Spring 2016 Sleep Section Bulletin

Spring 2016 Sleep Section Bulletin

Marilyn Woodard Barclay, RCBS, RRT, CPFT, RPSGT retired
Corvallis, OR

Cheyne Stokes Breathing

Marilyn Barclay, BSRT, RRT, CPFT

A breathing pattern characterized by progressively deeper and possibly faster breaths followed by a decreasing rate to the point of apnea was first described in the 1800s by John Cheyne and William Stokes. This pattern, known as Cheyne Stokes breathing (CSB), repeats the cycle every 30 seconds to two minutes and can occur during wakefulness or sleep. When it occurs during sleep it is also known as central sleep apnea syndrome (CSAS).

Patients with heart failure, stroke, hyponatremia, traumatic brain injury, or tumors may develop CSB. Sleeping at high altitude, morphine use, carbon monoxide poisoning, and toxic metabolic encephalopathy may also result in CSB.

Anatomy and physiology of breathing control

The medulla oblongata is the center for normal breathing patterns. It receives information from the cerebral cortex, pons, upper airways, phrenic nerve, and peripheral and central chemoreceptors. Based on the information received, the medulla oblongata sends instructions to the dorsal and ventral respiratory groups, which are also located within the medulla. The dorsal respiratory group (DRG) also receives information from the vagus and glossopharyngeal nerves, which stimulate inspiration. The DRG sends messages to the phrenic nerve, which activates the diaphragm and intercostals. These actions control the rate and depth of inspiration.

The ventral respiratory group (VRG) is inactive during normal breathing. Impulses from the VRG are sent to the laryngeal and pharyngeal muscles during stressed breathing.

The pneumotaxic and apneustic centers are located in the pons, which lies above the medulla oblongata. The pons modifies messages from the medulla oblongata, allowing the pneumotaxic and apneustic centers to alter respiratory rate and tidal volume.

Peripheral chemoreceptors located in the common carotid artery (carotid bodies) and aortic arch (aortic bodies) also play an important role in regulating breathing. These bodies are in direct contact with blood and are affected by pH, PaCO2, and dissolved oxygen.

Central chemoreceptors are located on the outer surface of the medulla oblongata. These chemoreceptors are in contact with cerebral spinal fluid and arterial blood. Changes in PaCO2 levels in the cerebral spinal fluid (CSF) affect the pH of the fluid. The pH of the CSF signals the central chemoreceptors to send messages to increase or decrease respiration.1

Why does Cheyne Stokes breathing occur?

Several factors influence the pathogenesis of CSB. When cardiac output is low, as in congestive heart failure (CHF), there is a significant increase in the time it takes blood from the lungs to reach the brain. When the medullary neurons are subjected to increases in PaCO2 they stimulate increased respiration. Since it takes a long time for the blood with decreased PaCO2 to return to the medullary neurons, respiration will have continued longer than necessary. The medullary neurons then cause respiration to diminish, but the PaCO2 levels continue to fall and ventilation is depressed to the point of apnea. The PaCO2 starts to climb and the process begins once again.

CSB is believed to be influenced by a hypersensitive chemoreflex response to CO2 along with delayed circulation of blood.2 Chemoreceptor response is increased due to elevated sympathetic tone. It has been shown that nighttime fluid shifting also contributes to CSB, as well as to obstructive sleep apnea (OSA), in patients with CHF. 3 Hyperventilation and reduced CO2 levels while awake may reduce CO2 reserve, contributing to hypersensitivity.4

Should we treat Cheyne Stokes breathing in patients with CHF?

