|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
 |
ABSTRACT |
|---|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
The anatomical relationships between lymphoid, bony, and other tissues affecting the shape of the upper airway in children with obstructive sleep apnea syndrome (OSAS) have not been established. We therefore compared the upper airway structure in 18 young children with OSAS (age 4.8 ± 2.1 yr; 12 males and 6 females) and an apnea index of 4.3 ± 3.9, with 18 matched control subjects (age, 4.9 ± 2.0 yr; 12 males and 6 females). All subjects underwent magnetic resonance imaging under sedation. Axial and sagittal T1- and T2-weighted sequences were obtained. Images were analyzed with image-processing software to obtain linear, area, and volumetric measurements of the upper airway and the tissues comprising the airway. The volume of the upper airway was smaller in subjects with OSAS in comparison with control subjects (1.5 ± 0.8 versus 2.5 ± 1.2 cm3; p < 0.005) and the adenoid and tonsils were larger (9.9 ± 3.9 and 9.1 ± 2.9 cm3 versus 6.4 ± 2.3 and 5.8 ± 2.2 cm3; p < 0.005 and p < 0.0005, respectively). Volumes of the mandible and tongue were similar in both groups; however, the soft palate was larger in subjects with OSAS (3.5 ± 1.1 versus 2.7 ± 1.2 cm3; p < 0.05). We conclude that in children with moderate OSAS, the upper airway is restricted both by the adenoid and tonsils; however, the soft palate is also larger in this group, adding further restriction.
Keywords: obstructive sleep apnea syndrome (OSAS); magnetic resonance imaging (MRI)
| |
INTRODUCTION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Obstructive sleep apnea syndrome (OSAS) is estimated to affect 2% of children (1). The disorder most commonly occurs between 2 and 6 yr of age and correlates with lymphoid hyperplasia during childhood (2, 3). Other important factors promoting OSAS in children include craniofacial anomalies and neuromuscular disorders that could affect the size, shape, and collapsibility of the upper airway during sleep.
Traditional methods used in children to assess the upper airway and tissues surrounding the airway include lateral neck radiographs and cephalometry measurements (2). However, these methods are essentially two-dimensional and provide little information about lateral structures of the nasopharyngeal and oropharyngeal regions. Newer techniques such as acoustic reflection, ultrafast computed tomography, and magnetic resonance imaging (MRI) are readily available, and are used in adults for more detailed analysis of the upper airway structure (7). Of the above-cited methods, MRI provides superior resolution of tissues composing the upper airway; it is accurate, reproducible, and free of ionizing radiation. However, MRI has not been used in the past to systematically evaluate the upper airway in children with OSAS.
We hypothesized that the upper airway as assessed by MRI in children with OSAS is smaller because of adenoid and/or tonsillar overgrowth in comparison with control subjects. To this end we quantified total upper airway volume and cross-sectional area at expected sites of upper airway restriction in the nasopharyngeal and oropharyngeal regions. In addition, we measured the sizes of soft tissues and skeletal structures that define the upper airway. Finally, we validated our methods by examining the accuracy and reliability of these measurements.
| |
METHODS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Subjects with OSAS
Eighteen children were recruited from the pool of patients evaluated for sleep-disordered breathing at the Children's Hospital of Philadelphia (Philadelphia, PA). After OSAS was confirmed by polysomnography, patients were allowed to undergo MRI of the upper airway under sedation. The study was approved by the Institutional Review Board of the Children's Hospital of Philadelphia. Informed consent was obtained from parents of the subjects.
Control Subjects
Eighteen children with normal growth and development were
matched to subjects with OSAS by age, sex, ethnicity, weight, and height.
Control subjects were selected from patients who underwent head
MRI at the Children's Hospital of Philadelphia for other medical indications. Exclusion criteria included (1) subjects with scores 
1 (as
assessed by a standard questionnaire, see below), (2) evidence of a brain
tumor or a seizure disorder requiring therapy, (3) genetic disorders associated with any craniofacial anomaly, and (4) chronic respiratory disease such as asthma or bronchopulmonary dysplasia.
