PEDIATRICS Vol. 123 Supplement May 2009, pp. S222-S225 (doi:10.1542/peds.2008-2952E)
SUPPLEMENT ARTICLE |
Assessment of Sleep-Disordered Breathing in Pediatric Neuromuscular Diseases
Division of Respirology, Children's Hospital of Eastern Ontario, University of Ottawa, Ottawa, Ontario, Canada
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ABSTRACT |
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 TOP ABSTRACT OBSTRUCTIVE SLEEP APNEANOCTURNAL HYPOVENTILATIONCONSEQUENCES OF UNTREATED SDBASSESSMENT OF SDBCONCLUSIONSREFERENCES |
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This is a summary of the presentation on the assessment of sleep-disordered breathing in pediatric neuromuscular diseases, presented as part of the program on pulmonary management of pediatric patients with neuromuscular disorders at the 30th annual Carrell-Krusen Neuromuscular Symposium on February 20, 2008.
Abbreviations: OSA—obstructive sleep apnea • REM—rapid eye movement • SDB—sleep-disordered breathing • FEV1—forced expiratory volume in 1 second • IVC—inspiratory vital capacity • MIP—maximal inspiratory pressure
Sleep-associated respiratory disorders are a major cause of morbidity and mortality in children with neuromuscular disease. They have a prevalence of >40%,1 a 10-fold greater occurrence than in the general population.2 Gas-exchange abnormalities and disrupted sleep architecture may occur in >80% of patients with neuromuscular disease.3 Neuromuscular weakness can result in 2 different types of nocturnal respiratory problems: obstructive sleep apnea (OSA) and nocturnal hypoventilation. Both will be defined here, and pathophysiology specific to neuromuscular disease will be reviewed. The challenges of diagnosis of these conditions and the tools available to evaluate their presence will be explored.
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OBSTRUCTIVE SLEEP APNEA |
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TOPABSTRACTOBSTRUCTIVE SLEEP APNEANOCTURNAL HYPOVENTILATIONCONSEQUENCES OF UNTREATED SDBASSESSMENT OF SDBCONCLUSIONSREFERENCES |
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OSA is defined as partial or complete upper airway obstruction during sleep, associated with at least 1 of the following: (1) sleep disruption; (2) hypoxemia; (3) hypercapnia; or (4) daytime symptoms.4 On observation, there is continued chest and abdominal motion in the absence of airflow during sleep. In contrast to the common pathophysiologic mechanism of adenotonsillar hypertrophy contributing to OSA,5 individuals with neuromuscular disease may also have weakness of the pharyngeal dilator muscles in the upper airway, which contribute to increased upper airway resistance during sleep because these muscles are required to maintain airway patency.6 This becomes most evident in rapid eye movement (REM) sleep,6 when these muscles are atonic. In addition, OSA may be compounded by the presence of obesity or upper airway abnormalities including retrognathia and macroglossia, which are also risk factors for OSA that contribute to a reduced airway diameter.
In neuromuscular disease, the presence of OSA often precedes the development of nocturnal hypoventilation. One retrospective study that studied the presentation of sleep-disordered breathing (SDB) in Duchenne muscular dystrophy evaluated 34 subjects, of whom 32 had polysomnography; 64% had symptoms of SDB, including daytime lethargy, headache or somnolence, and/or nighttime snoring or sleep disturbance. Interestingly, the presence or absence of symptoms did not predict SDB.7 In addition, the presence of OSA was detected in this group during the first decade of life, as compared with nocturnal hypoventilation, which appeared in the second decade.
