睡眠体位对不同睡眠阶段阻塞性睡眠呼吸暂停低通气综合征患者睡眠参数及其结构的影响

目的：观察体位疗法对阻塞性睡眠呼吸暂停低通气综合征患者夜间多导睡眠图监测参数的影响.方法：[1]选择2001-10/2003-01在南京医科大学第一附属医院睡眠中心就诊的阻塞性睡眠呼吸暂停低通气综合征患者38例.患者对实验目的均知情,并同意配合.[2]采用多导睡眠监测系统对患者行整夜多导睡眠监测.连续进行2 d的监测.第1夜,分别记录睡眠第1阶段（21：30～24：00）、第2阶段（0：00～2：30）和第3阶段（2：30～5：00）.监测项目：总清醒时间、整夜睡眠结构包括快动眼睡眠和非快动眼睡眠中的Ⅰ～Ⅳ期以及占总睡眠时间的百分比、呼吸暂停次数、最长呼吸暂停时间、呼吸暂停低通气指数、最低脉氧饱和度及血压.第2夜,给患者穿上背后带小口袋的特制背心,并于口袋中放置一只高尔夫球.同时加强巡视督促取侧卧位.再次观察记录上述各指标,进行治疗前后比较.[3]数据间差异比较采用多因素随机方差分析.结果：阻塞性睡眠呼吸暂停低通气综合征患者38例均进入结果分析.[1]不同睡眠阶段多导睡眠图监测结果：呼吸暂停低通气指数、最长呼吸暂停时间、平均动脉压：睡眠第2和3阶段明显大于/长于睡眠第1阶段（P＜0.05～0.01）,睡眠第3阶段明显高于睡眠第2阶段（P＜0.01）;最低血氧饱和度：睡眠第2和3阶段明显小于睡眠第1阶段（P＜0.05）.睡眠结构：睡眠各阶段差异不明显.[2]治疗前后多导睡眠图监测参数比较：呼吸暂停低通气指数、最长呼吸暂停时间、平均动脉压：治疗后明显小于/短于治疗前（P＜0.01）.最低血氧饱和度：治疗后明显高于治疗前（P＜0.01）.睡眠结构：睡眠各阶段差异不明显.结论：采取高尔夫球背心的睡眠侧卧位体位疗法可明显改善阻塞性睡眠呼吸暂停低通气综合征不同睡眠阶段多导睡眠图监测参数,且不影响睡眠结构.     

血氧气流记录与多导睡眠图的应用比较

目的:研究和评价血氧气流记录仪诊断不同程度阻塞性睡眠呼吸暂停低通气综合征的准确性。方法:62例研究对象同时进行整夜标准多导睡眠和血氧气流记录监测,以标准多导睡眠图监测的呼吸暂停低通气指数为诊断阻塞性睡眠呼吸暂停低通气综合征的金标准,评估血氧气流记录监测呼吸暂停低通气指数和最低血氧饱和度的准确性。结果:血氧气流记录与标准多导睡眠图测得的呼吸暂停低通气指数和最低血氧饱和度密切相关(r=0.964和0.816,P=0.000)。以呼吸暂停低通气指数≥5为诊断界值,血氧气流记录与标准多导睡眠图比较诊断阻塞性睡眠呼吸暂停低通气综合征的灵敏度为93.3%,特异度为76.5%。正常和轻度阻塞性睡眠呼吸暂停低通气综合征组血氧气流记录-呼吸暂停低通气指数与标准多导睡眠图-呼吸暂停低通气指数差异无统计学意义(P>0.05),中重度阻塞性睡眠呼吸暂停低通气综合征组血氧气流记录-呼吸暂停低通气指数较标准多导睡眠图-呼吸暂停低通气指数减低(P<0.05)。不同严重程度阻塞性睡眠呼吸暂停低通气综合征组血氧气流记录-最低血氧饱和度与标准多导睡眠图-最低血氧饱和度差异无统计学意义(P>0.05)。结论:血氧气流记录具有诊断阻塞性睡眠呼吸暂停低通气综合征的能力,可用于阻塞性睡眠呼吸暂停低通气综合征的初步诊断;血氧气流记录在评价中重度阻塞性睡眠呼吸暂停低通气综合征时可能低估病情,不宜单独用于判断阻塞性睡眠呼吸暂停低通气综合征的严重程度。     