More than 50% of patients with heart failure also have OSA or central apnea with the CSB pattern.5 These patients may exhibit both types of apnea in the same night.6 While OSA is considered a condition that should be treated7, some researchers believe CSB mechanisms may be more protective than detrimental.8

During the hyperventilation portion of CSB, end expiratory lung volume increases9 and oxygen stores increase, which increases peripheral oxygen saturation and decreases the time of the circulatory feedback loop.10

The deep breaths associated with CSB may reduce sympathetic activity11, while hypocapnia may assist myocardial oxygen extraction and reduce cardiotoxic events.12 The apnea portion of CSB has been shown to create intrinsic positive end-expiratory pressures in the range of 5-10 mmHg, mimicking continuous positive airway pressure (CPAP).13

The large randomized study, CANPAP, showed that although CPAP attenuated CSB, improved nocturnal oxygenation, increased the ejection fraction, lowered norepinephrine levels, and increased exercise capacity, it did not improve survival.14 After analyzing the CANPAP data, Arzt et al. noted that there were “responders” and “non-responders” to CPAP in these heart failure/CSB patients. Non-responders were older, had more severe sleep disordered breathing, and a larger central apnea component than the responders.15 A previous study also demonstrated this phenomenon, with the non-responders exhibiting a higher apnea-hypopnea index (AHI) and more central apnea.16 It appears that CPAP is of limited value in the treatment of patients with heart failure and CSB.

Effective medication treatment of heart failure seems an excellent starting point. Beta-blockers improve CSB and heart failure. Diuretics might improve CSB by decreasing pulmonary congestion and fluid shifting. The respiratory stimulant theophylline was suggested as a treatment, but it increased mortality in patients with heart failure due to left ventricular dysfunction. Nighttime oxygen therapy decreases sympathetic hyperactivity and may correct the minute volume/PCO2 ratio in CSB.17

Kasai et al. demonstrated that bi-level ventilation improved left ventricular ejection fraction (LVEF) and mitral regurgitation.18 Another study found that bi-level improved LV function as well as CSB.19 However, compliance with bi-level therapy was lacking and thus it cannot be recommended over CPAP.

Inhalation of CO2 has been shown to reduce the frequency of central apneas in patients with CSB, but more studies are needed to address the side effects of increased ventilation, work of breathing, and increased sympathetic nerve actitvity.20

Adaptive servo-ventilation (ASV) provides varying levels of pressure support using feedback from the patient’s previous breaths. If hyperventilation is detected pressure support is reduced. During periods of hypoventilation, pressure support is increased.21 This allows the respiratory rate and airflow to remain stable. A study by Kasai et al. showed improved cardiac function, exercise capacity, and quality of life when compared to CPAP.22 Although improved survival has not been established, some studies show improved LV ejection and decreased AHI in patients using ASV compared to patients using CPAP.23

On May 15, 2015, ResMed released a field safety notice based on early results of their SERVE-HF study: “In patients with symptomatic, chronic heart failure and with a reduced left ventricular ejection fraction (LVEF < 45%), using ASV to treat their moderate to severe central sleep apnea syndrome may be harmful . . . for this particular at risk population, there is a 33.5% increased risk of cardiovascular death, compared to control patients who are not on ASV therapy.”

In August, 2015, this statement was amended to read”. . . patients with symptomatic, chronic heart failure with reduced left ventricular ejection fraction (LVEF < 45%) and moderate to severe predominant central sleep apnea.”

In summary

CSB is an interesting physiologic response consisting of hypersensitive chemoreceptors and a lag in feedback loop response. Fifty percent of patients with heart failure have OSA or CSA with a CSB pattern. Some believe that CSB in heart failure may be beneficial rather than pathologic. Medication therapy, including beta-blockers, diuretics, and nocturnal oxygen therapy, provide positive benefit. Long-term use of inhaled CO2 to correct CSB needs more study. PAP therapy, outside of the narrow confines stated above, is still the treatment of choice. Studies exploring the long-term effectiveness of CPAP are still needed.

In order to provide our patients with the best care, it is important for practitioners to keep up to date with the literature and be prepared to change prescribing practices as knowledge increases.