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NOCTURNAL HYPOVENTILATION |
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TOPABSTRACTOBSTRUCTIVE SLEEP APNEANOCTURNAL HYPOVENTILATIONCONSEQUENCES OF UNTREATED SDBASSESSMENT OF SDBCONCLUSIONSREFERENCES |
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In all individuals, there is a relative hypoventilation that occurs during sleep as a result of blunting of the hypoxic and hypercapnic drive to breathe. Therefore, there is a 25% reduction in tidal volume, a rise in arterial partial pressure of carbon dioxide of 3 to 4 mm Hg, and a reduction in arterial partial pressure of oxygen of similar magnitude.8 In neuromuscular disease, this is exacerbated by weakness of the inspiratory muscles, with consequent "underbreathing" that further impairs gas exchange.9 This also first manifests in REM sleep because of muscle hypotonia.6 Furthermore, the presence of kyphoscoliosis can restrict lung capacity and, therefore, contributes to an impairment of ventilation.9
Initially, compensation for hypoventilation occurs with an arousal response that prevents prolonged oxygen desaturation or hypercapnia.10 Unfortunately, it is at the expense of a good night's sleep, with sleep fragmentation resulting in daytime fatigue and hypersomnolence. With time and progression of disease, the ventilatory chemosensitivity is reset, and the arousal response becomes blunted, allowing longer periods of REM sleep, during which alveolar hypoventilation occurs.10 Eventually, respiratory drive becomes depressed, and severe hypoventilation then becomes present during both day and night. Respiratory failure is the major cause of death in this population.10
Being a continuum, defining what constitutes clinically significant nocturnal hypoventilation is not straightforward. Although all definitions include the presence of hypercapnia and some degree of oxygen desaturation, specifics vary according to group and patient age. An adult consensus conference published in Chest in 1999 defined nocturnal hypoventilation as symptoms plus the presence of either an arterial carbon dioxide level of >60 mm Hg or >5 minutes asleep spent with oxygen saturation at <88%.11 This definition was split by the International Classification of Sleep Disorders, published in 2007, into 2 categories: sleep-induced hypoventilation and sleep-induced hypoxemia.12 The former was defined as a rise in arterial carbon dioxide of >45 mm Hg or "disproportionately increased relative to levels during wakefulness."12 Sleep-induced hypoxemia was defined as oxygen desaturation to <90% for at least 5 minutes with a nadir of at least 85% or >30% of total sleep time with oxygen saturation at <90%. In children, the definition is more complicated, and there has been no clear consensus on a definition.
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CONSEQUENCES OF UNTREATED SDB |
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TOPABSTRACTOBSTRUCTIVE SLEEP APNEANOCTURNAL HYPOVENTILATIONCONSEQUENCES OF UNTREATED SDBASSESSMENT OF SDBCONCLUSIONSREFERENCES |
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Both OSA and nocturnal hypoventilation are associated with significant morbidity and mortality rates. The neurobehavioral consequences of disrupted sleep are well documented, including a profound impact on cognitive function.13,14 Pulmonary hypertension can result from vasomotor recruitment of the pulmonary circulation in response to hypoxemia and hypercapnia.15 SDB also has significant impact on growth. Failure to thrive can result from impaired insulin-like growth factor 1 and growth-hormone release.16–18 These effects are largely reversible with treatment of SDB. A significant impact on quality of life has also been demonstrated with treatment.19,20
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ASSESSMENT OF SDB |
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TOPABSTRACTOBSTRUCTIVE SLEEP APNEANOCTURNAL HYPOVENTILATIONCONSEQUENCES OF UNTREATED SDBASSESSMENT OF SDBCONCLUSIONSREFERENCES |
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There are a variety of tests that can be performed to predict the presence of SDB, with varying degrees of utility. The ideal marker should be one that can be used in a clinical setting as a part of routine assessment of the patient with a neuromuscular disorder. To a great extent, this remains elusive. Alternatively, nocturnal tests can be used to screen for the presence of SDB. Polysomnography, or formal sleep study, remains the gold standard for diagnosis but is not widely available.
Daytime Tests
Daytime symptoms of SDB, especially hypoventilation, are vague and may be attributable to other facets of neuromuscular disease. They may include morning lethargy and headaches, anorexia, and poor growth.10 Although in severe cases clinical features are evident, many patients with slower disease progression develop symptoms insidiously.10 As a result, the symptoms are often only appreciated once they are corrected with treatment.
In a prospective study of 60 adults and children with various neuromuscular diseases, all were evaluated for SDB. The majority of subjects had symptoms of SDB, including disturbed sleep, snoring, and restless legs.1 Despite the high prevalence of moderate-to-severe SDB (42%), symptoms were not predictive of its presence.
Similarly, clinical signs of SDB are difficult to recognize. Although snoring and obstructed breathing may be suggestive of OSA,21,22 hypoventilation and apneas may be more difficult to detect.
