悬雍垂腭咽成形术治疗阻塞性睡眠呼吸 暂停综合征46 例疗效分析

目的：通过对睡眠呼吸暂停综合征病人（obstructlve sleep apnea syndrome,OSAS）睡眠呼吸参数的比较,探讨UPPP治疗OSAS的效果。方法：经多导睡眠图（Polysomnography,PSG）确诊为OSAS的病人46例,选择呼吸紊乱指数（apnea and hypopnea index,AHI）、呼吸暂停指数（apnea index,AI）及睡眠中的最低SaO2值作为评价OSAS轻重程度的指标。计算轻中度组、重度组在手术前后的AHI缓解率、最低SaO2缓解率厦显效率,并作为衡量UPPP手术治疗效果的指标。分析患者在手术前后AHI、最低SaO2的相关性;分析轻中度组和重度组的缓解率、最低SaO2缓解率及治愈率的相关性。结果：1利用UPPP手术治疗OSAS,患者手术前后AHI、最低SaO2具有相关性。2在分组资料中,轻中度组和重度组的缓解率、最低SaO2缓解率及显效率都具有显著相关性。结论：（1）UPPP是治疗OSAS的有效方法;（2）轻中度组的治疗效果要好于重度组。     

阻塞性睡眠呼吸暂停综合征临床监测分析

目的:探讨阻塞性睡眠呼吸暂停综合征患者的临床特征及评价疗效。方法:回顾分析70例阻塞性睡眠呼吸暂停综合征患者PSG监测数据。结果:随着呼吸紊乱指数的增加,年龄、体重指数、最长呼吸暂停时间、最低SaO_2%、平均SaO_2%下降等指标在轻度与中、重度SAS之间差异显著;70例患者中伴有高血压52.9%、糖尿病5.7%、冠心病21.4%。结论:OSAS是一种具有潜在危险的疾痛,对OSAS早期诊断治疗是预防发生严重并发症的关键。     

老年抑郁症患者自杀意念与生活事件、家庭功能及多导睡眠图参数的关系研究

摘要 目的：研究老年抑郁症患者自杀意念与生活事件、家庭功能及多导睡眠图参数的关系并予以分析。方法：选取从2019年1月～2020年10月期间我院收治的154例老年抑郁症患者纳入研究。将其按照是否存在自杀意念分作自杀意念组83例和无自杀意念组71例。比较分析两组生活事件、家庭功能及多导睡眠图参数等方面的差异,并以Spearman相关性分析明确老年抑郁症患者自杀意念与生活事件、家庭功能及多导睡眠图参数的关系。结果：自杀意念组正性事件、负性事件评分均高于无自杀意念组（均P＜0.05）。自杀意念组各项家庭功能评分均高于无自杀意念组（均P＜0.05）。自杀意念组N3期非快速眼动睡眠时间以及N3期非快速眼动睡眠占比均低于无自杀意念组（均P＜0.05）。经Spearman相关性分析可得,老年抑郁症患者自杀意念与各项生活事件评分、家庭功能评分均呈正相关,而与N3期非快速眼动睡眠时间以及N3期非快速眼动睡眠占比呈负相关（均P＜0.05）。结论：老年抑郁症自杀意念与生活事件、家庭功能及多导睡眠图参数密切相关,临床可通过对这些方面的观测来评估老年抑郁症的病情,以预防和减少老年抑郁症患者自杀行为的发生。     

动态心电图对睡眠呼吸暂停综合征的诊断价值及与心律失常的关系分析

目的:评估动态心电图对睡眠呼吸暂停综合征(SAS)的诊断价值并分析其与心律失常的关系。方法:选取2017年2月～2019年2月我院收治的SAS患者80例记为病变组,另取同期于我院进行体检的健康人员80例记为对照组。两组均进行动态心电图检查,并以多导睡眠监测仪检查结果为金标准,分析动态心电图诊断SAS的灵敏度、特异度以及准确度。比较两组动态心电图监测结果,心律失常以及ST-T缺血性改变发生情况。结果:动态心电图诊断SAS的灵敏度、特异度、准确度分别为92.31%、75.00%、90.00%。病变组最高心率、房性早搏次数、室性早搏次数均高于对照组,而最低心率低于对照组(均P0.05)。病变组心律失常及ST-T缺血性改变发生率均高于对照组(均P0.05)。结论:动态心电图对SAS的诊断价值较高,具有良好的灵敏度、特异度。临床工作中可通过动态心电图监测,从而及时检出心律失常及ST-T缺血性改变,进一步有效预防猝死的发生。     

