Review Article

Correlation between Sleep Duration and Risk of Stroke Sazal Patyar, MS (Pharm), PhD,* and Rakesh Raman Patyar, MSc, PhD†

Modern lifestyle and job requirements have changed the sleep habits of most of the adult population. Various population-based studies have associated an increase in mortality with either shortened sleep or long sleep duration. Thus a U-shaped relationship between sleep duration and all-cause mortality in both men and women has been suggested. Several studies have found an association between sleep duration and risk of cardiovascular diseases also. Efforts to understand the etiology of stroke have indicated an association between sleep and stroke too. Obstructive sleep apnea, a sleep-related disorder, has been reported to significantly increase the risk of stroke. Moreover, many studies have shown that both short and long sleep durations are related to increased likelihood of diabetes and hypertension, which themselves are risk factors for stroke. Therefore, this review focuses on the correlation between sleep duration and risk of stroke based on the experimental and epidemiologic studies. Although a few experimental studies have reported that partial sleep deprivation may reduce stroke incidence and severity, yet, most experimental and observational studies have indicated a strong association between short/long sleep durations and higher risk of stroke. Key Words: Sleep—sleep deprivation— diabetes—hypertension—stroke. Ó 2015 by National Stroke Association

Stroke is one of the leading causes of morbidity and mortality worldwide. It is defined as an abrupt onset of a neurologic deficit because of disturbance in the blood supply to the brain. World Health Organization (WHO) has defined stroke as ‘‘rapidly developed clinical signs of focal disturbance of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than vascular origin.’’ As per a study conducted by WHO, cerebrovascular disease (stroke) accounts for 9.6% of all deaths. Furthermore, it is the leading cause of

From the *Department of Pharmacology, School of Pharmaceutical Sciences, Lovely Professional University, Phagwara; and †Department of Cardiology, Advanced Cardiac Centre, Postgraduate Institute of Medical Education & Research, Chandigarh, India. Received November 10, 2014; revision received December 27, 2014; accepted December 31, 2014. Address correspondence to Sazal Patyar, School of Pharmaceutical Sciences, Lovely Professional University, Phagwara, India. E-mail: [email protected]; [email protected]. 1052-3057/$ - see front matter Ó 2015 by National Stroke Association http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2014.12.038

disability in adults.1 The medical or surgical therapy (except aspirin) used for the treatment of acute ischemic stroke has very limited efficacy. However, various clinical studies have indicated that the incidence and high mortality of cerebrovascular diseases can be prevented to a large extent. Thus, the growing disease burden of stroke points toward prevention as an effective strategy, which in turn highlights the need for awareness regarding stroke risk factors and warning signs.2 Risk factors for stroke include advanced age, hypertension, previous stroke or transient ischemic attack, diabetes, high cholesterol, cigarette smoking, and atrial fibrillation.3 Recently, sleep has been associated with stroke as most of the previously mentioned risk factors are modified by sleep and sleep-related disorders. So, the aim of this review was to highlight the correlation between sleep duration and risk of stroke.

Sleep Sleep is a naturally recurring state of relatively suspended sensory activity, which is characterized by

Journal of Stroke and Cerebrovascular Diseases, Vol. -, No. - (---), 2015: pp 1-7

1

S. PATYAR AND R.R. PATYAR

2

reduced consciousness and inactivity of nearly all voluntary muscles. There are 2 main types of sleep: nonrapid eye movement (NREM) sleep (also known as quiet sleep) and rapid eye movement (REM) sleep (also known as active sleep or paradoxical sleep). Sleep is divided into various stages. Stage 1 is the beginning of sleep cycle and is a relatively light stage of sleep. It can be considered as a transition period between wakefulness and sleep. In stage 1, the brain produces high-amplitude theta waves, which are very slow brain waves. This period of sleep lasts only a brief time (around 5-10 minutes). Stage 2 is the second stage of sleep and lasts for approximately 20 minutes. The brain begins to produce bursts of rapid, rhythmic brain wave activity known as sleep spindles. Stage 3 is a transitional period between light sleep and a very deep sleep. Deep, slow brain waves known as delta waves begin to emerge during this period. Stage 4 is sometimes referred to as delta sleep because of the slow brain waves known as delta waves that occur during this time. It is a stage of deep sleep that lasts for approximately 30 minutes. Stage 5 is known as REM sleep, which is characterized by eye movement, increased respiration rate, and increased brain activity. It is also referred to as paradoxical sleep because while the brain and other body systems become more active, muscles become more relaxed. Sleep does not progress through these stages in sequence; however, it begins in stage 1 and progresses into REM sleep through the stages 2, 3, and 4.4 Sleep is necessary for normal physiological and psychological functioning. The effect of altered sleep quality and quantity has a significant bearing on the psychological and physiological profile of an individual.