  1. Hess DR, Neil RM, Galvin W, Mishoe S. Respiratory Care; Principles and Practice. Burlington: Jones & Barlett Learning; 2016. 1170-1174.
  2. Plataki M, Sands S, Malhotra A. Clinical consequences of altered chemorelex control. Respir Physiol Neurobiol 2013;189:354-363.
  3. Yumino D, Redolfi S, Ruttanaumpawan P, Tomlinson G, Bradley TD. Nocturnal rostral fluid shift; a unifying concept for the pathogenesis of obstructive and central sleep apnea in men with heart failure. Circulation 2010;121:1598-1605.
  4. Manisty CH, Willson K, Wensel R, Whinnett ZI, Davies JE, Oldfield WL, Mayet J, Francis DP. Development of respiratory control instability in heart failure; a novel approach to dissect the pathophysiological mechanisms. J Physiol 2006;577:387-401.
  5. Naughton MT. Pathophysiology and treatment of Cheyne-Stokes respiration. Thorax 1998;53:514-518.
  6. Tkacova R, Niroumand M, Lorenzi-Filho G, et al. Overnight shift from obstructive to central apneas in patients with heart failure; role of PCO2 and circulatory delay. Circulation 2001;103:238-243.
  7. Bradley TD, Floras JS. Obstructive sleep apnoea and its cardiovascular consequences. Lancet 2009;373:82-93.
  8. Naughton MT. Cheyne-Stokes respiration; friend or foe? Thorax 2012;67:357-360.
  9. Brack T, Jubran A, Laghi F, et al. Fluctuations in end-expiratory lung volume during Cheyne-Stokes respiration. Am J Respir Crit Care Med 2005;171:1408-1413.
  10. Sands SA, Edwards BA, Kee K, et al. Loop gain as a means to predict a positive airway pressure suppression of Cheyne-Stokes respiration in heart failure patients. Am J Respir Crit Care Med 2011;184:1067-1075.
  11. Van de Borne P, Oren R, Abouassaly C, et al. Effect of Cheyne-Stokes respiration on muscle sympathetic nerve activity in severe congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy. Am J Cardiol 1998;81:432-436.
  12. Porter JM, Markos F, Snow HM, et al. Effects of respiratory and metabolic pH changes and hypoxia on ropivacaine-induced cardiotoxicity in dogs. Br J Anesth 2000;84:92-94.
  13. Christie RV, Meakins JC. The intrapleural pressure in congestive heart failure and its clinical significance. J Clin Invest 1934;13:323-345.
  14. Bradley TD, Logan AG, Kimoff RJ, Series F, Morrison D, Perguson K, Belenkie I, Pfeifer M, Fleetham J, Hanly P, Smlovitch M, Tomlinson G, Floras JS, CANPAP Investigators. Continuous positive airway pressure for central sleep apnea and heart failure. N Engl J Med 2005;353:2025-2033.
  15. Arzt M, Floras JS, Logan AG, Kimoff RJ, Series F, Morrison D, Ferguson K, Belenkie I, Pfeifer M, Fleetham J, Hanly P, Smilovitch M, Ryan C, Tomlinson G, Bradley TD, et al. Suppression of central sleep apnea by continuous positive airway pressure and transplant-free survival in heart failure; a post hoc analysis of the Canadian Continuous Positive Airway Pressure for Patients with Central Sleep Apnea and Heart Failure Trial (CANPAP), Circulation 2007;115:3173-3180.
  16. Javaheri S. Effects of continuous positive airway pressure on sleep apnea and ventricular irritability in patients with heart failure. Circulation 2000;101:392-397.
  17. Andreas S, Bingeli C, Mohacsi P, Luscher TF, Noll G. Nasal oxygen and muscle sympathetic nerve activity in heart failure. Chest 2003;123:366-371.
  18. Kasai T, Narui K, Dohi T, Ishiwata S, Yoshimura K, Nishiyama S, Yamaguchi T, Momomura S. Efficacy of nasal bi-level positive airway pressure in congestive heart failure patients with Cheyne-Stokes respiration and central sleep apnea. Circ J 2005;69:913-921.
  19. Noda A, Izawa H, Asano H, Nakata S, Hirashiki A, Murase Y, Lino S, Nagata K, Murohara T, Koike Y, Yokota M. Beneficial effect of bilevel positive airway pressure on left ventricular function in ambulatory patients with idiopathic dilated cardiomyopathy and central sleep apnea-hypopnea; a preliminary study. Chest 2007;131:1694-1701.
  20. Wan ZH, Wen FJ, Hu K. Dynamic CO2 inhalation; a novel treatment for CSR-CSA associated with CHF. Sleep Breath 2013;17:487-493.
  21. Kazimierczak A, Krzensinki P, Krzyzanowski K, et al. Sleep-disordered breathing in patients with heart failure: new trends in therapy. Biomed Res Int 2013;2013:459613.
  22. Kasai T, Usui Y, Yoshioka T, Yanagisawa N, Takata Y, Narui K, Yamaguchi T, Yamashina A, Momomura SI, JASV Investigators. Effect of flow-triggered adaptive servo-ventilation compared with continuous positive airway pressure in patients with chronic heart failure with coexisting obstructive sleep apnea and Cheyne-Stokes respiration. Circ Heart Fail 2010:3:140-148.
  23. Philipee C, Stoica-Herman M, Drouot X, et al. Compliance with and effectiveness of adaptive servoventilation versus continuous positive airway pressure in the treatment of Cheyne-Stokes respiration in heart failure over a six month period. Heart 2006;92(3):337-342.

