18
Decreased Vibratory Amplitude
The amplitude of vocal fold vibration is defined as the degree of horizontal displacement of the vocal folds during vibratory activity as viewed on videostroboscopy. During normal phonation, the vocal folds remain closed, while subglottal pressure builds with continued exhalation, until subglottal pressure increases enough to blow them apart. As air flows through the glottis, medial to lateral excursion of the vocal folds occurs. The amplitude of vibration is generally measured as the degree of displacement from the midline to the maximum lateral point of excursion in the vibratory cycle. Although there is no “normal” value for amplitude, it is generally accepted that an excursion of roughly one third of the width of the vocal fold should occur in normal subjects at a habitual pitch and loudness (Video Clip 3). The amplitude of vibration can vary due to physiologic factors (pitch, intensity) and pathologic factors (vocal fold lesions/stiffness, paresis, and vocal fold tension) (Video Clips 5 and 6). Both of these factors will be addressed in this section (see also Chapter 16).
Decreased vibratory amplitude is one of the most common findings associated with vocal fold pathology. When the amplitude of vocal fold vibration is asymmetric (specifically, a reduction in amplitude on one vocal fold compared with that of the “normal” side), this is almost always associated with vocal fold pathology. Certain general factors, however, have an influence on vibratory amplitude of the vocal folds, and they can be broken down into physiologic and pathologic factors (Table 18.1).
Physiologic Factors Associated with Reduced Vibratory Amplitude
Normal Reductions in Vibratory Amplitude
When assessing vibratory amplitude, it is helpful to first observe for symmetry. Symmetrically reduced vibratory amplitude can, and often is, due to normal variations in pitch and intensity of phonation. For example, when a singer is demonstrating his or her full vocal range during a typical videostroboscopic exam, one should expect the amplitude of vibration to decrease an equal amount in both vocal folds as the patient sings progressively higher notes on the scale (Video Clips 4 and 5). This is due to a tightening or stiffening of the vocal fold as pitch is increased, resulting in reduced excursion of the vocal fold from the midline during phonation. One must always be cognizant of the pitch of the patient’s voice when assessing amplitude of vibration and take this into account.
Physiologic factors that result in reduced vibratory amplitude: |
Decreased subglottal pressure (usually due to reduced intensity/volume of vocalization) |
Increased fundamental frequency/pitch |
Pathologic factors that result in reduced vibratory amplitude: |
Shortening of the vibratory portion of the membranous vocal fold |
Stiffness of the vocal folds |
Increased mass of the vocal folds |
Increased tension of the vocal folds |
Incomplete vocal fold closure |
In the same way, as the patient phonates in a softer voice (lower intensity), the amplitude should be reduced in a symmetric fashion. Reduced volume/intensity is associated with a reduction in the subglottal pressure generated during phonation. As subglottal pressure decreases, the amplitude of vibration is reduced. In essence, the reduction in airflow causes a decrease in the displacement of the vocal folds in a medial to lateral direction (Video Clip 6).
If one takes into account both of the two factors discussed above (intensity and fundamental frequency), then one should expect that the maximum amplitude of vibration would be expected to occur with loud, low-pitched phonation (low fundamental frequency at a high intensity). This is an excellent method to observe the maximum pliability of the vocal folds. Conversely, a patient using a soft, high-pitched voice (low intensity at a high frequency) is going to demonstrate a maximum reduction in vibratory amplitude. This is especially true if there is incomplete closure as well—as seen in falsetto voice (Video Clip 4).
The wide variation in vibratory amplitude observed in the same patient over the full spectrum of his or her phonatory range and intensity sometimes makes absolute determinations of “normal” vibratory amplitude problematic. As stated before, if there appears to be no pathology of the vocal folds present and the amplitude “reduction” appears symmetric, it is probably just due to increased pitch and/or reduced intensity of the patient’s phonation. The exceptions to this rule are the disorders of muscle tension, such as adductor spasmodic dysphonia and muscle tension dysphonia (discussed later).
Pathologic Factors That Result in Reduced Vibratory Amplitude
Shortening of the Vibratory Portion of the Membranous Vocal Folds
This is not commonly seen clinically and is usually related to a congenital or traumatic anterior glottic web. The formation of an anterior web between the vocal folds creates a nonvibratory segment, as vocal fold approximation cannot occur in this region. This results in a shortened segment of the remaining membranous vocal fold. This shortened segment is incapable of achieving the extent of excursion during vibration that a longer, normal vocal fold can achieve. As a result of this, the amplitude of vibration is dampened.
Stiffness of the Vocal Folds
This condition is one of the most common reasons for a reduction in vibratory amplitude. The stiffness can be due to several pathologic factors including scarring, infiltration by carcinoma, and submucosal benign lesions that are tightly bound to the epithelium and/or vocal ligament such as cysts or fibrous bands. It is generally easy to differentiate between these different entities (Video Clips 32 to 35).
One of the most concerning findings on a videostroboscopy examination is a vocal fold with an epithelial lesion (leukoplakia/erythroplakia/papillomatous changes) that demonstrates severely reduced or absent amplitude/mucosal wave. The surface changes of the epithelium are generally obvious on routine laryngoscopy. In these cases, the findings on videostroboscopy are potentially important clinically. The reduction in amplitude is suggestive of carcinomatous infiltration into the lamina propria, which creates a stiff, nonvibratory vocal fold. Another possible reason for the reduction of amplitude in these cases involves the increase in mass due to the epithelial lesion (see later), therefore both potential factors should be kept in mind when examining these patients (Video Clip 35).