Physical examination may yield some clues to the presence of SDB, although findings are not specific for this condition. The presence of adenotonsillar hypertrophy, mouth breathing, nasal obstruction, and hyponasal speech may suggest the presence of OSA. Cor pulmonale and digital clubbing may be present in severe disease. Most often, however, physical examination will be noncontributory. Clinical diagnosis correlates poorly with polysomnography and is correct for only 30% to 56% of patients.23
Questionnaires aimed at diagnosis of OSA in the pediatric population have been developed but are indeterminate in almost half of those queried.24,25 In addition, parents are often unable to predict the severity of OSA on the basis of their observations.26 It is likely even more difficult to predict hypoventilation given the vague symptoms and clinical signs.
Pulmonary function tests likely are the best clinical predictors of nocturnal hypoventilation. Hukins and Hillman27 conducted a prospective study of 19 subjects over the age of 12 years with Duchenne muscular dystrophy. A forced expiratory volume in 1 second (FEV1) below 40% predicted was sensitive for the presence of SDB (91%) but not specific. An FEV1 below 20% predicted is associated with daytime carbon dioxide retention.
In another prospective study, predictive thresholds were determined for different degrees of nocturnal hypoventilation.28 Hypoventilation confined to REM sleep was predicted by an inspiratory vital capacity (IVC) at <60% and maximal inspiratory pressure (MIP) at <45 cm H2O. Hypoventilation continuously through the night, regardless of sleep stage, was predicted by IVC at <40% predicted and MIP at <40 cm H2O. Finally, diurnal respiratory failure was predicted by IVC at <25% predicted and MIP at <35 cm H2O. The IVC is a surrogate measure of forced vital capacity, which in a small prospective series of children with congenital and limb girdle muscular dystrophies was predictive for nocturnal hypoventilation at <40% predicted, with a high sensitivity and specificity.29
Measurement of daytime capillary or arterial blood gases can reliably predict nocturnal hypoventilation if arterial carbon dioxide is at >45 mm Hg on a daytime sample.27 Some would argue, however, that when evidence of daytime hypercapnia is present, nocturnal hypoventilation is almost certainly present, and an opportunity to intervene at an earlier point when findings were limited to nocturnal events may have been missed.
Nocturnal Tests
Polysomnography, or formal sleep study, remains the gold standard for assessment of SDB.4,23 It is the only technique that involves comprehensive noninvasive monitoring of both cardiorespiratory function and sleep. It involves continuous monitoring by a sleep technologist of electroencephalogram, electromyogram, chest and abdominal movement, airflow, oxygen saturation, and carbon dioxide level, as well as video. In addition to SDB, it can also be used to differentiate seizures, periodic limb movements, and other parasomnias. Importantly, there is no significant variability in respiratory parameters from night to night, making it a robust test for the assessment of SDB.30 It has some drawbacks, however, in that it is an expensive and labor-intensive test that is not readily available in all centers, and there may be long wait times to obtain a study. It is also disruptive for families, and the monitoring may interfere with normal sleep, in particular limiting REM sleep, during which SDB will first manifest.
Given the limitations of polysomnography, the search for a simpler and less involved method of screening for SDB has been ongoing. Homemade audiotapes and videotapes lack sensitivity or specificity for diagnosis.31,32 Studies conducted during naps of a few hours' duration are unlikely to contain REM, particularly when conducted in an unfamiliar environment. They therefore have low sensitivity, and they run the risk of underestimating the severity of SDB.33
Overnight oximetry is a more widely available test that can be performed overnight in a patient's home in a noninvasive manner. Patterns of desaturation on oximetry may be suggestive of SDB. Repetitive clusters of "saw-tooth" desaturation may occur in REM sleep in the presence of OSA, whereas prolonged periods of desaturation may be evident with hypoventilation.10 In a cross-sectional study of 349 "healthy" children referred to a sleep laboratory for possible OSA, Brouillette et al34 found that although oximetry has a positive predictive value of 97%, the severity of SDB was not discernible. Oximetry also did not distinguish between hypoventilation and OSA, an important consideration for guiding treatment. Furthermore, a "normal" pulse oximetry reading did not rule out SDB, because respiratory events that resulted in arousals rather than desaturation were not detected. In addition, technical problems including motion artifact and a long built-in averaging time of the device can result in overestimation or underestimation of respiratory events.