Bi-Level Positive Airway Pressure: Advanced Platforms 

David Wolfe, MSEd, RRT-SDS, RPSGT
Crouse Hospital, Syracuse, NY

Hybrid models of bi-level positive airway pressure (PAP) are presently available. However, the various modes and features are sometimes complicated and difficult to understand — and that’s especially true when trying to decide when to use which mode.

Depending on the manufacturer, the mode/feature that averages a patient’s volume is called average volume assured pressure support (AVAPS) or intelligent volume assured pressure support (iVAPS). Basically, this feature should be used on hypercapnic patients. Patients who are normocapnic or hypocapnic would benefit more from adaptive/automatic servo ventilation (ASV).

iVAPS targets alveolar ventilation, whereas AVAPS targets tidal volume. This volume/ventilation is based on the patient’s ideal body weight (IBW). Generally, as the patient’s volume/ventilation decreases, the pressure support (PS) will first increase to return the volume/ventilation back to what is set according to the patient’s IBW. If the PS is unable to return the volume/ventilation back to normal, the back-up rate will be activated.

AVAPS and iVAPS can be used for so-called “underachievers;” that is, patients who are hypoventilating (hypercapnic) and may have COPD, obesity hypoventilation syndrome, neuromuscular disorders, or restrictive diseases. Compared to traditional bi-level PAP, one advantage to these features/modes is that they automatically adjust to changing patient needs.

Instead of targeting a certain volume based on IBW, ASV aims to achieve about 90% of the patient’s recent ventilation. Although the manufacturer’s algorithms differ, the goal is to avoid central hypopneas and apneas by automatically adjusting PS in response to the patient’s recent ventilation. The response to this change in ventilation, with a change in PS, is quicker than it is for AVAPS/iVAPS. A back-up rate will be activated if the PS cannot achieve the targeted ventilation. Manufacturers also offer an auto-expiratory PAP (EPAP) to address flow limitation.

ASV is indicated for central sleep apnea patients who are “overachievers”; that is, those who are hyperventilating or ventilating normally. Central apneas may be in the form of Cheyne-Stokes Breathing (CSB), PAP-emergent sleep apnea (complex sleep apnea), mixed apneas, and periodic breathing. ASV should not be used, or used cautiously, in some CSB patients, according to a recent study.

