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CHAPTER 6 Sleep and Stroke G.J CHAPTER 6 Sleep and Stroke G.J. Meskill*, C. Guilleminault** *Comprehensive Sleep Medicine Associates, Houston, TX, USA **The Stanford Center for Sleep Sciences and Medicine, Redwood City, CA, USA OUTLINE Introduction 115 Stroke, Parasomnias, and Sleep- Related Movement Disorders 120 Sleep Apnea is a Risk Factor for Stroke 115 Diagnosis 120 Pathophysiology 116 Treatment 122 Stroke Increases the Risk of Sleep Apnea 118 Conclusions 123 Stroke and the Sleep–Wake Cycle 118 References 124 INTRODUCTION Stroke, defined as a focal neurological deficit of acute onset and vascular origin, is the sec- ond leading cause of death worldwide and is a major source of physical, psychological, and monetary hardship. There are more than 15 million cases worldwide annually, and 795,000 in the United States alone. In total, 137,000 stroke patients will die from stroke complications, and more than 50% will have physical and mental impairment.1 Factoring healthcare services, medications, and productivity loss, strokes cost the United States $34 billion annually.2 SLEEP APNEA IS A RISK FACTOR FOR STROKE Obstructive sleep apnea (OSA) is characterized by recurrent episodes of partial or complete interruption in breathing during sleep due to increased upper airway resistance. OSA has been identified as an independent risk factor for several cardiovascular and cerebrovascular Sleep and Neurologic Disease. http://dx.doi.org/10.1016/B978-0-12-804074-4.00006-6 Copyright © 2017 Elsevier Inc. All rights reserved. 115 116 6. SLEEP AND STROKE morbidities, including hypertension, ischemic heart disease, heart failure, atrial fibrillation, and hypertrophic cardiomyopathy.3–6 The incidence of OSA varies due to significant differ- ences in the sensitivity of testing sites, testing modalities (e.g., in-laboratory polysomnog- raphy vs. home sleep testing), and changes in the American Academy of Sleep Medicine (AASM) scoring rules over time. The severity of OSA is measured by the numbers of apneas and hypopneas per hour of sleep, otherwise termed the Apnea-Hypopnea Index (AHI). A re- cent source estimates that 1 in 5 adults has at least mild OSA.4 An epidemiologic study of the citizens of Sao Paulo, Brazil demonstrated that moderate OSA, defined as an AHI > 15, was present in 25% of men and 9% of women.7 OSA and stroke have a bidirectional relationship: individuals with OSA have a greater risk of stroke, and stroke survivors have a greater incidence of OSA. Studies have shown that 50–75% of patients with stroke or TIA have OSA.8–10 Despite this relationship, as many as 80% of all patients with OSA are neither diagnosed nor treated. Barriers to diagnosis include patient resistance, provider awareness, and access to diagnostic facilities.11 After adjusting for independent cardiovascular risk factors such as hypertension, atrial fibrillation, diabetes, hyperlipidemia, and smoking status, the hazard ratio of myocardial in- farction and stroke in patients with OSA was observed in one study to be 2.0 (AHI > 5), and 3.3 in patients with severe OSA (AHI > 30).12 Another study demonstrated that in patients with moderate OSA (AHI > 20), regardless of the presence of obesity, the odds ratio of stroke occurrence was 4.3.13 The Sleep Heart Health Study showed that the increased incidence of stroke in men with OSA compared to men without OSA is 2.26.14 Meta-analysis of more than 20 studies has demonstrated that more than 50% of patients with stroke have sleep-disordered breathing (SDB), which includes both OSA and Central Sleep Apnea (CSA), with an AHI > 10.15 Another metaanalysis evaluating 29 stroke articles (ischemic, hemorrhagic, and TIA) suggested that the incidence of SDB was 72% in stroke patients.16 While SDB improves in the subacute period after a stroke (6 months after stroke onset), as many as 50% of stroke patients continue to have OSA months to years following stroke.17 Higher AHI values, particularly in men, are associated with higher risk of stroke.18 While correlation between OSA and stroke has been clearly demonstrated, to date there have been no randomized controlled trials on this topic. PATHOPHYSIOLOGY There are two types of strokes: ischemic (85%) and hemorrhagic (15%). An ischemic stroke is a cerebrovascular event in which an intracranial artery is occluded, leading to cerebral ischemia and cell death. An ischemic event that resolves spontaneously before cellular death occurs is considered a transient ischemic attack (TIA). Previously, TIA was defined as an event whose symptoms resolved in less than 24 h. This definition has been replaced because many such events were found to be associated with lesions on diffusion-weighted magnetic resonance imaging (MRI). A hemorrhagic stroke is a cerebrovascular event in which an