Cerebral Hemodynamics during Sleep Cerebral circulation is characterized by changes in cerebral blood flow (CBF) and cerebral metabolic rate. Several positron emission tomography studies conducted on sleep stages have indicated that CBF changes dramatically with alterations of mental states. It has been reported that during the transition from quiet sleep to active sleep, CBF increases, regardless of the nature of the accompanying blood pressure change in all species.5-7 However, during the transition from wakefulness to quiet sleep, the change in CBF is variable, depending on the species.8 Generally, in these conditions, there is a reduction in relative regional cerebral blood flow (rCBF) in brain regions directly involved in executive function. Recently, a positron emission tomography study has reported a relatively increased CBF in the occipital lobes and decreased CBF in the bilateral cerebellum, the bilateral posterior parietal cortex, the right premotor cortex, and the left thalamus during sleep. However, decrease in rCBF has been reported in premotor cortex, thalamus, and cerebellum during stage 1 sleep.9 Earlier studies too have reported a significant decrease in CBF during slow

wave sleep (SWS), an increase during REM sleep in the brain stem and limbic areas but decrease in frontal cortex.10,11 Sympathetic nerves innervating the cerebral vessels have been suggested to play a protective role during the large arterial pressure surges of active sleep. It has been demonstrated that tonic sympathetic nerve activity constricts the cerebral circulation and restrains baseline CBF in sleep.12 Cerebral metabolic rate and CBF decrease during stages 3 and 4 NREM sleep, whereas the partial pressure of arterial CO2 increases because of a reduction in alveolar ventilation. It has been reported that the cerebral circulation during sleep is regulated by metabolic factors depending on the brain activity at a regional level, PO2, PCO2, pH changes, and autoregulation.13

Sleep and Major Risk Factors for Stroke Circadian Variation The incidence of stroke has shown a 24-hour pattern irrespective14 of stroke subtype, patient demographics, clinical features, and the presence or the absence of predisposing risk factors.15,16 Various studies have indicated an association between circadian variations and stroke onset because the stroke onset peaks in morning hours.17,18 Circadian rhythms are responsible for changes in blood pressure and rhythmic occurrence of some cardiovascular diseases.19 Most circadian rhythms are controlled by the body’s biological clock and are influenced by sleep. During NREM sleep sympathetic activity decreases and parasympathetic activity predominates thereby causing a decrease in heart rate, blood pressure, cardiac output, peripheral vascular resistance, and respiratory frequency. On the other hand, during REM sleep, variations in the activity of both the sympathetic and parasympathetic systems have been reported with phasic oscillations and surges resulting in a net increased parasympathetic tone and decreased sympathetic influence. Thus, REM sleep is characterized by increased cerebral cortical and spinal blood flow as well as variable heart rate and arterial blood pressure. As mostly normotensive and uncomplicated essential hypertensive individuals experience a nocturnal dip in blood pressure followed by a morning ‘‘surge,’’20,21 it has been suggested that this morning surge may disrupt vulnerable plaques causing rupture and thrombosis leading to a cardiovascular or cerebrovascular incident.21,22 As circadian rhythms are influenced by sleep, the duration of sleep produces circadian variations, which thereby alter the stroke incidence. Recently, a study has reported that rotating night shift work disrupts circadian rhythms and is an independent risk factor for ischemic stroke.23

Advanced Age Advancing age is considered as a risk factor for stroke as high incidence rates have been observed in the elderly

