Weakness or paralysis of the vocal cord’s thyroarytenoid (TA) muscle, but with normal function of the vocal cord’s other muscles. The TA muscle “inhabits” the vocal cord and normally provides bulk and internal tone to the cord. The following are indicators of TA-only paresis:
- Movement: The vocal cord opens normally for breathing and closes normally for voicing.
- Position and appearance: Position is normal. Typically, the margin of the cord is slightly concave, the ventricle is capacious, and the conus area below the free margin is lacking in bulk.
- Appearance during voicing (under strobe lighting): Closure at the posterior commissure is complete and symmetrical bilaterally. Under strobe light, one sees flaccidity as indicated by increased amplitude of vibration; the lateral excursions become exaggerated and the mucosal wave increases. One may also see chaotic fluttering.
- Voice quality: Weak and air-wasting and often indistinguishable from a case of complete vocal cord paralysis—TA, LCA (lateral cricoarytenoid), and PCA (posterior cricoarytenoid).
Photos of TA-only paresis:
Paresis, TA-only: before and after an Implant
Vocal Cord Paresis (Thyroarytenoid Muscle) Accentuated by Disuse
This woman illustrates that vocal cords are inhabited by muscle (thyroarytenoid muscle, to be precise). If that muscle atrophies due to paresis (partial loss of nerve supply), this alone can weaken the voice. That is what happened to her 10 years ago, in her fifties, after thyroid surgery. Initially the left cord did not move (paralysis). Then movement returned and along with it, her voice gradually gained in strength. When recovery was maximal, the vocal cord abducted (opened) and adducted (closed) normally. She also regained “90%” of her voice; while the muscle within the vocal cord did not recover fully, there was sufficient strength and tone to mostly “keep up” with the demands of her moderate voice use. Technically, she began with paralysis (of TA, LCA, and PCA) but after recovery, had a TA-only paresis as shown in photos 1-3 below. All was well for 10 years as she had a perfectly functional voice.
Ten years later, now in her sixties, she developed a bad URI (not Covid-19) and voice deteriorated in the midst of hard bouts of coughing. At the same time, due to retirement, and self-quarantine, she was using voice very little. Two months later, still using voice very little and even intentionally “resting it,” her voice is extremely weak. The explanation is that by figuratively putting her voice in bed, she has added disuse atrophy to the longstanding paresis. How do we know this? The answer is in photos 4-5 below. And the appropriate initial treatment? Voice building exercises.
TA-only Paresis before and after Voice Gel Injection
Just Bowing? No, TA-only Paresis
TA-only Paresis, before and after Recovery
Another TA-only Paresis
Arytenoid Mismatch Makes for Gravelly Voice Quality Is Hard to Fix in Some Cases of Vocal Cord Paralysis
One could medialize more aggressively posteriorly on the left, hoping to raise the level of the cord, but often attempts to compensate for arytenoid mismatch such as that seen here are only modestly successful. Arytenoid superstructure is not useful for assessment of match; instead, the examiner should judge match at the vocal processes.