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Beta spectral power during sleep is associated with impaired recall of extinguished fear. 睡眠中的β光谱功率与消除恐惧的记忆受损有关。
IF 5.3 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2023-10-11 DOI: 10.1093/sleep/zsad209
Dan Denis, Ryan Bottary, Tony J Cunningham, Sean P A Drummond, Laura D Straus

The failure to retain memory for extinguished fear plays a major role in the maintenance of posttraumatic stress disorder (PTSD), with successful extinction recall necessary for symptom reduction. Disturbed sleep, a hallmark symptom of PTSD, impairs fear extinction recall. However, our understanding of the electrophysiological mechanisms underpinning sleep's role in extinction retention remains underdetermined. We examined the relationship between the microarchitecture of sleep and extinction recall in healthy humans (n = 71, both male and females included) and a pilot study in individuals with PTSD (n = 12). Participants underwent a fear conditioning and extinction protocol over 2 days, with sleep recording occurring between conditioning and extinction. Twenty-four hours after extinction learning, participants underwent extinction recall. Power spectral density (PSD) was computed for pre- and post-extinction learning sleep. Increased beta-band PSD (~17-26 Hz) during pre-extinction learning sleep was associated with worse extinction recall in healthy participants (r = 0.41, p = .004). Beta PSD was highly stable across three nights of sleep (intraclass correlation coefficients > 0.92). Results suggest beta-band PSD is specifically implicated in difficulties recalling extinguished fear.

未能保留对消除恐惧的记忆在创伤后应激障碍(PTSD)的维持中起着重要作用,成功的消除恐惧回忆是减少症状所必需的。睡眠障碍是创伤后应激障碍的标志性症状,会削弱恐惧消退的记忆。然而,我们对睡眠在消光保持中所起作用的电生理机制的理解仍不明确。我们研究了健康人睡眠微结构与灭绝回忆之间的关系(n = 71,包括男性和女性)和一项针对PTSD患者的试点研究(n = 12) 。参与者接受了为期2天的恐惧调节和消退方案,在调节和消退之间进行睡眠记录。灭绝学习24小时后,参与者进行了灭绝回忆。计算消光前和消光后学习睡眠的功率谱密度。在灭绝前学习睡眠期间,β频带PSD(~17-26 Hz)的增加与健康参与者更差的灭绝回忆有关(r = 0.41,p = .004)。βPSD在三个晚上的睡眠中高度稳定(组内相关系数 > 0.92)。结果表明β带PSD与回忆消除的恐惧的困难特别相关。
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引用次数: 0
Contactless monitoring for the elderly: potential and pitfalls. 老年人非接触式监测:潜力和陷阱。
IF 5.6 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2023-10-11 DOI: 10.1093/sleep/zsad227
Ju Lynn Ong, Kelly Glazer Baron
1Sleep and Cognition Laboratory, Centre for Sleep and Cognition, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore and 2Department of Family and Preventive Medicine, University of Utah, Salt Lake City, UT USA *Corresponding author. Ju Lynn Ong, Sleep and Cognition Laboratory, Centre for Sleep and Cognition, Yong Loo Lin School of Medicine, National University of Singapore, Tahir Foundation Building, MD1, 12 Science Drive 2, Singapore 117549. Email: julynn.ong@nus.edu.sg.