SLEEP AND STROKE

population. Aging affects the cardiovascular system, which increases the risks of both ischemic stroke and intracerebral hemorrhage. It has been demonstrated that 20%-24% reduction in rCBF occurs in normal aging individuals for which both age-related brain atrophy and increased cerebral vascular resistance secondary to cerebral arteriosclerosis are held responsible. In addition to this, sleep duration and the alterations during sleep too act as predisposing factors. Insomnia and hypertension are common problems in the elderly. Sleep deprivation in elderly has been associated with hypertension in Western population, which itself is an important risk factor for stroke.24,25 Short duration of sleep has been associated with an increased risk of stroke events in hypertensive patients, which is further discussed in the following section titled ‘‘hypertension.’’ The sleep stage analyses have indicated a nocturnal increase in serum interleukin 6 levels in association with stage 1-2 and REM sleep with no difference in the levels during SWS. As aging involves a relative increase in REM sleep at the expense of SWS, the abnormal increase in interleukin 6 is being implicated as a risk factor for stroke in geriatric population.24,25 Furthermore, it has been seen that elderly people have lower oxygen retention during sleep in the supine position, which may be because of reduced hypoventilation. This may be because of decreased lung elasticity resulting from advancing age, depressed respiratory regulation caused by autonomic dysfunction, or due to underventilation caused by cardiac, lung, and brain diseases. Thus, advancing age often acts as a risk factor for stroke and heart disease.26 Recently, a study conducted in elders has observed that arterial oxyhemoglobin (SaO2) levels decline in most people during sleep, and the compensatory vascular responses prevent cerebral oxyhemoglobin saturation (rcSO2) from falling during sleep. Thus, elderly persons with lower baseline rcSO2 levels and greater declines in cerebral oxygenation during sleep may have greater cardiovascular burden and are at greater risk for stroke or other forms of disabling cerebrovascular disease.27

Hypertension Hypertension is a major risk factor for stroke as high blood pressure puts stress on the blood vessel walls and causes blood clots or hemorrhage. Various ambulatory blood pressure studies have indicated that even small increases in blood pressure, particularly night-time blood pressure levels, are associated with significant increases in cardiovascular morbidity and mortality. Furthermore, sleep deprivation and insomnia have been reported to increase the incidence and the prevalence of hypertension.28 Blood pressure level and sleeps are closely associated. The different sleep stages modulate autonomous functions such as blood pressure and heart rate. Sleep

3

apnea increases blood pressure and may cause low levels of oxygen in the blood while carbon dioxide levels rise, which may lead to blood clots or strokes.28 Experimental evidence has associated short-term sleep restriction with impairment in blood pressure regulation. An experimental study has demonstrated that an impaired daily rhythm was closely related to the development of hypertension, and regulation of sympathetic nerve alterations may prove helpful in the treatment of hypertension and circadian rhythm disorder.29 The Coronary Artery Risk Development in Young Adults cohort study has shown reduced sleep duration as a predictor of higher blood pressure levels.30 The National Health and Nutrition Examination Survey has reported that short sleep duration of less than 5 hours is associated with increased risk of hypertension. Another study has showed that poor sleep quality is related with nondipping hypertension and serves as an independent predictor of nondipping in newly diagnosed stage 1 hypertensive patients.31 Higher morning hypertension has been associated with stroke risk independently of ambulatory blood pressure, nocturnal blood pressure falls, and silent infarct in elderly hypertensive patients.32 Some other studies also have linked insomnia with short sleep duration to increased risk of hypertension.33 Recent studies have shown that reduced sleep duration may be associated with an increased risk of hypertension with possibly stronger effects among women than those among men. A population-based study has confirmed this association while suggesting a stronger association among premenopausal women.34

Diabetes The increasing incidence of diabetes along with the contemporaneous decrease in sleep duration has indicated that diabetes is a risk factor for stroke modifiable by sleep duration. A study conducted among adults in the United States has reported that both short (,7 hours) and long sleep (.8 hours) are positively associated with the risk of obesity, diabetes, hypertension, and cardiovascular diseases.35 The United States Nurses’ Health Study conducted in middle-aged women who were not diabetic at baseline reported an increased risk of incident symptomatic diabetes among those reporting sleep durations of less than 5 hours and more than 9 hours over 10 years, but the risk became insignificant after adjustment for confounders.36 Similarly, various studies have shown that both short and long sleep durations are related to increased likelihood of diabetes.37-40 The underlying mechanism in experimentally induced sleep loss in healthy volunteers is decreased insulin sensitivity without adequate compensation in beta-cell function, which results in impaired glucose tolerance and increased diabetes risk. Second, it is suggested that lack of sleep downregulates the satiety hormone leptin,

S. PATYAR AND R.R. PATYAR

4

Figure 1.

