Miller S A, Ospina L H, Mullins A E, Parekh A, Kam K, Fowler C R, Varga A W, Kimhy D
Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Mount Sinai Integrative Sleep Center, Division of Pulmonary, Critical Care, and Sleep Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
medRxiv. 2025 Aug 21:2025.08.18.25333917. doi: 10.1101/2025.08.18.25333917.
People with schizophrenia (SZ) display neurocognitive deficits that have been identified as predictors of poor functioning and disability. Previous reports have noted that these deficits are strikingly similar to the cognitive sequalae of poor sleep. Consistent with this observation, extensive animal and basic human research have strongly support the deleterious effects of poor sleep on neurocognition. Notably, insomnia and disturbed sleep (DS) are highly ubiquitous among people with SZ. Yet, there is scarce information about the potential impact of poor sleep on neurocognition in this population, with available studies using correlational or cross-sectional designs.
We will employ an experimental, within-person, cross-over design to characterize sleep architecture, duration, continuity and quality along with their neurocognitive, functional, electrophysiological, and clinical sequalae in individuals with SZ. Participants will complete two overnight lab-based polysomnography examinations (two weeks apart) employing two sleep schedules: 1) undisturbed sleep (8 hours); and 2) perturbed sleep (4 hours). As part of each overnight sleep schedule, participants will complete brief EEG-indexed sleep-sensitive memory tasks pre- and post-sleep, a post-sleep neurocognitive test battery, as well as a three-day post-sleep digital phenotyping of physical activity, daily functioning, mood, symptoms, medication side-effects, and suicidal ideation via smartphones and actigraphy.
Despite their chronic and ubiquitous nature, the impact of insomnia and DS on neurocognition in SZ remain poorly understood and modeled. This lack of information hinders our ability to develop accurate treatment models and effective interventions for neurocognitive deficits in SZ. Our aim is to address these gaps in knowledge.
精神分裂症患者存在神经认知缺陷,这些缺陷已被确定为功能不良和残疾的预测指标。先前的报告指出,这些缺陷与睡眠不足的认知后遗症极为相似。与这一观察结果一致,大量的动物研究和基础人类研究有力地支持了睡眠不足对神经认知的有害影响。值得注意的是,失眠和睡眠障碍在精神分裂症患者中极为普遍。然而,关于睡眠不足对该人群神经认知的潜在影响的信息却很少,现有研究采用的是相关性或横断面设计。
我们将采用实验性的个体内交叉设计,以描述精神分裂症患者的睡眠结构、持续时间、连续性和质量,以及它们的神经认知、功能、电生理和临床后遗症。参与者将完成两次基于实验室的夜间多导睡眠图检查(相隔两周),采用两种睡眠方案:1)不受干扰的睡眠(8小时);2)受干扰的睡眠(4小时)。作为每个夜间睡眠方案的一部分,参与者将在睡眠前后完成简短的脑电图索引睡眠敏感记忆任务、睡眠后神经认知测试组,以及通过智能手机和活动记录仪对身体活动、日常功能、情绪、症状、药物副作用和自杀意念进行为期三天的睡眠后数字表型分析。
尽管失眠和睡眠障碍具有慢性和普遍性,但它们对精神分裂症患者神经认知的影响仍知之甚少且缺乏模型。这种信息匮乏阻碍了我们为精神分裂症患者的神经认知缺陷开发准确的治疗模型和有效干预措施的能力。我们的目标是填补这些知识空白。