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引用次数: 0
Scaling up sleep education and cognitive behavioral therapy for insomnia training across multiple health disciplines. 在多个健康学科中加强失眠训练的睡眠教育和认知行为疗法。
IF 5.6 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2023-10-11 DOI: 10.1093/sleep/zsad204
Ivan Vargas
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引用次数: 0
Comparative outcomes in obstructive sleep apnea therapy: mean disease alleviation as a more appropriate measure-it's about time. 阻塞性睡眠呼吸暂停治疗的比较结果:平均病情缓解是一种更合适的衡量标准,现在是时候了。
IF 5.6 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2023-10-11 DOI: 10.1093/sleep/zsad210
Olivier M Vanderveken, Frédéric Gagnadoux
1Department of Otorhinolaryngology, Head and Neck Surgery, Antwerp University Hospital, Edegem, Belgium, 2Department of Otorhinolaryngology, Head and Neck Surgery, Translational Neurosciences, Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium, 3Department of Respiratory and Sleep Medicine, Angers University Hospital, Angers, France and 4INSERM, CNRS, MITOVASC, Equipe CarME, SFR ICAT, University of Angers, Angers, France *Corresponding author. Olivier M. Vanderveken, MD, PhD, Full Professor and Chair, ENT-HNS Department, Antwerp University Hospital, Drie Eikenstraat 655, 2650 Edegem, Belgium. Email: olivier.vanderveken@uantwerp.be.
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引用次数: 0
Applying advanced menstrual cycle affective science methods to study mood regulation and sleep. 应用先进的月经周期情感科学方法研究情绪调节和睡眠。
IF 5.6 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2023-10-11 DOI: 10.1093/sleep/zsad102
Katherine M Sharkey, Allison Stumper, Jessica R Peters
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引用次数: 0
Cardiovascular burden of narcolepsy: what have we learned and what do we still need to know? 发作性睡病的心血管负担:我们学到了什么,还需要知道什么?
IF 5.6 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2023-10-11 DOI: 10.1093/sleep/zsad213
Lucie Barateau, Yves Dauvilliers
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引用次数: 2
Giving weight to incretin-based pharmacotherapy for obesity-related sleep apnea: a revolution or a pipe dream? 给予基于肠促胰岛素的药物治疗肥胖相关睡眠呼吸暂停:革命还是白日梦?
IF 5.3 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2023-10-11 DOI: 10.1093/sleep/zsad224
Ronald R Grunstein, Thomas A Wadden, Julia L Chapman, Atul Malhotra, Craig L Phillips

Obesity is a chronic disease affecting over 670 million adults globally, with multiple complications including obstructive sleep apnea (OSA). Substantial weight loss in patients with obesity-related OSA can reduce or even eliminate OSA as well as reduce sleepiness and improve cardio-metabolic health. Evidence suggests that these improvements exceed those that occur with device-based OSA therapies like continuous positive airway pressure which continue to be the first-line of therapy. Resistance to weight management as a first-line strategy to combat OSA could arise from the complexities in delivering and maintaining adequate weight management, particularly in sleep clinic settings. Recently, incretin-based pharmacotherapies including glucagon-like peptide 1 (GLP-1) receptor agonists alone or combined with glucose-dependent insulinotropic polypeptide (GIP) receptor agonists have been developed to target glycemic control in type 2 diabetes. These medications also slow gastric emptying and reduce energy intake. In randomized, placebo-controlled trials of these medications in diabetic and non-diabetic populations with obesity, participants on active medication lost up to 20% of their body weight, with corresponding improvements in blood pressure, lipid levels, physical functioning, and fat mass loss. Their adverse effects are predominantly gastrointestinal-related, mild, and transient. There are trials currently underway within individuals with obesity-related OSA, with a focus on reduction in weight, OSA severity, and cardio-metabolic outcomes. These medications have the potential to substantially disrupt the management of OSA. Pending coming data, we will need to consider pharmacological weight loss as a first-line therapy and how that influences training and management guidelines.