Pathways associating sleep duration with the risk of stroke.

upregulates the appetite-stimulating hormone ghrelin, and increases hunger and food intake.41 Furthermore, short sleep duration has been associated with an elevated risk of incident-impaired fasting glucose through insulin resistance.42 A multiethnic cohort study has supported the role of short sleep as an independent risk factor for type 2 diabetes in whites and Hispanics.43 However, a prospective population study has reported no association between sleep problems at baseline and diabetic risk in a 32-year follow-up.44

Association between Sleep Duration and Risk of Stroke Sleep duration is influenced by a wide range of factors including professional demands, social or domestic responsibilities, and sleep disorders. Poor or insufficient sleep is associated with adverse health outcomes, including poor attention, performance deficit, type 2 diabetes, cardiovascular disease, and premature death.45 Various studies have associated the sleep duration with higher risk of stroke (Fig 1; Tables 1 and 2). Although there is scarcity of experimental evidence in this regard, yet, the clinical observations have supported this association. The summarized findings of experimental and epidemiologic studies are as follows:

Experimental Findings It has been reported that sleep disturbances impair functional stroke recovery. It has been suggested that sleep deprivation and sleep disturbances produce detri-

mental effects on functional and morphologic/structural outcomes after stroke. This indicates a potential role of sleep in the modulation of recovery processes and neuroplasticity.46 Another study has reported that prolonged exposures to the intermittent hypoxia during sleep, which characterizes sleep apnea, result in increased brain susceptibility to acute ischemic events thereby resulting in increased susceptibility to stroke.47 As sleep apnea causes sleep discontinuity, the observations of this study implicate the role of sleep duration in stroke. Experimental sleep deprivation has been reportedly found to induce a functional alteration of the monocyte proinflammatory cytokine response.48 Previous studies have also reported that sleep deprivation produces a proinflammatory and pro-oxidative environment and activates classical stress responses, which lead to poor ischemic outcomes.49-52 Thus, it can be hypothesized that acute sleep deprivation would exacerbate neuroinflammation and neurodegeneration after global ischemia. A potential role of sleep-modulating treatments on stroke outcomes has been suggested as the results of an experimental study have demonstrated that at the early phase of stroke, sleep disruption including sleep deprivation aggravates brain damage and increases expression of genes that inhibit poststroke axonal sprouting.53 Sleepenhancing drugs like g-hydroxybutyrate (sodium oxybate) have demonstrated neuroprotective action against ischemia/brain damage in rat models54-58 and have been shown to accelerate motor recovery after stroke in a mouse model.59

SLEEP AND STROKE

5

Table 1. Important experimental studies associating sleep duration with the risk of stroke Experimental studies Zunzunegui et al Wang et al Irwin et al; Ferrie et al; Lorton et al; Mullington et al; Toth et al Bralet et al; Lavyne et al; Vergoni et al; Ottani et al; Ottani et al Gao et al

Outcomes Sleep deprivation and sleep disturbances impair functional stroke recovery46 Prolonged exposures to the intermittent hypoxia during sleep result in increased susceptibility to stroke47 Sleep deprivation produces a pro-inflammatory and pro-oxidative environment and activates classical stress responses, which lead to poor ischemic outcomes48-52 Sleep-enhancing drug g-hydroxybutyrate (sodium oxybate) demonstrated neuroprotective action against ischemia/brain damage thereby implicating the role of sleep54-58 Gamma-hydroxybutyrate–accelerated functional recovery after focal cerebral ischemia has been shown to accelerate motor recovery after stroke in a mouse model.59