不同通气模式在阻塞性睡眠呼吸暂停低通气综合征临床滴定中的应用研究

目的:探讨极重度阻塞性睡眠呼吸暂停低通气综合征患者无创呼吸机治疗方法及临床疗效.方法:极重度阻塞性睡眠呼吸暂停低通气综合征患者60例依据呼吸机治疗模式不同分为4组,每组15例,分别给予持续气道内正压通气(A组)、自动调压正压通气(B组)、双水平气道正压(C组)和自动调压双水平气道正压(D组)通气模式治疗并观察其治疗效果,进行比较.结果:4组诊断夜多导睡眠图监测结果比较差异无统计学意义(P>0.05);与治疗前多导睡眠图监测结果比较,经不同模式无创呼吸机治疗后,4组患者最长呼吸暂停时间、睡眠呼吸暂停低通气指数、最低脉搏血氧饱和度、平均脉搏血氧饱和度,<90%的氧减时间等指标均有所改善(P<0.05),但A组各项指标改善最明显(P<0.01).结论:极重度阻塞性睡眠呼吸暂停低通气综合征患者采用持续气道内正压通气模式治疗临床疗效最佳.     

83例睡眠鼾症多导睡眠图观察研究

目的 研究多导睡眠图和动态SaO2监测诊断睡眠呼吸暂停综合征(SAS)的意义。方法 运用多导睡眠仪整夜9h检测睡眠打鼾并疑有睡眠呼吸障碍门诊和住院病人83例。结果 52例诊断为不同程度的阻塞性睡眠呼吸暂停低通气综合征(OSAHS)，表明睡眠呼吸暂停或/和低通气，间断性SaO2下降，重症心率分布宽度增高，肢动频繁。结论 每小时呼吸暂停或/和低通气数、累计数、持续时间、呼吸紊乱指数(RDI)是OSAHS诊断和分度的可靠指标。SaO2≤90%时间占睡眠总时间的比例为单纯动态Sa02监测OSAHS提供诊断和分组的参考指标。     

便携式睡眠监测仪与多导睡眠监测仪临床应用比较

目的探讨便携式睡眠监测仪对筛选呼吸暂停综合征的有效性。方法应用便携式睡眠监测仪和多导睡眠监测仪同步监测疑似阻塞性睡眠呼吸暂停低通气综合征患者35例,记录相关数据并进行比较。结果本组中31例监测纪录有效,多导睡眠仪结果与便携式睡眠监测仪相关数据有相关性,其中呼吸暂停次数、呼吸低通气次数、呼吸暂停低通气紊乱指数与平均血氧饱和度明显相关。结论 2种监测方法对诊断睡眠呼吸暂停综合征具有良好一致性,便携式睡眠监测仪可用于大规模筛查睡眠呼吸暂停综合征。     

黄连温胆汤对睡眠低通气治疗作用的研究

目的:观察黄连温胆汤治疗睡眠呼吸暂停低通气的临床效果,并分析其疗效的机制.方法:采用多导睡眠图技术,对诊断为阻塞性睡眠呼吸暂停低通气综合征并以低通气为主的54例患者,随机分为2组,分别予中药黄连温胆汤和都可喜治疗.治疗2周后,从减轻临床症状、缩短低通气持续时间、提高血氧饱和度等方面,进行对照分析.结果:黄连温胆汤能明显改善患者的睡眠紊乱、胸闷、舌象等临床表现.复查多导睡眠图结果,黄连温胆汤治疗后,平均睡眠时间延长47min,低通气总时间缩短10min,90%以下血氧饱和度总时间减少15min,疗效明显优于都可喜(P＜0.01).但2种治疗方法对阻塞性睡眠呼吸暂停的治疗效果欠佳.结论:黄连温胆汤对睡眠呼吸暂停低通气综合征,特别是以低通气和低氧为主的患者,有一定的效果.     

