Effect of Uvulopalatopharyngoplasty on Upper Airway Collapsibility in Obstructive Sleep Apnea

Schwartz, Alan R.; Schubert, Norman; Rothman, Warren; Godley, Frederick A.; Marsh, Bernard R.; Eisele, David W.; Nadeau, John; Permutt, Lisa; Gleadhill, I.; Smith, Philip L.

doi:10.1164/ajrccm/145.3.527

Cited by 159 publications

(103 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, the magnitude of the change in Pcrit was predictive of the change in sleep-disordered breathing index following surgery. Because the present modeling study and the Schwartz clinical study addressed different populations, no direct comparisons can be made regarding the absolute values for Pcrit, although the magnitudes of the effects were comparable (ie, Pcrit 0.2 to −3.1 cm H 2 O in Schwartz et al 34 vs Pcrit −13 to −18 cm H 2 O in present study). Of note, because the Pcrit values in normal subjects are somewhat variable in the literature, our simulations are most useful for examining the relative changes in Pclose measures, since the absolute values will depend on the initial Pclose applied to the model.…”

Section: Discussionmentioning

confidence: 59%

See 1 more Smart Citation

The Impact of Anatomic Manipulations on Pharyngeal Collapse

Huang

White

Malhotra

2005

Chest

View full text Add to dashboard Cite

Obstructive sleep apnea (OSA) is a common disease with important neurocognitive and cardiovascular sequelae. Existing therapies are unsatisfactory, leading investigators to seek alternative forms of anatomic manipulation to influence pharyngeal mechanics. We have developed a two-dimensional computational model of the normal human upper airway based on signal averaging of MRI. Using the finite element method, we can perform various anatomic perturbations on the structure in order to assess the impact of these manipulations on pharyngeal mechanics and collapse. By design, the normal sleeping upper airway model collapses at −13 cm H 2 O. This closing pressure becomes more negative (ie, less collapsible) when we perform mandibular advancement (−21 cm H 2 O), palatal resection (−18 cm H 2 O), or palatal stiffening (−17 cm H 2 O). Where clinical data are available in the literature, the results of our model correspond reasonably well. Furthermore, our model provides information regarding the site of obstruction and provides hypotheses for clinical studies that can be undertaken in the future (eg, combination therapies). We believe that, in the future, finite element modeling will provide a useful tool to help advance our understanding of OSA and its response to various therapies. Keywords breathing; computational model; lung; MRI; obstructive sleep apnea; pharyngeal collapse Obstructive sleep apnea (OSA) is an important disorder due to both its high prevalence and its well-established sequelae. 1,2 Although effective therapies exist for sleep apnea, [3][4][5][6] investigators continue to seek alternative methods to manipulate pharyngeal mechanics/ anatomy with the ultimate goal of improving currently available therapeutic modalities. [3][4][5][6][7][8] Various different methods of manipulating pharyngeal mechanics have been used to treat snoring in individuals with largely normal upper airway anatomy and to treat sleep apnea in those with a compromised pharyngeal lumen. These methods include weight loss, oral appliances, and upper airway surgery. 9-11 However, these techniques have also been problematic due to variable efficacy and minimal ability to predict therapeutic response. A number of investigators have attempted to determine which patients are most likely to respond to treatment, but without great success. [12][13][14][15][16] We believe that improvements in our Our group has been involved in the development of a computational model to better understand the behavior of the human upper airway. 17 We have used finite element analysis, which is a mathematical technique to quantitatively analyze the behavior of a given mechanical structure. We have previously published our two-dimensional model that uses anatomically correct structure from MRI of normal human subjects. 17 With this model, we have used the critical closing pressure (Pcrit) as our outcome measure to assess the collapsibility of the upper airway. 18 Using finite element analysis, we sought to determine the impact of mandibular advancement, pa...

show abstract

Section: Discussionmentioning

confidence: 59%

“…Schwartz et al 34 reported on the Pcrit of patients undergoing UPPP measured before and after surgery. In this population with severe sleep-disordered breathing, consistent reductions were seen in Pcrit in patients undergoing surgery.…”

Section: Discussionmentioning

confidence: 99%

The Impact of Anatomic Manipulations on Pharyngeal Collapse

Huang

White

Malhotra

2005

Chest

View full text Add to dashboard Cite

show abstract

“…The severity of upper airway obstruction during sleep is related to quantitative differences in pharyngeal collapsibility, as reflected by elevations in the critical closing pressure (Pcrit). Moreover, as Pcrit fell below a minimally negative threshold of approximately 25 cm H 2 O, sleep apnea remitted, suggesting that changes in Pcrit play a pivotal role in the pathogenesis of this disorder (see Figure 1, right) (25,(57)(58)(59)(60)(61). In further studies, investigators have demonstrated that Pcrit is determined by mechanical and neural factors that regulate pharyngeal collapsibility (62)(63)(64)(65)(66)(67).…”

Section: Obesity and Upper Airway Neuromechanical Control Modeling Upmentioning

confidence: 95%

Obesity and Obstructive Sleep Apnea: Pathogenic Mechanisms and Therapeutic Approaches

