Sleep Apnea Syndromes: Gozal D

Kushida CA, Chediak A, Berry RB, Brown LK, Gozal D, Iber C, Parthasarathy S, Quan SF, Rowley JA, Anonymous00026, Anonymous00027. · Stanford University Center of Excellence for Sleep Disorders, 401 Quarry Road, Suite 3301, Stanford, CA 94305-5730, USA. · J Clin Sleep Med. · Pubmed #18468315 links to  free full text

Abstract: Positive airway pressure (PAP) devices are used to treat patients with sleep related breathing disorders (SRBDs), including obstructive sleep apnea (OSA). After a patient is diagnosed with OSA, the current standard of practice involves performing attended polysomnography (PSG), during which positive airway pressure is adjusted throughout the recording period to determine the optimal pressure for maintaining upper airway patency. Continuous positive airway pressure (CPAP) and bilevel positive airway pressure (BPAP) represent the two forms of PAP that are manually titrated during PSG to determine the single fixed pressure of CPAP or the fixed inspiratory and expiratory positive airway pressures (IPAP and EPAP, respectively) of BPAP for subsequent nightly usage. A PAP Titration Task Force of the American Academy of Sleep Medicine reviewed the available literature. Based on this review, the Task Force developed these recommendations for conducting CPAP and BPAP titrations. Major recommendations are as follows: (1) All potential PAP titration candidates should receive adequate PAP education, hands-on demonstration, careful mask fitting, and acclimatization prior to titration. (2) CPAP (IPAP and/or EPAP for patients on BPAP) should be increased until the following obstructive respiratory events are eliminated (no specific order) or the recommended maximum CPAP (IPAP for patients on BPAP) is reached: apneas, hypopneas, respiratory effort-related arousals (RERAs), and snoring. (3) The recommended minimum starting CPAP should be 4 cm H2O for pediatric and adult patients, and the recommended minimum starting IPAP and EPAP should be 8 cm H2O and 4 cm H2O, respectively, for pediatric and adult patients on BPAP. (4) The recommended maximum CPAP should be 15 cm H2O (or recommended maximum IPAP of 20 cm H2O if on BPAP) for patients < 12 years, and 20 cm H2O (or recommended maximum IPAP of 30 cm H2O if on BPAP) for patients > or = 12 years. (5) The recommended minimum IPAP-EPAP differential is 4 cm H2O and the recommended maximum IPAP-EPAP differential is 10 cm H2O (6) CPAP (IPAP and/or EPAP for patients on BPAP depending on the type of event) should be increased by at least 1 cm H2O with an interval no shorter than 5 min, with the goal of eliminating obstructive respiratory events. (7) CPAP (IPAP and EPAP for patients on BPAP) should be increased from any CPAP (or IPAP) level if at least 1 obstructive apnea is observed for patients < 12 years, or if at least 2 obstructive apneas are observed for patients > or = 12 years. (8) CPAP (IPAP for patients on BPAP) should be increased from any CPAP (or IPAP) level if at least 1 hypopnea is observed for patients < 12 years, or if at least 3 hypopneas are observed for patients > or = 12 years. (9) CPAP (IPAP for patients on BPAP) should be increased from any CPAP (or IPAP) level if at least 3 RERAs are observed for patients < 12 years, or if at least 5 RERAs are observed for patients > or = 12 years. (10) CPAP (IPAP for patients on BPAP) may be increased from any CPAP (or IPAP) level if at least 1 min of loud or unambiguous snoring is observed for patients < 12 years, or if at least 3 min of loud or unambiguous snoring are observed for patients > or = 12 years. (11) The titration algorithm for split-night CPAP or BPAP titration studies should be identical to that of full-night CPAP or BPAP titration studies, respectively. (12) If the patient is uncomfortable or intolerant of high pressures on CPAP, the patient may be tried on BPAP. If there are continued obstructive respiratory events at 15 cm H2O of CPAP during the titration study, the patient may be switched to BPAP. (13) The pressure of CPAP or BPAP selected for patient use following the titration study should reflect control of the patient's obstructive respiration by a low (preferably < 5 per hour) respiratory disturbance index (RDI) at the selected pressure, a minimum sea level SpO2 above 90% at the pressure, and with a leak within acceptable parameters at the pressure.) (14) An optimal titration reduces RDI < 5 for at least a 15-min duration and should include supine REM sleep at the selected pressure that is not continually interrupted by spontaneous arousals or awakenings. (15) A good titration reduces RDI < or = 10 or by 50% if the baseline RDI < 15 and should include supine REM sleep that is not continually interrupted by spontaneous arousals or awakenings at the selected pressure. (16) An adequate titration does not reduce the RDI < or = 10 but reduces the RDI by 75% from baseline (especially in severe OSA patients), or one in which the titration grading criteria for optimal or good are met with the exception that supine REM sleep did not occur at the selected pressure. (17) An unacceptable titration is one that does not meet any one of the above grades. (18) A repeat PAP titration study should be considered if the initial titration does not achieve a grade of optimal or good and, if it is a split-night PSG study, it fails to meet AASM criteria (i.e., titration duration should be > 3 hr).

