卒中后睡眠表型与执行功能障碍：迈向睡眠-网络-执行框架

文献信息

中文摘要

背景： 卒中后睡眠障碍与执行功能障碍常共存，但将睡眠紊乱与认知恢复联系起来的机制仍知之甚少。一个主要挑战是表型异质性：失眠、睡眠碎片化、阻塞性睡眠呼吸暂停、嗜睡和昼夜节律紊乱在生物学驱动因素和认知后果上各不相同。方法：为构建可检验的网络层面解释，我们对临床卒中研究、卒中神经影像研究、非卒中睡眠网络证据和干预研究进行了针对性综合，并按每条证据流与所提出通路的接近程度进行映射。结果：该综合表明，卒中后局灶性病变、神经机能联系不能和结构失连接可破坏显著性网络、默认模式网络和额顶网络的完整性与协调。临床研究支持睡眠紊乱与卒中后认知较差之间的关联，而神经影像发现显示卒中后认知障碍中存在大尺度网络组织改变。来自非卒中人群的证据进一步提示，睡眠剥夺、失眠和睡眠碎片化可损害网络分离、默认模式调节、额顶募集以及显著性网络介导的切换。结论：因此我们提出，睡眠碎片化、失眠和觉醒不稳定可能作为功能性应激源作用于本已脆弱的卒中后网络架构。低效切换可能使默认模式活动在情境不适当时持续存在，并在执行需求期间减少或延迟额顶参与，从而促成冲突监测、工作记忆、处理速度和认知灵活性的损害。尚无研究在单一卒中队列中直接检验这一完整通路。因此，该框架应被视为可证伪的机制性假说，而非已确立的因果模型。未来研究应在同一卒中队列中结合客观睡眠表型分型、动态与有效连接、任务态神经影像、领域特异性执行功能测量以及纵向或干预设计。

英文摘要

Post-stroke sleep disturbance and executive dysfunction frequently coexist, yet the mechanisms linking disturbed sleep to cognitive recovery remain poorly understood. A major challenge is phenotypic heterogeneity: insomnia, sleep fragmentation, obstructive sleep apnea, hypersomnolence, and circadian disruption differ in their biological drivers and cognitive consequences. To develop a testable network-level account, we conducted a targeted synthesis of clinical stroke studies, stroke neuroimaging research, non-stroke sleep-network evidence, and intervention studies, mapping each evidence stream according to its proximity to the proposed pathway. The synthesis indicates that focal lesions, diaschisis, and structural disconnection after stroke can disrupt the integrity and coordination of the salience, default mode, and frontoparietal networks. Clinical studies support an association between disturbed sleep and poorer post-stroke cognition, while neuroimaging findings demonstrate altered large scale network organization in post-stroke cognitive impairment. Evidence from non-stroke populations further suggests that sleep loss, insomnia, and sleep fragmentation can impair network segregation, default mode regulation, frontoparietal recruitment, and salience-network-mediated switching. We therefore propose that sleep fragmentation, insomnia, and arousal instability may act as functional stressors on an already vulnerable post-stroke network architecture. Inefficient switching may permit context-inappropriate persistence of default mode activity and reduce or delay frontoparietal engagement during executive demand, thereby contributing to impaired conflict monitoring, working memory, processing speed, and cognitive flexibility. No study has directly tested this complete pathway within a single stroke cohort. The framework should therefore be regarded as a falsifiable mechanistic hypothesis rather than an established causal model. Future studies should combine objective sleep phenotyping, dynamic and effective connectivity, task based neuroimaging, domain specific executive measures, and longitudinal or interventional designs within the same stroke cohorts.