肥胖是一种影响全球6.7亿多成年人的慢性疾病,有多种并发症,包括阻塞性睡眠呼吸暂停(OSA)。肥胖相关OSA患者的体重大幅减轻可以减少甚至消除OSA,减少嗜睡,改善心脏代谢健康。有证据表明,这些改善超过了基于设备的OSA治疗,如持续气道正压通气,后者仍然是治疗的一线。对将体重管理作为对抗OSA的一线策略的抵制可能源于提供和维持足够的体重管理的复杂性,尤其是在睡眠临床环境中。最近,基于肠促胰岛素的药物疗法,包括胰高血糖素样肽1(GLP-1)受体激动剂单独或与葡萄糖依赖性促胰岛素多肽(GIP)受体激动药联合,已被开发用于靶向2型糖尿病的血糖控制。这些药物还能减缓胃排空,减少能量摄入。在糖尿病和非糖尿病肥胖人群中进行的这些药物的随机安慰剂对照试验中,服用活性药物的参与者体重减轻了20%,血压、脂质水平、身体功能和脂肪量减少也相应改善。它们的不良反应主要是与胃肠道相关的、轻微的和短暂的。目前正在对肥胖相关OSA患者进行试验,重点是减轻体重、OSA严重程度和心脏代谢结果。这些药物有可能严重干扰OSA的治疗。在等待即将到来的数据之前,我们需要将药物减肥视为一线治疗,以及它如何影响训练和管理指南。
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引用次数: 0
Novel insights into the role of eye movements during REM sleep in memory consolidation. 对快速眼动睡眠中眼球运动在记忆巩固中的作用的新见解。
IF 5.6 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2023-10-11 DOI: 10.1093/sleep/zsad178
Michele Ferrara, Aurora D'Atri, Federico Salfi
A large and consistent literature converges in pointing out how hippocampus-dependent memories benefit from slow wave activity during non-rapid eye movement sleep (NREM). The declarative memory traces are repeatedly reactivated during slow-wave sleep (SWS), promoting long-term storage at the cortical level [1, 2]. Sleep also supports the consolidation of procedural memory underlying problem-solving and the acquisition of new rules or cognitive strategies [3–5], but in this context, the specific role of SWS is more controversial. While some studies support the possible involvement of SWS [6, 7], others propose rapid eye movement (REM) sleep as the main responsible for the sleep-dependent integration of information supporting creative problem solving [8]. Meanwhile, the iterative and synergic interleaving of REM and NREM stage characteristics has been recently conceptualized to explain the sleep effect on creative problem-solving skills [3]. However, evidence of specific cortical processes representing the actual reactivation of this kind of memories during paradoxical sleep is still scarce. Another gap in the literature addressing the relationship between REM sleep and memory function is represented by the common practice of considering paradoxical sleep as a homogeneous state, especially in human studies [9]. However, from decades, two neurophysiologically distinct REM substates have been identified [9, 10], namely the tonic and phasic REM sleep, and the available literature suggested a functional heterogeneity of these two substates in memory consolidation [11–13]. In the August issue of SLEEP, van den Berg and collaborators [14] addressed some of these open and scarcely explored questions, providing novel insight into the role of the electroencephalographic (EEG) activity during human tonic and phasic REM sleep in the consolidation of novel problem-solving skills. Two different groups of healthy young participants (n = 20 per group) performed the Tower of Hanoi task before and after (1) an undisturbed 8-hour period of sleep, or (2) a same-length wake period. Each group also took part in another similar condition (in counterbalanced order) in which a non-learning control task was performed. The study [14] adopted a quite novel approach to address the involvement of REM sleep in memory consolidation, evaluating the event-related spectral perturbations (ERSP) time-locked to the eye movement (EM) peaks. This analysis allowed the authors to estimate specific oscillatory EEG components surrounding EMs during REM sleep, unraveling stable cortical patterns associated with EMs in the post-learning night compared with the control (non-learning) condition. Furthermore, the authors [14] classified the EMs during REM sleep into “bursts,” defining phasic REM state, and “isolated” EMs, proposed as a proxy of tonic REM state. This categorization led to evaluating the differential contribution of phasic and tonic REM sleep to the consolidation of problem-solvin