Gozal D. · No affiliation provided · Am J Respir Crit Care Med. · Pubmed #18832555 No free full text.

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Spruyt K, Gozal D. · No affiliation provided · Sleep Med Rev. · Pubmed #18790409 No free full text.

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Gozal D, Kheirandish L. · No affiliation provided · Am J Respir Crit Care Med. · Pubmed #15941842 links to  free full text

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Gozal D. · No affiliation provided · Sleep. · Pubmed #12938801 No free full text.

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Gozal D. · No affiliation provided · Rev Mal Respir. · Pubmed #12709632 No free full text.

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Gozal D. · No affiliation provided · Am J Respir Crit Care Med. · Pubmed #12421736 links to  free full text

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Gozal D. · No affiliation provided · Chest. · Pubmed #11834635 links to  free full text

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Bhattacharjee R, Kheirandish-Gozal L, Pillar G, Gozal D. · Kosair Children's Hospital Research Institute, Louisville, KY 40202, USA. · Prog Cardiovasc Dis. · Pubmed #19249448 No free full text.

Abstract: Obstructive Sleep Apnea Syndrome (OSAS) is a common condition in children, and is characterized by intermittent partial or complete occlusion of the upper airway during sleep, leading to profound disturbances in homeostatic gas exchange, frequent arousals and disturbed sleep architecture. Pediatric OSAS is associated with a multitude of end-organ morbidities, most of which have been uncovered in the last decade. Of particular interest are the cardiovascular complications that may develop in children with OSAS, since they are posited to have not only an immediately significant impact on cardiovascular health during childhood, but may also affect cardiovascular outcomes later during adult life. In this review, we will present the specific cardiovascular complications that have thus far been described in children with OSAS, with reference to pertinent mechanisms, and potential implications.

Sans-Capdevila O, Gozal D. · Hospital Universitari Sant Joan de Déu, Esplugues de Llobregat, España. · Rev Neurol. · Pubmed #19085884 links to  free full text

Abstract: INTRODUCTION AND DEVELOPMENT: Sleep disorders in general, and more specifically those related to obstructive sleep apnea syndrome (OSAS) in children, are associated with cognitive and behavioural dysfunctions. Both restriction and fragmentation of sleep as well as intermittent hypoxia are involved in the pathophysiological alterations triggered by this neurobiological comorbidity. The mechanisms that eventually give rise to these neurobehavioural disorders appear to involve a number of biological pathways, particularly oxidative stress and systemic inflammation. CONCLUSIONS: The role played by inter-individual susceptibility, together with the environmental conditions and lifestyle, may account for the larger part of the variance in the phenotype. Moreover, the usual clinical prototype of the patient referred to a children's sleep unit due to snoring has evolved a lot in the past 15 years. We have gone from the patient who presents adenotonsillar hypertrophy with no associated obesity (as was the case in the early nineties) to the prototype of a patient who visits our sleep unit with a slight or moderate adenotonsillar hypertrophy, and with an obese biotype that is very similar to that of the adult patient with OSAS. For this reason we therefore propose the use of the terms type I and type II OSAS in children, and their different manifestations and clinical course are discussed.

