Insomnia, alcoholism and relapse

Insomnia and alcoholism are significantly associated in community surveys and patient samples. Insomnia occurs in 36-72% of alcoholic patients and may last for weeks to months after initiating abstinence from alcohol. Some correlates of insomnia in alcoholic patients are identical to those observed in non-alcoholic insomniacs, including anxiety and depression, tobacco smoking, and the use of alcohol to aid sleep. Other studies suggest that as the severity of alcoholism increases, so does the likelihood of insomnia in alcoholic patients. In the sleep laboratory, alcoholic patients who complain of insomnia have disrupted sleep continuity when compared to alcoholic patients without insomnia complaints. Recently sober alcoholics are also more likely than non-alcoholics to have sleep-disordered breathing and increased periodic leg movements, which might contribute to insomnia in some alcoholic patients. The co-occurrence of insomnia and alcoholism is clinically significant because alcoholism can exacerbate the adverse consequences of insomnia (e.g. mood changes and performance decrements) and because insomnia among patients entering treatment for alcoholism has been significantly associated with subsequent alcoholic relapse. Baseline polysomnographic correlates of subsequent relapse include prolonged sleep latency, decreased sleep efficiency and total sleep time, increased rapid eye movement sleep pressure, and decreased slow wave sleep. Whether treatment of insomnia in alcoholic patients reduces relapse rates is unknown, but preliminary treatment guidelines that accommodate the special characteristics of alcoholic patients are provided, with a goal to reduce daytime impairment and psychological distress.     

Acute effects of low doses of melatonin on the sleep of young healthy subjects

This study was undertaken to evaluate the acute effects of single low doses of melatonin given to healthy volunteers in the evening. Six healthy male volunteers (age range 22-24 years) participated in this study, after signing an informed consent form. They received in a double-blind fashion placebo or 0.3 or 1.0 mg melatonin at three fixed times: 18:00, 20:00, and 21:00 hr. Polysomnographic recordings began immediately thereafter, with their being allowed to sleep. Prior to each experimental session and in the following morning, subjects completed a sleep quality questionnaire, the Profile of Mood States, the Stanford Sleepiness Scale, and underwent a visual reaction test. Significant decrease on sleep latencies was found following melatonin treatment at 18:00 and 20:00 hr. In addition, melatonin tended to improve sleep efficiency and to reduce intermittent wakefulness. However, at 21:00 hr, 0.3 mg melatonin increased latency to sleep onset and 1.0 mg melatonin had no effect on sleep variables. Furthermore, melatonin given at different times did not alter subjective sleepiness, mood, and reaction time in the following morning. The results from the present study support the notion that administration of low doses of melatonin, mimicking the nocturnal physiological concentration of this hormone may exert immediate sleep-inducing effects.     

Serial Polysomnograms in Creutzfeldt-Jakob Disease

Abstract: This is a report of the case of a patient with Creutzfeldt-Jakob disease, whose electroencephalograms and polysomnograms were repeatedly recorded throughout the course of the illness with details of the alterations of periodic synchronous discharges. In the advanced stage of the disease, the appearance of peculiar paroxysms was noted, predominantly in the early morning. Furthermore, apnea of the central type was observed during the same time period. Discussions were held on the mechanisms inducing the EEG paroxysms and apneas.     

Developmental aspects of sleep in Prader Willi Syndrome

Background : Children with Prader Willi syndrome (PWS) are at risk of sleep disordered breathing involving central and obstructive components. PWS patients are known to have abnormal responses to hypoxia and hypercapnoea, an increased incidence of Obstructive Sleep Apnoea [OSA] and hypersomnolence when older. As infants, many present with delay in central control of breathing during sleep and resultant hypoxia. This may have long term consequences for the phenotype. Methods : Polysomnography (PSG) and multiple sleep latency testing [MSLT] was performed on PWS children attending a multidisciplinary clinic. Sleep disorders and age of presentation were identified. EEG spectral analysis on infants was undertaken and compared to a group of typically developing infants. Genotype was established. Results : Results suggest that in children less than 2 years central hypoventilation is present in 100%. 10% of children older than five had normal studies and the rest had OSA+/central hypoventilation. 10% had central hypoventilation and hypersomnolence. Twenty‐five children under 12 months of age were analysed separately. Improvements in central hypoventilation were seen in some infants as they matured. The relationship between this and development of mature EEG patterns was examined and is significantly different to EEG spectral analysis of normal infants studied at 3, 6 and 12 months. This was also related to the genotype of each infant. Conclusion : Infants with Prader Willi have a delay in neural maturity as reflected by EEG development of defined EEG sleep stages. All infants with Prader Willi should have a sleep study in infancy and appropriate therapy instigated if required. Hypersomnolence is generally associated with other sleep disorders.     

