Absence of effects of prolonged simvastatin therapy on nocturnal sleep in a large randomized placebo-controlled study

1It has been suggested that lipophilic HMG CoA reductase inhibitors, like lovastatin and simvastatin, may cause sleep disturbance. 2Six hundred and twenty-one patients at increased risk of coronary heart disease were randomized in a single centre to receive 40 mg daily simvastatin, 20 mg daily simvastatin or matching placebo. To assess the effects of prolonged use of simvastatin on nocturnal sleep quality and duration, a sleep questionnaire was administered to 567 patients (95% of 595 survivors) at an average of 88 weeks (range: 44–129 weeks) after randomization. 3The main outcome measures were sleep-related problems and use of sleep-enhancing medications reported during routine study follow-up visits, and responses to the sleep questionnaire about changes in sleep duration and about various sleep events during the preceding month. 4No differences were observed between the treatment groups in the frequency of sleep-related problems reported, in the proportion of follow-up visits at which such problems were reported, or in the use of sleep-enhancing medications. The numbers who stopped study treatment were similar in the different treatment groups, and no patient stopped principally because of insomnia. In response to the sleep questionnaire, there were no significant differences between the treatment groups in reports of various sleep events during the preceding month, except that slightly fewer patients allocated simvastatin reported waking often. No differences in sleep duration were observed. 5This placebo-controlled trial does not indicate any adverse effects of prolonged treatment with simvastatin on systematically sought measures of sleep disturbance.     

Effect of forward rapidly rotating shift work on circadian rhythms of arterial pressure, heart rate and oral temperature in air traffic controllers

Twenty-four-hour records of arterial pressure (AP), heart rate(HR), oral temperature (OT) and physical and mental performancewere obtained in air traffic controllers during morning (n=16),afternoon (n=17) and night (n=19) shifts. Data were analyzedby the cosinor method. The results obtained during the morningshift were as follows (mesor/amplitude/;acrophase): systolicAP (mm Hg)—113.6/10.0/16:03 h; diastolic AP—71.1/8.2—15:19h; mean AP—85.6/8.8/15:41 h; HR (beats/min)—77.5/8.9/16:00h; OT (dg C)—36.71/0.21/15:49 h; right-hand grip strength(kg)—49.8/2.0/17:43 h; left-hand grip strength—46.1/2.0/16.08h; mental performance (calculations/min)—14.9/1.1/16:39h. During the night shift either no change of the circadianacrophases (HR, right-hand grip strength) or acrophase delaysranging from about 2 h (systolic AP, OT, mental performance)up to 3 h (diastolic and mean AP, left-hand grip strength) wereobserved. Our data suggest that the shift system studied doesnot significantly alter the circadian rhythms, and does notinduce a desynchronization, particularly as concerns arterialpressure and oral temperature.     

Is monoamine oxidase inhibitor induced myoclonus serotoninergically mediated?

Summary In the present study a single case observation of myoclonus during sleep-wave transition was monitored in a depressed patient treated with the monoamine oxidase inhibitor, phenelzine. The myoclonus had a rhythm of 1 c/second and lasted for two years, the duration of phenelzine treatment. Myoclonus appeared neither during wakefulness nor during sleep, but at wake-sleep-wake transitions. This switch myoclonus was associated with phasic muscle hyperactivity during REM sleep.Methysergide a 5-HT suppressor, decreased the switch myoclonus frequency and the REM muscle hyperactivity, indicating serotoninergic involvement in the mechanism of phenelzine induced myoclonus.     

妊娠期阻塞性睡眠呼吸暂停筛查的研究进展

阻塞性睡眠呼吸暂停（OSA）是妊娠人群中常见的睡眠呼吸障碍性疾病,不仅与多种不良妊娠结局相关,也可能对母婴远期健康产生重要影响。目前诊断OSA的金标准多导睡眠监测在妊娠人群中难以大规模开展,导致绝大多数妊娠期OSA未能得到及时诊断。寻求其他筛查策略和筛查工具准确识别具有OSA风险的孕妇并进行及时诊治,对于改善不良妊娠结局具有重要意义。本文针对妊娠期OSA患病率、筛查现状、筛查时机、目标人群、筛查工具的研究进展进行综述,以期为妊娠期OSA的筛查提供参考和理论依据。     

