The thyroarytenoid is the bulk of the true vocal fold, whose medial fibres form the vocalis muscle that is the vibrating body of the voice. It shortens and thickens the vocal cord to produce lower frequencies of voice and adducts it for phonation and airway protection. Paralysis from recurrent laryngeal nerve injury produces the breathy, weak voice of vocal cord palsy.
| Origin | Inner surface of the thyroid cartilage |
|---|---|
| Insertion | Anterolateral surface of the arytenoid cartilage |
| Nerve Supply | Recurrent laryngeal nerve (CN X) |
| Blood Supply | Superior and inferior laryngeal arteries |
| Actions | Shortens and relaxes the vocal cord; Adducts the vocal cord to close the glottis; The medial portion (vocalis) fine-tunes vocal cord tension during phonation |
|---|
The vocalis portion works alongside the cricothyroid muscle in an antagonistic pair that controls vocal cord length and tension, with the cricothyroid lengthening and the vocalis shortening the cord, together producing the full range of vocal frequencies.
Recurrent laryngeal nerve paralysis produces thyroarytenoid and vocalis weakness causing a breathy, weak voice from incomplete glottic closure. Unilateral RLN palsy is managed with vocal cord medialization (injection augmentation or thyroplasty) to push the paralysed cord to the midline and allow the normal cord to make contact. Bilateral RLN palsy produces airway obstruction requiring tracheostomy.
Not externally palpable. Assessed by laryngoscopy showing cord mobility and glottic closure pattern.
Thyroarytenoid and vocalis denervation from RLN injury producing breathy voice and aspiration risk, managed with vocal cord medialization for unilateral palsy and tracheostomy for bilateral palsy.