The Association of Sleep Apnea and Cardiorespiratory Fitness With Long-Term Major Cardiovascular Events

ObjectiveTo determine the risk of long-term major adverse cardiovascular events (MACE) when sleep-disordered breathing (SDB) and decreased cardiorespiratory fitness (CRF) co-occur.MethodsWe included consecutive patients who underwent symptom-limited cardiopulmonary exercise tests between January 1, 2005, and January 1, 2010, followed by first-time diagnostic polysomnography within 6 months. Patients were stratified based on the presence of moderate-to-severe SDB (apnea/hypopnea index ≥15 per hour) and decreased CRF defined as <70% predicted peak oxygen consumption (VO₂). Long-term MACE was a composite outcome of myocardial infarction (MI), coronary artery bypass graft (CABG), percutaneous coronary intervention (PCI), stroke or transient ischemic attack (TIA), and death, assessed until May 21, 2018. Cox-proportional hazard models were adjusted for factors known to influence CRF and MACE.ResultsOf 498 included patients (60±13 years, 28.1% female), 175 (35%) had MACE (MI=17, PCI=14, CABG=13, stroke=20, TIA=12, deaths=99) at a median follow-up of 8.7 years (interquartile range=6.5 to 10.3 years). After adjusting for age, sex, beta blockers, systemic hypertension, diabetes mellitus, coronary artery disease, cardiac arrhythmia, chronic obstructive pulmonary disease, smoking, and use of positive airway pressure (PAP), decreased CRF alone (hazard ratio [HR]=1.91, 95% confidence interval [CI], 1.15 to 3.18; P=.01), but not SDB alone (HR=1.26, 95% CI, 0.75 to 2.13, P=.39) was associated with increased risk of MACE. Those with SDB and decreased CRF had greater risk of MACE compared with patients with decreased CRF alone (HR=1.85; 95% CI, 1.21 to 2.84; P<.005) after accounting for these confounders. The risk of MACE was attenuated in those with reduced CRF alone after additionally adjusting for adequate adherence to PAP (HR=1.59; 95% CI, 0.77 to 3.31; P=.21).ConclusionThe incidence of MACE, especially mortality, was high in this sample. Moderate-to-severe SDB with concurrent decreased CRF was associated with higher risk of MACE than decreased CRF alone. These results highlight the importance of possibly including CRF in the risk assessment of patients with SDB and, conversely, that of screening for SDB in patients with low peak VO₂.     

阻塞性睡眠呼吸暂停低通气综合征手术治疗38例临床分析

目的探讨保留悬雍垂的腭咽成型术治疗阻塞性睡眠呼吸暂停低通气综合征（OSAHS）的临床效果。方法回顾性分析手术治疗38例OSAHS患者临床资料，并随访其疗效。结果38例患者术后随访6个月并行PSG检查，治愈11例，显效16例，有效5例，总有效率84．2％。28例术后随访1年，20例有效。所有患者均未发生严重并发症。结论合理选择OSAHS患者，并进行术前仔细评估，针对不同阻塞平面进行手术可获得较满意疗效。     

椎-基动脉缺血发作与睡眠呼吸障碍

Therelationshipbetweencerebro－vasculardiseases（CVD）andSRBDhasattractedpeople’sattentionmoreandmoreinthepastyears．WepresentinthispapertherelationshipofVBIandSRBDwhichhasnoteverbeenreportedbefore．１Subjectandmethod１．１SubjectFortyfivepatients，male３２，female１３，withanageof２７～７４yearsandanaveragedurationofillnessof２．１years（５daysto１０years）．１．２Criteriaofdiagnosis犤１犦（１）Transientvertigoattacksaccom－paniedbyotherVBIsymptomssuchasdiplopia，scintillation，visua…     

