Correlates of daytime sleepiness in patients with asthma

BACKGROUND AND PURPOSE: Patients with asthma often complain of daytime sleepiness, which is usually attributed to a direct effect of asthma on nocturnal sleep quality. We investigated this and other potential explanations for daytime sleepiness among asthmatics. PATIENTS AND METHODS: One hundred fifteen adult asthmatics were assessed for perceived daytime sleepiness (one question item), subjective sleepiness (Epworth Sleepiness Scale score, ESS), obstructive sleep apnea risk (Sleep Apnea scale score within Sleep Disorders Questionnaire, SA-SDQ), asthma severity step, relevant comorbid conditions, and current asthma medications. RESULTS: Among all subjects, 55% perceived excessive daytime sleepiness and 47% had ESS>10. Most subjects reported snoring (n=99, or 86%) and many snored habitually (n=44, 38%). The ESS correlated with SA-SDQ (P<0.0001), male gender (P=0.01), and asthma severity step (P=0.04). In a multiple regression model, the ESS was independently associated with SA-SDQ (P=0.0003) and male gender (P=0.02), but not with asthma severity step (P=0.51). There were no correlations between ESS and age, body mass index (BMI), forced expiratory volume in one second as percent of predicted value (FEV(1)%), comorbidities, or medication used to treat asthma. CONCLUSIONS: Sleepiness is common in asthmatics and may reflect occult obstructive sleep apnea more often than effects of asthma itself, other comorbid conditions, or asthma medications.     

卒中后睡眠障碍的研究进展

随着对卒中研究的深入,逐渐发现睡眠障碍这一常见并发症与卒中的关系比预期的更加密切和复杂。例如,在卒中发作急性期,患者睡眠结构破坏,总睡眠时间缩短、睡眠效率降低、入睡潜伏期延长,而进入慢性期后随着受损脑组织结构和功能的恢复,患者的睡眠质量依然可以恢复到相对正常的状态。卒中病灶位于不同脑区可能出现不同形式的睡眠障碍,如睡眠呼吸暂停、日间过度嗜睡、发作性睡病、睡眠期运动异常和异态睡眠等。随着多导睡眠检测技术的广泛应用,临床医师与科研人员对卒中后睡眠障碍展开更多深入的研究。     

Cognitive dysfunction in patients with obstructive sleep apnea (OSA): partial reversibility after continuous positive airway pressure (CPAP)

The aims of this study were to assess cognitive function in obstructive sleep apnea (OSA) patients and to evaluate the effect of short- and long-term treatment with continuous positive airway pressure treatment (CPAP). A battery of neuropsychological tests, the Epworth Sleepiness Scale (ESS), and the Beck Inventory Scale were administered to 23 patients with severe OSA (age: 56.5+/-6.13; AHI: 54.9+/-13.37) and to 23 age- and education-matched controls. The OSA patients were evaluated in a baseline condition and in two follow-up treatment sessions (after 15 days and 4 months of CPAP, respectively). At baseline, OSA patients had a significant impairment, compared to controls, in tests of sustained attention, visuospatial learning, executive function, motor performance, and constructional abilities. The longitudinal evaluation showed that after a 15-days CPAP treatment attentive, visuospatial learning, and motor performances returned to normal levels. A 4-months CPAP treatment did not result in any further improvement in cognitive tests. Performance on tests evaluating executive functions and constructional abilities was not affected by short- and long-term treatment with CPAP. The findings of this study confirm the hypothesis of partial reversibility of cognitive dysfunction in OSA patients after CPAP.     

An alternative measure of sleep fragmentation in clinical practice: the sleep fragmentation index