视频脑电图鉴别诊断癫痫患者睡眠障碍、认知障碍的临床价值研究

目的:探讨视频脑电图诊断癫痫患者睡眠障碍、认知障碍的临床价值。方法:选取2014年1月~2016年12月在我院神经内科进行诊治的癫痫患者236例作为癫痫组,另选取同期的健康患者家属或者其他健康体检者236例作为正常对照组,对两组进行视频脑电图联合睡眠参数分析;并对癫痫组视频脑电图联合认知参数进行分析。结果:癫痫组睡眠Ⅰ~Ⅱ期时间显著长于正常对照组且具有统计学差异(P=0.000),睡眠Ⅲ~Ⅳ期时间显著短于正常对照组且具有统计学差异(P=0.000),睡眠时相转换频率、觉醒指数均显著高于正常对照组且均具有统计学差异(P=0.000);清醒期、睡眠期不同痫样放电指数(IED)的WAIS-RC IQ和WMS-RC MQ均具有统计学差异(P0.05),10%IED≤50%者的WAIS-RC IQ和WMS-RC MQ均显著低于1%IED≤10%者且均具有统计学差异(P0.05),IED 10%可能是痫样放电影响患者认知功能的最低阈值。结论:视频脑电图在癫痫患者睡眠障碍、认知障碍识别中具有重要的临床价值。     

卒中后抑郁大鼠多导睡眠图研究

目的:探讨卒中后抑郁(PSD)大鼠多导睡眠图的检测方法和变化特征。方法:雄性SD(Sprague Dawley)大鼠随机分为3组:对照组、卒中组、PSD组,通过结扎双侧颈总动脉结合孤养法、慢性不可预知应激刺激,建立PSD模型,同时将电极缝制在大鼠头皮下进行多导睡眠图监测。结果:多导睡眠图可清晰地记录大鼠活动、脑电、肌电、眼动等情况;PSD组大鼠快眼动睡眠潜伏期(REM latency,RL)为(108.2±16.1)s,较对照组(152.5±20.5)s和卒中组(145.1±18.7)s缩短,差异有统计学意义(P0.01);PSD组大鼠快眼动睡眠时间百分比(5.2%±1.2%),较对照组(8.3%±1.4%)和卒中组(7.9%±1.6%)降低,差异有统计学意义(P0.01)。结论:头皮下缝制电极法适合大鼠多导睡眠图监测应用;多导睡眠图可以做为PSD模型的一个检测指标。     

手术治疗摩洛哥儿童睡眠呼吸障碍的临床研究

目的:观察鼻内镜下腺样体切除术或联合扁桃体切除术对摩洛哥儿童睡眠呼吸障碍的疗效,探讨儿童睡眠呼吸障碍治疗的手术适应症。方法:136例病例分成2组,治疗组85例睡眠呼吸障碍伴慢性扁桃体炎、或扁桃体Ⅲ°肥大的儿童,行鼻内镜下腺样体切除加扁桃体切除术;对照组51例睡眠呼吸障碍伴单纯扁桃体扁桃体Ⅱ°肥大的儿童,采用鼻内镜下腺样体切除,术后随访3个月。结果:治疗组总有效率为100%(85/85),对照组84.31%(43/51),差异有统计学意义(P0.05);两组患儿的Conners儿童行为量表评分较术前明显下降,差异有统计学意义(P0.05)。结论:鼻内镜下腺样体切除术联合扁桃体切除术,明显改善患儿睡眠和呼吸,生活质量明显提高,是治疗摩洛哥儿童睡眠呼吸障碍的一线治疗方案。     