Epidemiologic findings Both short and long sleep durations have been associated with increased risk of stroke.60 Various studies have examined an association between sleep duration/ patterns and risk of stroke. The epidemiologic data relating to these studies are summarized in Table 2. Excessive daytime sleepiness has been reported as a significant risk factor for stroke.61 Prolonged sleep duration (increased REM sleep) has been associated with increase in the incidence of stoke. The Japan Collaborative Cohort Study for Evaluation of Cancer Risk conducted in Japanese men and women concluded that long sleep duration was associated with increased mortality from stroke.60 According to the First National Health and Nutrition Examination Survey Epidemiologic Follow-up Study, stroke risk was higher in people who reported sleeping longer than 8 hours at night, as compared to those sleeping between 6 and 8 hours.62 It has been suggested that the increased risks for coronary heart diseases, stroke, and mortality among long sleepers might be because of other sleep disorders, such as sleep disordered breathing.62

The Caerphilly Cohort Study has concluded that sleep disorders including insomnia are predictive of ischemic cerebrovascular disease and possibly ischemic cardiac events. The study has reported that the risk of an ischemic stroke is increased in men whose sleep is frequently disturbed, and the daytime sleepiness is associated with a significant increase in ischemic heart disease events.63 A study conducted in the framework of WHO ‘‘Monitoring Trends and Determinants on Cardiovascular Diseases–psychosocial’’ program reported a 2-7–fold relative risk of stroke development in males with sleep disturbances.64 A prospective study conducted in postmenopausal women in the Women’s Health Initiative Observational Study cohort has observed an association of ischemic stroke (60%-70% increase in risk) with long sleep that was stronger than the association with short sleep (10%-20% increase in risk). Although this was consistent with previous studies, the modest increase in ischemic stroke risk associated with short sleep (#6 hours/night) indicates adverse effects of sleep deprivation.65

Table 2. Important epidemiologic studies associating sleep duration with the risk of stroke Epidemiologic studies NHANES-I The Caerphilly Cohort Study WHO program ‘‘MONICA–psychosocial’’ WHI-OS Jichi Medical School Cohort Study JACC study Multiethnic cross-sectional study of US adults A case-control study by Davies et al A study by Eguchi et al

Outcomes Increased risk of stroke in long sleepers62 Insomnia increases the risk of ischemic stroke63 Sleep disturbances increase the relative risk of stroke development in males up to 2-7 fold64 Increased risk of ischemic stroke risk with long sleep65 Higher risk of stroke in men sleeping less than 6 hours67 Long sleep duration is associated with increased mortality from stroke60 Insufficient rest or sleep was found to be positively associated with stroke68 Excessive daytime sleepiness is a significant risk factor for stroke61 Shorter sleep duration is an independent risk for future incidence of stroke events in hypertensive patients, especially those with silent cerebral infarcts66

Abbreviations: JACC, Japan Collaborative Cohort Study for Evaluation of Cancer Risk; MONICA, Monitoring Trends and Determinants on Cardiovascular Diseases; NHANES, National Health and Nutrition Examination Survey; WHI-OS, Women’s Health Initiative Observational Study; WHO, World Health Organization.

S. PATYAR AND R.R. PATYAR

6

Recently, a study has demonstrated shorter sleep duration as an independent risk for future incidence of stroke events in hypertensive patients, especially those with silent cerebral infarcts.66 Jichi Medical School Cohort Study, a population-based prospective study conducted in Japan, observed a higher risk of stroke in men sleeping less than 6 hours/day than those sleeping 7-7.9 hours. While in women, there was no material association between sleep duration and stroke.67 Similarly, in a multiethnic cross-sectional study of US adults, insufficient rest or sleep was found to be positively associated with stroke.68

Conclusion Both experimental and epidemiologic studies have reported a strong association between short/long sleep durations and higher risk of stroke. There is scarcity of experimental evidence in this regard, but the clinical observations have very strongly supported this association. From the findings of experimental and epidemiologic studies, it may be concluded that sleep duration affects the stroke incidence directly and indirectly through the modulation of certain risk factors for stroke like circadian variations, sleep disordered breathing, hypertension, and diabetes. This implication of sleep suggests that prevention of sleep disturbances, improvement of sleep quality, and sleep-modulating treatments may play a potential role in the management of stroke.

