Different studies support the statement that patients with POSA are more likely to have a lower BMI, neck circumference, and AHI than their non-positional counterparts. The mechanism underlying this, however, is still unclear. Saigusa et al. performed awake pharyngeal magnetic resonance imaging and cephalometric radiography on 10 positional and 10 non-positional Japanese patients that were matched for BMI, AHI, and age. The authors found both craniofacial and soft tissue volume differences in positional patients compared to those who were non-positional. Positional patients had more backward positioning of the lower jaw with smaller lower facial height and craniofacial volume. They were also noted to have a smaller volume of lateral pharyngeal wall soft tissue [8].

Teerapraipruk et al. also concur that craniofacial structural changes may play an important role in POSA given that in their population of Asian patients, the average BMI noted in both positional and non-positional patients was lower than the average BMI noted in the Western population [9]. It is possible that a subgroup of patients initially develops OSA that is positional, but when left untreated or undiagnosed, they increase in weight as a consequence of their disease and further develop an OSA that is more severe and non-positional in nature.

Spiegel et al. performed a randomized 2-period, 2-condition crossover clinical study in 12 healthy young men where subjects underwent 2 days of sleep restriction and 2 days of sleep extension. It was found that sleep restriction was associated with increased levels of ghrelin, a hunger-stimulating hormone, and decreased levels of the hunger-suppressing hormone leptin. As a result, increases in hunger and appetite were noted in this sleep-deprived population [10]. It can be postulated that patients with OSA who suffer from fragmented sleep may experience the metabolic changes described above with an increase in weight and subsequently become obese. Patients may also have decreased energy secondary to sleep deprivation, rendering physical activity more difficult and less desirable, which compounds the issue of weight gain and obesity.

Sunnergren et al. believe that the underlying etiology may be neurological [11]. The airway remains open during sleep due to reflexes that dilate the upper airway musculature. These reflexes would be most active in the supine position to counteract gravity and muscular hypotonia. A literature review by Svanborg et al. reports on various studies looking at neurological and electrophysiological findings in the upper airway of non-apneic snorers and patients with OSA [12]. Snoring occurs as a result of vibration of the upper airway soft tissues. Studies have reported that long-term soft tissue vibration can cause local nerve lesions and injury [13, 14]. Svanborg et al. then theorized that repeated snoring over time may cause neuronal lesions with compromise to the dilator reflexes of the upper airway [15]. A study was performed using concentric needle electromyography (EMG) in the palatopharyngeus muscle of 12 OSA patients and 15 non-apneic snorers and 5 controls. Ten out of 12 OSA patients had local motor neuropathy, while only 3 out of 15 non-apneic snorers and none of the controls had neuropathy. They used this finding to hypothesize that progression from non-apneic snoring to OSA may be due to neurogenic injury [15]. Sunnergren et al. have further theorized that the severity of upper airway neuropathy may not only determine progression of non-apneic snoring to OSA but also place POSA as an intermediary between snoring and OSA. The more severe the neuropathy, the more likely that a patient would have problems dilating their upper airway in all sleeping positions and not just supine [11].