心源性睡眠呼吸异常：心衰患者睡眠期间陈-施呼吸 机制探讨的初步报告*

目的: 探讨心衰患者陈施呼吸的发生率及发生机制。方法: 连续入选2015年3月~2015年5月于阜外医院行睡眠呼吸监测的患者56例,分为心衰组和非心衰组。结果: 两组睡眠呼吸暂停的发生率均较高,心衰组11例患者中呼吸暂停低通气指数（AHI）>5的有10例,平均AHI指数23.93±14.63;非心衰组45例患者中AHI>5的有33例,平均AHI指数16.20±18.76;心衰组中枢性睡眠呼吸暂停（CSA）次数占睡眠呼吸暂停总数的比例明显大于非心衰组病人,分别为80.21%±30.55%和27.16%±35.71%,P<0.01。结论: 心脏的循环功能和肺脏的呼吸功能是联合一体化,相互联系、互为因果而又互相影响。慢性心力衰竭的循环障碍促成了潮式呼吸的发生,所以称之为心源性呼吸睡眠异常。     

阻塞性睡眠呼吸暂停综合征相关蛋白FNDC5的生物信息学分析

有研究认为血清FNDC5水平或与阻塞性睡眠呼吸暂停综合征的发生及发展有关,因此利用生物信息学工具对FNDC5的结构、性质、功能作出必要的预测和分析,以发现FNDC5与阻塞性睡眠呼吸暂停综合征的相关关系及机理,为进一步研究提供理论依据。利用NCBI、STRING、Protscale、SignalP、TMHMM、PSORT、SOPMA、SWISS-MODEL、NetNGlyc、NetOGlyc、Netphos、ProtParam等数据库或软件,进行预测和分析。FNDC5具有亲水性,稳定性差,非分泌蛋白,有跨膜结构域,二级结构弹性较大,在体内分布较为广泛。FNDC5拥有多个糖基化位点和蛋白磷酸化位点,与其产生相互作用的蛋白可参与脂肪代谢及炎症反应。就FNDC5及其互作蛋白参与的信号通路及生物学过程来看,FNDC5可通过肥胖发展、炎症反应、内分泌调节等途径导致或加重阻塞性睡眠呼吸暂停综合征。对FNDC5结构的预测表明,可通过生物或化学方法对其结构进行改造,可能会在机制上对阻塞性睡眠呼吸暂停综合征进行预防或治疗。     

睡眠呼吸暂停综合征患者血脂水平的研究

目的:了解阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血浆脂质代谢情况。方法:分别检测健康对照组、睡眠呼吸暂停综合征患者组甘油三酯、总胆固醇、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇、载脂蛋白A、载脂蛋白B、脂蛋白a、载脂蛋白E含量。进行统计学对比及分析。结果:睡眠呼吸暂停综合征患者的甘油三酯、总胆固醇、高密度脂蛋白、总胆固醇/高密度脂蛋白、载脂蛋白A、载脂蛋白B及载脂蛋白E与健康对照组比较有显著差异,且与其睡眠监测指标有明显相关。结论:OSAHS可导致血浆脂质代谢紊乱,与动脉粥样硬化发生及发展的存在重要的相关性,是独立于年龄、体重、饮食、遗传等原因的冠心病、高血压、脑卒中等心脑血管疾病的发病因素之一。因此,提高对OSAHS的警惕是非常重要的。     

The cytogenetics of 90 patients with idiopathic mental retardation/malformation syndromes and of 90 normal subjects