阻塞性睡眠呼吸暂停综合征的口腔矫治器治疗

目的:探讨口腔矫治器对阻塞性睡眠呼吸暂停综合征(OSAS)的治疗效果。方法:11例经多导睡眠图监测确诊OSAS的患者,用德国EBKODENT器材制作可调节型的软塑料口腔矫治器(OA),患者佩戴2～3个月后复查,了解患者的自觉症状,并再次进行多导睡眠图监测,比较治疗前后患者的睡眠结构以及呼吸情况的各项指标。结果:11例患者均感到夜间睡眠质量明显提高。患者的呼吸暂停时间和低通气时间在睡眠时间中所占的比例有明显下降,呼吸暂停指数和低通气指数也显著降低;而最低血氧饱和度和平均血氧饱和度则显著增高。患者的睡眠结构以及呼吸情况的各项指标有了明显的改善。结论:OA对于轻中度的OSAS具有明显的治疗效果。     

无人值守整夜多导睡眠图评估睡眠呼吸暂停低通气综合征患者300例

目的探讨无人值守整夜多导睡眠图监测睡眠呼吸暂停低通气综合征的可行性。方法选择2001—06／2003—12建湖县人民医院呼吸科门诊及住院的疑似睡眠呼吸暂停综合征患者300例，男271例，女29例。均知情同意。采用SRM-9601多导睡眠呼吸监测系统进行无人值守整夜睡眠呼吸暂停低通气综合征监测。回顾性总结多导睡眠图监测成功率。结果纳入对象300例中一次监测成功291例，成功率97．00％。经多导睡眠图诊断为睡眠呼吸暂停低通气综合征255例（85．0％）。结论无人值守整夜多导睡眠图监测一次成功率及确诊率均较高。     

长期经鼻持续气道正压通气对阻塞性睡眠呼吸暂停低通气综合征患者睡眠质量的改善作用

目的:阻塞性睡眠呼吸暂停低通气综合征可引起高血压与睡眠分裂。长期经鼻持续气道正压通气治疗是否可改善通气功能、睡眠质量,并能够降低继发性高血压?方法:选择1997-07/2004-03在福建医科大学附属第一医院呼吸科鼾症工作室明确诊断患有阻塞性睡眠呼吸暂停低通气综合征,并能坚持在家长期使用经鼻持续气道正压通气治疗的患者66例。患者呼吸紊乱指数>20,即均为中、重度患者。携带经鼻持续气道正压通气呼吸机回家,每晚使用≥6h,应用12～34个月。观察患者治疗前、治疗时及治疗后睡眠时最低动脉血氧饱和度,睡前及清晨血压,低通气指数,呼吸暂停指数,呼吸紊乱指数及最长呼吸暂停时间,并调查治疗前后Epworth评分(根据患者嗜睡出现频率:从不嗜睡0分,偶尔嗜睡1分,有时嗜睡2分,经常嗜睡3分的积分判断嗜睡程度)及匹兹堡睡眠质量指数(包括睡眠质量、入睡时间、睡眠时间、睡眠效率、睡眠障碍、安眠药物和日间功能,每个成分按0,1,2,3计分,各域分相加为总分越高示睡眠质量越差)。治疗时对患者随访3年。结果:按意向处理分析,3年随访,66例患者均进入结果分析。①Epworth评分和匹兹堡睡眠质量指数:治疗后明显低于治疗前[(7.54±2.21),(2.85±1.56)分,(13.67±4.72),(8.61±3.75)分,P<0.01]。②多导睡眠图监测参数:治疗后低通气指数、呼吸暂停指数、呼吸紊乱指数、最长呼吸暂停时间均较治疗前改善(P<0.05)。③最低血氧饱和度:治疗时和治疗后均明显高于治疗前(P<0.05),尤以治疗时明显(P<0.05);治疗后明显低于治疗时(P<0.05)。④血压:治疗后明显低于治疗前(P<0.05)。结论:长期坚持经鼻持续气道正压通气治疗,可以显著改善中、重度阻塞性睡眠呼吸暂停低通气综合征患者的睡眠质量,消除睡眠时呼吸暂停和低通气,纠正夜间低氧血症,治疗因阻塞性睡眠呼吸暂停低通气综合征所引起的高血压。     