Companies offering these advanced platforms also have some form of leak recognition and compensation, automatic or variable trigger and cycle thresholds, and inspiratory time adjustments, depending on the mode. With more complicated patients seen in the sleep center, more advanced modes and features are being utilized. Understanding these modes is important for the advancing respiratory therapist and sleep technologist.

Sleep, Memory, and Learning: An Overview of the Future of Theory and Practice in Sleep Medicine

Abdullah Alismail, MS, RRT-NPS, RRT-SDS
Assistant Professor, Cardiopulmonary Sciences Department, Loma Linda University, Loma Linda, CA

The mystery of the human brain continues to be a challenge for researchers, scientists, practitioners, educators, and physicians. The advancement of research and brain imaging techniques has resulted in never before seen or studied anatomical and physiologic processes providing better insights into many aspects of sleep and its relationships to memory and learning. To date, much research has been devoted to understanding the brain as a function of a system that has trillions of networks and pathways, resulting in diverse fields of study.

For example, the study of pediatric neuroimaging (developmental neuroimaging) has increased dramatically in the last decade, Blakemore reported an increased number of articles from 1996-2010.1 Other technologies have also been developed that provide a better understanding of the brain, including, but not limited to, the fMRI, ERP, and EEG.

An example of these technologies is the CLARITY project at Stanford that is using a hydrogel process to create a transparent brain.2 A report on the distribution of technologies used in the literature and published studies, which was published in the Journal of Cognitive Neuroscience by Rosen et al., spanned current imaging practices from fMRI to EEG.3 EEG came in second as the most common technique being used by researchers after fMRI.3 These technologies, among others, have seemingly unwrapped many mysteries of this three pound organ we call the brain.

The phenomenon of “sleep” began to attract the attention of researchers in health care, science, and education independently as they studied sleep as an emergent indicator of specific outcomes. One example of this focused study is in the area of memory and learning. Research has shown that memories consolidate during sleep.4-9 This attracted educators, psychologists, and neuroscientists, among others, to further investigate sleep in many diverse fields of study.

This paper will highlight some important aspects of the discoveries made in the areas of memory, learning, and sleep and how they relate to research in the practice of sleep medicine and the respiratory care profession.

Sleep, memory, and learning

Research into sleep and memory has increased dramatically. Researchers are discovering that improving sleep quality is basically a therapy for many disorders.10-12 These findings are not only on patients with sleep disorders, but also on normal healthy subjects. In addition, there are other disorders that are not yet considered sleep-related but demonstrate sleep-related pathologies. Maski K et al. reported that improving sleep quality in children with autism spectrum disorder results in improving cognitive function.10 Other studies have shown that targeting sleep spindles can improve cognitive function and deficits, not only in healthy individuals, but also in patients with schizophrenia.11,13,14 Neurodegenerative diseases have been linked to sleep disorders such as Alzheimer’s and dementia as well.15,16

From a neuroscience perspective we have seen expanded discoveries such as long-term potentiation (LTP) as an example of synaptic plasticity. An increase in LTP in the neuron will enhance learning and memory. Moreover, synaptic plasticity occurs at an early age and during sleep where memory and attention are being affected.17,18 Synaptic plasticity has been associated with learning and memory as well.19,20 Studies have shown that sleep loss has a similar impact on LTP as sleep has on memory consolidation, connecting sleep and memory.21

It is also postulated that memories are stored in a place on the neuron called the dendritic spines as learning occurs. Morphological changes occur with learning and LTP induction (increase in high frequency signals in the synapse).22 The changes of the dendritic spines are also affected by neurodegenerative diseases such as dementia.23 In our field of sleep, several studies have also investigated memory and improvement of cognitive function in patients with several sleep disorders who are undergoing therapy.24-26

