TA + LCA paresis

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.

Other variants of vocal cord paresis include LCA-only, TA-only, PCA-only, and IA-only (interarytenoid muscle).

Photos of TA + LCA paresis:

LCA-only paresis

LCA-only paresis refers to weakness or paralysis of the vocal cord’s lateral cricoarytenoid (LCA) muscle, but with normal function of the vocal cord’s other muscles. 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 LCA-only paresis:

  • Movement: The vocal cord opens normally for breathing. From a distance, it can appear to close normally for voicing, but more acute and up-close inspection often shows a faint lag or reduction of crispness of approach to the midline, and inspection of the posterior commissure at close range shows that in fact it does not fully adduct.
  • Position and appearance: Position is normal during breathing, but again, the vocal cord does not come fully to the midline for voicing. A tell-tale indicator of LCA-only paresis 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 (as illustrated by a pair of photos below).
  • Appearance during voicing (under strobe lighting): Persistent slight gap between the vocal cords posteriorly, with the laterally turned vocal process, but no flaccidity of the cord with vibration. Normal tone and bulk of the vocal cord itself.
  • Voice quality: Weak and air-wasting, but without the luffing and diplophonia often apparent when the thyroartyenoid (TA) muscle is also paralyzed.

Other variants of vocal cord paresis include TA-only, TA + LCA, PCA-only (posterior cricoarytenoid muscle), and IA-only (interarytenoid muscle).

Photos of LCA-only paresis:

Palate paralysis

Loss of motion of the muscle in the soft palate, so that the palate does not properly elevate. Normally, the soft palate elevates to seal the nasopharynx when swallowing or when pronouncing any non-nasal sounds (in English, all sounds except for “n,” “m,” and “ng”). However, if the vagus nerve is damaged high in its course, near the base of skull, then the palate on that side can lose its ability to lift, and it remains down during the aforementioned tasks.

A patient with palate paralysis might experience not only hypernasality (speech resonance quality resembling that heard with cleft palate) but also nasal regurgitation, especially of liquids (“water comes out my nose when I swallow”), and also nasal emissions (a slight hissing sound that comes through the nose when the person produces strong consonants).


Vocal cord paralysis, unilateral

Neurogenic inability of one vocal cord to move. Unilateral vocal cord paralysis is associated with weak voice of a degree that can vary between individuals. Symptoms may include one or more of the following: weak, air-wasting dysphonia; inability to be heard in noisy locations; a tendency of the voice to be somewhat stronger in the morning but to “fade” with use; and a tendency to cough when drinking thin liquids.

See also: vocal cord paralysis, bilateral.



Vocal cord paralysis, bilateral

A neurological disorder in which the nerve supply to both vocal cords is absent. This may be as the result of injury through external trauma, thyroid surgery, or blunt or penetrating trauma to the neck. Sometimes vocal cord immobility due to scarring—from an endotracheal tube, for instance—is mistaken for vocal cord paralysis, though the distinction is usually easy to determine, provided that an appropriately intense and directed workup is done. In particular, this workup must include topical anesthesia to the larynx so as to enable an extremely close visualization of the posterior commissure and subglottis, which may uncover evidence of scarring.

See also: intubation injury, stenosis, vocal cord synechia, and vocal cord paralysis, unilateral.


Tonic variant spasmodic dysphonia

A variant of spasmodic dysphonia in which the spasms (and their effect on the voice) are sustained rather than intermittent. Tonic variant spasmodic dysphonia is to be distinguished from classic variant spasmodic dysphonia.

Individuals with a tonic variant of adductor spasmodic dysphonia have a sustained strained-sounding voice. Individuals with a tonic variant of abductor spasmodic dysphonia have a voice that is more or less continuously breathy. Tonic variant spasmodic dysphonia goes undiagnosed or misdiagnosed far more frequently than does classic variant spasmodic dysphonia.



Four subtypes of adductor spasmodic dysphonia, tonic variant :

Non dysphonic variant

Cry variant

Stage whisper variant

Vocal fry variant

Superior laryngeal nerve (SLN) paralysis

Paralysis of one of four main nerves serving the larynx, and two of the four if the paralysis is bilateral. SLN paralysis may be idiopathic or perhaps the result of neck surgery. The SLN internal branch supplies sensation to the interior of the upper part of the larynx; the external branch supplies motor innervation to the cricothyroid muscle.

Individuals with SLN paralysis, whether unilateral or bilateral, seem to compensate for the sensory deficits, provided that motor swallowing abilities are intact. On the other hand, they have symptoms of loss of upper voice and poor vocal projection. These two symptoms are easily verified by clinician elicitation and judgment of response.

Laryngeal dystonia

Laryngeal dystonia is a benign neurological condition affecting the larynx associated either with voice disturbance or, much less commonly, with breathing disturbance or, yet more infrequently, with both. The voice disturbance is referred to as spasmodic dysphonia. The breathing manifestation is called respiratory dystonia.

Intermittent whisper phonation

Intermittent whisper phonation is a term that describes the vocal phenomenology of abductor spasmodic dysphonia (AB-SD).