Schwartz

Patil²,

Laffan

et al. 2008

Proceedings of the American Thoracic Society

571

395

View full text Add to dashboard Cite

Obstructive sleep apnea is a common disorder whose prevalence is linked to an epidemic of obesity in Western society. Sleep apnea is due to recurrent episodes of upper airway obstruction during sleep that are caused by elevations in upper airway collapsibility during sleep. Collapsibility can be increased by underlying anatomic alterations and/or disturbances in upper airway neuromuscular control, both of which play key roles in the pathogenesis of obstructive sleep apnea. Obesity and particularly central adiposity are potent risk factors for sleep apnea. They can increase pharyngeal collapsibility through mechanical effects on pharyngeal soft tissues and lung volume, and through central nervous system-acting signaling proteins (adipokines) that may affect airway neuromuscular control. Specific molecular signaling pathways encode differences in the distribution and metabolic activity of adipose tissue. These differences can produce alterations in the mechanical and neural control of upper airway collapsibility, which determine sleep apnea susceptibility. Although weight loss reduces upper airway collapsibility during sleep, it is not known whether its effects are mediated primarily by improvement in upper airway mechanical properties or neuromuscular control. A variety of behavioral, pharmacologic, and surgical approaches to weight loss may be of benefit to patients with sleep apnea, through distinct effects on the mass and activity of regional adipose stores. Examining responses to specific weight loss strategies will provide critical insight into mechanisms linking obesity and sleep apnea, and will help to elucidate the humoral and molecular predictors of weight loss responses.

show abstract

“…The critical closing pressure (P crit ) has been used to characterize upper airway function. In both children and adults with sleep-disordered breathing, ranging from primary snoring to obstructive sleep apnea, the value of P crit correlates with the degree of obstruction (21,27,28) and decreases after surgical treatment of obstructive apnea (21,26). Although this model is useful, recent studies have shown that, during natural sleep, the model is modified by the effect of upper airway neuromotor reflexes in response to factors such as subatmospheric pressure and CO 2 (6,9,10).…”

Section: Pfrmentioning

confidence: 99%

Upper Airway Dynamic Responses in Children with the Obstructive Sleep Apnea Syndrome

et al. 2005

View full text Add to dashboard Cite

Normal children have a smaller upper airway than adults, but, nevertheless, snore less and have less apnea. We have previously shown that normal children have an upper airway that is resistant to collapse during sleep. We hypothesized that this resistance to collapse is due to preservation of upper airway neuromotor responses during sleep. Furthermore, we hypothesized that upper airway responses would be diminished in children with the obstructive sleep apnea syndrome (OSAS). We therefore compared the upper airway pressure-flow relationship during sleep between children with OSAS and controls. Measurements were made by correlating maximal inspiratory airflow with the level of nasal pressure applied via a mask. Neuromotor upper airway activation was assessed by evaluating the upper airway response to 1) hypercapnia and 2) intermittent, acute negative pressure. We found that children with OSAS had no significant response to either hypercapnia or negative pressure during sleep, compared with the normal children. After treatment of OSAS by tonsillectomy and adenoidectomy, there was a trend for normalization of upper airway responses. We conclude that upper airway dynamic responses are decreased in children with OSAS but recover after treatment. We speculate that the pharyngeal airway neuromotor responses present in normal children are a compensatory response for a relatively narrow upper airway. Further, we speculate that this compensatory response is lacking in children with OSAS, most likely due to either habituation to chronic respiratory abnormalities during sleep or to mechanical damage to the upper airway. In children, OSAS is related to adenotonsillar hypertrophy. Most children with OSAS have large tonsils and adenoids, and improve after T&A (1). Nevertheless, studies suggest that childhood OSAS is not due to anatomic abnormalities alone. Most obvious is the fact that patients with OSAS do not obstruct during wakefulness, when upper airway muscle tone is high. Although the upper airway may be narrower in children with OSAS than in those without, there is overlap between the groups (2). A small percentage of children with adenotonsillar hypertrophy but no other known risk factors for OSAS are not cured by T&A (1). Furthermore, a small percentage of children who were cured of their OSAS by T&A have been reported to develop a recurrence during adolescence (3,4). Thus, it appears that childhood OSAS is a dynamic process resulting from a combination of structural and neuromotor abnormalities, rather than from structural abnormalities alone. The upper airway above the level of the cartilaginous airway is a collapsible muscular tube that usually remains patent but has the potential to collapse to facilitate such functions as speech and swallowing. It comprises more than 30 pairs of muscles (5). Thus, neuromotor control of this area is important to maintain airway patency. Upper airway collapsibility during sleep is modulated by the central ventilatory drive (6). The upper airway dilatory muscles are respiratory musc...

show abstract

Effect of Uvulopalatopharyngoplasty on Upper Airway Collapsibility in Obstructive Sleep Apnea

Cited by 159 publications

References 7 publications

The Impact of Anatomic Manipulations on Pharyngeal Collapse

The Impact of Anatomic Manipulations on Pharyngeal Collapse

Obesity and Obstructive Sleep Apnea: Pathogenic Mechanisms and Therapeutic Approaches

Upper Airway Dynamic Responses in Children with the Obstructive Sleep Apnea Syndrome

Contact Info

Product

Resources

About