The addition of capnography to oximetry has been proposed as an additional tool to aid in the diagnosis of SDB, but it has not been evaluated rigorously. In 1 adult case series of nocturnal oximetry and capnography, all of those who had hypercapnia also showed evidence of desaturation.35 No comparison was made to polysomnography. In pediatric patients, a retrospective review by Kirk et al36 of 609 pediatric polysomnographies was intended to show good agreement between end-tidal and transcutaneous carbon dioxide monitoring and did, but the authors also found that 12% of the subjects with a low apnea-hypopnea index had abnormally high carbon dioxide levels, which were clinically significant. The role of capnography, therefore, is not entirely clear but may be a helpful adjunct to overnight oximetry.
More sophisticated forms of ambulatory testing have been proposed for overnight assessment of SDB, largely specifically investigating OSA. Only those that replicate most of the sleep laboratory assessment have been successful.37–42 It is important to realize, however, that with the exception of a single pilot study of patients with Duchenne muscular dystrophy,43 they have not been evaluated for the purpose of detecting hypoventilation. There are several new technologies emerging, however, that may be able to serve this need.
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CONCLUSIONS |
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TOPABSTRACTOBSTRUCTIVE SLEEP APNEANOCTURNAL HYPOVENTILATIONCONSEQUENCES OF UNTREATED SDBASSESSMENT OF SDBCONCLUSIONSREFERENCES |
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The diagnosis of SDB remains challenging. It is a common problem, with insidious onset of symptoms. With the exception of pulmonary function tests (FEV1 or forced vital capacity of <40% predicted or IVC of <60% predicted), there currently are no reliable clinical indices that can be evaluated during the day to predict SDB. Polysomnography remains the gold standard for diagnosis of SDB. Other nocturnal tests may be helpful for screening. Establishment of a diagnosis of SDB is important, however, given its significant impact on morbidity and mortality and its amenability to treatment. A high index of suspicion for SDB, therefore, is required by those caring for children with neuromuscular disease and risk of SDB.
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FOOTNOTES |
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Accepted Jan 5, 2009.
Address correspondence to Sherri L. Katz, MDCM, FRCPC, MSc, Children's Hospital of Eastern Ontario, Division of Respirology, University of Ottawa, Ottawa, Ontario, Canada K1H 8L1. E-mail: skatz{at}cheo.on.ca
The author has indicated she has no financial relationships relevant to this article to disclose.
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REFERENCES |
|---|
|
TOPABSTRACTOBSTRUCTIVE SLEEP APNEANOCTURNAL HYPOVENTILATIONCONSEQUENCES OF UNTREATED SDBASSESSMENT OF SDBCONCLUSIONSREFERENCES |
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1. Labanowski M, Schmidt-Nowara W, Guilleminault C. Sleep and neuromuscular disease: frequency of sleep-disordered breathing in a neuromuscular disease clinic population. Neurology. 1996;47 (5):1173 –1180
2. Brunetti L, Rana S, Lospalluti ML, Pietrafesa A, Francavilla R, Fanelli M, Armenio L. Prevalence of obstructive sleep apnea syndrome in a cohort of 1,207 children of southern Italy.
Chest. 2001;120
(6):1930
–1935
3. Gozal D. Pulmonary manifestations of neuromuscular disease with special reference to Duchenne muscular dystrophy and spinal muscular atrophy. Pediatr Pulmonol. 2000;29 (2):141 –150[CrossRef][Web of Science][Medline]
4. American Thoracic Society. Standards and indications for cardiopulmonary sleep studies in children. Am J Respir Crit Care Med. 1996;153 (2):866 –878[Web of Science][Medline]
5. Lind MG, Lundell BP. Tonsillar hyperplasia in children: a cause of obstructive sleep apneas, CO2 retention, and retarded growth.