Sleep and academic performance of schoolchildren and adults is an area of research that has drawn the attention of many educators. Academic performance may be measured in many ways, such as grade point average, teacher and parent feedback, and self-reporting. Curcio G et al. presented an overview of the current literature on the relationship between sleep loss and academic performance and learning capacity.27 They reported an association between sleep loss and different types of memory and learning. Neurocognitive functions and behavioral consequences were also observed.27

Kopasz et al. suggest that research and outcomes in sleep and memory could significantly assist academia.28 A relatively new journal entitled Mind, Brain, and Education reflects the multidisciplinary approach being taken to the study of sleep. This journal recently devoted an entire issue to sleep and learning. Researchers investigated the effect of circadian rhythm and cognition29, partial sleep deprivation and school schedule30, effect of sleep on part time students31, and morningness and eveningness (those who prefer morning vs. evening hours to perform certain tasks).32 One of the missions of this journal is to bring professionals together, including sleep therapists and neuroscientists, to investigate the role of sleep and how it can improve education.

Moving “beyond the technologist level” in polysomnography

With the aforementioned direction and results of this multi-professional approach to polysomnography, a logical question arises for our profession: How can we integrate this new information and contribute to this developing field of study? This was but a brief overview of what others have learned and applied to the various areas of sleep-related research. From this overview, we can see how we, as sleep professionals, can play a major role in the areas being investigated by scientists and other professionals.

Additional areas of study and discussion may include the appropriate level of education for the sleep specialist. Currently, sleep education is provided by respiratory care programs that have opted to add a sleep specialty track to their curriculum through CoARC. Sleep technologists may also graduate from an approved CAAHEP program that offers an associate or certificate-level degree in polysomnography.

Given this movement in research and science to uncover brain mysteries related to memory, learning, and sleep, our participation is critical. As respiratory care practitioners move to a higher entry level of education into the profession, our students should have additional education in sleep research and new updates within the field. This could be achieved by additional interaction with groups such as the AARC Sleep Section and additional collaboration between sleep centers and education programs. We should promote sleep research to empower our students to participate on a higher level and join others in this journey into new insights to the sleep profession.


