Rethinking the muscles of obstructive sleep apnea

Sleep medicine has long held the view that obstructive sleep apnea (OSA) is caused by sleep-related loss of tone in the tongue-protruding genioglossus muscle. Strong evidence points to abnormal muscle laxity as being the most fundamental cause of OSA: neuromuscular blockade induces relatively more airway instability in healthy airways compared to OSA airways, suggesting that healthy airways maintain some degree of tonic muscular activity during sleep [1,2]. However, multiple lines of evidence suggest that using genioglossus to maintain airway patency during wakefulness is a compensatory strategy used when the normal method of maintaining airway patency has failed, and this compensatory strategy fails during sleep when the tongue relaxes [3]. The idea that OSA is caused by abnormal relaxation of the tongue during sleep does not explain many features associated with OSA: low hyoid bone, retrognathia, high Mallampati score, temporomandibular joint (TMJ) disorders, downward facial growth, etc. We need an understanding of OSA that can explain these phenomena. In this editorial, I will briefly review some of the evidence that disputes the idea that genioglossus is the primary dilator of the pharynx and point toward a revised view of the muscles in OSA.

Arguments that genioglossus is not the primary dilator of the pharynx

1. If sleep-related loss of genioglossus tone were the core problem in OSA, hypoglossal nerve stimulation would be a perfect treatment. Instead, it is successful in only about 1/3 of unselected patients [4].

2. Healthy people have low resting genioglossus tone while awake that reduces even further during sleep. People with OSA have significantly increased resting genioglossus tone while awake, which is variable during sleep [5].

3. Stimulation of genioglossus pulls the hyoid bone forward and upward [6]. Hence, the higher tone in genioglossus in people with OSA should elevate the hyoid bone, yet the hyoid bone descends. This strongly suggests that the low hyoid bone position in OSA is due to loss of the primary means of support of the hyolaryngeal complex (hyoid and thyroid cartilage) from the skull base, and increased activation of genioglossus is a compensatory strategy for this loss.

Reasons stylopharyngeus laxity is likely a large part of OSA pathophysiology

1. Stylopharyngeus originates from the styloid process and inserts into the thyroid cartilage and tonsillar capsule (Figures 1(a,b)), with variable interconnections with the superior and middle pharyngeal constrictors [7].

1. Stylopharyngeus is the only muscle positioned to support the lateral pharyngeal walls. Lateral wall collapse strongly correlates with OSA severity and hypoxemic events [8].

2. Loss of tone in stylopharyngeus can anatomically explain tonsillar prolapse into the airway in OSA [9].

3. Stylopharyngeus’ lateral tension on the oropharyngeal isthmus reduces Mallampati score (Figure 1b), nicely explaining its correlation with OSA risk.

4. The differences in transverse cross-sectional airway shapes in healthy vs OSA subjects [10] can be explained by differential tone of stylopharyngeus and genioglossus, with increased tone of stylopharyngeus in normal airways, and decreased tone of stylopharyngeus and increased tone of genioglossus in OSA airways (Figure 1c).

5. Guilleminault et al. [11] showed that loss of stylopharyngeus activity was associated with obstructive events in sleep despite continued genioglossus activity. Stylopharyngeus showed continued activity in healthy subjects even during phasic REM, which is the time of most profound muscle hypotonia.

Figure 1. (a) Stylopharyngeus and the tandem action of palatopharyngeus and levator veli palatini support the thyroid cartilage from the skull base. (b)Stylopharyngeus and palatopharyngeus both insert in the tonsillar capsule (approximately at the blue dot) and on the thyroid cartilage. Through the interconnections in the tonsillar capsule, stylopharyngeus can keep the tonsils out of the airway, widen the oropharyngeal isthmus, and lower the Mallampati score. Not shown are the hyoid bone and stylopharyngeus’ interconnections with the pharyngeal constrictors, which will also widen the pharynx laterally. Figure is based on a public domain illustration available at: https://commons.wikimedia.org/wiki/File:Ротова_порожина.jpg, which was extensively modified by Dr. Dewald. (c) Differences in cross-sectional airway shapes can be explained by predominantly laterally oriented tension on the pharyngeal walls by stylopharyngeus (STP, red arrow) in healthy airways and predominantly anteriorly oriented tension by genioglossus (GG, Orange arrow) in OSA. Cross-sectional airway shapes based on reference [10].

Rethinking airway stability

The thyroid cartilage is the entrance to the lower airway and is directly supported from the cranial base by stylopharyngeus and the tandem combination of palatopharyngeus and levator veli palatini (Figure 1). There are secondary supports via connections with the hyoid bone and its attachments as well as through the pharyngeal constrictor muscles and their attachments. Every breath we take exerts significant downward force on the thyroid cartilage when negative pressure in the chest is generated [12]. If stylopharyngeus is dysfunctional, downward respiratory forces will be transmitted to the superior pharyngeal constrictor, which attaches to the mandible and the medial pterygoid plates. Excessive downward respiratory forces on the mandible could have serious ramifications for the stability of the TMJ. Downward forces on the medial pterygoid plates could lead to deformation and excessive lower facial height. Lack of lateral tension on the medial pterygoid plates could lead to a narrow palate.

We need to figure out why stylopharyngeus is not working properly, and how to fix it, if we are to properly address the problems of OSA, aberrant facial development, and TMJ disorders.