Arch Otolaryngol. 1982;108
(10):650
–654
6. Culebras A. Sleep disorders and neuromuscular disease. Semin Neurol. 2005;25 (1):33 –38[CrossRef][Web of Science][Medline]
7. Suresh S, Wales P, Dakin C, et al. Sleep-related breathing disorder in Duchenne muscular dystrophy: disease spectrum in the paediatric population. J Paediatr Child Health. 2005;41 (9–10):500 –503[CrossRef][Web of Science][Medline]
8. Lumb AB. Nunn's Applied Respiratory Physiology. 5th ed. Oxford, United Kingdom: Butterworth-Heinemann; 2000:345 –356
9. Panitch HB. Respiratory issues in the management of children with neuromuscular disease. Respir Care. 2006;51 (8):885 –893[Web of Science][Medline]
10. Perrin C, Unterborn JN, Ambrosio CD, Hill NS. Pulmonary complications of chronic neuromuscular diseases and their management. Muscle Nerve. 2004;29 (1):5 –27[CrossRef][Web of Science][Medline]
11. Clinical indications for noninvasive positive pressure ventilation in chronic respiratory failure due to restrictive lung disease, COPD, and nocturnal hypoventilation: a consensus conference report.
Chest. 1999;116
(2):521
–534
12. American Sleep Disorders Association, Diagnostic Classification Steering Committee. International Classification of Sleep Disorders: Diagnostic and Coding Manual, ICDS-R. Westchester, IL: American Academy for Sleep Medicine; 2005.
13. Gozal D. Sleep-disordered breathing and school performance in children.
Pediatrics. 1998;102
(3 pt 1):616
–620
14. Suratt PM, Peruggia M, D'Andrea L, et al. Cognitive function and behavior of children with adenotonsillar hypertrophy suspected of having obstructive sleep-disordered breathing. Pediatrics. 2006;118 (3). Available at: www.pediatrics.org/cgi/content/full/118/3/e771
15. Tal A, Leiberman A, Margulis G, Sofer S. Ventricular dysfunction in children with obstructive sleep apnea: radionuclide assessment. Pediatr Pulmonol. 1988;4 (3):139 –143[Web of Science][Medline]
16. Gianotti L, Pivetti S, Lanfranco F, et al. Concomitant impairment of growth hormone secretion and peripheral sensitivity in obese patients with obstructive sleep apnea syndrome.
J Clin Endocrinol Metab. 2002;87
(11):5052
–5057
17. Nieminen P, Löppönen T, Tolonen U, Lanning P, Knip M, Löppönen H. Growth and biochemical markers of growth in children with snoring and obstructive sleep apnea. Pediatrics. 2002;109 (4). Available at: www.pediatrics.org/cgi/content/full/109/4/e55
18. Freezer NJ, Bucens IK, Robertson CF. Obstructive sleep apnoea presenting as failure to thrive in infancy. J Paediatr Child Health. 1995;31 (3):172 –175[Web of Science][Medline]
19. Baydur A, Layne E, Aral H, et al. Long term noninvasive ventilation in the community for patients with musculoskeletal disorders: 46 year experience and review.
Thorax. 2000;55
(1):4
–11
20. Tzeng AC, Bach JR. Prevention of pulmonary morbidity for patients with neuromuscular disease.
Chest. 2000;118
(5):1390
–1396
21. Guilleminault C, Korobkin R, Winkle R. A review of 50 children with obstructive sleep apnea syndrome. Lung. 1981;159 (5):275 –287[Web of Science][Medline]
22. Brouillette RT, Fernbach SK, Hunt CE. Obstructive sleep apnea in infants and children. J Pediatr. 1982;100 (1):31 –40[CrossRef][Web of Science][Medline]
23. Messner AH. Evaluation of obstructive sleep apnea by polysomnography prior to pediatric adenotonsillectomy.
Arch Otolaryngol Head Neck Surg. 1999;125
(3):353
–356
24. Brouilette R, Hanson D, David R, et al. A diagnostic approach to suspected obstructive sleep apnea in children. J Pediatr. 1984;105 (1):10 –14[CrossRef][Web of Science][Medline]
25. Carroll JL, McColley SA, Marcus CL, Curtis S, Loughlin GM. Inability of clinical history to distinguish primary snoring from obstructive sleep apnea syndrome in children.
Chest. 1995;108
(3):610
–618
26. Preutthipan A, Chantarojanasiri T, Suwanjutha S, Udomsubpayakul U. Can parents predict the severity of childhood obstructive sleep apnoea? Acta Paediatr. 2000;89 (6):708 –712[CrossRef][Web of Science][Medline]
27. Hukins CA, Hillman DR. Daytime predictors of sleep hypoventilation in Duchenne muscular dystrophy.
Am J Respir Crit Care Med. 2000;161
(1):166
–170
28. Ragette R, Mellies U, Schwake C, Voit T, Teschler H. Patterns and predictors of sleep disordered breathing in primary myopathies.