Summary A cytogenetic study, done on randomized coded slides, of 90 patients with idiopathic mental retardation and at least 3 other developmentally independent congenital anomalies and of 90 normal subjects is reported. Audiatorography, Q-banding and C-staining were used in the analysis of chromosomally abnormal cases. Eight patients were found to have chromosome abnormalities. Four had substantial chromosome aberrations that would be expected to cause abnormal phenotype. These were CD165 (46,18q-); CD25 (46,18q+) (partial trisomy of 10q); CD175 (46,4q+) and CD95 (46,mar22). In addition, 4 patients were found to have chromosomal anomalies that could not account for their conditions. Three of these were considered to have heterochromatic variants. Patient CD167 had an 9qh+ chromosome which had been inherited from her mother. Case CD137 had a No. 19 chromosome with additional centric heterochromatin. A similar chromosome was found in her mother, maternal grandmother and 2 of 3 half sibs. In patient CD125 a telocentric No. 13 was found. In addition, CD80 was shown to have an XYY constitution.In the normal subjects, no unbalanced chromosome rearrangements were found. Four persons, however, had minor chromosome anomalies. Three were considered to have heterochromatic variants. These were CD54 (46,22p+); CD149 (46,21p+) and CD19 (46,tel22). One normal subject (CD51) was found to be a balanced t(13q14q) carrier. The translocation chromosome had been inherited from his father.     

Mechanisms of breathing instability in patients with obstructive sleep apnea.

The response to chemical stimuli (chemical responsiveness) and the increases in respiratory drive required for arousal (arousal threshold) and for opening the airway without arousal (effective recruitment threshold) are important determinants of ventilatory instability and, hence, severity of obstructive apnea. We measured these variables in 21 obstructive apnea patients (apnea-hypopnea index 91 +/- 24 h(-1)) while on continuous-positive-airway pressure. During sleep, pressure was intermittently reduced (dial down) to induce severe hypopneas. Dial downs were done on room air and following approximately 30 s of breathing hypercapneic and/or hypoxic mixtures, which induced a range of ventilatory stimulation before dial down. Ventilation just before dial down and flow during dial down were measured. Chemical responsiveness, estimated as the percent increase in ventilation during the 5(th) breath following administration of 6% CO(2) combined with approximately 4% desaturation, was large (187 +/- 117%). Arousal threshold, estimated as the percent increase in ventilation associated with a 50% probability of arousal, ranged from 40% to >268% and was <120% in 12/21 patients, indicating that in many patients arousal occurs with modest changes in chemical drive. Effective recruitment threshold, estimated as percent increase in pre-dial-down ventilation associated with a significant increase in dial-down flow, ranged from zero to >174% and was <110% in 12/21 patients, indicating that in many patients reflex dilatation occurs with modest increases in drive. The two thresholds were not correlated. In most OSA patients, airway patency may be maintained with only modest increases in chemical drive, but instability results because of a low arousal threshold and a brisk increase in drive following brief reduction in alveolar ventilation.     

Sleep quality in adult patients with sleep related bruxism

Sleep related bruxism (SB) is the grinding of teeth during sleep and may also be associated with various sleep disorders. However, little is known about sleep structures and disturbances of SB. This study aims to further understand sleep architectures using overnight polysomnography (PSG) in patients with SB. We analyze sleep parameters and architectures in 33 healthy subjects and 25 patients with SB. PSG and sleep questionnaires measured sleep variables including proportions of rapid eye movement (REM) sleep, non-REM sleep (N1, N2 and N3), latency to sleep onset, sleep efficiency, wake after sleep onset (WASO), apnea hypopnea index (AHI), respiratory disturbance index (RDI), and periodic limb movement index (PLMI) during sleep for both groups. Sleep efficiency and the proportion of N3 in the SB group were significantly lower than in the control group (P < 0.05). In addition latency to onset of sleep and WASO were markedly increased in the SB group (P < 0.05). AHI, RDI, and PLMI showed no differences between the groups. Epworth Sleepiness Scale was significantly higher in the SB group than in the control group (P < 0.05). In contrast to previous studies, we conclude that patients with SB are not good sleepers based on PSG study. Further studies are required to assess the relationship between sleep quality and the severity of SB.