睡眠体位衣的制作及临床应用

目的 观察体位型睡眠呼吸暂停低通气综合征患者夜间睡眠时睡眠体位衣的临床应用效果.方法 选取愿意接受睡眠体位衣治疗的体位型睡眠呼吸暂停低通气综合征患者60例,在多导睡眠图监测下穿睡眠体位衣进行治疗,并与治疗前多导睡眠图各项参数进行比较.结果 治疗前后侧卧位呼吸暂停低通气指数比较无显著差异;与治疗前比较,治疗后仰卧位呼吸暂停低通气指数、最低血氧饱和度、＜90％的氧减时间、氧减指数等各项参数有显著差异.结论 睡眠体位衣对体位型睡眠呼吸暂停低通气综合征治疗效果较好,适宜临床推广.     

BDNF in sleep,insomnia, and sleep deprivation

The protein brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family of growth factors involved in plasticity of neurons in several brain regions. There are numerous evidence that BDNF expression is decreased by experiencing psychological stress and that, accordingly, a lack of neurotrophic support causes major depression. Furthermore, disruption in sleep homeostatic processes results in higher stress vulnerability and is often associated with stress-related mental disorders. Recently, we reported, for the first time, a relationship between BDNF and insomnia and sleep deprivation (SD). Using a biphasic stress model as explanation approach, we discuss here the hypothesis that chronic stress might induce a deregulation of the hypothalamic-pituitary-adrenal system. In the long-term it leads to sleep disturbance and depression as well as decreased BDNF levels, whereas acute stress like SD can be used as therapeutic intervention in some insomniac or depressed patients as compensatory process to normalize BDNF levels. Indeed, partial SD (PSD) induced a fast increase in BDNF serum levels within hours after PSD which is similar to effects seen after ketamine infusion, another fast-acting antidepressant intervention, while traditional antidepressants are characterized by a major delay until treatment response as well as delayed BDNF level increase.

• Key messages

• Brain-derived neurotrophic factor (BDNF) plays a key role in the pathophysiology of stress-related mood disorders.

• The interplay of stress and sleep impacts on BDNF level.

• Partial sleep deprivation (PSD) shows a fast action on BDNF level increase.

     

Lung aeration during sleep in patients with obstructive sleep apnoea

Background: Previous studies have indicated that patients with obstructive sleep apnoea (OSA) have altered ventilation and lung volumes awake and the results suggest that this may be a determinant of severity of desaturations during sleep. However, little is known about regional lung aeration during sleep in patients with OSA. Methods: Twelve patients with OSA were included in the study. Computed tomography was used to study regional lung aeration during wakefulness and sleep. Lung aeration was calculated in ml gas/g lung tissue in four different regions of interest (ROI_1–4), along the border of the lung from ventral to dorsal. Results: Lung aeration in the dorsal (dependent) lung region (ROI₄) was lower during sleep compared to wakefulness 0·78 ± 0·19 versus 0·88 ± 0·19 (mean ± SD) ml gas/g lung tissue (P = 0·005). Associations were found between awake expiratory reserve volume and change in lung aeration from wakefulness to sleep in ROI₄ (r = ?0·69; P = 0·012). In addition, the change in lung aeration in the dorsal region correlated to sleep time (r = 0·69; P = 0·014) but not to time in supine position. The difference in lung aeration between inspiration and expiration (i.e. ventilation), was larger in the ventral lung region when expressed as ml gas per g lung tissue. In two patients it was noted that, during on‐going obstructive apnoea, lung aeration tended to be increased rather than decreased. Conclusions: Aeration in the dorsal lung region is reduced during sleep in patients with OSA. The decrease is related to lung volume awake and to sleep time.     

