Central sleep apnea (CSA) is a heterogeneous and relatively rare sleep breathing disorder characterized by recurrent reductions in respiratory drive and airflow during sleep. Its complex and not fully understood pathophysiology reflects challenges in respiratory control mechanisms. CSA is associated with cardiovascular, neurologic, systemic, and genetic conditions, and remains a key area for further research, particularly in improving diagnosis and understanding mechanisms. This article outlines the definition, diagnostic approaches, classification, and provides an overview of the underlying pathophysiology of CSA.
Breathing problems are the root cause of the most common and serious of the sleep disorders. Respiratory dysfunction can manifest only during sleep or can be present in wakefulness and made worse by sleep. This article identifies foundational concepts and principles of the control of breathing to explain why the respiratory system is vulnerable in sleep. The relation of these foundational concepts and principles to the spectrum of clinical sleep-related breathing problems are identified. Ultimately, understanding such mechanisms is the basis of rational strategies to improve breathing in sleep and the clinical course.
This chapter presents a comprehensive overview of central sleep apnea (CSA) and central hypoventilation disorders in the pediatric population. It places particular emphasis on children with complex medical conditions and genetic syndromes, including congenital central hypoventilation syndrome (CCHS) and rapid-onset obesity with hypothalamic dysfunction, hypoventilation, and autonomic dysregulation (ROHHAD) syndrome.In addition, the chapter examines related conditions such as Prader-Willi syndrome and other hypoventilation disorders arising from structural or functional abnormalities, including Chiari malformations and Leigh syndrome. It reviews current knowledge of the pathogenesis, epidemiology, clinical presentation, and diagnostic evaluation of these disorders in children, and concludes with evidence-based guidance for their management and treatment.
At elevations above roughly 2500 m, susceptible individuals manifest central sleep apnea due to high-altitude periodic breathing (high-altitude central sleep apnea [HA-CSA]) characterized by a typical periodic breathing pattern. Mechanistically, HA-CSA develops when sleep-related decreases in respiratory drive, triggered by hypocapnia, resulting from hypoxia-induced hyperventilation, interact with increased loop gain during non-rapid eye movement sleep. Clinically, severity is mitigated by descent or supplemental oxygen. Pharmacologic strategies such as acetazolamide are effective, and sleep quality may improve with judicious hypnotic use independent of CSA severity. This article integrates the description of HA-CSA mechanisms, clinical expression, ethnic and chronic-exposure perspectives, and management strategies.
Central apnea is cessation of breathing resulting from insufficient respiratory drive from the central respiratory network to the muscles of respiration. In this article, we present the pathophysiology, treatment of central apnea in preterm infants using the construct of loop-gain. We also present and discuss the diagnostic criteria, pathophysiology, assessment and treatment of central apnea of infancy, and the importance of polysomnography. Lastly, we present the pros and cons of monitoring devices and techniques and algorithms used to detect and measure the frequency of central apnea in preterm and term infants.
Central sleep apnea (CSA) is a disorder characterized by a lack of drive to breathe during sleep. Rare in the general population, it is most commonly seen in patients with heart failure, but is also prevalent, though often under-recognized, in conditions such as chronic kidney disease (CKD), acromegaly, and to a lesser extent, hypothyroidism. While there is a relative paucity of data compared to obstructive sleep apnea, there is evidence to suggest CSA may have an impact on morbidity and mortality in CKD, driven by the deleterious impact of intermittent hypoxia on kidney pathology.
Idiopathic central sleep apnoea (ICSA) is a form of periodic hyperventilation followed by central apnea that occurs in the absence of a clear etiologic factor. ICSA generally develops beyond the 5th decade of life and may occur in the presence of cardiovascular risk factors. The natural history and prognostic implications of ICSA are not well understood. In this context, the role of long-term suppressive treatment has not been established. For patients presenting with suspected ICSA, we suggest a careful evaluation for underlying metabolic or physiologic disturbances, monitoring of symptoms and consideration of referral to an expert center.