Thorax. 2002;57
(8):724
–728
29. Dohna-Schwake C, Ragette R, Mellies U, Straub V, Teschler H, Voit T. Respiratory function in congenital muscular dystrophy and limb girdle muscular dystrophy 2I.
Neurology. 2004;62
(3):513
–514
30. Katz ES, Greene MG, Carson KA, et al. Night-to-night variability of polysomnography in children with suspected obstructive sleep apnea. J Pediatr. 2002;140 (5):589 –594[CrossRef][Web of Science][Medline]
31. Lamm C, Mandeli J, Kattan M. Evaluation of home audiotapes as an abbreviated test for obstructive sleep apnea syndrome (OSAS) in children. Pediatr Pulmonol. 1999;27 (4):267 –272[CrossRef][Web of Science][Medline]
32. Sivan Y, Kornecki A, Schonfeld T. Screening obstructive sleep apnoea syndrome by home videotape recording in children. Eur Respir J. 1996;9 (10):2127 –2131[Abstract]
33. Saeed MM, Keens TG, Stabile MW, Bolokowicz J, Davidson Ward SL. Should children with suspected obstructive sleep apnea syndrome and normal nap sleep studies have overnight sleep studies?
Chest. 2000;118
(2):360
–365
34. Brouillette RT, Morielli A, Leimanis A, Waters KA, Luciano R, Ducharme FM. Nocturnal pulse oximetry as an abbreviated testing modality for pediatric obstructive sleep apnea.
Pediatrics. 2000;105
(2):405
–412
35. Kotterba S, Patzold T, Malin JP, Orth M, Rasche K. Respiratory monitoring in neuromuscular disease: capnography as an additional tool? Clin Neurol Neurosurg. 2001;103 (2):87 –91[CrossRef][Web of Science][Medline]
36. Kirk VG, Batuyong ED, Bohn SG. Transcutaneous carbon dioxide monitoring and capnography during pediatric polysomnography. Sleep. 2006;29 (12):1601 –1608[Web of Science][Medline]
37. Kirk VG, Bohn SG, Flemons WW, Remmers JE. Comparison of home oximetry monitoring with laboratory polysomnography in children.
Chest. 2003;124
(5):1702
–1708
38. Goodwin JL, Enright PL, Kaemingk KL, et al. Feasibility of using unattended polysomnography in children for research: report of the Tucson children's assessment of sleep apnea study (TuCASA). Sleep. 2001;24 (8):937 –944[Web of Science][Medline]
39. Weese-Mayer DE, Corwin MJ, Peucker MR, et al. Comparison of apnea identified by respiratory inductance plethysmography with that detected by end-tidal CO(2) or thermistor. The CHIME Study Group.
Am J Respir Crit Care Med. 2000;162
(2 pt 1):471
–480
40. De Groote A, Groswasser J, Bersini H, Mathys P, Kahn A. Detection of obstructive apnea events in sleeping infants from thoracoabdominal movements. J Sleep Res. 2002;11 (2):161 –168[CrossRef][Web of Science][Medline]
41. Poels PJP, Schilder AGM, von den Berg S, Hoes AW, Joosten KF. Evaluation of a new device for home cardiorespiratory recording on children.
Arch Otolaryngol Head Neck Surg. 2003;129
(12):1281
–1284
42. Jacob SV, Morielli A, Mograss MA, Ducharme FM, Schloss MD, Brouillette RT. Home testing for pediatric obstructive sleep apnea syndrome secondary to adenotonsillar hypertrophy. Pediatr Pulmonol. 1995;20 (4):241 –252[Web of Science][Medline]
43. Kirk VG, Flemons WW, Adams C, Rimmer KP, Montgomery MD. Sleep-disordered breathing in Duchenne muscular dystrophy: a preliminary study of the role of portable monitoring. Pediatr Pulmonol. 2000;29 (2):135 –140[CrossRef][Web of Science][Medline]
PEDIATRICS (ISSN 1098-4275). ©2009 by the American Academy of Pediatrics
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