阻塞性睡眠呼吸暂停与甘油三酯葡萄糖指数的相关性

目的 探讨阻塞性睡眠呼吸暂停（OSA）与甘油三酯葡萄糖（TyG）指数的相关性。方法 选取2021年1月—2022年12月中南大学湘雅二医院行睡眠呼吸监测的270例OSA患者。根据甘油三酯和空腹血糖计算TyG指数,根据TyG指数的三分位数将患者分为Q1组、Q2组、Q3组,根据睡眠呼吸暂停低通气指数（AHI）将患者分为轻度组、中度组、重度组。采用多元线性分析评估TyG指数与AHI之间的关系,有序Logistic回归分析TyG指数与OSA严重程度之间的关系。结果 TyG指数越高的患者AHI、体质量指数（BMI）、总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白胆固醇（LDL-C）、空腹血糖越高,而血清高密度脂蛋白胆固醇（HDL-C）水平则越低（P <0.05）。TyG指数越高的患者肥胖和糖尿病、冠心病比例越高,男性比例越高,年龄更低（P <0.05）。随着患者AHI的增加,TyG指数、BMI增加,TG、空腹血糖上升,最低血氧饱和度下降（P <0.05）,OSA越严重的患者肥胖、高血压和冠心病比例越高（P <0.05）。Pearson相关性分析结果显示,TyG指数与AHI水平呈正相关（r =0.282,P <0.05）。多元线性回归分析结果显示,AHI（b =0.002）、BMI（b =0.017）、TG（b =0.361）、空腹血糖（b =0.109）和性别（b =0.083）是TyG的影响因素（P <0.05）。有序Logistic模型结果显示：轻度OSA［O^R=0.396（95% CI：0.207,0.757）］和中度OSA［O^R=0.281（95% CI：0.163,0.484）］患者的TyG等级较重度OSA低,说明OSA严重程度增加是TyG指数升高的影响因素。非肥胖患者［O^R=0.424（95% CI：0.253,0.710）］、不吸烟患者［O^R=0.506（95% CI：0.283,0.904）］、非糖尿病患者［O^R=0.268（95% CI：0.156,0.460）］、非冠心病患者［O^R=0.452（95% CI：0.253,0.807）］、女性［O^R=0.409（95% CI：0.221,0.760）］的TyG等级较低,故吸烟、肥胖、糖尿病、冠心病、男性是TyG指数升高的影响因素（P <0.05）。结论 TyG指数与OSA严重程度相关,可以考虑将TyG指数用于OSA患者胰岛素抵抗的观察,从而进行干预,使患者获益。     

腰椎间盘突出症与腰椎间盘突出症合并阻塞性睡眠呼吸暂停患者的对比研究

目的 探究腰椎间盘突出症（LDH）与阻塞性睡眠呼吸暂停（OSA）之间的关联,为LDH的临床诊治策略及治疗方案提供参考依据。方法 选取2018年1月—2020年3月中国医科大学附属第一医院骨科行外科手术治疗的485例LDH患者,按是否合并OSA进行分组研究。结果 485例LDH患者中合并OSA的307例,发生率为63.3%。LDH合并OSA组主观症状、临床症状、日常活动受限程度日本骨科协会（JOA）腰痛评分低于单纯LDH组（P <0.05）;两组膀胱功能JOA评分比较,差异无统计学意义（P> 0.05）;LDH合并OSA组视觉模拟评分法（VAS）评分高于单纯LDH组（P <0.05）。Pfirrmann 5级评分法中4、5级例数构成比LDH合并OSA组较单纯LDH组高（P <0.05）。两组患者的硬膜撕裂率、神经受损率、血肿率、切口感染率等并发症发生率比较,差异无统计学意义（P>0.05）。单纯LDH组与LDH合并OSA组术后3、6、12和24个月静息状态下JOA和VAS评分比较,采用重复测量设计的方差分析,结果：(1)不同时间点的JOA和VAS评分有差异（...     

