A man notes end-of-day hoarseness, which over time progresses to hoarseness earlier and earlier in the day. An otolaryngologist treats him with a proton pump inhibitor and subsequently excises leukoplakia from the left vocal cord, which is benign appearing on histopathologic exam. His voice becomes worse over the next three years, although his otolaryngologist reports that his vocal cords look better. His otolaryngologist feels this ongoing hoarseness may be something he just needs to tolerate. Ultimately though, I see him and after assessing his vocal capabilities and endoscopy find that he has a malignancy within the false vocal cord which is compressing the true vocal cord during phonation and impairing his vocal cord vibrations.
In this case, vocal capabilities pattern matching yields the following. His voice is gravelly during reading, gravelly being another descriptive term for roughness. On maximum phonation time testing the duration is 8 seconds and the quality is very rough. While maximum phonation time testing can be utilized to determine approximately how much air is converted to sound, the degree of harmonic sound production can also be noted. When he attempts to yell, it is mostly air that comes out and is not very loud.
Roughness suggests that there is an asymmetry and likely two sound sources even at his comfortable speaking pitch. During phonation, the unilateral false vocal cord mass is compressing the ipsilateral vocal cord, but not the opposite cord. This compression from the false cord tumor on the superior surface, near the anterior part of the left cord, both tensions the ipsilateral vocal cord and shortens the effective vibrating length on that side so that the left vocal cord tends to vibrate at a higher pitch than the right. We may attribute his shortened phonation time to partial loss of vibratory energy secondary to a damping effect from the false vocal cord mass pressing on the true vocal cord. This pressure also stiffens the left vocal cord.
When we try to test his upper vocal range, attempting to go higher in pitch, we hear a higher volume with more air leak and less roughness. As his pitch rises (cricothyroid muscle stretching the vocal cords) supraglottic squeeze pushes the mass more firmly onto the ipsilateral vocal cord, such that the left true cord stops vibrating entirely, essentially becoming extremely stiff from compression. Even though there is a complete closed phase, additional airflow is required to keep the opposite vocal cord vibrating against the compressed left cord and we hear breathiness. At one point there is a single, nearly clear, high note (A3#) that he squeaks out from a short segment of a vocal cord that vibrates normally.
Vocal capabilities pattern matching directs our endoscopic exam to take place at both low and high pitch and seek an explanation for the roughness in the low range and the breathiness at high volume and attempted high range. The compression from the false cord mass becomes the obvious source of his vocal impairment because it accounts for both these audible findings.
The left false vocal cord mass is easily seen and likely larger than three years ago when he was initially treated.
Ultimately an excisonal biopsy of the false vocal cord reveals the carcinoma enlarging beneath the mucosa. Similar findings may occur with supraglottic masses such as a dilated saccular cyst or a laryngocoele. This compression may be present in only a portion of the vocal range.
It is easy enough to focus one’s selective attention on the physical surface characteristics of the vocal cord and miss an even larger mass of the false vocal cord, particularly if the false cord’s surface is smooth. In this case, the left true vocal cord leukoplakia attracted the examiner’s visual attention so much that even during surgery, the false vocal cord was moved out of sight by the operative laryngoscope. Often such a mass is obvious in hindsight. However, if one listens to where the voice is impaired and then visualizes the vocal cord’s vibrations during that impairment, the etiology for hoarsness will be identified.
Even if the true vocal cord leukoplakia in this patient was impairing vibration to some degree, failure of the voice to improve after excision would warrant a reevaluation of vocal cord vibration to determine the etiology of the ongoing impairment. The most obvious visual finding may distract the examiner, when not correlating hoarseness with vocal cord vibration impairment.