Overnight Polysomnography
For subjects with OSAS, polysomnography was performed 0-4 wk before MRI. Subjects were studied in the Sleep Disorders Center at the Children's Hospital of Philadelphia. Scoring of respiratory variables was performed on the basis of standards set by the American Thoracic Society and previous published data about children (15, 16; details in online data supplement). Sleep stages were determined by the criteria of Rechtschaffen and Kales (17).
Sleep Questionnaire
A questionnaire regarding symptoms of sleep-disordered breathing,
based on the questionnaire developed by Brouillette and coworkers
(18), was used to assess the likelihood of OSAS in control subjects
and subjects with OSAS. On the basis of the questionnaire no subject
with a score < 1 would be expected to have OSAS; a score between
1 and 3.5 is considered indeterminate, and a score > 3.5 is considered highly predictive of obstructive sleep apnea.
Magnetic Resonance Imaging
MRI studies were performed in the Department of Radiology at the Children's Hospital of Philadelphia. All studies were performed under sedation with intravenous pentobarbital (2-6 mg/kg), administered in increments until sleep was achieved; a maximum of 200 mg was administered. All subjects were monitored continuously by pulse oximetry and observed by a critical care physician until recovery (~ 1 h).
MRI was performed with a 1.5T Siemens (Iselin, NJ) Vision system. Images were acquired with a commercially available head coil. The patient's head was positioned supine in the soft tissue Frankfort plane. Axial and sagittal sequential T1-weighted (TR [repetition time], 650 ms; TE [echo time], 14 ms) and T2-weighted (TR, 6,000 ms; TE, 90 ms) images with 3-mm slice thickness and 1 NEX (number of excitations) were obtained from the orbital cavity to the larynx and from the midline bilaterally, respectively (see online data supplement for MRI sequences).
Image Processing and Anatomic Measurements
Measurements from MR images were made with image processing software (Volumetric Image Display and Analysis [VIDA]; Department of Radiology, University of Iowa, Ames, IA) (9, 10, 13). Airway, soft tissue, and bony structure segmentation was performed by manual tracing.
Axial Measurements
From an axial T1-weighted image at the level of the maximal tonsillar cross-sectional area (Figure 1A), we determined the cross-sectional area of the oropharyngeal airway, tonsils, pterygoids, and parapharyngeal fat pads. The oropharyngeal airway was defined radiologically as being bounded anteriorly by the soft palate or tongue, laterally by the tonsils, and posteriorly by the pharyngeal constrictor muscle. At this level we also performed a series of linear measurements along a transverse line crossing the center of the tonsils (e.g., intertonsillar width, bilateral tonsillar width, bilateral fat pad width, bilateral pterygoid width, and intermandibular distance). In addition, we measured at other axial levels the largest adenoid cross-sectional area, maxilla width, and the internal distance between mandibular heads.
|
Sagittal Measurements
From a midsagittal T1-weighted image (Figure 1B), we determined the cross-sectional area of the nasopharyngeal airway, adenoid, soft palate, tongue, mandible, and hard palate. The nasopharyngeal airway was defined radiologically as being bounded anteriorly by the vomer, posteriorly by the adenoid, and inferiorly by a horizontal line above the hard and soft palate. In addition, we obtained a series of linear measurements along an oblique line connecting the mental spine, the center of the soft palate, and the clivus (i.e., tongue oblique, soft palate oblique, airway oblique, adenoid oblique, and mental spine-clivus oblique). We measured the length of the hard palate, defined from anterior nasal spine to end of the palatine bone.
Volumetric Measurements
Adjacent axial slices were used to determine the volumes of the following: combined upper airway (nasopharynx and oropharynx), adenoid, tonsils, tongue, soft palate, and mandible. Volumetric measurements (except tonsils and adenoid) were made from axial T1-weighted slices spanning from the base of the orbital cavities to the epiglottis. For measurements of adenoid and tonsils we used T2-weighted images because of their better resolution of lymphoid tissue. Tonsillar volume is the combined volume of right and left tonsils.
Validation Studies
(See online data supplement.) Accuracy of measurements was determined by using a set of commercial phantoms for lengths, areas, and volumes spanning the measurements used in the study. Intraclass correlation coefficient (ICC) was computed to assess the reliability of MRI measurements (19, 20).