Gozal D, Kheirandish-Gozal L. · Division of Pediatric Sleep Medicine, Department of Pediatrics, and Kosair Children's Hospital Research Institute, University of Louisville, Louisville, Kentucky, USA. · Curr Opin Pediatr. · Pubmed #19005334 No free full text.

Abstract: PURPOSE OF REVIEW: To delineate some of the major morbid phenotypes that have emerged in pediatric obstructive sleep apnea (OSA), address new concepts in our understanding of OSA-associated morbidities, and elaborate on innovative therapeutic schemes that may improve outcomes for this condition. In addition, the conceptual framework whereby a childhood condition such as OSA can be linked to specific adult diseases will be presented. RECENT FINDINGS: OSA in children is a frequent condition that affects up to 3% of nonobese, otherwise healthy children. In recent years, increased awareness of OSA and changes in obesity rates in children have contributed to significant changes in disease prevalence and clinical presentation, such that distinct morbidity-related phenotypes have become apparent. Furthermore, oxidative stress and systemic inflammatory pathways are mechanistically involved in the pathophysiology of OSA-associated morbidity. Adenotonsillectomy, the treatment of choice for pediatric OSA, may not be as efficacious as previously thought. Alternative nonsurgical therapies have started to emerge and may become an essential component of treatment. SUMMARY: Pediatric OSA, particularly when obesity is concurrently present, is associated with substantial end-organ morbidities that primarily but not exclusively affect central nervous and cardiovascular systems. These morbidities are pathophysiologically mediated by inflammatory and free radical mediators. Although adenotonsillectomy remains the first line of treatment, more critical assessment of its role is needed, and incorporation of nonsurgical approaches to pediatric OSA seems warranted.

Kheirandish-Gozal L, Gozal D. · Division of Pediatric Sleep Medicine, Department of Pediatrics, University of Louisville, Louisville, Kentucky, USA. · Curr Opin Pediatr. · Pubmed #19005333 No free full text.

Abstract: PURPOSE OF REVIEW: To review some of the inherent problems in defining the diagnosis of pediatric obstructive sleep apnea (OSA) and propose a novel approach to clinical evaluation and referral of habitually snoring children. RECENT FINDINGS: OSA has emerged in the last 30 years as a highly prevalent condition in children. However, the diagnostic uncertainties associated with the clinical presentation and physical examination, and changes in the clinical phenotype over time dictated by the escalation of obesity in children, along with the objective difficulties in accessing appropriately equipped sleep laboratories, have led to substantial underrecognition and to implementation of empirically driven treatment interventions for which scientific validity and efficacy remain undefined. SUMMARY: Current tools for the diagnosis of OSA in children are labor-intensive, and onerous, and remain unvalidated. Novel diagnostic approaches linking objective physiological, biological, or both, measures to defined outcomes of pediatric OSA need to be developed and validated to enable wider and earlier recognition of this condition.

Gozal D. · Kosair Children's Hospital Research Institute and Division of Pediatric Sleep Medicine, Department of Pediatrics, University of Louisville School of Medicine, Louisville, KY 40202, USA. · Semin Pediatr Neurol. · Pubmed #18555196 links to  free full text

Abstract: Recent increases in our awareness to the high prevalence of sleep disorders in general and of sleep-disordered breathing among children, in particular, has led to concentrated efforts aiming to understand the pathophysiological mechanisms, clinical manifestations, and potential consequences of such conditions. In this review, I will briefly elaborate on some of the pathogenetic elements leading to the occurrence of obstructive sleep apnea (OSA) in children, focus on the psychobehavioral consequences of pediatric OSA, and review the evidence on the potential mechanisms underlying the close association between central nervous system morbidity and the episodic hypoxia and sleep fragmentation that characterize OSA.

