Mehmet Murat Sumer* Health Sciences Faculty, Atilim University, Turkey *Corresponding author: Mehmet Murat Sumer, Health Sciences Faculty, Atilim University, Turkey Submission: June 06, 2018; Published: September 27, 2018 Stroke and Sleep Disorders Introduction Stroke, remains one of leading causes of death and significant disability worldwide although incidence and early stroke mortality have been decreasing [1-4]. Cardinal risk factors are hypertension, cardiac disorders mainly valve disorders and atrial fibrillation, hyperlipidaemia, diabetes, smoking [5,6]. Recently, the role of sleep pathology in the development of cardiovascular and metabolic diseases has been highlightted [7-9]. Sleep, although characterized by quiescence and diminished responsiveness, is not only simple state of rest, but rather a cyclic state of periodic transitions between rapid-eye-movement (REM) and non-REM (NREM) sleep, which are precisely regulated by the central nervous system [10]. Along with the brain and other organs or physiological streams, the cardiovascular system achieves homeostatic restoration during sleep, mainly through autonomic circulatory control [11]. The decrease in blood pressure during sleep, “dipping,” is a key biomarker of cardiovascular health, secondary to changes in activity and posture and also under the influence of sleep and circadian rhythms [12]. During NREM or slow wave sleep, the largest portion (up to 80%) of normal adult sleep, the autonomic system is stabilized with vagal dominance, reduced sympathetic tone, and heightened baroreceptor gain, contributing to a significant reduction in blood pressure and heart rate, with the greatest drop occurring during NREM sleep [13,14]. REM sleep-occupying about 20% of total sleep-is dominated by marked fluctuations in sympathovagal balance (irregularly peaking sympathetic surges against a background of tonic vagal inhibition), which lead to abrupt changes in blood pressure and heart rate [11,15]. A compromised cardiovascular system is at risk for pathological events such as myocardial ischemia or arrhythmias during REM sleep. Sleep thus acts as a gatekeeper through cyclic oscillations between NREM and REM sleep. Non-dipping-loss of the typical blood pressure drop during sleep-is associated with a host of poor cardiac, neurological, metabolic, and renal outcomes [16]. Sleep fragmentation causes non-dipping [17]. Non-dipping is common in older adults and is associated with an increased risk of stroke [18]. Reduced dipping is associated with brain atrophy, worse functional status, and lower daytime cerebral blood flow [19]. Common sleep disorders such as sleep apnea, insomnia, and PLMS (Periodic limb movement during sleep) activate multiple mechanisms including intermittent hypoxia-reoxygenation injury, inflammation, insulin resistance, hypothalamic-pituitary- adrenal axis activation, hemodynamic swings, cardiac arrhythmia, and hypercoagulability, all of which have the potential to provoke cardiovascular diseases [20]. Obstructive Sleep Apnea (OSA) is the most frequent sleep disorder. The prevalence of moderate-to-severe OSA in the adult general population is 4-14% and increasing with age [21,22]. Experimental and observational studies have provided evidence that OSA promotes the development of cardiovascular diseases, including stroke [20,23]. Moderate to severe OSA is associated with silent ischemic changes, including white matter changes and lacunae as well as cerebral microbleeds [24,25]. Carotid and intracranial atherosclerosis are also accelerated in OSA [26]. It is unclear whether continuous positive airway pressure (CPAP) has a therapeutic effect on these changes [27]. Hypertension and insulin resistance might mediate the development of stroke in OSA. Moderate-to-severe OSA is significantly associated with prevalent and incident hypertension [28]. Effective CPAP therapy, alone or in addition to antihypertensive medication, significantly reduces blood pressure [29,30]. OSA may also increase the risk for development of type 2 diabetes by mechanisms such as increased insulin resistance and high cortisol secretion [31]. Concomitant obesity might have Mini Review 1/4 Copyright © All rights are reserved by Mehmet Murat Sumer. Volume - 2 Issue - 1 Examines in Physical Medicine and Rehabilitation: Open Access C CRIMSON PUBLISHERS Wings to the Research ISSN 2637-7934 Abstract Sleep disorders are highly prevalent in patients at risk for stroke and may be modifiable risk factors for stroke. Obstructive sleep apnea increases the risk of stroke independently, but the reported lack of therapeutic effectiveness of Continuous positive airway pressure for stroke prevention and cardiovascular protection should be cautiously interpreted. Short or long sleep duration, and insomnia with objective short sleep duration, could be risk factors for stroke and mortality. Sleep-related movement disorders, including Periodic limb movement during sleep and Restless leg syndrome are also potential risk factors for stroke. The overall findings suggest that systematic screening and proper management of sleep disturbances can substantially contribute to stroke risk modification at the population level.