Data Analysis
We hypothesized that children with OSA have a smaller upper airway in comparison with matched control subjects. Therefore, the primary outcome variable set was defined as (1) axial oropharyngeal cross-sectional airway area at the level of the maximal tonsillar cross-sectional area, (2) midsagittal nasopharyngeal cross-sectional airway area, and (3) upper airway volume. Secondary outcome measures included lengths, areas, and volumes of the tissues surrounding the upper airway and were considered hypothesis generating.
Means and standard deviations were used to summarize continuous variables. For comparisons between the groups for MRI data, demographics, and questionnaire data, we used a two-tailed unpaired t test, the Wilcoxon rank test, or 
2 test as appropriate. The Pearson
correlation was used to assess the linear correlation of volume percent
difference of each OSAS-control pair and the corresponding apnea-
hypopnea index. A p value < 0.05 was considered significant.
| |
RESULTS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
We studied 18 children with OSAS, (mean age, 4.8 ± 2.1 yr; range, 1.9-9.3 yr) and 18 control subjects (mean age, 4.9 ± 2.1 yr; range 1.8-8.7 yr). Children with OSAS were not significantly different from control subjects with respect to age, sex, ethnicity, height, or weight (Table 1). All controls had normal development and cognitive function, intact tonsils and adenoid, and no respiratory disorders or craniofacial anomalies. The primary indications for head MRI in control subjects were as follows: single seizure/febrile convulsion (10 subjects), migraine/headache (4 subjects), head concussion (2 subjects), torticollis (1 subject), and eye injury (1 subject). Thus, none of these clinical indications would be expected to affect the upper airway anatomy.
|
Polysomnography
For subjects with OSAS the mean total sleep time during polysomnography was 7.3 ± 1.0 h. The mean respiratory variable values during this period were as follows: apnea index, 4.3 ± 3.9; apnea-hypopnea index, 11.2 ± 6.8; baseline arterial oxygen saturation (SaO2), 95 ± 1%; and SaO2 nadir: 80 ± 10%. Thus, these data suggest moderate OSAS in this group.
Sleep Questionnaire
All controls had an apnea score < 1, indicating absence of
obstructive sleep apnea in this group (18), and as a group had a mean apnea score of 2.8 ± 0.8. This score was significantly lower than the apnea score noted in the OSAS group, of 3.2 ± 1.0 (p < 0.0001).
Magnetic Resonance Imaging
The amount of sedation given before MRI was similar to both groups. A mean of 3.8 ± 1.1 and 4.0 ± 1.2 mg of pentobarbital per kilogram was given to subjects with OSAS and control subjects, respectively. Representative midsagittal and axial images of a control subject and a subject with OSAS are presented in Figure 2. The MRI measurements of the various tissues forming the upper airway of control subjects and children with OSAS are presented graphically in Figures 3-5.
|
|
|
|
Airway. The upper airway volume of children with OSAS was significantly smaller in comparison with the control group, 1.5 ± 0.8 versus 2.5 ± 1.2 cm3 (p < 0.005). Similarly, midsagittal nasopharyngeal airway cross-sectional area was smaller in the children with OSAS, 0.6 ± 0.3 versus 1.1 ± 0.5 cm2 (p < 0.005), as was the axial oropharyngeal cross-sectional airway area at the level of maximal tonsillar cross-sectional area, 0.4 ± 0.3 versus 0.7 ± 0.5 cm2 (p < 0.02).
Soft tissues. The cross-sectional areas of the pterygoids, parapharyngeal fat pads, tongue, and soft palate obtained from the axial and midsagittal images are presented along with the volumetric measurements of the tongue and soft palate in Figure 3. The axial and sagittal cross-sectional areas of the soft tissues were similar in both groups, as was the volume of the tongue. However, we noted a significantly larger soft palate volume in the OSAS group, 3.5 ± 1.1 versus 2.7 ± 1.2 cm3 (p < 0.05).
Adenoid and tonsils. As can be noted from all the measurements obtained in Figure 4, both the adenoid and tonsils were significantly larger in children with OSAS. The mean adenoid volume in children with OSAS was 9.9 ± 3.9 cm3 in comparison with 6.4 ± 2.3 cm3 in control subjects (p < 0.005) and mean tonsillar volume in children with OSAS was 9.1 ± 2.9 versus 5.8 ± 2.2 cm3 in control subjects (p < 0.0005).