BACKGROUND AND PURPOSE: Micro-arousals (MA) are commonly considered as sleep components reflecting sleep fragmentation. However, their elucidation is time-consuming, with considerable inter-observer variability. The aim of our study was to investigate the usefulness of a sleep fragmentation index (SFI) to detect sleep disruption in a large sample of patients. PATIENTS AND METHODS: Five-hundred ninety-eight polysomnographic studies made in controls and patients were examined. The SFI was calculated as the total number of awakenings and sleep stage shifts divided by total sleep time. RESULTS: In the whole group a significant correlation was found between the SFI and the MA index (MAI) (P<0.001) with good agreement across a wide range of values. When patients were stratified according to final diagnosis a significant relation was noted for patients with insomnia (P<0.001), parasomnia (P<0.001), circadian schedule disorders (P<0.001) and sleep related breathing disorders (P< 0.001). Lower values were found in controls (P<0.01) and in patients with periodic limb movement disorder and/or restless legs syndrome (P<0.05). In 111 patients having two consecutive recording nights, a good reproducibility was present with no differences between nights (P=ns) and with significant correlation (P<0.001). CONCLUSIONS: The SFI seems to be an accurate, reproducible and easy method to detect sleep fragmentation in patients with sleep disorders. Further studies are needed to validate the usefulness of this tool in clinical practice.     

失眠症患者睡眠质量的主观评估与多导睡眠图参数对比分析

目的 探讨失眠症患者对睡眠质量的主观评估,并通过对多导睡眠图(PSG)睡眠参数的定量分析,对失眠症患者的睡眠状况进行客观评估,进一步将二者进行对比分析.方法 对失眠症患者和健康人各100例运用匹兹堡睡眠质量指数问卷(PSQI)进行评定,并分别进行多导睡眠图的整夜睡眠描记,次日晨起后询问夜间睡眠情况.结果 失眠症组PSQI各成分得分及总分均高于对照组,差异有统计学意义(P＜0.01).与对照组相比,失眠症组的睡眠潜伏期(min)延长(失眠症组43.69±11.54,对照组16.01±10.44)、总睡眠时间(min)减少(失眠症组314.65±91.89,对照组446.41±77.81)、睡眠效率降低(失眠症组64.51%±18.59%,对照组91.32%±3.58%)、快眼动睡眠时间(min)减少(失眠症组33.26±15.61,对照组93.21±21.63),差异有统计学意义(P＜0.01).失眠症组对总睡眠时间的评估较PSG检测值显著减低、对睡眠潜伏期的评估较PSG检测值显著增高,自我评估与实际睡眠情况不一致.结论 失眠症患者睡眠质量较差.失眠症患者的PSG各睡眠参数有特征性的改变,利用PSG检查发现失眠症患者对失眠情况的主客观评估不一致,存在过高估价睡眠潜伏期和过低估价睡眠时间的倾向.     

30例睡眠呼吸暂停综合征临床分析

目的：了解睡眠呼吸暂停综合征（SAS）患者的常见临床症状和白天主观困倦程度。方法：采用SAS8项症状问卷,Epworth量表对30例SAS患者和28例正常对照者进行调查。结果：病例组以睡眠时打鼾,夜间憋醒易醒白天打瞌睡等症状较常见,病例组白天主观困倦程度显著高于对照组。结论：SAS患者白天主观困倦程度较高,需要进行适当的医学干预。     

急性脑血管病并睡眠呼吸暂停综合征的危险因素

目的 探讨急性脑血管病合并睡眠呼吸暂停综合征的危险因素,为预防和降低急性脑血管病并发SAS的发生率,改善脑血管病的预后提供依据.方法 对126例急性脑血管病患者进行多导睡眠图(PSG)监测,应用条件Logistic回归模型分析可能影响并发SAS的因素.结果 选入回归方程的因素有肥胖、脂代谢紊乱、饮酒、肢体瘫痪程度,其危险度比分别为3.17、4.27、9.14、4.04.结论 肥胖、脂代谢紊乱、饮酒、肢体瘫痪是急性脑血管病并发SAS的危险因素,而不同性质和不同卒中病灶与并发SAS并不相关.     