Capdevila OS, Kheirandish-Gozal L, Dayyat E, Gozal D. · Department of Pediatrics, University of Louisville, Kentucky, USA. · Proc Am Thorac Soc. · Pubmed #18250221 links to  free full text

Abstract: Obstructive sleep apnea (OSA) in children has emerged not only as a relatively prevalent condition but also as a disease that imposes a large array of morbidities, some of which may have long-term implications, well into adulthood. The major consequences of pediatric OSA involve neurobehavioral, cardiovascular, and endocrine and metabolic systems. The underlying pathophysiological mechanisms of OSA-induced end-organ injury are now being unraveled, and clearly involve oxidative and inflammatory pathways. However, the roles of individual susceptibility (as dictated by single-nucleotide polymorphisms), and of environmental and lifestyle conditions (such as diet, physical, and intellectual activity), may account for a substantial component of the variance in phenotype. Moreover, the clinical prototypic pediatric patient of the early 1990s has been insidiously replaced by a different phenotypic presentation that strikingly resembles that of adults afflicted by the disease. As such, analogous to diabetes, the terms type I and type II pediatric OSA have been proposed. The different manifestations of these two entities and their clinical course and approaches to management are reviewed.

Gozal D, Kheirandish-Gozal L. · Kosair Children's Hospital Research Institute, University of Louisville School of Medicine, 570 South Preston Street, Suite 204, Louisville, KY 40202, USA. · Am J Respir Crit Care Med. · Pubmed #17975198 links to  free full text

Abstract: Sleep-disordered breathing and obstructive sleep apnea (OSA) are highly prevalent disorders throughout the lifespan, which may affect up to 2-10% of the population, and have now been firmly associated with an increased risk for cardiovascular and neurobehavioral complications. Nevertheless, the overall pathophysiologic mechanisms mediating end-organ injury in OSA remain undefined, particularly due to the very frequent coexistence of other disease states, such as obesity, that clearly complicate the potential cause-effect relationships. Two major, and to some extent overlapping, mechanisms have been proposed to explain the morbid consequences of OSA, namely increased generation and propagation of reactive oxygen species and initiation and amplification of inflammatory processes. The evidence supporting the validity of these concepts as well as that detracting from such mechanisms will be critically reviewed in the context of clinical and laboratory-based approaches. In addition, some of the contradictory issues raised by such evaluation of the literature will be interpreted in the context of putative modifications of the individual responses to OSA, as determined by genetic variants among susceptibility-related genes, and also by potential environmental modulators of the phenotypic expression of any particular end-organ morbidity associated with OSA.

Redline S, Budhiraja R, Kapur V, Marcus CL, Mateika JH, Mehra R, Parthasarthy S, Somers VK, Strohl KP, Sulit LG, Gozal D, Wise MS, Quan SF. · Department of Pediatrics, Case Western Reserve University, Cleveland, OH, WA 44106-6033, USA. · J Clin Sleep Med. · Pubmed #17557426 No free full text.

Abstract: The American Academy of Sleep Medicine Task Force on Respiratory Scoring reviewed the evidence that addresses: the validity of specific sensors in detecting airflow, tidal volume, oxyhemoglobin saturation, and CO2; the reliability of specific scoring approaches for quantifying sleep related breathing disorders (SRBD); and the validity of using various definitions of the apnea hypopnea index (AHI) as assessed by the strength and consistency of associations with several comorbidities (hypertension, cardiovascular disease, sleepiness, impaired quality of life, and accidents). The evidence was based on a literature search of relevant articles published through December 2004, which resulted in identifying and extracting data from 182 articles, which were graded using standardized approaches. Diverse physiological sensors have been utilized to quantify airflow limitation in patients with suspected SRBD. Although thermistry appears appropriate for identifying apneas, the available evidence did not indicate it provides valid quantification of airflow reduction. The emerging evidence evaluating the accuracy of signal detection against the gold standard measurements (e.g., pneumotachography) suggested the superiority of inductance plethysmography and nasal pressure transducers for detection of hypopneas, with some evidence that recordings from a nasal pressure transducer may better approximate flow/volume than uncalibrated inductance plethysmography. However, since the nasal pressure transducer has only recently been incorporated into large-scale studies, there are as of yet few data that address the predictive value of transducer-identified events relative to clinical or physiological outcomes. Very few studies directly compared the validity of alternative approaches for defining the duration, amplitude change, and use of corroborative data from desaturation or arousal for defining hypopneas. Many observational studies utilizing various designs and approaches for event detection have shown significant associations between measures of SRBD and health outcomes. Data from the 2 largest sleep cohort studies, the Sleep Heart Health Study and the Wisconsin Sleep Cohort, both used definitions of hypopneas based on "discernible" reductions of inductance plethysmography signals with associated desaturation and showed that the derived AHIs using these hypopnea definitions correlated with various indices of morbidity. However, it is not clear whether alternative definitions would provide comparable if not better prediction, or whether optimal approaches for event identification would vary for different outcomes. Despite these limitations, forming a consensus on optimal approaches for recording and measuring respiratory events is an important step toward generating data from different clinical or research laboratories that can be compared. However, additional research is needed, including direct comparisons of alternative measuring approaches for predicting clinical outcomes, with a need to address these issues in large samples across the age spectrum and with inclusion of promising new technology.