A scarred vocal fold can frequently appear “normal” on routine laryngoscopy because of the lack of epithelial changes. A scarred vocal fold results in stiffness because of deposition of fibrous tissue in the superficial lamina propria. The elimination of this potential space and the resulting loss of pliability leads to a reduction or loss of vibratory amplitude on stroboscopy. Loss of vibratory activity in the context of a suggestive history (laryngeal biopsy, aggressive resection of a benign lesion, external beam radiation) is critical in making the clinical diagnosis of scar (Video Clips 32 and 33).
Certain submucosal lesions (cyst and fibrous band) can be subtle on routine laryngoscopy, in contrast with more common and obvious benign vocal fold pathology (polyps, nodules). With vocal fold cysts, the lesion is either on the infraglottic (mucous retention) or superior surface (epidermal inclusion) of the vocal fold, and its outline may be indistinct. Vocal fold cysts are located in the superficial lamina propria and are frequently adherent to the epithelium and/or vocal ligament, resulting in stiffness and a substantial reduction in vibratory amplitude and mucosal wave (Video Clips 26 and 34). Fibrous bands are another form of vocal fold pathology, and these lesions represent an accumulation of fibrous tissue within the superficial lamina propria. This material is typically amorphous in nature and often has thin extensions anteriorly and posteriorly within the vocal fold giving it a fusiform shape. The deposition of fibrous tissue is similar to scar formation, but the tissue is organized into a lesion that is discrete from the surrounding tissue. Because this tissue behaves much like scar in terms of vibratory activity, there is a reduction or (more typically) a complete absence of vibratory amplitude.
Increased Mass of the Vocal Folds
Increased mass of the vocal folds is typically related to more extensive vocal fold pathology of either the epithelium or of the superficial lamina propria. Typical examples are large mass lesions such as papilloma, large hyperkeratotic plaques, and polyps. The lesion acts as a resistive force in the displacement of the vocal folds, and this effect is magnified when the lesion also causes incomplete closure of the vocal folds (which is quite common) as is discussed later. Another example of a lesion that may lead to reduced or absent vibratory amplitude is Reinke’s edema (also referred to as polypoid corditis). Interestingly, the mucosal wave in these lesions is often increased because of the increased pliability of the polypoid/myxoid component of the superficial lamina propria. When the polypoid degeneration results in significant increase in mass, this may reduce the amplitude of vibration (Video Clip 36). In a similar fashion, acute edema of the vocal folds due to infection or inflammation will lead to a reduction of vibratory amplitude (Video Clip 37).
Increased Tension of the Vocal Folds
Unlike all of the previously mentioned causes of reduced vibratory amplitude, the category of increased vocal fold tension consists principally of muscle tension disorders and not an actual pathophysiologic derangement of the vocal fold itself. Examples include adductor spasmodic dysphonia and muscle tension dysphonia. Adductor spasmodic dysphonia (adductor SD) is a neurologic disorder (dystonia) that results in excessive and forceful closure of the vocal folds during most phonatory tasks. The effect is most marked on words beginning with vowels and nasal consonants. Muscle tension dysphonia (MTD) is a functional disorder that presents with a consistently strained voice across phonatory tasks (Video Clip 20). With videostroboscopic studies, the amplitude of vibration with adductor SD and MTD is markedly diminished or completely absent. It is often difficult to assess vibratory parameters in many of these cases due to the lack of vocal fold visualization during phonation secondary to supraglottic compression. The excessive lateral compressive forces prevent displacement of the vocal fold and thus dampen or completely extinguish vibratory amplitude. During singing, patients with adductor SD may have normal vibratory amplitude, as the spasmodic activity can be absent during activities outside of the realm of connected speech. In addition, patients with MTD may have a normalization of vibratory amplitude if the muscle tension patterns are eliminated using voice therapy techniques that “unload” the abnormal muscular compressive forces. (See Chapter 25 for a full discussion of these conditions.)
Incomplete Vocal Fold Closure
Incomplete vocal fold closure can be caused by vocal fold paralysis and paresis. In severe cases, there may be a large (3 mm or more) glottal gap during phonation, and this may prevent any vibration whatsoever. In less severe cases, incomplete vocal contact results in diminished subglottal pressure buildup, so that the displacement force of the vocal folds during phonation is decreased. The reduction in displacement of the vocal folds during phonation results in diminished amplitude of vibration in the vocal fold (Video Clips 25, 27, and 28).
Conclusion
The amplitude of vocal fold vibration depends on the interaction between the superficial tissues at the margin of the vocal fold (superficial lamina propria), the mass of the vocal fold, the length of the vocal fold, the subglottic pressure, and the medial compressive forces generated by muscular contraction. The differential diagnosis of a decrease in vibratory amplitude includes pathology that impacts any of these factors.
Suggested Reading
Hirano M, Bless DM. Videostroboscopic Examination of the Larynx. San Diego, CA: Singular Publishing Group; 1993