     

Rest-activity circadian rhythm and sleep quality in patients with binge eating disorder

Recent findings suggest that altered rest-activity circadian rhythms (RARs) are associated with a compromised health status. RARs abnormalities have been observed also in several pathological conditions, such as cardiovascular, neurological, and cancer diseases. Binge eating disorder (BED) is the most common eating disorder, with a prevalence of 3.5% in women and 2% in men. BED and its associate obesity and motor inactivity could induce RARs disruption and have negative consequences on health-related quality of life. However, the circadian RARs and sleep behavior in patients with BED has been so far assessed only by questionnaires. Therefore, the purpose of this study was to determine RARs and sleep parameters by actigraphy in patients with BED compared to a body mass index-matched control group (Ctrl). Sixteen participants (eight obese women with and eight obese women without BED diagnosis) were recruited to undergo 5-day monitoring period by actigraphy (MotionWatch 8®, CamNtech, Cambridge, UK) to evaluate RARs and sleep parameters. In order to determine the RARs, the actigraphic data were analyzed using the single cosinor method. The rhythmometric parameters of activity levels (MESOR, amplitude and acrophase) were then processed with the population mean cosinor.

The Actiwatch Sleep Analysis Software (Cambridge Neurotecnology, Cambridge, UK) evaluated the sleep patterns. In each participant, we considered seven sleep parameters (sleep onset: S-on; sleep offset: S-off; sleep duration: SD; sleep latency: SL; movement and fragmentation index: MFI; immobility time: IT; sleep efficiency: SE) calculated over a period of five nights.

The population mean cosinor applied to BED and Ctrl revealed the presence of a significant circadian rhythm in both groups (p < 0.001). The MESOR (170.0 vs 301.6 a.c., in BED and Ctrl, respectively; p < 0.01) and amplitude (157.66 vs 238.19 a.c., in BED and Ctrl, respectively p < 0.05) differed significantly between the two groups. Acrophase was not different between BED and Ctrl, as well as all sleep parameters. Both groups displayed a low level of sleep quality (SE 80.7% and 75.7% in BED and Ctrl, respectively). These data provided the first actigraphy-based evidence of RARs disruption and sleep behavior disorder in patients with BED. However, while sleep disorders could be reasonably ascribed to overweight/obesity and the related lower daily physical activity, RARs disruption in this pathology should be ascribed to factors other than reduced physical activity. The circadian timing approach can represent a novel potential tool in the treatment of patients with eating disorders. These data provide exploratory evidence of behavioral association in a small population of patients that, if confirmed in a wider number of subjects and across different populations, may lead to a revision and enhancement of interventions in BED patients.     

Generalized epilepsy with spike-wave paroxysms as an epileptic disorder of the function of sleep promotion

A new hypothesis is offered regarding the pathomechanism of generalized epilepsy with spike-wave paroxysms (GESw) based on the pertaining literature and personal investigations. The first section is devoted to a critical overview of the development of theories regarding GESw. The centrencephalic theory, the debate on subcortical versus cortical origin, the "corticoreticular" hypothesis of Gloor and, finally, the "dyshormic" concept of Niedermeyer are outlined. In the next section it is shown that there is a particular optimum zone between sleep and wakefulness and between REM and slow wave sleep which highly favours the occurrence of spike-wave paroxysms. According to our investigations into the dynamics within this critical zone, the spike-wave paroxysms always appear with characteristic fluctuations of the level of consciousness where the changes towards awakening are always followed by rebounds towards sleep. Hence, the dynamic properties of this unstable border zone become especially interesting in the genesis of spike-wave paroxysms. It has been shown that even without epilepsy, a dynamics can be observed in the micro-oscillations in the depth of sleep which could be interpreted according to the reciprocal induction regulation model. In our concept the process of falling asleep emerges from rebounds of the sleep promoting system in response to sensory inputs streaming in from the external environment. According to this model, arousal influences in sleep have a sleep promoting effect. We interpret in this way all synchronized EEG reactions elicited by sensory stimuli and we consider K-complex type synchronization reactions as a "building stone" of the process of falling asleep which contains the whole process in concentrated form. The manifold similarities between the K-complex and the spike-wave pattern are demonstrated. On this basis spike-wave paroxysms can be regarded as an epileptic "caricature" of the sleep induction momentum reflected in the K-complex phenomenon. Hence, the GESw is the epileptic disorder of the sleep promotion function. This hypothesis resolves and explains many contradictory features of our knowledge about this mechanism and gives a new biologically oriented framework for further research. In the light of the hypothesis it has been attempted to interpret some of the characteristic features of the GESw: the genetic determination, the age dependency, the link with the sleep-waking cycle as well as the functional-anatomical characteristics and the symptoms of the seizures.     