  1. Blakemore SJ. Imaging brain development: the adolescent brain. Neuroimage 2012;61(2):397-406.
  2. Chung K, Deisseroth K. CLARITY for mapping the nervous system. Nat Methods 2013;10(6):508-513.
  3. Rosen BR, Savoy RL. fMRI at 20: has it changed the world? Neuroimage 2012;62(2):1316-1324.
  4. Stickgold R, Scott L, Rittenhouse C, Hobson JA. Sleep-induced changes in associative memory. J Cogn Neurosci 1999;11(2):182-193.
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  8. Ellenbogen JM, Payne JD, Stickgold R. The role of sleep in declarative memory consolidation: passive, permissive, active or none? Curr Opin Neurobiol 2006;16(6):716-722.
  9. Stickgold R, Walker MP. Sleep-dependent memory consolidation and reconsolidation. Sleep Med 2007;8(4):331-343.
  10. Maski K, Holbrook H, Manoach D, Hanson E, Kapur K, Stickgold R. Sleep dependent memory consolidation in children with autism spectrum disorder. Sleep 2015;38(12):1955-1963.
  11. Manoach DS, Stickgold R. Sleep, memory and schizophrenia. Sleep Med 2015;16(5):553-554.
  12. Frank MG. Sleep and synaptic plasticity in the developing and adult brain. Curr Top Behav Neurosci 2015;25:123-149.
  13. Wamsley EJ, Tucker MA, Shinn AK, Ono KE, McKinley SK, Ely AV, et al. Reduced sleep spindles and spindle coherence in schizophrenia: mechanisms of impaired memory consolidation? Biol Psychiatry 2012;71(2):154-161.
  14. Goder R, Graf A, Ballhausen F, Weinhold S, Baier PC, Junghanns K, et al. Impairment of sleep-related memory consolidation in schizophrenia: relevance of sleep spindles? Sleep Med 2015;16(5):564-569.
  15. Djonlagic I, Guo M, Matteis P, Carusona A, Stickgold R, Malhotra A. Untreated sleep-disordered breathing: links to aging-related decline in sleep-dependent memory consolidation. PloS one 2014;9(1):e85918.
  16. Pace-Schott EF, Spencer RM. Sleep-dependent memory consolidation in healthy aging and mild cognitive impairment. Curr Top Behav Neurosci 2015;25:307-330.
  17. Mormann F, Fell J, Axmacher N, Weber B, Lehnertz K, Elger CE, et al. Phase/amplitude reset and theta-gamma interaction in the human medial temporal lobe during a continuous word recognition memory task. Hippocampus 2005;15(7):890-900.
  18. Romcy-Pereira RN, Leite JP, Garcia-Cairasco N. Synaptic plasticity along the sleep-wake cycle: implications for epilepsy. Epilepsy Behav 2009;14Suppl1:47-53.
  19. Yang G, Lai CS, Cichon J, Ma L, Li W, Gan WB. Sleep promotes branch-specific formation of dendritic spines after learning. Science 2014;344(6188):1173-1178.
  20. Wallace E, Kim do Y, Kim KM, Chen S, Blair Braden B, Williams J, et al. Differential effects of duration of sleep fragmentation on spatial learning and synaptic plasticity in pubertal mice. Brain Res 2015;1615:116-128.
  21. Gronli J, Soule J, Bramham CR. Sleep and protein synthesis-dependent synaptic plasticity: impacts of sleep loss and stress. Front Behav Neurosci 2013;7:224.
  22. Matsuzaki M. Factors critical for the plasticity of dendritic spines and memory storage. Neurosci Res 2007;57(1):1-9.
  23. Yuste R, Bonhoeffer T. Morphological changes in dendritic spines associated with long-term synaptic plasticity. Annu Rev Neurosci 2001;24:1071-1089.
  24. Lau EY, Choi EW, Lai ES, Lau KN, Au CT, Yung WH, et al. Working memory impairment and its associated sleep-related respiratory parameters in children with obstructive sleep apnea. Sleep Med 2015;16(9):1109-1115.
  25. Kushida CA, Nichols DA, Holmes TH, Quan SF, Walsh JK, Gottlieb DJ, et al. Effects of continuous positive airway pressure on neurocognitive function in obstructive sleep apnea patients: The Apnea Positive Pressure Long-term Efficacy Study (APPLES). Sleep 2012;35(12):1593-1602.
  26. Pan YY, Deng Y, Xu X, Liu YP, Liu HG. Effects of continuous positive airway pressure on cognitive deficits in middle-aged patients with obstructive sleep apnea syndrome: a meta-analysis of randomized controlled trials. Chinese Med J 2015;128(17):2365-2373.
  27. Curcio G, Ferrara M, De Gennaro L. Sleep loss, learning capacity and academic performance. SleepMed Rev 2006;10(5):323-337.
  28. Kopasz M, Loessl B, Hornyak M, Riemann D, Nissen C, Piosczyk H, et al. Sleep and memory in healthy children and adolescents – a critical review. SleepMed Rev 2010;14(3):167-177.
  29. Valdez P, Ramírez C, García A. Circadian rhythms in cognitive processes: implications for school learning. MindBrain Educ 2014;8(4):161-168.
  30. Anacleto TS, Adamowicz T, Simões da Costa Pinto L, Louzada FM. School schedules affect sleep timing in children and contribute to partial sleep deprivation. MindBrain Educ 2014;8(4):169-174.
  31. Laberge L, Ledoux E, Auclair J, Gaudreault M. Determinants of sleep duration among high school students in part-time employment. Mind Brain Educ 2014;8(4):220-226.
  32. Schulke BB, Zimmermann LK. Morningness-eveningness and college advising: a road to student success? Mind Brain Educ 2014;8(4):227-230.

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