发作性睡病夜间睡眠结构特征的探讨

目的了解发作性睡病患者夜间睡眠结构特点。方法对10例符合发作性睡病国际睡眠疾病分类最低诊断标准的发作性睡病患者和13例正常对照者连续进行两夜夜间多导睡眠图监测,比较两组各项睡眠参数,并分析发作性睡病患者的夜间睡眠结构特点。结果发作性睡病组患者的夜间睡眠潜伏期和快速眼动睡眠潜伏期缩短(P<0．01),在整个睡眠过程中睡眠始发快速眼动时段出现比例明显升高(P<0．01),唤醒指数和睡眠纺锤波密度增高(P<0．05),睡眠转换次数和清醒次数及S1期睡眠比例增加(P<0．01),S2期和S3 S4期比例减少(P<0．01),快速眼动密度增加(P<0．01);全夜快速眼动睡眠时段持续时间无逐渐延长趋势。与对照组受试者睡眠生理参数相比,差异具有显著性意义(P<0．05或P< 0．01)。结论发作性睡病患者夜间睡眠结构的特征为快速眼动活动增强,睡眠维持机制紊乱,中枢唤醒水平降低。     

失眠症患者的多导睡眠图研究

目的 探讨失眠症患者多导睡眠图睡眠参数的变化特征。方法 对６２例单纯性失眠症患者和２２名正常人进行多导睡眠图描记,并进行各睡眠参数比较。结果 与正常人比较,失眠症患者睡眠潜伏期长（２１．７分）,觉醒次数多（５．４次）,实际睡眠时间少（３３０．６）,睡眠效率低（７３．３％）。睡眠结构快眼动（ＲＥＭ）时间减少（１７．１％）,ＲＥＭ活动度和密度低,自我估价与实际睡眠时间不一致（５２．９％;Ｐ〈０．０５￣     

抑郁症患者睡眠行为及睡眠生理障碍的研究

目的　探讨抑郁症患者睡眠行为及睡眠生理的变化。方法　采用调查表对 32例抑郁症患者的睡眠行为障碍和睡眠生理进行调查 ,检测其全夜多导睡眠图 ,并与 2 1名正常人进行对照。结果　 (1)抑郁症组的入睡困难、早醒、睡眠维持障碍及睡眠过多的发生率高于对照组 (P <0 0 5～0 0 1) ;(2 )与对照组比较 ,抑郁症组存在睡眠潜伏期长 [(36 1± 17 2 )min],醒觉时间、觉醒次数、醒觉睡眠比高 ,睡眠效率和睡眠维持率低 (P <0 0 5～ 0 0 1) ,快速眼动睡眠潜伏期短 [(6 1 8± 31 2 )min]等。结论　抑郁症患者存在睡眠行为与睡眠生理相一致的异常改变 ,其睡眠障碍的病理机制可能同源于抑郁症的发病机制。     

情感性精神障碍患者的睡眠脑电图试验研究

目的 探讨情感性精神障碍患者睡眠脑电图的特点。方法 对１０例躁狂中层得、１０例抑郁症患者的睡眠脑电图进行全夜测试,并与１６名正常受试者进行对照。结果 与对组相比,抑郁症组睡眠脑电图改变主要有快动（ＲＥＭ）睡眠潜伏期缩短等;躁狂症组实际睡眠时间秒,睡眠效率下降。两组比较,抑郁症组比躁狂症组ＲＥＭ潜伏期更短。而躁狂症组比抑郁症组实际睡眠时间更少。结论 睡眠脑电图中的ＲＥＭ指标有可能是情感性精神障碍患者     

Sleep in Children with Asperger Syndrome

The prevalence of sleep disturbances in 52 children with Asperger syndrome (AS) as compared with 61 healthy controls (all subjects aged 5–17 years) was investigated. Problems with sleep onset and maintenance, sleep-related fears, negative attitudes toward sleeping, and daytime somnolence were more frequent among children with AS than among controls. Short sleep duration (<9 h) was almost twofold (59% vs. 32%), and the risk for sleep onset problems more than fivefold (53% vs. 10%) more common in the AS group than in the control group. Child-reported sleeping problems were also more prevalent in the AS group than in controls (58% vs. 7%). The results suggest that sleep disturbances should be routinely evaluated in children with AS.     