Facial skeletal structure. Figure 5 demonstrates the skeletal findings of our study. The mandible width, length (as implied by mental spine-clivus distance), and volume were similar in both groups. Similarly, maxilla width, hard palate length, and sagittal cross-sectional area did not differ between groups. Thus, the similar skeletal findings in this set of measurements do not suggest a primary skeletal difference between subjects with OSAS and control subjects.
Linear correlation of volume percent difference and apnea- hypopnea index. Linear correlations between a volume percent difference of each matched OSAS-control pair and apnea-hypopnea index are presented in Figure 6A and 6B. We noted no correlation between percent difference in airway volume and apnea-hypopnea index (Figure 6A), and a positive correlation between the percent difference of the combined tonsil and adenoid volume and apnea-hypopnea index (r = 0.51, p = 0.03; Figure 6B).
|
Validation of Methods
Analysis of data obtained from phantom MRI measurements indicated, in general, that accuracy increases with the size of the object measured. The ICC values for 13 representative parameters obtained include 1 measurement with a value of 0.78, indicating substantial reliability, and 12 with values greater than 0.88, indicating almost perfect reliability (20).
| |
DISCUSSION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
We used MRI to study the upper airway and surrounding tissues as well as the lower face skeletal structure in young children with OSAS. This is the first study of children with OSAS to use MRI to delineate the airway in detail, the tissues surrounding the airway, and the three-dimensional relationships of these tissues. Our volumetric measurements indicate that the adenoid and tonsils as well as the soft palate are significantly larger in children with OSAS concomitant with significantly smaller upper airway volume.
OSAS is common in children, with a prevalence of about 2% (1). OSAS may occur in all age groups. However, the peak incidence occurs between 2 and 6 yr of age, concomitant with rapid growth of the lymphoid tissue during these years (3). Diagnosis and management of OSAS are important because untreated OSAS may lead to altered neurodevelopmental performance (21), growth retardation (21, 24), pulmonary hypertension (25), and corpulmonale (21, 26).
Our validation studies show that MRI provides both highly accurate and reliable measurements of the various tissues composing the upper airway. However, a disadvantage of MRI compared with ultra-fast computed tomography (CT) scan is its relatively long acquisition time (e.g., 2 min versus 10 s for each sequence) and therefore its sensitivity to motion artifact. To minimize movement during MR scanning, light sedation is given routinely to all children in our institution younger than 8 yr of age. We are aware that sedation could have reduced muscle tone impacting on airway measurements in our subjects. We assume that because the same sedation protocol was used for both groups, airway measurements would be affected in a similar fashion. Sedation should not have affected the volumetric measurements of muscle, lymphoid, and bone tissues.
To obtain the most reliable comparison, we performed a case control study and matched subjects by age, height, weight, sex, and ethnicity. All of these may influence the anatomy of the structures studied, especially in respect to skeletal growth (3). On the basis of volumetric measurements of the upper airway and cross-sectional area measurements of the midsagittal and axial images, we conclude that the upper airway in children with moderate OSAS is significantly restricted in both the nasopharyneal and oropharyngeal regions. The main factors contributing to this restriction are oversized adenoid and tonsils, which were noted to be 55 and 58% larger in volume, respectively, in comparison with control subjects.
Moreover, the positive correlation between the percent difference of the combined tonsil and adenoid volume and the apnea-hypopnea index found in the present study suggests that volumetric measurements of these tissues may be a useful way to predict severity of OSAS in these subjects. We found, however, no correlation of percent difference in airway volume alone with severity of OSAS. It is possible that airway shape, rather than simply volume, is a stronger predictor in determining airway resistance and airway collapsibility.
We also noted the volume of the soft palate to be about 30% larger in subjects with OSAS, adding additional restriction to the airway. This finding, not previously reported in children, has been observed in adults with OSAS (27). Histological evaluation of the soft palate of adults who underwent uvulopalatopharyngoplasty for OSAS indicated significant inflammatory changes and edema (27, 28). In another study, adults treated for OSAS with continuous positive airway pressure showed significant reduction in soft palate volume measured by MRI after several weeks of therapeutic use (29). Increased volume of the soft palate, hypothesized to be caused by chronic vibratory injury due to snoring and leading to edema and inflammation in adults, may be true in children as well.
