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Objectives: The exact pathophysiology leading to pharyngeal collapse in obstructive sleep apnea syndrome (OSAS) remains incompletely understood. Prior research has shown that normal men have a longer pharyngeal airway than women, and it has been hypothesized that this difference may play a role in the gender-related differences in OSAS. In the current study, we sought to study the potential relationship between the length of the collapsible pharyngeal segment, the upper airway length (UAL), and the severity of OSAS., Study Design: The hospital records were searched for all patients who had had polysomnography and also had had a computed tomography of the neck. A total of 24 such patients were identified who participated (15 men and nine women)., Measurements and Results: The UAL, the distance between the lower posterior part of the hard palate bone to the upper posterior part of the hyoid bone, was measured for all participants in the midsagittal plane. A correlation coefficient (Pearson r) of 0.406 was found between Respiratory Disturbance Index (RDI) and UAL (p = 0.049). When UAL was normalized to body height, a correlation coefficient (r) of 0.423 was found (p = 0.039). A gender-related difference in UAL was also found. Men with OSAS were found to have longer UAL even when normalized to body height (p = 0.003, unpaired t test) as compared with OSAS women., Conclusion: This study provides potential clinical relevance to prior studies in normal subjects, by demonstrating that men with OSAS have longer UAL than women with OSAS, independent of body size. In addition, the significant correlation between UAL and OSAS severity suggests that UAL may play a role in the pathophysiology of OSAS. These findings are consistent with our predictions from computational modeling studies.

Objective: Obstructive sleep apnea has a strong male predominance in adults but not in children. The collapsible portion of the upper airway is longer in adult men than in women (a property that may increase vulnerability to collapse during sleep). We sought to test the hypothesis that in prepubertal children, pharyngeal airway length is equal between genders, but after puberty boys have a longer upper airway than girls, thus potentially contributing to this change in apnea propensity., Methods: Sixty-nine healthy boys and girls who had undergone computed tomography scans of their neck for other reasons were selected from the computed tomography archives of Rambam and Carmel hospitals. The airway length was measured in the midsagittal plane and defined as the length between the lower part of the posterior hard palate and the upper limit of the hyoid bone. Airway length and normalized airway length/body height were compared between the genders in prepubertal (4- to 10-year-old) and postpubertal (14- to 19-year-old) children., Results: In prepubertal children, airway length was similar between boys and girls (43.2 +/- 5.9 vs 46.8 +/- 7.7 mm, respectively). When normalized to body height, airway length/body height was significantly shorter in prepubertal boys than in girls (0.35 +/- 0.03 vs 0.38 +/- 0.04 mm/cm). In contrast, postpubertal boys had longer upper airways (66.5 +/- 9.2 vs 52.2 +/- 7.0 mm) and normalized airway length/body height (0.38 +/- 0.05 vs 0.33 +/- 0.05 mm/cm) than girls., Conclusions: Although boys have equal or shorter airway length compared with girls among prepubertal children, after puberty, airway length and airway length normalized for body height are significantly greater in boys than in girls. These data suggest that important anatomic changes at puberty occur in a gender-specific manner, which may be important in explaining the male predisposition to pharyngeal collapse in adults.

Study Objectives: Obstructive sleep apnea (OSA) is characterized by repetitive pharyngeal collapse during sleep. Several techniques have been proposed to assess the collapsibility of the upper airway in awake humans, but sleep-wake comparisons have rarely been attempted and there are few studies comparing OSA patients to control subjects. We sought to compare two collapsibility measurement techniques between normal and apneic subjects, and between wakefulness and sleep., Design: We conducted three studies. First, we examined whether collapsibility assessed by negative pressure pulses (NPPs) during wakefulness reflected values during sleep in 21 normal subjects. Second, we determined in these normal subjects whether collapsibility during sleep assessed by NPPs was predictive of collapsibility measured by inspiratory resistive loading (IRL). Finally, we compared upper-airway collapsibility between apnea patients (n = 22) and normal volunteers (n = 38) during wakefulness by NPPs., Setting: Clinical and research laboratories at the Brigham and Women's Hospital., Participants: Two populations of normal subjects (n = 21 and n = 38) and OSA patients (n = 22)., Measurements and Results: Collapsibility during wakefulness, as measured by NPPs, correlated significantly with collapsibility during sleep (r = 0.62; p = 0.003). There was also a significant correlation between the two measures of collapsibility (IRL and NPP) during sleep (r = 0.53; p = 0.04). Both measures revealed a significant increase in pharyngeal collapsibility during sleep as compared to wakefulness. Finally, apnea patients had significantly greater pharyngeal collapsibility than control subjects during wakefulness (p = 0.017)., Conclusions: These data suggest that upper-airway collapsibility measured during wakefulness does provide useful physiologic information about pharyngeal mechanics during sleep and demonstrates clear differences between individuals with and without sleep apnea.

Although pharyngeal muscles respond robustly to increasing PCO(2) during wakefulness, the effect of hypercapnia on upper airway muscle activation during sleep has not been carefully assessed. This may be important, because it has been hypothesized that CO(2)-driven muscle activation may importantly stabilize the upper airway during stages 3 and 4 sleep. To test this hypothesis, we measured ventilation, airway resistance, genioglossus (GG) and tensor palatini (TP) electromyogram (EMG), plus end-tidal PCO(2) (PET(CO(2))) in 18 subjects during wakefulness, stage 2, and slow-wave sleep (SWS). Responses of ventilation and muscle EMG to administered CO(2) (PET(CO(2)) = 6 Torr above the eupneic level) were also assessed during SWS (n = 9) or stage 2 sleep (n = 7). PET(CO(2)) increased spontaneously by 0.8 +/- 0.1 Torr from stage 2 to SWS (from 43.3 +/- 0.6 to 44.1 +/- 0.5 Torr, P < 0.05), with no significant change in GG or TP EMG. Despite a significant increase in minute ventilation with induced hypercapnia (from 8.3 +/- 0.1 to 11.9 +/- 0.3 l/min in stage 2 and 8.6 +/- 0.4 to 12.7 +/- 0.4 l/min in SWS, P < 0.05 for both), there was no significant change in the GG or TP EMG. These data indicate that supraphysiological levels of PET(CO(2)) (50.4 +/- 1.6 Torr in stage 2, and 50.4 +/- 0.9 Torr in SWS) are not a major independent stimulus to pharyngeal dilator muscle activation during either SWS or stage 2 sleep. Thus hypercapnia-induced pharyngeal dilator muscle activation alone is unlikely to explain the paucity of sleep-disordered breathing events during SWS.