References 1. World Health Organization. World Health Report 2002. Reducing risks, promoting healthy life. Geneva: WHO 2002. 2. Straus SE, Majumdar SR, McAlister FA. New evidence for stroke prevention: scientific review. J Am Med Assoc 2002;288:1388-1395. 3. Stroebele N, M€ uller-Riemenschneider F, Nolte CH, et al. Knowledge of risk factors, and warning signs of stroke: a systematic review from a gender perspective. Int J Stroke 2011;6:60-66. 4. Silber MH, Ancoli-Israel S, Bonnet MH, et al. The visual scoring of sleep in adults. J Clin Sleep Med 2007;3: 121-131. 5. Grant DA, Franzini C, Wild J, et al. Continuous measurement of blood flow in the superior sagittal sinus of the lamb. Am J Phys 1995;269:R274-R279. 6. Zoccoli G, Bach V, Cianci T, et al. Brain blood flow and extracerebral carotid circulation during sleep in rat. Brain Res 1994;641:46-50. 7. Grant DA, Franzini C, Wild J, et al. Cerebral circulation in sleep: vasodilatory response to cerebral hypotension. J Cereb Blood Flow Metab 1998;18:639-645. 8. Franzini C. Brain metabolism and blood flow during sleep. J Sleep Res 1992;1:3-16. 9. Kjaer T, Law I, Ltschiøtz GW, et al. Regional cerebral blood flow during light sleep—a H215O-PET study. J Sleep Res 2002;11:201-207.

10. Maquet P, Delgueldre C, Delfiore G. Functional neuroanatomy of human slow wave sleep. J Neurosci 1997; 17:2807-2812. 11. Maquet P, Peters JM, Aerts J. Functional neuroanatomy of human non rapid eye movement sleep and dreaming. Nature 1996;383:163-166. 12. Loos N, Grant DA, Wild J, et al. Sympathetic nervous control of the cerebral circulation in sleep. J Sleep Res 2005;14:275-283. 13. Corfield DR, Meadows GE. Control of cerebral blood flow during sleep and the effects of hypoxia. AdvExp Med Biol 2007;588:65-73. 14. Manfredini R, Boari B, Smolensky MH. Circadian variation in stroke onset: identical temporal pattern in ischemic and hemorrhagic events. Chronobiol Int 2005; 22:417-453. 15. Casetta I, Granieri E, Fallica E, et al. Patient demographic and clinical features and circadian variation in onset of ischemic stroke. Arch Neurol 2002;59:48-53. 16. Guy AY, Bornstein NM. Are there any unique epidemiological and vascular risk factors for ischaemic strokes that occur in the morning hours? Eur J Neurol 2000;7:179-181. 17. Marler JR, Price TR, Clark GL. Morning increase in onset of ischemic stroke. Stroke 1989;20:473-476. 18. Marsh EE III, Biller J, Adams HP Jr. Circadian variation in onset of acute ischemic stroke. Arch Neurol 1990;47: 1178-1180. 19. McNamara P, Seo SP, Rudic RD, et al. Regulation of CLOCK and MOP4 by nuclear hormone receptors in the vasculature: a humoral mechanism to rest a peripheral clock. Cell 2001;105:877-889. 20. Kawano Y, Tochikubo O, Minamisawa K, et al. Circadian variation of haemodynamics in patients with essential hypertension: comparison between early morning and evening. J Hypertens 1994;12:1405-1412. 21. Millar-Craig MW, Bishop CN, Raftery EB. Circadian variation of blood-pressure. Lancet 1978;1:795-797. 22. Johnstone MT, Mittleman M, Tofler G, et al. The pathophysiology of the onset of morning cardiovascular events. Am J Hypertens 1996;9:22S-28S. 23. Brown DL, Feskanich D, Sa nchez BN, et al. Rotating night shift work and the risk of ischemic stroke. Am J Epidemiol 2009;169:1370-1377. 24. Musselman DL, Evans DL, Nemeroff CB. The relationship of depression to cardiovascular disease: epidemiology, biology, and treatment. Arch Gen Psychiatry 1998; 55:580-592. 25. Hall MH, Muldoon MF, Jennings JR, et al. Self-reported sleep duration is associated with the metabolic syndrome in midlife adults. Sleep 2008;31:635-643. 26. Hjalmarsen A, Hykkerud DL. Severe nocturnal hypoxaemia in geriatric inpatients. Age Ageing 2008;37:526-529. 27. Carlson BW, Neelon VJ, Carlson JR, et al. Cerebrovascular disease and patterns of cerebral oxygenation during sleep in elders. Biol Res Nurs 2009;10:307-317. 28. Calhoun DA, Harding SM. Sleep and hypertension. Chest 2010;138:434-443. 29. Suzuki J, Ogawa M, Tamura N, et al. A critical role of sympathetic nerve regulation for the treatment of impaired daily rhythm in hypertensive Dahl rats. Hypertens Res 2010;33:1060-1065. 30. Knutson KL, Van Cauter E, Rathouz PJ, et al. Association between sleep and blood pressure in midlife: the CAR DIA sleep study. Arch Intern Med 2009;169:1055-1061. 31. Erden I, Erden EC, Ozhan H, et al. Poor-quality sleep score is an independent predictor of nondipping hypertension. Blood Press Monit 2010;15:184-187.