Other soft tissues (excluding the tonsils) contributing to the width of the lateral pharyngeal wall, such as the pterygoid muscles, pharyngeal constrictor muscles, and parapharyngeal fat pads, were similar in size in both groups studied. These tissues did not contribute to airway restriction by thickening the lateral pharyngeal wall as reported in adults with OSAS (13). It is possible that these structures develop as risk factors later in life and contribute to the adult form of OSAS.
Several studies applying cephalometry to children with OSAS reported various facial skeleton differences, including retroposed mandible and maxilla, low positioned hyoid bone, and alterations in face length and width (30). On the basis of these, it has been suggested that OSAS may be caused by a combination of both adenotonsillar hypertrophy and abnormalities in the development of the lower face skeleton (32, 33). However, another prospective study showed that most cephalometric differences found in children reversed soon after adenotonsillectomy, suggesting that some of these differences detected by cephalometry may be secondary or compensatory and not a primary cause of OSAS (34).
Our set of skeletal measurements of children with no apparent craniofacial anomaly does not suggest a primary skeletal difference between our OSAS and control groups. The reason we did not find such a difference in our subjects can only be speculated at this time. We used different techniques and made measurements different from those performed in cephalometry, including lateral measurements obtained by axial images. Our subjects were sedated and in the supine position during imaging, compared with the upright awake subject studied by cephalometry. It is conceivable that an altered mandibular- skull or hyoid-tongue orientation detected in subjects in the upright postion by cephalometry is positional in nature and could not be confirmed in our study of children in the supine position. Finally, differences in skeletal measurements may be related to subject-control matching criteria. It would be helpful in future to analyze cephalometric and MR images simultaneously to draw more definite conclusions.
In summary, we used MRI to study the upper airway in normal children and in children with moderate OSAS. We noted no significant lower face skeletal differences between these groups. The upper airway was restricted in children with OSAS by overgrowth of the adenoid and tonsils as well as a larger soft palate. Our data suggest a positive correlation between the percent difference in adenoid and tonsil volumes (OSAS to control) and the apnea-hypopnea index. Because OSAS represents a spectrum of disorders with a range of severity it will be essential in future to determine more precisely the relationships between these structures and the risk for, and severity of, OSAS at a given age.
| |
Footnotes |
|---|
Correspondence and requests for reprints should be addressed to Raanan Arens, M.D., Division of Pulmonary Medicine, Children's Hospital of Philadelphia, 34th Street and Civic Center Blvd., Philadelphia, PA 19104-4399. E-mail: arens{at}email.chop.edu
(Received in original form January 25, 2001 and in revised form April 18, 2001).
This article has an online data supplement, which is accessible from this issue's table of contents online at www.atsjournals.orgAcknowledgments: The authors thank the children and families who participated in the study, and Tamara D. Lee BSRT and Mimi Carroll for performing the MRI studies.
Supported by grants HL-62408, HL-60287, and MO1-RR00240 from the National Institutes of Health.
| |
References |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
1.
Redline S,
Tishler PV,
Schluchter M,
Aylor J,
Clark K,
Graham G.
Risk
factors for sleep-disordered breathing in children: associations with
obesity, race, and respiratory problems.
Am J Respir Crit Care Med
1999;
159:
1527-1532
2. Fujioka M, Young LW, Girdany BR. Radiographic evaluation of adenoidal size in children: adenoidal-nasopharyngeal ratio. Am J Roentgenol 1979; 133: 401-404 [Abstract].
3.
Jeans WD,
Fernando DC,
Maw AR,
Leighton BC.
A longitudinal study
of the growth of the nasopharynx and its contents in normal children.
Br J Radiol
1981;
54:
117-121
4. Fernbach SK, Brouillette RT, Riggs TW, Hunt CE. Radiologic evaluation of adenoids and tonsils in children with obstructive sleep apnea: plain films and fluoroscopy. Pediatr Radiol 1983; 13: 258-265 [Medline].
5. Brooks LJ, Stephens BM, Bacevice AM. Adenoid size is related to severity but not the number of episodes of obstructive sleep apnea in children. J Pediatr 1998; 132: 682-686 [Medline].
6. Guilleminault C, Partinen M, Praud JP, Quera-Salva MA, Powell N, Riley R. Morphometric facial changes and obstructive sleep apnea in children. J Pediatr 1989; 114: 997-999 [Medline].