抑郁症住院患者适应性睡眠改变的研究

目的　了解抑郁症住院患者适应性睡眠改变的情况。方法　连续两晚测量 14例抑郁症住院患者的多导睡眠图 ,比较其两晚的睡眠参数。结果　患者的睡眠总时间、睡眠潜伏期、醒起时间、运动觉醒时间、醒觉次数、睡眠效率、睡眠结构、快动眼 (REM)睡眠潜伏期、REM强度、REM密度、REM时间、REM周期数等指标 ,第 1晚与第 2晚的差异均无显著性 (P均 >0 0 5 )。结论　抑郁症住院患者存在适应性睡眠改变的相对缺乏 ,其第 1晚的睡眠资料不应轻易地丢弃。     

The effects of lamotrigine on sleep in patients with epilepsy

PURPOSE: The older antiepileptic drugs (AEDs) have a variety of effects on sleep, including marked reduction in REM, slow-wave sleep (SWS) and sleep latency, and increased percentage of light sleep. The effects of the newer AEDs on sleep are unknown. Our purpose was to study the effect of lamotrigine (LTG) on sleep. METHODS: Ten adults with focal epilepsy, in whom the decision was made to add LTG to either phenytoin (PHT) or carbamazepine (CBZ) for control of seizures, were the subjects of this study. Patients underwent pre- and posttreatment polysomnography (PSG) and completed sleep questionnaires. Polygraphic variables and Epworth Sleepiness Scale (ESS) scores, a subjective measure of sleep propensity, were compared by using the Wilcoxon sign rank test. RESULTS: Seven patients were taking CBZ, and three were treated with PHT. All subjects were titrated to an LTG dose of 400 mg/day. Treatment with LTG produced a significant decrease in SWS and an increase in stage 2 sleep percentage. No significant difference in ESS or any of the other polygraphic variables was observed. However, LTG treatment was associated with a reduction in arousals and stage shifts and an increase in REM periods. No subjects reported insomnia with treatment. CONCLUSIONS: LTG appears to be less disruptive to sleep than some of the older AEDs.     

Association between actigraphy-based sleep duration variability and cardiovascular risk factors – Results of a population-based study

BackgroundAlthough a few studies suggest an adverse effect of sleep duration variability on cardiovascular risk factor, others did not and this association remains controversial. Moreover, most studies were non-representative of the general population, used different sleep duration variability measures, and relied on self-reported sleep duration. We aimed to assess the association between different, actigraphy-based sleep duration variability measures and cardiovascular risk factors in a population-based sample.MethodsIn a middle-aged population-based cohort, 2598 subjects had data on sleep duration variability measured by actigraph over 14 days. Multivariable logistic regressions were performed to assess the relationship between different sleep duration variability measures [ie, night-to-night variability (NNV), range between shortest and longest sleep duration (RSL), range between average weekday and weekend sleep duration (RWW)] and cardiovascular risk factors including obesity, diabetes and hypertension.ResultsSubjects with highest sleep duration variability - measured as NNV, RSL and RWW, were more likely to be obese. These associations robust in most but not all sensitivity analyses, and no associations between sleep duration variability measures and diabetes or hypertension were found.ConclusionThere is a possible association between high sleep duration variability and obesity, although results were not robust in all sensitivity analyses. Further, no associations between sleep duration variability and other cardiovascular risk factor such as diabetes or hypertension were found.     

Few changes observed in polysomnographic-assessed sleep before and after completion of chemotherapy

Objective

Sleep disturbance is prevalent among patients undergoing chemotherapy and is strongly associated with cancer-related fatigue (CRF). However, little objective evidence has been gathered on the patterns of sleep before and following chemotherapy.

Methods

Twenty-six patients scheduled to receive chemotherapy were recruited. Sleep parameters were assessed by in-lab polysomnography (PSG) for two consecutive nights prior to first chemotherapy, approximately 3 weeks following the patients' last chemotherapy, and 3 months following the last treatment. Fatigue was measured on the first night of each of the two-night PSG assessments. We focus on Slow-Wave Sleep (SWS) as we hypothesized that a decrease of this restorative phase of sleep might be implicated in CRF.

Results

Repeated-measures analyses examining changes from baseline to the later time points in the proportion of time asleep spent in each of the four sleep architecture stages (Stage 1, Stage 2, SWS, and REM sleep) were non-significant, all Ps > 0.41. Canonical correlation analysis showed that the proportion of time spent in SWS was not significantly correlated with any of the three CRF measures at any of the three assessment points, P = 0.28.

Conclusions

Sleep architecture is not affected by cancer treatment. No evidence of an association between CRF and SWS, or alterations in SWS, was found.