Tauman R, Gozal D. · Kosair Children's Hospital Research Institute, and Division of Pediatric Sleep, Medicine, Department of Pediatrics, University of Louisville, Louisville, KY 40202, USA. · Paediatr Respir Rev. · Pubmed #17098639 No free full text.

Abstract: The prevalence and severity of obesity in children and adolescent is dramatically increasing worldwide with a corresponding increase in the prevalence of obesity-associated morbidities particularly those involving OSAS and metabolic and cardiovascular sequelae. Obstructive sleep apnea and obesity hypoventilation syndrome are important and serious consequences of obesity, and may in fact mediate components of the association between obesity and metabolic and cardiovascular morbidities, most likely via potentiation of inflammatory cascades. It is anticipated that the increased prevalence of obesity in children and adolescents in our society will be accompanied by a steady increase in the incidence of OSAS. In this review, we will examine our current understanding of sleep-disordered breathing and associated morbidities in obese children, and summarize the range of therapeutic modalities currently available for this high-risk population.

Gozal D, Kheirandish-Gozal L. · Kosair Children's Hospital Research Institute, Division of Pediatric Sleep Medicine, Department of Pediatrics, University of Louisville, Louisville, KY 40202, USA. · Paediatr Respir Rev. · Pubmed #16798597 No free full text.

Abstract: The prevalence of obstructive sleep apnea (OSA) is clearly increasing in the pediatric population. However, the polysomnographic criteria for treatment still remain to be defined by appropriate scientific methodology. Furthermore, the overall efficacy of currently available interventions such as surgical removal of enlarged tonsils and adenoids (T&A) is unknown, such that we are currently unable to precisely define who the high risk patients are, and the cost and benefits associated with any given treatment. Here, we review the available approaches to the management of OSA in the pediatric population, and examine the potential complementary role of anti-inflammatory therapy, mask ventilation, and intra-oral appliances in the context of mild OSA or residual OSA following T&A.

Kheirandish L, Gozal D. · Child and Youth Project and Division of Paediatric Sleep Medicine, Department of Paediatrics, University of Louisville School of Medicine, Louisville, KY 40202, USA. · Dev Sci. · Pubmed #16764612 No free full text.

Abstract: It is well known that adults with sleep disturbances frequently exhibit a wide range of neurocognitive decrements, and that these deficits are potentially reversible with effective treatment. However, the consequences of respiratory sleep disturbances on neurocognitive function in children have only recently been evaluated, and suggest a strong causal association between the episodic hypoxia and sleep fragmentation that characterize the disease and the emergence of reduced memory, attention and intelligence as well as a link to problematic and hyperactive behaviours and mood disturbances. This article takes a critical look at the current literature on these issues, reviews the major findings and discusses such findings in conjunction with those derived from pertinent animal models.