Genes for normal sleep and sleep disorders

Sleep and wakefulness are complex behaviors that are influenced by many genetic and environmental factors, which are beginning to be discovered. The contribution of genetic components to sleep disorders is also increasingly recognized as important. Point mutations in the prion protein, period 2, and the prepro-hypocretin/orexin gene have been found as the cause of a few sleep disorders but the possibility that other gene defects may contribute to the pathophysiology of major sleep disorders is worth in-depth investigations. However, single gene disorders are rare and most common disorders are complex in terms of their genetic susceptibility, environmental effects, gene-gene, and gene-environment interactions. We review here the current progress in the genetics of normal and pathological sleep.     

Overview of sleep medicine and sleep respiratory disorders centers in Japan

Sleep medicine in Japan evolved gradually, beginning with sleep research being conducted in the late 1960's exclusively on the university basis. Japan Sleep Society was founded in 1977 mainly by psychiatrists. Recently public awareness regarding sleep related breathing disorders has been raised as a result of a media campaign in Japan. However, the medical service system is unable to appropriately meet the needs of caring for sleep-disordered patients due to insufficient reimbursement and the lack of well-trained technical personnel. So far only several sleep centers existed in Japan. To make sleep be included in the mainstream of the health care system, the educational system and throughout society, many tasks remains to be done by healthcare professionals and government.     

Age and gender variations of sleep in subjects without sleep disorders

Objective. Although sleep is a biomarker for general health and pathological conditions, its changes across age and gender are poorly understood.

Methods. Subjective evaluation of sleep was assessed by questionnaires in 5,064 subjects, and 2,966 were considered without sleep disorders. Objective evaluation was performed by polysomnography in 2,160 subjects, and 1,147 were considered without sleep disorders. Only subjects without sleep disorders were included (aged 40–80 years).

Results. Aging was strongly associated with morning preference. Older subjects, especially women, complained less about sleepiness, and pathological sleepiness was significantly lower than in younger subjects. Self-reported sleep quality and daytime functioning improved with aging. Sleep latency increased with age in women, while sleep efficiency decreased with age in both genders. Deep slow-wave sleep decreased with age, but men were more affected. Spectral power densities within slow waves (< 5 Hz) and fast spindles (14–14.75 Hz) decreased, while theta-alpha (5-1 Hz) and beta (16.75–25 Hz) power in non-rapid eye movement sleep increased with aging. In REM sleep, aging was associated with a progressive decrease in delta (1.25–4.5 Hz) and increase in higher frequencies.

Conclusions. Our findings indicate that sleep complaints should not be viewed as part of normal aging but should prompt the identification of underlying causes.     

Apolipoprotein E polymorphisms and sleep quality in obstructive sleep apnea syndrome

BackgroundThe purpose of this study was to evaluate the influence of polymorphism on sleep parameters of Obstructive Sleep Apnea Syndrome (OSAS) patients.MethodsPatients were genotyped after a full-night polysomnography using the large Epidemiologic Sleep Study of São Paulo population-based sample.ResultsIndividuals who carry the APOE ε2 allele showed longer sleep latency, lower sleep efficiency and higher numbers of arousals/hour, when compared to ε3 allele homozygous and carriers of ε4 allele (p < 0.05). These findings remained significant even after correction for potential confounders, such as sex, age and African genetic ancestry.ConclusionThe APOE polymorphisms may modulate the effects of intermittent hypoxia and sleep fragmentation in the sleep architecture of OSAS patients, and that the presence of the ε2 allele may serve as a biological marker for the identification of a subgroup of patients who are more likely to suffer with OSAS detrimental effects on sleep, impacting not only the daily functioning, but also their quality of life.