Several new treatment strategies have become available for patients with sleep disordered breathing

Sleep and Biological Rhythms -     

Correlations between objective and subjective sleep and circadian markers in remitted patients with bipolar disorder

Bipolar disorder (BD) is a chronic psychiatric condition characterized by recurrences of depressive and (hypo)manic episodes. Patients in remission report a wide range of sleep and circadian disturbances that correlate with several outcomes measures such as functioning or physical health. The most appropriate way to measure these abnormalities in clinical practice requires further investigation since the external validity of self-reports, as compared to more physiological measures (such as polysomnography or actigraphy), has been questioned. Despite the fact that questionnaires are inexpensive, fast and easy to use, they need to be validated against objective measures. This study aims to validate three sleep and circadian questionnaires, namely the Pittsburgh Sleep Quality Index (PSQI), the Composite Scale of Morningness (CSM) and the Circadian Type Inventory (CTI) – against actigraphy in BD patients in remission. Twenty-six carefully assessed BD patients in remission completed the PSQI, the CTI and the CSM, and wore an actigraph (AW7, Camntech) for 21 consecutive days. Phase preference assessed by the CSM strongly correlated with actigraphic phase markers (M10 onset ρ?=??0.69 and L5 onset ρ?=??0.63). Sleep duration and sleep latency assessed by the PSQI and by actigraphy were also highly correlated (ρ?=??0.76; ρ?=?0.50). Moderate correlation coefficients were observed between questionnaires and actigraphy for markers that explored the stability of rhythms, sleep quality, sleep latency and sleep disturbances (|ρ|?>?0.40) although these were not significant after correcting for multiple testing. No correlation was observed between markers for the amplitude of rhythms. While the external validity of the CTI clearly requires further investigation, this study supported the external validity of the CSM and the PSQI for phase preference, sleep duration and latency. We conclude that the CSM and the PSQI could be useful in routine practice and research when actigraphy is not easily available.     

Neural-mechanical coupling of breathing in REM sleep

Smith, C. A., K. S. Henderson, L. Xi, C.-M. Chow, P. R. Eastwood, and J. A. Dempsey. Neural-mechanical coupling of breathing in REM sleep. J. Appl.Physiol. 83(6): 1923-1932, 1997.During rapid-eye-movement (REM) sleep theventilatory response to airway occlusion is reduced. Possiblemechanisms are reduced chemosensitivity, mechanical impairment of thechest wall secondary to the atonia of REM sleep, or phasic REM eventsthat interrupt or fractionate ongoing diaphragm electromyogram (EMG)activity. To differentiate between these possibilities, we studiedthree chronically instrumented dogs before, during, and after15-20 s of airway occlusion during non-REM (NREM) and phasic REMsleep. We found that 1) for a given inspiratory time the integrated diaphragm EMG(Di) was similar or reduced in REM sleep relativeto NREM sleep; 2) for a givenDi in response to airway occlusion and thehyperpnea following occlusion, the mechanical output (flow or pressure)was similar or reduced during REM sleep relative to NREM sleep;3) for comparable durations ofairway occlusion the Di and integratedinspiratory tracheal pressure tended to be smaller and more variable inREM than in NREM sleep, and 4)significant fractionations (caused visible changes in trachealpressure) of the diaphragm EMG during airway occlusion inREM sleep occurred in ~40% of breathing efforts. Thus reducedand/or erratic mechanical output during and after airwayocclusion in REM sleep in terms of flow rate, tidal volume, and/or pressure generation is attributable largely to reduced neural activity of the diaphragm, which in turn is likely attributable to REM effects, causing reduced chemosensitivity at the level of theperipheral chemoreceptors or, more likely, at the central integrator.Chest wall distortion secondary to the atonia of REM sleep maycontribute to the reduced mechanical output following airway occlusionwhen ventilatory drive is highest.