Bass JL, Corwin M, Gozal D, Moore C, Nishida H, Parker S, Schonwald A, Wilker RE, Stehle S, Kinane TB. · Department of Pediatrics, Newton-Wellesley Hospital, MassGeneral Hospital for Children, Harvard Medical School, Newton, Massachusetts 02462, USA. · Pediatrics. · Pubmed #15342857 links to  free full text

Abstract: OBJECTIVE: A review of the evidence concerning the effect of chronic or intermittent hypoxia on cognition in childhood was performed by using both a systematic review of the literature and critical appraisal criteria of causality. Because of the significant impact of behavioral disorders such as attention-deficit/hyperactivity disorder on certain cognitive functions as well as academic achievement, the review also included articles that addressed behavioral outcomes. METHODS: Both direct and indirect evidence were collected. A structured Medline search was conducted from the years 1966-2000 by using the OVID interface. Both English- and non-English-language citations were included. Significant articles identified by the reviewers up to 2003 were also included. To be included as direct evidence, an article needed to be an original report in a peer-reviewed journal with data on cognitive, behavioral, or academic outcomes in children up to 14 years old, with clinical conditions likely to be associated with exposure to chronic or intermittent hypoxia. Indirect evidence from other reviews and publications in closely related fields, including experimental studies in adults, was used to help formulate conclusions. Two reviewers screened abstracts and titles. Each article included as direct evidence received a structured evaluation by 2 reviewers. Adjudication of differences was performed by a group of 2 reviewers and a research consultant. After this review, tables of evidence were constructed that were used as the basis for group discussion and consensus development. Indirect evidence assigned by topic to specific reviewers was also presented as part of this process. A formal procedure was used to rank the studies by design strength. The critical appraisal criteria for causation described in Evidence Based Pediatrics and Child Health (Moyer V, Elliott E, Davis R, et al, eds. London, United Kingdom: BMJ Books; 2000:46-55) were used to develop consensus on causality. RESULTS: A total of 788 literature citations were screened. For the final analysis, 55 articles met the criteria for inclusion in the direct evidence. Of these, 43 (78.2%) reported an adverse effect. Of the 37 controlled studies, 31 (83.8%) reported an adverse effect. Adverse effects were noted at every level of arterial oxygen saturation and for exposure at every age level except for premature newborns. The studies were classified into 5 clinical categories: congenital heart disease (CHD), sleep-disordered breathing (SDB), asthma, chronic ventilatory impairment, and respiratory instability in infants. Two of these categories, CHD and SDB, which accounted for 42 (76.4%) of the included articles, fulfilled the Evidence Based Pediatrics and Child Health criteria for causation. The indirect evidence included 8 reviews, 1 meta-analysis, and 10 original reports covering the fields of adult anoxia, animal research, SDB in adults, natural and experimental high-altitude studies, perinatal hypoxic-ischemic encephalopathy, anemia, and carbon-monoxide poisoning. The studies of high-altitude and carbon-monoxide poisoning provided evidence for causality. CONCLUSIONS: Adverse impacts of chronic or intermittent hypoxia on development, behavior, and academic achievement have been reported in many well-designed and controlled studies in children with CHD and SDB as well as in a variety of experimental studies in adults. This should be taken into account in any situation that may expose children to hypoxia. Because adverse effects have been noted at even mild levels of oxygen desaturation, future research should include precisely defined data on exposure to all levels of desaturation.

Gozal D, O'Brien LM. · Kosair Children's Hospital Research Institute, Department of Pediatrics, University of Louisville School of Medicine, USA. · Paediatr Respir Rev. · Pubmed #14980299 No free full text.

Abstract: Frequent and loud snoring is a very frequent condition in prepubertal children affecting approximately 10% of all 2-8 year old children. If polysomnographical evaluations are performed in these snoring children, approximately 10% will be diagnosed with obstructive sleep apnoea (OSA). The pathophysiology of OSA in children is still poorly understood. Indeed, while adenotonsillar hypertrophy is certainly a major contributor to OSA, other factors need to be implicated for OSA to develop. In recent years, it has become apparent that OSA and snoring are not as innocuous as previously thought. Indeed, epidemiological and pre-post treatment analyses have identified substantial morbidities that primarily affect cardiovascular and neurobehavioural systems, namely pulmonary hypertension, systemic elevation of arterial blood pressure, nocturnal enuresis, reduced somatic growth, behavioural problems that resemble attention deficit-hyperactivity disorder, as well as learning and cognitive deficits. These problems are associated with marked increases in healthcare-related costs. More importantly, if timely diagnosis and intervention are not implemented, some of these morbid complications may not be completely reversible, leading to long-lasting residual consequences.