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引用次数: 0
In response to the Letter to the Editor regarding "Earlier chronotype in midlife as a predictor of accelerated brain aging: a population-based longitudinal cohort study." 针对致编辑的关于“中年早期时间型是大脑加速衰老的预测因素:一项基于人群的纵向队列研究”的信
IF 5.6 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2023-10-11 DOI: 10.1093/sleep/zsad212
Hyeon Jin Kim, Regina E Y Kim, Soriul Kim, Seung Ku Lee, Hyang Woon Lee, Chol Shin
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引用次数: 0
Long-term efficacy and safety of tonic motor activation for treatment of medication-refractory restless legs syndrome: A 24-Week Open-Label Extension Study. 强直性运动激活治疗药物难治性不宁腿综合征的长期疗效和安全性:一项为期24周的开放标签扩展研究。
IF 5.6 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2023-10-11 DOI: 10.1093/sleep/zsad188
Asim Roy, Joseph Ojile, Jerrold Kram, Jonathan Olin, Russell Rosenberg, J Douglas Hudson, Richard K Bogan, Jonathan D Charlesworth
Abstract Study Objectives To evaluate long-term efficacy and safety of tonic motor activation (TOMAC) for treatment of medication-refractory moderate-to-severe primary restless legs syndrome (RLS). Methods In the parent study (RESTFUL), adults with refractory RLS were randomized to active TOMAC or sham for 4 weeks followed by 4 weeks of open-label active TOMAC. In the extension study, earlier RESTFUL completers comprised the control group (n = 59), which was followed for 24 weeks with no TOMAC intervention, and later RESTFUL completers compromised the treatment group (n = 44), which received 24 additional weeks of open-label active TOMAC followed by no intervention for 8 weeks. The primary endpoint was Clinician Global Impressions-Improvement (CGI-I) responder rate at week 24 compared to RESTFUL entry. Results CGI-I responder rate improved from 63.6% (95% CI, 49.4 to 77.9%) at RESTFUL completion to 72.7% (95% CI, 58.2 to 83.7%) at week 24 for the treatment group versus 13.6% (95% CI, 7.0 to 24.5%) at week 24 for the control group (p < 0.0001). Mean change in International RLS Rating Scale (IRLS) score improved from −7.4 (95% CI, −5.6 to −9.2) at RESTFUL completion to -11.3 points (95% CI, −8.8 to −13.9) at week 24 for the treatment group versus −5.4 (95% CI, −3.7 to −7.2) at week 24 for control group (p = 0.0001). All efficacy endpoints partially reverted during cessation of treatment. There were no grade 2 or higher device-related adverse events. Conclusions TOMAC remained safe and efficacious for >24 total weeks of treatment with partial reversion of benefits upon cessation. Clinical Trial Extension Study Evaluating NTX100 Neuromodulation System for Medication-Refractory Primary RLS; clinicaltrials.gov/ct2/show/NCT05196828; Registered at ClinicalTrials.gov with the identifier number NCT05196828.
研究目的:评价强直性运动激活(TOMAC)治疗药物难治性中重度原发性不宁腿综合征(RLS)的长期疗效和安全性。在扩展研究中,早期的RESTFUL完成者包括对照组(n=59),对照组随访24周,没有TOMAC干预,而后期的RESTFUL完成者损害了治疗组(n=44),治疗组接受了额外24周的开放标签活性TOMAC,随后8周没有干预。主要终点是与RESTFUL条目相比,临床医生在第24周的整体印象改善(CGI-I)应答率。结果:治疗组的CGI-I应答率从RESTFUL完成时的63.6%(95%CI,49.4至77.9%)提高到第24周的72.7%(95%CI,58.2至83.7%),而对照组在第24周为13.6%(95%CI)(p<0.0001)治疗组在第24周时为-8.8至-13.9,而对照组在第二十四周时为-5.4(95%CI,-3.7至-7.2)(p=0.0001)。在停止治疗期间,所有疗效终点均部分恢复。没有发生2级或更高级别的器械相关不良事件。结论:TOMAC在超过24周的治疗中仍然安全有效,停止治疗后疗效部分逆转。临床试验:评价NTX100神经调控系统治疗药物不良原发性RLS的扩展研究;clinicaltrials.gov/ct2/show/NCT051966828;在ClinicalTrials.gov注册,识别号为NCT05196828。
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引用次数: 2
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Sleep
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