7.
Brown IG,
Zamel N,
Hoffstein V.
Pharyngeal cross-sectional area in
normal men and women.
J Appl Physiol
1986;
61:
890-895
8.
Fredberg JF,
Wohl MEB,
Glass GM,
Dorkin HL.
Airway area by acoustic reflections measured at the mouth.
J Appl Physiol
1980;
48:
749-758
9.
Schwab RJ,
Gefter WB,
Pack AI,
Hoffman EA.
Dynamic imaging during respiration in normal subjects.
J Appl Physiol
1993;
74:
1504-1514
10. Schwab RJ, Gefter WB, Hoffman EA, Gupta KB, Pack AI. Dynamic upper airway imaging during awake respiration in normal subjects and patients with sleep disordered breathing. Am Rev Respir Dis 1993; 148: 1385-1400 [Medline].
11. Ryan CF, Lowe AA, Li D, Fluthom JA. Three dimensional upper airway CT in obstructive sleep apnea. Am Rev Respir Dis 1991; 144: 428-432 [Medline].
12.
Burger CD,
Stanson AW,
Daniels BK,
Sheedy PF,
Shepard JW.
Fast-computed tomographic evaluation of the effect of route of breathing
on upper airway size and function in normal men.
Chest
1993;
103:
1032-1037
13. Schwab RJ, Gupta KB, Gefter WB, Hoffman EA, Pack AI. Upper airway soft tissue anatomy in normals and patients with sleep disordered breathing: significance of the lateral pharyngeal walls. Am J Respir Crit Care Med 1995; 152: 1673-1689 [Abstract].
14. Schwab RJ, Pack AI, Gupta KB, Metzger LJ, Oh E, Getsy JE, Hoffman EA, Gefter WB. Upper airway and soft tissue structural changes induced by CPAP in normal subjects. Am J Respir Crit Care Med 1996; 154: 1106-1116 [Abstract].
15. American Thoracic Society. Standards and indications for cardiopulmonary sleep studies in children. Am J Respir Crit Care Med 1996;153: 866-878.
16. Marcus CL, Omlin KJ, Basinski DJ, Bailey SL, Rachal AB, Von Pechmann WS, Keens TG, Ward SL. Normal polysomnogram values for children and adolescents. Am Rev Respir Dis 1992; 146: 1235-1239 [Medline].
17. Rechtschaffen A, Kales A. A manual of standardized terminology, techniques and scoring systems for sleep stages on human subjects. Washington DC: National Institutes of Health; 1968, Publ. No. 204.
18. Brouillette R, Hanson D, David R, Klemka L, Szatkowski A, Fernbach S, Hunt C. A diagnostic approach to suspected obstructive sleep apnea in children. J Pediatr 1984; 105: 10-14 [Medline].
19. Fleiss JK. The design and analysis of clinical experiments. New York: John Wiley & Sons; 1986, Chapter 1.
20. Landis JR, Koch GG. The measurement of observer agreement for categorical data. Biometrics 1977; 33: 159-174 [Medline].
21. Brouillette RT, Fernbach SK, Hunt CE. Obstructive sleep apnea in infants and children. J Pediatr 1982; 100: 31-40 [Medline].
22. Rhodes SK, Shimoda KC, Waid LR, O'Neil PM, Oexmann MJ, Collop NA, Willi SM. Neurocognitive deficits in morbidly obese children with obstructive sleep apnea. J Pediatr 1995; 127: 741-744 [Medline].
23.
Gozal D.
Sleep disordered breathing and school performance in children.
Pediatrics
1998;
102:
616-620
24. Marcus CL, Carroll JL, Koerner CB, Hamer A, Lutz J, Loughlin GM. Determinants of growth in children with obstructive sleep apnea syndrome. J Pediatr 1994; 125: 556-562 [Medline].
25. Perkin RM, Anas NG. Pulmonary hypertension in pediatric patients. J Pediatr 1984; 105: 511-522 [Medline].
26. Menashe VD, Ferrehi F, Miller M. Hypoventilation and cor pulmonale due to chronic upper airway obstruction. J Pediatr 1965; 67: 198-203 .