Lipton AJ, Gozal D. · Kosair Children's Hospital Sleep Medicine and Apnea Center, Department of Pediatrics, University of Louisville School of Medicine, USA. · Sleep Med Rev. · Pubmed #12586531 No free full text.

Abstract: Obstructive sleep apnea syndrome (OSAS) is a frequent, albeit underdiagnosed problem in children. If left untreated, OSAS may lead to substantial morbidities affecting multiple target organs and systems. The immediate consequences of OSAS in children include behavioral disturbance and learning deficits, pulmonary hypertension, as well as compromised somatic growth. However, if not treated promptly and early in the course of the disease, OSAS may also impose long-term adverse effects on neurocognitive and cardiovascular function, thereby providing a strong rationale for effective treatment of this condition. This review provides a detailed description of the current treatment modalities for pediatric OSAS, and uncovers the potential limitations of the available data on these issues. Furthermore, we postulate that OSAS will persist relatively often after tonsillectomy and adenoidectomy, and that critical studies need to be conducted to identify such patients and refine the clinical management algorithm for pediatric OSAS.

O'Brien LM, Gozal D. · Kosair Children's Hospital Research Institute, Department of Pediatrics, University of Louisville School of Medicine, KY 40202, USA. · Paediatr Respir Rev. · Pubmed #12065176 No free full text.

Abstract: The pathophysiology of obstructive sleep apnoea (OSA), a common condition in children, is poorly understood. While adenotonsillar hypertrophy is certainly a major contributor, other factors are needed for OSA to develop. OSA has been associated with substantial morbidities primarily affecting cardiovascular and neurobehavioural systems which may not be completely reversed with appropriate treatment. This paper reviews the available information and attempts to provide the rationale for early diagnosis and treatment of OSA in children.

Beebe DW, Gozal D. · Division of Psychology, Children's Hospital Medical Center, Cincinnati, OH 45229, USA. · J Sleep Res. · Pubmed #11869421 No free full text.

Abstract: Obstructive sleep apnea (OSA) is accompanied by significant daytime cognitive and behavioral deficits that extend beyond the effects of sleepiness. This article outlines a causal model by which to understand these psychological effects among OSA patients. The model proposes that sleep disruption and blood gas abnormalities prevent sleep-related restorative processes, and further induce chemical and structural central nervous system cellular injury. This, in turn, leads to dysfunction of prefrontal regions of the brain cortex (PFC), manifested behaviorally in what neuropsychologists have termed 'executive dysfunction'. Executive dysfunction is proposed to markedly affect the functional application of cognitive abilities, resulting in maladaptive daytime behaviors. The proposed model (1) accounts for the specific psychological phenotype associated with OSA, (2) accommodates developmental components in this phenotype, (3) bridges between physical and psychological phenomena, (4) suggests mechanisms by which the nocturnal disorder might have effects on daytime functioning, (5) is empirically testable, (6) generates unique research hypotheses, and (7) has practical implications. The model is intended to act as a catalyst for future research and as a preliminary guide for clinicians.

Gozal D. · Department of Pediatrics, Kosair Children's Hospital Sleep Medicine and Apnea Center, University of Louisville School of Medicine, Louisville, Kentucky 40202, USA. · Sleep Breath. · Pubmed #11868138 No free full text.

Abstract: Sleep-disordered breathing (SDB) is a frequent, albeit underdiagnosed, problem in children. If left untreated, SDB may lead to substantial morbidities affecting multiple target organs and systems. This review provides a detailed and current description of the current status of our understanding of SDB-associated morbidity in children, and provides recommendations of future research directions necessary for increasing our knowledge and awareness on the short- and long-term consequences of SDB during childhood.