SLEEP AND STROKE 32. Kario K, Ishikawa J, Pickering TG, et al. Morning hypertension: the strongest independent risk factor for stroke in elderly hypertensive patients. Hypertens Res 2006; 29:581-587. 33. Vgontzas AN, Liao D, Bixler EO, et al. Insomnia with objective short sleep duration is associated with a high risk for hypertension. Sleep 2009;32:491-497. 34. Stranges S, Dorn JM, Cappuccio FP, et al. A populationbased study of reduced sleep duration and hypertension: the strongest association may be in premenopausal women. J Hypertens 2010;28:896-902. 35. Buxton OM, Pavlova M, Reid EW, et al. Sleep restriction for 1 week reduces insulin sensitivity in healthy men. Diabetes 2010;59:2126-2133. 36. Ayas NT, White DP, Al-Delaimy WK, et al. A prospective study of self-reported sleep duration and incident diabetes in women. Diabetes Care 2003;26:380-384. 37. Yaggi HK, Araujo AB, McKinlay JB. Sleep duration as a risk factor for the development of type 2 diabetes. Diabetes Care 2006;29:657-661. 38. Cappuccio FP, D’Elia L, Strazzullo P, et al. Quantity and quality of sleep and incidence of type 2 diabetes: a systematic review and meta-analysis. Diabetes Care 2010; 33:414-420. 39. Gangwisch JE, Heymsfield SB, Boden-Albala B, et al. Sleep duration as a risk factor for diabetes incidence in a large U.S. sample. Sleep 2007;30:1667-1673. 40. Rod NH, Vahtera J, Westerlund H, et al. Sleep disturbances and cause-specific mortality: results from the GAZEL Cohort Study. Am J Epidemiol 2011;173:300-309. 41. Morselli L, Leproult R, Balbo M, et al. Role of sleep duration in the regulation of glucose metabolism and appetite. Best Pract Res Clin Endocrinol Metab 2010; 24:687-702. 42. Rafalson L, Donahue RP, Stranges S, et al. Short sleep duration is associated with the development of impaired fasting glucose: the Western New York Health Study. Ann Epidemiol 2010;20:883-889. 43. Beihl DA, Liese AD, Haffner SM. Sleep duration as a risk factor for incident type 2 diabetes in a multiethnic cohort. Ann Epidemiol 2009;19:351-357. 44. Bjorkelund C, Bondyr-Carlsson D, Lapidus L, et al. Sleep disturbances in midlife unrelated to 32-year diabetes incidence: the prospective population study of women in Gothenburg. Diabetes Care 2005;28:2739-2744. 45. Gallicchio L, Kalesan B. Sleep duration and mortality: a systematic review and meta-analysis. J Sleep Res 2009; 18:148-158. 46. Zunzunegui C, Gao B, Cam E, et al. Sleep disturbance impairs stroke recovery in the rat. Sleep 2011;34:1261-1269. 47. Wang Y, Guo SZ, Bonen A, et al. Monocarboxylate transporter 2 and stroke severity in a rodent model of sleep apnea. J Neurosci 2011;31:10241-10248. 48. Irwin MR, Wang M, Campomayor CO, et al. Sleep deprivation and activation of morning levels of cellular and genomic markers of inflammation. Arch Intern Med 2006;166:1756-1762. 49. Ferrie JE, Kivimaki M, Akbaraly TN, et al. Associations between change in sleep duration and inflammation: findings on C-reactive protein and interleukin 6 in the Whitehall II Study. Am J Epidemiol 2013;178:956-961. 50. Lorton D, Lubahn CL, Estus C, et al. Bidirectional communication between the brain and the immune system: implications for physiological sleep and disorders

7

51.