Quisi与睡眠脑电图检测抑郁症的比较研究

目的评价Quisi检测抑郁症的作用和适应证。方法对19例抑郁症患者和21名正常受试者分别作Quisi和睡眠脑电图检测。并以日本SEEG-1500型睡眠脑电图为检测标准,与德国Quisi进行比较研究。结果在正常对照组中,除睡眠第二阶段百分比,Quisi少于多导睡眠图(Polysomnography,PS)外(Quisi为48±8,正常人PSG56±9,t=2.48,P<0.05),其余12项指标差异均无显著性。抑郁症组中睡眠第一阶段百分比,Quisi也少于PSG(Quisi为11±4,PSG为13±3,t=2.0,P<0.05),其余12项指标差异也无显著性。结论Quisi检测抑郁症作用与PSG相似,在心理咨询、外出巡诊和家庭病床上有应用前途,但不适用于发作性疾病的评估。     

AG200睡眠监测阻塞定位技术和螺旋CT评估OSAHS上气道狭窄的价值

目的研究睡眠监测阻塞定位仪(Apneagraphy,AG200)结合螺旋CT在评估阻塞性睡眠呼吸暂停低通气综合征(OSAHS)上气道狭窄中的临床应用价值。方法 28例睡眠打鼾患者,采用睡眠监测阻塞定位仪进行整夜睡眠呼吸监测,分析呼吸紊乱指标、出现呼吸暂停低通气事件时的阻塞平面,不同平面的阻塞次数和总阻塞次数。以螺旋CT测量清醒状态下上气道的软腭后区、舌后区气道的横截面积。将AG200测定上气道狭窄平面与CT测量判断平面进行比较。结果①28例AG200监测,6例排除OSAHS。22例符合OSAHS,其中轻度4例,中度10例,重度8例。②28例CT测量,4例无狭窄平面,16例腭后区狭窄2,例舌后区狭窄6,例腭后区、舌后区双重狭窄。③22例OSAHS中AG200测压均为上部和下部联合阻塞,上部阻塞为主18例,下部阻塞为主4例,其中1例上部阻塞为100%。④22例OSAHS中,AG200测压腭后区阻塞为主占81.8%(18/22),CT测量腭后区狭窄占68.2%(15/22),差异无统计学意义(P>0.05)。AG200测压下部阻塞为主占27.6%(6/22),CT测量舌后区阻塞占18.2%。结论 AG200对OSAHS定性定位诊断具有重要作用,结合CT测量可以很好地评估上气道腭后区狭窄。     

Case-control study of subjective and objective differences in sleep patterns in older adults with insomnia symptoms

Older adults have high prevalence rates of insomnia symptoms, yet it is unclear if these insomnia symptoms are associated with objective impairments in sleep. We hypothesized that insomnia complaints in older adults would be associated with objective differences in sleep compared with those without insomnia complaints. To test this hypothesis, we conducted a cross‐sectional study in which older adults with insomnia complaints (cases, n = 100) were compared with older adults without insomnia complaints (controls, n = 100) using dual‐night in‐lab nocturnal polysomnography, study questionnaires and 7 days of at‐home actigraphy and sleep diaries. Cases were noted to have reduced objective total sleep time compared with controls (25.8 ± 8.56 min, P = 0.003). This was largely due to increased wakefulness after sleep onset, and not increased sleep latency. When participants with sleep‐related breathing disorder or periodic limb movement disorder were excluded, the polysomnography total sleep time difference became even larger. Cases also had reduced slow‐wave sleep (5.10 ± 1.38 min versus 10.57 ± 2.29 min, effect size −0.29, P = 0.04). When comparing self‐reported sleep latency and sleep efficiency with objective polysomnographic findings, cases demonstrated low, but statistically significant correlations, while no such correlations were observed in controls. Cases tended to underestimate their sleep efficiency by 1.6% (±18.4%), while controls overestimated their sleep efficiency by 12.4% (±14.5%). In conclusion, we noted that older adults with insomnia complaints have significant differences in several objective sleep findings relative to controls, suggesting that insomnia complaints in older adults are associated with objective impairments in sleep.