Weakness or paralysis of both the thyroarytenoid (TA) and lateral cricoarytenoid (LCA) muscles of one vocal cord, but with normal function of that cord’s posterior cricoarytenoid (PCA) muscle. The TA muscle “inhabits” the vocal cord and normally provides bulk and internal tone to the cord. The LCA muscle helps to bring the vocal cord to the midline for voice production and, more specifically, to bring the “toe” of the arytenoid cartilage to the midline. The following are indicators of TA + LCA paresis:
- Movement: Position is normal during breathing, but the vocal cord does not move closer than the intermediate position for voicing. In other words, it is further lateral than the paramedian position one would see with paralysis of all three muscles: TA + LCA + PCA.
- Position and appearance: Due to the TA paralysis, the margin of the cord is slightly concave, the ventricle is capacious, and the conus area below the free margin is lacking in bulk. Due to the LCA paralysis, there is lateral turning of the vocal process. This lateral turning is seen best in low voice, and is a little less apparent with very high voice.
- Appearance during voicing (under strobe lighting): Flaccidity as indicated by increased amplitude of vibration; the lateral excursions become exaggerated and the mucosal wave increases. One may also see chaotic fluttering. The gap between the cords is particularly large because of the unopposed lateral pull of the intact PCA muscle. TA and LCA paresis is often mistaken for complete vocal cord paralysis (TA + LCA + PCA). To avoid this mistake, the examiner must notice this lateral position. The examiner can also try to make any such lateral pulling more evident by asking the patient to inhale sharply or, better yet, to sniff, which exaggerates the abductory movements of the patient’s vocal cords.
- Voice quality: Exceedingly weak and air-wasting. After successful medialization, the obligate falsetto and luffing may disappear, while some of the breathy-pressed quality may persist.