52. 53. 54.

55.

56.

57.

58.

59.

60.

61.

62.

63.

64.

65.

66.

67.

68.

with disrupted sleep. Neuroimmunomodulation 2006; 13:357-374. Mullington JM, Haack M, Toth M, et al. Cardiovascular, inflammatory, and metabolic consequences of sleep deprivation. Prog Cardiovasc Dis 2009;51:294-302. Toth LA. Sleep, sleep deprivation and infectious disease: studies in animals. Adv Neuroimmunol 1995;5:79-92. Gao B, Cam E, Jaeger H, et al. Sleep disruption aggravates focal cerebral ischemia in the rat. Sleep 2010;33:879-887. Bralet J, Beley P, Bralet AM, et al. Influence of various agents on the development of brain edema in the rat following microembolism: protective effect of gammabutyrolactone. Stroke 1979;10:653-656. Lavyne MH, Hariri RJ, Tankosic T, et al. Effect of low dose gamma-butyrolactone therapy on forebrain neuronal ischemia in the unrestrained, awake rat. Neurosurgery 1983;12:430-434. Vergoni AV, Ottani A, Botticelli AR, et al. Neuroprotective effect of gamma-hydroxybutyrate in transient global cerebral ischemia in the rat. Eur J Pharmacol 2000;397:75-84. Ottani A, Saltini S, Bartiromo M, et al. Effect of gammahydroxybutyrate in two rat models of focal cerebral damage. Brain Res 2003;986:181-190. Ottani A, Vergoni AV, Saltini S, et al. Effect of late treatment with gamma-hydroxybutyrate on the histological and behavioral consequences of transient brain ischemia in the rat. Eur J Pharmacol 2004;485:183-191. Gao B, Kilic E, Baumann CR, et al. Gamma-hydroxybutyrate accelerates functional recovery after focal cerebral ischemia. Cerebrovasc Dis 2008;26:413-419. Ikehara S, Iso H, Date C, et al. Association of sleep duration with mortality from cardiovascular disease and other causes for Japanese men and women: the JACC study. Sleep 2009;32:295-301. Davies DP, Rodgers H, Walshaw D, et al. Snoring, daytime sleepiness and stroke: a case-control study of firstever stroke. J Sleep Res 2003;12:313-318. Qureshi AI, Giles WH, Croft JB, et al. Habitual sleep patterns and risk for stroke and coronary heart disease: a 10-year follow-up from NHANES I. Neurology 1997; 48:904-911. Elwood P, Hack M, Pickering J, et al. Sleep disturbance, stroke, and heart disease events: evidence from the Caerphilly cohort. J Epidemiol Community Health 2006;60: 69-73. Gafarov VV, Gromova EA, Gagulin IV, et al. A study of the risk factors of stroke development in the framework of WHO program ‘‘MONICA–psychosocial’’. Zh Nevrol Psikhiatr Im S S Korsakova 2005;13:36-41. Chen JC, Brunner RL, Ren H, et al. Sleep duration and risk of ischemic stroke in postmenopausal women. Stroke 2008;39:3185-3192. Eguchi K, Hoshide S, Ishikawa S, et al. Short sleep duration is an independent predictor of stroke events in elderly hypertensive patients. J Am Soc Hypertens 2010; 4:255-262. Amagai Y, Ishikawa S, Gotoh T, et al. Sleep duration and incidence of cardiovascular events in a Japanese population: the Jichi Medical School cohort study. J Epidemiol 2010;20:106-110. Shankar A, Syamala S, Kalidindi S. Insufficient rest or sleep and its relation to cardiovascular disease, diabetes and obesity in a national, multiethnic sample. PLoS One 2010;5:e14189.

Correlation between Sleep Duration and Risk of Stroke.

Modern lifestyle and job requirements have changed the sleep habits of most of the adult population. Various population-based studies have associated ...
477KB Sizes 5 Downloads 26 Views