masses are described as translucent, noncapsulated and fluid-filled, with a blister-like appearance. 53 Pseudocysts occur most frequently in young, nonsmoking adult females and especially vocal professionals, and have been described as a focal type of unilateral edema in the SLLP, otherwise known as a type of unilateral localized (rather than diffuse) Reinke’s edema. 51,​ 52 The phonotrauma resulting in pseudocysts is thought to be a functional compensation for underlying scar or paresis that develops from viral infections, iatrogenic (e.g., surgical) injury, or idiopathic causes. It has been suggested that unilateral paresis causes asymmetrical vocal fold closure with subsequent imbalanced sheer stress on the paretic side. In the presence of hyperfunctional effortful closure to compensate for the glottal inefficiency, the asymmetrical stress patterns cause tissue injury developing into a pseudocyst. 52



Left vocal fold pseudocyst with reactive selling on right vocal fold; Pseudocysts appear as translucent exophytic masses that resemble a blister. These have classically been referred to as edematous p


Fig. 2.9 Left vocal fold pseudocyst with reactive selling on right vocal fold; Pseudocysts appear as translucent exophytic masses that resemble a blister. These have classically been referred to as edematous polyps but recent theory suggests their development is due to phonotrauma secondary to underlying vocal fold paresis.


(From Kendall K, Leonard R. Laryngeal Evaluation, 1st edition. New York: Thieme Publishers, 2010.)


Clinical Characteristics


The glottal configuration resulting from pseudocysts is an hourglass configuration. The glottal insufficiency subsequently affects aerodynamic, acoustic, and auditory-perceptual signs in a similar manner to other mid-membranous lesions. Perceptual signs attributed to these lesions include breathy voice quality and voice breaks with patient-reported symptoms including effortful phonation and vocal fatigue. Laryngeal endoscopy may reveal hyperfunctional characteristics similar to those seen in MTD. 52


Treatment


Voice therapy to rebalance the vocal subsystems can “unload” laryngeal hyperfunction causing the phonotrauma, but the voice is likely to remain dysphonic unless any underlying precipitating paresis is addressed. 52 The exophytic mass will often need surgical removal, although it is understood that if the underlying paresis is not addressed there can be a high rate of recurrence. 50,​ 53 It is also important to understand that published studies do not unanimously find 100% of patients diagnosed with pseudocysts have an underlying paresis. This suggests the likelihood that a subset of patients with pseudocyst-like exophytic lesions might present with phonotrauma as the primary and singular etiology. In such cases, a combination of trial voice therapy with subsequent medical management, if needed, would constitute an appropriate treatment approach.


2.4.9 Vocal Fold Cysts*


Description


Vocal fold cysts are unilateral or bilateral masses located most commonly at the mid-membranous region of the vocal fold. Cysts are epithelial-lined sacs that form in the SLLP. They can anchor to the BMZ or the vocal ligament, in which case they can significantly increase the stiffness of the vocal fold at the site of lesion. Cysts are a subtype of functional voice disorder that we label with an asterisk, because this lesion is also thought to have an organic origin in a number of cases or result from a synergistic combination of functional and organic causes.


Etiological Characteristics


Vocal fold cysts can be congenital or acquired. In congenital cysts, patients will often relate that they have a long history of dysphonia. In the authors’ clinical experiences and in a large number of reports, it is common that acquired cysts present in patients with heavy vocal demands or excessive voice use patterns, which along with their common mid-membranous location suggests a functional contribution to the development of cysts in many patients. There are two types of cysts that form in the vocal folds, mucous retention cysts and epidermoid cysts. Mucous retention cysts are thought to result from clogging of a mucous gland duct secondary to phonotrauma and/or some other irritant. Epidermoid cysts are thought to result from epithelial cells which become entrapped below the vocal fold surface. 35,​ 54 Vocal fold epithelium is constantly being remodeled secondary to phonation and old cells are normally shed off into the mucociliary blanket lining supraglottal region. Theoretically, if one or more cells become trapped within the vocal fold cover, they can migrate into the subepithelial space and potentially result in the formation of an epidermoid cyst.


Clinical Characteristics


Visually, cysts can take on varied clinical appearances depending on their size and depth (▶ Fig. 2.10; ▶ Fig. 2.11). Deeper cysts may appear as a small raised surface at the medial edge of a vocal fold, while more superficial or large cysts can appear as white or translucent masses below the surface of the epithelium which protrude into the glottis. Because the epithelium covers them, very small cysts may not be visible even though their effects on vibratory dynamics observed during stroboscopy can be seen. Cysts form deeper in the vocal fold cover than do VFN and VFP and some can anchor to the vocal ligament. For these reasons, they can create stiffer vocal fold segments than VFN and VFP and their impact on vibratory amplitude, mucosal wave, and symmetry tends to be greater. Large cysts or those that form closer to the BMZ can cause an excrescence on the medial edge of the vocal fold and in some cases result in a contralateral reactionary lesion. 55 Cysts result in a similar glottal configuration (hourglass), aerodynamic, acoustic, and auditory perceptual features as those that occur with VFN and VFP. The severity of these clinical signs will depend on the size of the cyst, its location along the medial edge of the vocal fold, and the presence of compensatory hyperfunction by the patient.