This article provides an overview of central sleep apnea (CSA) in the context of cardiovascular diseases (CVDs), highlighting its common association with conditions such as heart failure, atrial fibrillation, and cerebrovascular accidents. While the detailed pathophysiology is addressed elsewhere, the article notes that central apneas generally arise during sleep when arterial carbon dioxide levels drop below the apnea threshold, despite variability in underlying mechanisms. It also emphasizes that affected patients are typically normocapnic or hypocapnic rather than hypercapnic. The article focuses on key clinical aspects of CSA in CVD, including its epidemiology, clinical presentation, prognostic significance, and available treatment approaches.
Night shift work is designated a probable carcinogen based on epidemiologic studies in humans and mechanistic studies in animals. Increased cancer risk from night shift work is thought to result from the disruption of the normal circadian rhythms from exposure to light at night. Individual cancer risk due to night shift work varies, depending on individual sensitivity of the circadian system to light at night related disruption, pre-existing breast cancer risk, night shift schedules and environmental light at night exposures. Currently, there is no evidence for interventions to minimize or prevent breast cancer risk. Screening at-risk individuals seems appropriate.
Sleep patterns in women change across life stages, influenced by hormonal fluctuations during puberty, pregnancy, and menopause. Hormonal changes during the menstrual cycle can affect sleep quality, with premenstrual syndrome and premenstrual dysphoria disorder linked to poor sleep and daytime fatigue. Pregnancy disrupts sleep owing to elevated hormones, physical discomfort, and fetal movements. Menopause is associated with a high prevalence of sleep disturbances (40%-60%), including insomnia and sleep fragmentation, largely because of declining estrogen levels and vasomotor symptoms like hot flashes. After menopause, the prevalence of obstructive sleep apnea increases, with higher risks of cardiovascular complications.
This review examines gender differences in the major sleep disorders and specific areas in need of further research. Herein, we examine obstructive sleep apnea, obesity hypoventilation syndrome, insomnia, restless legs syndrome, and rapid eye movement sleep behavior disorder, highlighting differences in prevalence, symptoms, pathophysiology, diagnosis, and treatment between women and men. Hormonal influences, underdiagnosis, and atypical symptom presentation in women are recurring themes. The article also discusses current treatments and emerging therapies, including PAP therapy, weight-loss medications, digital cognitive behavioral therapy for insomnia, and neuromodulation. Across disorders, it emphasizes the need for improved screening tools.
Restless legs syndrome (RLS) affects about 1 in 4 pregnant women, typically emerging in the second or third trimester and resolving after delivery. Iron deficiency, family history, and multiparity are consistent risk factors, with transient RLS conferring increased long-term risk of chronic disease. Management prioritizes nonpharmacologic measures and iron repletion, reserving medication for severe, refractory cases. Oral or intravenous iron remains the safest and most effective therapy, while dopamine agonists, gabapentinoids, opioids, and benzodiazepines are last-line options. Collaborative care ensures maternal comfort while minimizing fetal exposure.
Obstructive sleep apnea (OSA) is increasingly recognized as an important comorbidity during pregnancy, with implications for both maternal and fetal health. Pregnancy-related anatomical, hormonal, and physiological changes, including upper airway edema, reduced functional residual capacity, increased respiratory drive, sleep fragmentation, and weight gain, collectively heighten susceptibility to sleep-disordered breathing. Evidence indicates that OSA can emerge or worsen as gestation progresses, with prevalence rising from early to late pregnancy across multiple cohorts. Although most cases are classified as mild, even mild OSA has been associated with hypertensive disorders, gestational diabetes, impaired fetal growth, and adverse perinatal outcomes.
Women show a disproportionately higher prevalence in several sleep disorders and mental health problems. This review highlights how women-specific biological and psychosocial characteristics may not only contribute to the onset of sleep disorders but also shape the strength and direction of their associations. Focusing on insomnia, restless legs syndrome, nightmare, and obstructive sleep apnea, we summarize evidence on sex differences in prevalence, risk factors, and mental health correlates across the female lifespan. Understanding these is essential for developing targeted sleep-focused approaches to improve mental health in women.
