我们认为觉醒和睡眠相关的运动过度癫痫是遗传性双胞胎疾病,一个没有,一个癫痫。他们在NREM睡眠期间共享增强的唤醒活动,睡眠-觉醒分离,最终导致类似症状的睡眠恐怖和与睡眠相关的运动过度发作。两个光谱背后的已知突变是不同的,但是有多重种群遗传-,家庭-甚至个人(两个条件发生在同一个人)重叠支持共同的遗传根源。在觉醒障碍的发作中,前扣带,前岛叶和前额叶皮层(显示参与恐惧和情绪处理)在睡眠的大脑中被激活。这些区域与成功手术的睡眠相关运动过度发作的癫痫发作区重叠,尤其是,属于与其中心一致的显著性网络。在睡眠恐怖和运动过度发作中发生的觉醒相关和类似的恐惧混乱,使它们类似于睡眠中出现的急性应激反应;由假警报触发。前扣带的激活,在这两种情况下的前额叶和岛屿区域,可以轻松动员下丘脑-垂体-肾上腺轴(在清醒状态下准备战斗-飞行反应);通过其往返于显着性网络的直接途径。这一假设从未被研究过。
We consider the disorders of arousal and sleep-related hypermotor epilepsy as genetic twin-conditions, one without, one with epilepsy. They share an augmented arousal-activity during NREM sleep with sleep-wake dissociations, culminating in sleep terrors and sleep-related hypermotor seizures with similar symptoms. The known mutations underlying the two spectra are different, but there are multifold population-genetic-, family- and even individual (the two conditions occurring in the same person) overlaps supporting common genetic roots. In the episodes of disorders of arousal, the anterior cingulate, anterior insular and pre-frontal cortices (shown to be involved in fear- and emotion processing) are activated within a sleeping brain. These regions overlap with the seizure-onset zones of successfully operated sleep-related hypermotor seizures, and notably, belong to the salience network being consistent with its hubs. The arousal-relatedness and the similar fearful confusion occurring in sleep terrors and hypermotor seizures, make them alike acute stress-responses emerging from sleep; triggered by false alarms. The activation of the anterior cingulate, prefrontal and insular regions in the episodes of both conditions, can easily mobilize the hypothalamo-pituitary-adrenal axis (preparing fight-flight responses in wakefulness); through its direct pathways to and from the salience network. This hypothesis has never been studied.