Vocal fold cyst. A unilateral cyst on the right vocal fold. The exophytic effect at the vibrating edge will result in an hourglass or incomplete closure pattern.


Fig. 2.10 Vocal fold cyst. A unilateral cyst on the right vocal fold. The exophytic effect at the vibrating edge will result in an hourglass or incomplete closure pattern.


(From Kendall K, Leonard R. Laryngeal Evaluation, 1st edition. New York: Thieme Publishers, 2010.)



Bilateral vocal fold cysts; Bilateral cysts occur less often than unilateral cysts. These are likely congenital as this adult patient reported a history of hoarseness since childhood.


Fig. 2.11 Bilateral vocal fold cysts; Bilateral cysts occur less often than unilateral cysts. These are likely congenital as this adult patient reported a history of hoarseness since childhood.


(From Fried M, Tan M. Clinical Laryngology. 1st edition. New York: Thieme Publishers, 2014.)


Treatment


The prognosis for cysts to resolve secondary to voice rest or voice therapy is poor, although some advocate for a trial of voice therapy prior to surgery. In most specialty voice centers, the front-line treatment for cysts is phonosurgery. The skill of the surgeon is important for cyst removal because they can easily rupture during removal, especially when anchored to the vocal ligament, and it is believed that material left within the vocal fold can develop into another cyst during the wound healing process. Some also believe that ruptured cysts can result in the development of scar or sulcus vocalis (see sections “Vocal Cord Scar” and “Vocal Fold Sulcus” later). Because cysts are often associated with phonotrauma, postsurgical voice therapy is appropriate to restore a physiological balance to the subsystems of voice and prevent reoccurrence of benign mid-membranous lesions.


2.4.10 Vocal Process Granulomas*


Description


Vocal process granulomas are unilateral or bilateral exophytic masses located on or just above the vocal process of the arytenoid, in the region of the cartilaginous glottis. Granulomas may form secondary to ulceration of tissue at the vocal processes in response to chronic irritation, which can include phonotrauma. We also qualify this subtype with an asterisk because granulomas are known to have multiple etiologies, which can include reflux irritation and iatrogenic injury from intubation. 56


Etiological Characteristics


Granulomas related to phonotrauma are thought to occur when the cartilaginous glottis oscillates at greater than normal amplitudes. The vocal fold tissue experiencing large amplitude oscillations and the greatest impact stress is typically at the mid-membranous region. When an individual speaks loudly, especially forcibly loud, they can recruit tissue oscillation in the cartilaginous glottis. Unlike anterior regions, underlying the epithelium and lamina propria at the cartilaginous glottis is hard cartilage, such that tissues at the vocal processes must oscillate over a hard surface instead of muscle. Chronic irritation subsequent to this type of phonation can cause ulceration at the vocal process and subsequent formation of granuloma tissue. At a microscopic level, granulomas are characterized by ulceration and cellular injury to the epithelium, with inflammation and edema in the vocal fold lamina propria. 57


Clinical Characteristics


The appearance of granulomas on endoscopy can be quite varied, ranging from small and round to large and irregular shape (▶ Fig. 2.12). Color varies from pearly white to dull yellow, and mucus tends to congregate at the site of the granuloma. In some cases, a reactive lesion or additional granuloma is present on the opposite vocal process with a groove shaped by the contours of the contralateral mass. Because laryngeal sensory receptors at the level of the glottis are located in the posterior regions, some patients with these lesions may complain of pain at rest, pain during phonation, or a globus sensation in the throat. Granulomas may not cause a dysphonia or disrupt vibratory dynamics due to their posterior placement, which typically does not interfere with oscillation of the membranous vocal folds. This means that aerodynamic, acoustic, and auditory-perceptual characteristics of voice in speakers with vocal process granulomas are often within normal limits. However, a secondary MTD can develop as a hyperfunctional response to the abnormal sensations produced by the granuloma, which would then produce clinical signs of symptoms associated with excessive muscle tension during phonation.



Vocal process granuloma; Granuloma on the left vocal fold with erythema and the development of possible granulation tissue on the left vocal process.


Fig. 2.12 Vocal process granuloma; Granuloma on the left vocal fold with erythema and the development of possible granulation tissue on the left vocal process.


(From Kendall K, Leonard R. Laryngeal Evaluation, 1st edition. New York: Thieme Publishers, 2010.)

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