27. Sekosan M, Zakkar M, Wenig BL, Olopade CO, Rubinstein I. Inflammation in the uvula mucosa of patients with obstructive sleep apnea. Laryngoscope 1996; 106: 1018-1020 [Medline].
28. Hamans EP, Van Marck EA, De Backer WA, Creten W, Van de Heyning PH. Morphometric analysis of the uvula in patients with sleep-related breathing disorders. Eur Arch Otorhinolaryngol 2000; 257: 232-236 [Medline].
29. Ryan CF, Lowe AA, Li D, Fleetham JA. Magnetic resonance imaging of the upper airway in obstructive sleep apnea before and after chronic nasal continuous positive airway pressure therapy. Am Rev Respir Dis 1991; 144: 939-944 [Medline].
30. Zucconi M, Caprioglio A, Calori G, Ferini-Strambi L, Oldani A, Castronovo C, Smirne S. Craniofacial modifications in children with habitual snoring and obstructive sleep apnoea: a case-control study. Eur Respir J 1999; 13: 411-417 [Abstract].
31. Shintani T, Asakura K, Kataura A. Adenotonsillar hypertrophy and skeletal morphology of children with obstructive sleep apnea syndrome. Acta Otolaryngol Suppl 1996; 523: 222-224 [Medline].
32. Kawashima S, Niikuni N, Chia-hung L, Takahasi Y, Kohno M, Nakajima I, Akasaka M, Sakata H, Akashi S. Cephalometric comparisons of craniofacial and upper airway structures in young children with obstructive sleep apnea syndrome. Ear Nose Throat J 2000;79:499-502, 505-506.
33. Shintani T, Asakura K, Kataura A. Evaluation of the role of adenotonsillar hypertrophy and facial morphology in children with obstructive sleep apnea. ORL J Otorhinolaryngol Relat Spec 1997; 59: 286-291 [Medline].
34. Agren K, Nordlander B, Linder-Aronsson S, Zettergren-Wijk L, Svanborg E. Children with nocturnal upper airway obstruction: postoperative orthodontic and respiratory improvement. Acta Otolaryngol 1998; 118: 581-587 [Medline].
This article has been cited by other articles:
 |
|
 |
|
  E. Dayyat, L. Kheirandish-Gozal, O. Sans Capdevila, M. M. A. Maarafeya, and D. Gozal Obstructive Sleep Apnea in Children: Relative Contributions of Body Mass Index and Adenotonsillar Hypertrophy Chest, July 1, 2009; 136(1): 137 - 144. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Pirila-Parkkinen, P. Pirttiniemi, P. Nieminen, U. Tolonen, U. Pelttari, and H. Lopponen Dental arch morphology in children with sleep-disordered breathing Eur J Orthod, April 1, 2009; 31(2): 160 - 167. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. G. Kaditis, M. G. Ioannou, K. Chaidas, E. I. Alexopoulos, M. Apostolidou, T. Apostolidis, G. Koukoulis, and K. Gourgoulianis Cysteinyl Leukotriene Receptors Are Expressed by Tonsillar T Cells of Children With Obstructive Sleep Apnea Chest, August 1, 2008; 134(2): 324 - 331. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. S. Katz and C. M. D'Ambrosio Pathophysiology of Pediatric Obstructive Sleep Apnea Proceedings of the ATS, February 15, 2008; 5(2): 253 - 262. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Muzumdar and R. Arens Diagnostic Issues in Pediatric Obstructive Sleep Apnea Proceedings of the ATS, February 15, 2008; 5(2): 263 - 273. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
O. S. Capdevila, L. Kheirandish-Gozal, E. Dayyat, and D. Gozal Pediatric Obstructive Sleep Apnea: Complications, Management, and Long-term Outcomes Proceedings of the ATS, February 15, 2008; 5(2): 274 - 282. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 O. Ronen, A. Malhotra, and G. Pillar Influence of Gender and Age on Upper-Airway Length During Development Pediatrics, October 1, 2007; 120(4): e1028 - e1034. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. S. Katz, C. L. Marcus, and D. P. White Influence of Airway Pressure on Genioglossus Activity during Sleep in Normal Children Am. J. Respir. Crit. Care Med., April 15, 2006; 173(8): 902 - 909. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. P. White Pathogenesis of Obstructive and Central Sleep Apnea Am. J. Respir. Crit. Care Med., December 1, 2005; 172(11): 1363 - 1370. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Arens Is It Time to Consider a New Treatment for Children with Sleep-disordered Breathing? Am. J. Respir. Crit. Care Med., August 1, 2005; 172(3): 264 - 265. [Full Text] [PDF]
