癫痫与睡眠之间的双向关系：一篇叙述性综述

文献信息

中文摘要

背景： 癫痫和睡眠障碍是高度流行的疾病，常共存，并通过共享的神经生物学机制产生相互不良影响。
目的： 我们对涉及癫痫与睡眠障碍之间双向关系的文献进行了叙述性综述，旨在对其神经生理学基础、临床意义和治疗后果提供全面的综合。
结果： 癫痫-睡眠关系由多种神经生物学机制介导，包括丘脑皮质网络动力学、昼夜节律钟基因调控、腺苷能和食欲素能张力、突触稳态以及类淋巴清除。这一关系的关键病理生理概念是，NREM睡眠通过丘脑皮质同步化促进发作间期癫痫样放电和癫痫发作传播，而REM睡眠则发挥保护作用。癫痫活动破坏睡眠宏观和微观结构，减少总睡眠时间、睡眠效率和REM睡眠，增加入睡后觉醒，并通过改变周期性交替模式率反映的NREM微观结构不稳定。相反，睡眠障碍降低癫痫发作阈值并促进疾病进展：睡眠剥夺是独立的癫痫发作诱发因素，共病阻塞性睡眠呼吸暂停通过间歇性缺氧和觉醒不稳定进一步降低癫痫发作阈值。还综述了与睡眠有特殊关系的特定癫痫综合征，包括睡眠相关过度运动性癫痫、睡眠中棘波激活的癫痫性脑病和自限性儿童局灶性癫痫。NREM异态睡眠与睡眠相关癫痫之间的鉴别诊断仍然具有挑战性；诊断检查应始终包括详细的临床病史以描述发作特征，随后进行视频多导睡眠监测，这是金标准。从治疗角度看，抗癫痫发作药物对睡眠结构产生异质性影响，多药治疗与较差的睡眠质量独立相关；因此，针对睡眠障碍代表了一种可改变策略，能够改善癫痫发作控制、认知功能和生活质量。
结论： 一种多学科方法，整合睡眠障碍的系统筛查、抗癫痫发作药物时机和选择的优化、共病阻塞性睡眠呼吸暂停的治疗以及行为睡眠干预，有可能显著改善癫痫患者的结局。在常规临床实践中更广泛地实施这些策略既是优先事项也是机遇。

英文摘要

BACKGROUND: Epilepsy and sleep disorders are highly prevalent conditions that frequently coexist, exerting reciprocal adverse effects through shared neurobiological mechanisms.
OBJECTIVE: We conducted a narrative review of the literature addressing the bidirectional relationship between epilepsy and sleep disorders, aiming to provide a comprehensive synthesis of its neurophysiological basis, clinical implications, and therapeutic consequences.
RESULTS: The epilepsy-sleep relationship is mediated by multiple neurobiological mechanisms, including thalamocortical network dynamics, circadian clock gene regulation, adenosinergic and orexinergic tone, synaptic homeostasis, and glymphatic clearance. A key pathophysiological concept underlying this relationship is that NREM sleep promotes interictal epileptiform discharges and seizure propagation through thalamocortical synchronization, whereas REM sleep exerts a protective effect. Epileptic activity disrupts both sleep macro- and microarchitecture, reducing total sleep time, sleep efficiency, and REM sleep, increasing wake after sleep onset, and destabilizing NREM microarchitecture as reflected by altered cyclic alternating pattern rates. Conversely, sleep disturbances lower the seizure threshold and contribute to disease progression: sleep deprivation is an independent seizure-precipitating factor, and comorbid obstructive sleep apnea further lowers the seizure threshold through intermittent hypoxia and arousal instability. Specific epileptic syndromes with a privileged sleep relationship are also reviewed, including sleep-related hypermotor epilepsy, epileptic encephalopathy with spike-wave activation in sleep, and self-limited childhood focal epilepsies. The differential diagnosis between NREM parasomnias and sleep-related epilepsies remains challenging; the diagnostic workup should always include a thorough clinical history characterizing the episodes, followed by video-polysomnography, which represents the gold standard. From a therapeutic standpoint, antiseizure medications exert heterogeneous effects on sleep architecture, and polytherapy is independently associated with worse sleep quality; targeting sleep disturbances therefore represents a modifiable strategy capable of improving seizure control, cognitive function, and quality of life.
CONCLUSION: A multidisciplinary approach integrating systematic screening for sleep disorders, optimization of antiseizure medication timing and selection, treatment of comorbid obstructive sleep apnea, and behavioral sleep interventions has the potential to meaningfully improve outcomes in patients with epilepsy. Wider implementation of these strategies in routine clinical practice is both a priority and an opportunity.