intra- cranial vessel ruptures, leading to brain injury. OSA occurs when changes in cortical regulation of upper airway musculature lead to recur- rent episodes of airway obstruction and disruptions in sleep. Relaxation of pharyngeal muscu- lature and the genioglossus during sleep leads to retroposition of these structures, narrowing PATHOPHYSIOLOGY 117 the diameter of the upper airway.18 These changes require increased inspiratory effort to gen- erate negative intrathoracic pressure in order to maintain consistent airflow. The resulting in- crease in airflow velocity through a narrowed lumen causes turbulence and pharyngeal soft tissue vibration (i.e., snoring). This increased airflow velocity creates a vacuum effect on the upper airway soft tissue, and when combined with intrathoracic negative pressure this can lead to partial or complete collapse of the upper airway. Resolution of this occlusion is achieved by intermittent interruptions in cortical sleep, which leads to increased pharyngeal muscle tone and restored patency of the upper airway. More subtle episodes of obstructive breathing, some- times termed “upper airway resistance syndrome,” may not lead to airway obstruction but the respiratory dynamics and increased negative intrathoracic pressure are the same.19 Dynamic fluctuations in intrathoracic pressure contribute to long-term cardiovascular con- sequences. Obstructive respirations during sleep have been demonstrated to cause a leftward shift of the cardiac interventricular septum and pulsus paradoxus.20 The increased negative pressure in the thoracic cavity leads to increased venous return on diastole, with right atrial and ventricular distention. Conversely, systole is resisted, leading to decreased ejection into the systemic circulation. This can lead to increased atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) secretion, inducing nocturnal polyuria as a defense mechanism to reduce cardiac load.21 Peripheral vasoconstriction has been observed to occur with SDB.22,23 In addition, when a patient with OSA experiences an obstructive respiratory event during sleep, pulmonary autonomic afferents are largely inhibited due to the prolonged increase in negative intrathoracic pressure, which is the result of inspiring against a closed or partially closed glottis.24 As a result, hyperventilation is prevented, baroreceptors are stimulated, and sympathetic vasomotor tone increases, leading to peripheral vasoconstriction.25 In the context of observed changes in intrathoracic pressure and their resultant effect on cardiac ejection fraction, these changes in the peripheral vasculature could be a response to maintain perfusion pressure. Conversely, given that cortical sleep is fragmented and airway patency is restored by cortical regulation of upper airway muscle tone, cardiac ejection is also normalized. While the peripheral vasculature remains constricted, transient episodes of capillary hypertension occur, which may contribute to end-organ damage. When obstructive apneas recur and cardiac ejection again becomes impaired, the lag between decreased cardiac output and peripheral vascular constriction may cause brief periods of cerebral hypotension, particularly in the distal vasculature. This is one proposed mechanism for the association between OSA and anterior ischemic optic neuropathy.26 As SDB becomes more significant, intermittent periods of hypoxia and hypercapniaoccur due to periodic airflow impairment. This hypoxia stimulates sympathetic activation, oxida- tive stress, metabolic derangement, and systemic inflammation.27 This has been demonstrat- ed in both obstructive and central sleep apnea, indicating that it is the hypoxemia and not the obstruction itself that activates sympathetic tone. In addition, metabolic and sleep dys- function increases the propensity for obesity, insulin resistance and diabetes mellitus, and nonalcoholic fatty liver disease.28 The changes in intrathoracic pressure dynamics, sympa- thetic activation, inflammatory regulation, and their resultant stress to the cardiovascular system contribute to the increased risk of congestive heart failure, hypertension,29 and atrial fibrillation,30 all of which are associated with increased risk of stroke.31–33 The apnea-induced hypoxia also triggers the activation of the so-called “diving reflex,” a protective mechanism in all mammals whereby cardiac vagal tone increases, resulting in transient bradycardia. This 118 6. SLEEP AND STROKE mechanism helps preserve blood flow to the heart and brain while limiting cardiac oxygen demand. In susceptible individuals, however, the diving reflex can trigger sinus pauses and bradyarrhythmias, such as AV block.34 When breathing resumes, cardiac output increases and sympathetic tone remains elevated, predisposing
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