调和阴阳法针灸对老年不寐患者睡眠质量及MT、NE、5-HT水平的影响

目的 探讨调和阴阳法针灸对老年不寐患者睡眠质量及褪黑素（MT）、去甲肾上腺素（NE）、5-羟色胺（5-HT）水平的影响。方法 选取2020年7月—2022年7月河北医科大学第一医院收治的老年不寐患者120例,采用随机数表法分为观察组和对照组,每组60例。对照组采取常规药物治疗,观察组在对照组基础上联合调和阴阳法针灸。比较两组临床疗效,同时评估其中医证候积分和匹兹堡睡眠质量指数（PSQI）评分,测定MT、NE、5-HT、多巴胺（DA）、γ-氨基丁酸（GABA）水平,观察记录不良反应发生情况。结果 观察组总有效率高于对照组（P <0.05）;观察组治疗前后入睡困难、多梦易醒、神疲食少、目赤口苦、舌红少津、脉弦数、舌苔黄评分的差值均高于对照组（P <0.05）。观察组与对照组治疗前及治疗后2、4周的PSQI评分比较,结果 ①不同时间点PSQI评分比较,差异有统计学意义（F =17.894,P =0.000）;②两组PSQI评分比较,差异有统计学意义（F =26.894,P =0.000）,观察组PSQI评分较低,相对睡眠质量较好;③观察组与对照组PSQI评分变化趋势比较,差异有统计学意义（F =45.247,P =0.000）。观察组治疗前后睡眠总时间、快速眼动睡眠期、睡眠潜伏期、醒觉时间、睡眠效率的差值均高于对照组（P <0.05）;观察组治疗前后MT、NE、5-HT的差值均高于对照组（P <0.05）;观察组治疗前后DA、GABA的差值均高于对照组（P <0.05）;两组不良反应总发生率比较,差异无统计学意义（P >0.05）。结论 调和阴阳法针灸治疗老年失眠症疗效显著,不仅能有效改善患者中医症状、睡眠质量及睡眠结构,还能改善血清MT、NE、5-HT、DA、GABA水平,安全性较高。     

基于两样本孟德尔随机化方法探讨睡眠与痛风的关联

[目的] 通过两样本孟德尔随机化设计,探讨睡眠与痛风之间的关联。[方法] 从一项包含763 813名参与者的全基因组关联研究(genome-wide association study,GWAS)中获取痛风遗传关联数据。以与打鼾、睡眠时间、睡眠类型、失眠及白日困倦程度等睡眠表型相关的单核苷酸多态性(single nucleotide polymorphism,SNP)作为工具变量,采用逆方差加权(inverse variance weighted,IVW)评估遗传学预测的不同睡眠表型与痛风发生风险的关系。采用MR-Egger回归和孟德尔随机多态性残差和离群值(MR pleiotropy residual sum and outlier,MR-PRESSO)检验进行敏感性分析,以评估工具变量的多效性。进一步采用加权中位数法、简单中位数法、最大似然比法等分析方法检验结果的稳健性与可靠性。[结果] IVW结果显示,遗传学预测的打鼾[优势比(odds ratio,OR)=3.12,95%置信区间(confidence interval,CI)(1.21～8.05),PFDR=0.045]和失眠[OR=1.09,95%CI(1.04～1.15),PFDR=0.005]与痛风发生风险呈正相关,而睡眠时间、睡眠类型及白日困倦程度与痛风发生之间不存在统计学关联。MR-Egger回归提示上述因果关联未受到水平多效性影响,加权中位数法、简单中位数法、最大似然比法得出与IVW相似的结果。[结论] 打鼾、失眠与痛风发生风险呈正相关,纠正打鼾和失眠可能对痛风有一定的预防作用。     

Human slow-wave sleep and the cerebral cortex

SUMMARY  Recent hypotheses about the roles of human slow-wave sleep (hSWS—delta EEG activity) are appraised. The possible linkage between hSWS and the functions of the prefrontal cortex (PFC) are explored with respect to normal subjects and to disorders involving PFC deficits.     

Neurobiological structure of the revised limit cycle reciprocal interaction model of REM cycle control

SUMMARY  New data bearing on the neurobiological basis of REM sleep and on mechanisms of EEG synchronization/desynchronization are presented. The revision of the limit cycle reciprocal interaction model (LCRIM) of REM cycle control incorporates new information on monoamine inhibition of mesopontine cholinergic neurons and of cholinergic mechanisms promoting REM sleep. New data also show cortical slow-wave activity is controlled by thalamocortical neurons' membrane potential level, which, in turn, is strongly controlled during sleep by brainstem cholinergic input arising from REM-on neurons. This new knowledge leads to a neurobiologi-cally justified integration of the LCRIM and of the two-process model of sleep control.