|
|
|
|
 |
|
 G M Nixon and R T Brouillette Sleep {middle dot} 8: Paediatric obstructive sleep apnoea Thorax, June 1, 2005; 60(6): 511 - 516. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Arens, S. Sin, J. M. McDonough, J. M. Palmer, T. Dominguez, H. Meyer, D. M. Wootton, and A. I. Pack Changes in Upper Airway Size during Tidal Breathing in Children with Obstructive Sleep Apnea Syndrome Am. J. Respir. Crit. Care Med., June 1, 2005; 171(11): 1298 - 1304. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. S. Katz and D. P. White Genioglossus Activity During Sleep in Normal Control Subjects and Children with Obstructive Sleep Apnea Am. J. Respir. Crit. Care Med., September 1, 2004; 170(5): 553 - 560. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. L. Marcus Pediatric Sleep Medicine Comes Into Its Own Pediatrics, May 1, 2004; 113(5): 1393 - 1394. [Full Text] [PDF]
|
|
|
|
|
|
C. L. Marcus Evaluating the Upper Airway during Wakefulness: What Can It Tell Us about Sleep? Am. J. Respir. Crit. Care Med., January 15, 2004; 169(2): 140 - 141. [Full Text] [PDF]
|
|
|
|
|
|
D. Gozal and M. M. Burnside Increased Upper Airway Collapsibility in Children with Obstructive Sleep Apnea during Wakefulness Am. J. Respir. Crit. Care Med., January 15, 2004; 169(2): 163 - 167. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. F. Fregosi, S. F. Quan, K. L. Kaemingk, W. J. Morgan, J. L. Goodwin, R. Cabrera, and A. Gmitro Sleep-disordered breathing, pharyngeal size and soft tissue anatomy in children J Appl Physiol, November 1, 2003; 95(5): 2030 - 2038. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. E. Montgomery-Downs, V. F. Jones, V. J. Molfese, and D. Gozal Snoring in Preschoolers: Associations with Sleepiness, Ethnicity, and Learning Clinical Pediatrics, October 1, 2003; 42(8): 719 - 726. [Abstract] [PDF]
|
|
|
|
|
|
E. S. Katz and D. P. White Genioglossus Activity in Children with Obstructive Sleep Apnea during Wakefulness and Sleep Onset Am. J. Respir. Crit. Care Med., September 15, 2003; 168(6): 664 - 670. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. J. Schwab, M. Pasirstein, R. Pierson, A. Mackley, R. Hachadoorian, R. Arens, G. Maislin, and A. I. Pack Identification of Upper Airway Anatomic Risk Factors for Obstructive Sleep Apnea with Volumetric Magnetic Resonance Imaging Am. J. Respir. Crit. Care Med., September 1, 2003; 168(5): 522 - 530. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Arens, J. M. McDonough, A. M. Corbin, N. K. Rubin, M. E. Carroll, A. I. Pack, J. Liu, and J. K. Udupa Upper Airway Size Analysis by Magnetic Resonance Imaging of Children with Obstructive Sleep Apnea Syndrome Am. J. Respir. Crit. Care Med., January 1, 2003; 167(1): 65 - 70. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. J. Tobin The Official Copy of AJRCCM Is Posted but Not Printed Am. J. Respir. Crit. Care Med., October 1, 2002; 166(7): 905 - 906. [Full Text]
|
|
|
|
|
|
M. J. TOBIN Sleep-Disordered Breathing, Control of Breathing, Respiratory Muscles, and Pulmonary Function Testing in AJRCCM 2001 Am. J. Respir. Crit. Care Med., March 1, 2002; 165(5): 584 - 597. [Full Text] [PDF]
|
|
|
|
|
|
M. J. TOBIN Pediatrics, Surfactant, and Cystic Fibrosis in AJRCCM 2001 Am. J. Respir. Crit. Care Med., March 1, 2002; 165(5): 619 - 630. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Proc. Am. Thorac. Soc. | Am. J. Respir. Cell Mol. Biol. |