癫痫是一种复杂的疾病,除了癫痫发作之外,多方面的疾病还以多种方式影响患者,包括心理,社会,和生活质量问题,但众所周知,癫痫也与睡眠相互作用。癫痫发作通常发生在睡眠和觉醒之间的边界,癫痫患者经常经历睡眠中断,非REM睡眠期间发作间癫痫样放电率增加。癫痫的网络理论没有解决睡眠的作用,但最近对癫痫与睡眠之间相互作用的强调表明,癫痫发作后的睡眠也可能参与癫痫发作的过程,并通过与长期记忆形成相关的过程随着时间的推移而变得更加严重(“癫痫发生”)。虽然人们普遍认为反复发作是由神经回路的异常功能引起的,癫痫的进展可能是由正常情况辅助的,睡眠过程中由病理信号驱动的神经回路的生理功能。研究记录了多个,在自发性癫痫发作之前的单个神经元表明,在癫痫发作开始之前激活的神经组件在癫痫发作后睡眠期间重新激活,类似于行为神经组件的重新激活,这被认为与长期记忆的形成有关,称为内存整合的过程。因此,睡眠过程中与癫痫相关的神经组件的重新激活被描述为与癫痫相关的整合(SRC)的组成部分。这些结果进一步表明,SRC可能被视为癫痫的网络相关方面,即使是在解剖学上限制神经解剖学起源的癫痫发作中。正如癫痫网络理论所建议的那样,作为干扰ictogenesis的一种手段,干扰SRC的疗法可能会提供一些抗癫痫的治疗益处,即使干扰针对的是最初不参与癫痫发作的结构。这里,通过提供记忆巩固的概述,我们展示了癫痫网络理论如何扩展到包括与学习相关的神经可塑性机制,被认为是MC基础的机制,它们与缉获相关合并的关系,并建议小说,针对癫痫发作后睡眠期间癫痫发作后网络激活干扰的抗癫痫治疗。
Epilepsy is a complex, multifaceted disease that affects patients in several ways in addition to seizures, including psychological, social, and quality of life issues, but epilepsy is also known to interact with sleep. Seizures often occur at the boundary between sleep and wake, patients with epilepsy often experience disrupted sleep, and the rate of inter-ictal epileptiform discharges increases during non-REM sleep. The Network Theory of Epilepsy did not address a role for sleep, but recent emphasis on the interaction between epilepsy and sleep suggests that post-seizure sleep may also be involved in the process by which seizures arise and become more severe with time (\"epileptogenesis\") by co-opting processes related to the formation of long-term memories. While it is generally acknowledged that recurrent seizures arise from the aberrant function of neural circuits, it is possible that the progression of epilepsy is aided by normal, physiological function of neural circuits during sleep that are driven by pathological signals. Studies recording multiple, single neurons prior to spontaneous seizures have shown that neural assemblies activated prior to the start of seizures were reactivated during post-seizure sleep, similar to the reactivation of behavioral neural assemblies, which is thought to be involved in the formation of long-term memories, a process known as Memory Consolidation. The reactivation of seizure-related neural assemblies during sleep was thus described as being a component of Seizure-Related Consolidation (SRC). These results further suggest that SRC may viewed as a network-related aspect of epilepsy, even in those seizures that have anatomically restricted neuroanatomical origins. As suggested by the Network Theory of Epilepsy as a means of interfering with ictogenesis, therapies that interfered with SRC may provide some anti-epileptogenic therapeutic benefit, even if the interference targeted structures that were not involved originally in the seizure. Here, we show how the Network Theory of Epilepsy can be expanded to include neural plasticity mechanisms associated with learning by providing an overview of Memory Consolidation, the mechanisms thought to underlie MC, their relation to Seizure-Related Consolidation, and suggesting novel, anti-epileptogenic therapies targeting interference with network activation in epilepsy following seizures during post-seizure sleep.