Shouse M N
Sleep Disturbance Research, Veterans Administration Medical Center, Sepulveda, California 91343.
Exp Neurol. 1988 Mar;99(3):664-77. doi: 10.1016/0014-4886(88)90183-5.
Pathological somatomotor system excitability and generalized seizures occur throughout the sleep-awake cycle but peak at different times in the amygdala kindling and systemic penicillin epilepsy models. Sleep loss increases seizure activity in both models during all waking and sleep states but does not alter the timing of seizure susceptibility in the sleep-wake cycle. Although the mechanism for sleep-deprivation seizures is unknown, we propose that sleep loss magnifies somatomotor system hyperexcitability patterns in all states, thereby increasing seizure vulnerability at all times but preferentially during seizure-prone intervals. To evaluate this hypothesis, the timing of ventral lateral thalamic and motor cortex excitability, indexed by amplitudes of primary evoked responses, was studied throughout the sleep-wake cycle in eight cats before and after nearly total sleep deprivation. Sleep loss was induced by 24-h exposure to a modified "flower pot" procedure; the control procedure consisted of 24-h exposure to a larger pedestal which did not affect sleep time. Findings confirmed the hypothesis, as follows: (i) Sleep deprivation increased ventral lateral thalamic and motor cortical excitability nonspecifically. (ii) Motor cortex hyperexcitability correlated best with penicillin seizure activity; both were elevated in slow-wave sleep and drowsiness after awakening from slow-wave sleep before sleep loss and were further increased by sleep loss. (iii) Ventral lateral thalamic hyperexcitability patterns correlated best with the timing of kindled seizure susceptibility; both peaked during transitions from slow-wave to REM sleep before and after sleep loss but were maximal after sleep loss. (iv) Sleep loss increased thalamocortical excitability and seizure susceptibility during stable REM sleep in both models, but values were lower than in other states. These results suggest a chronic neuropathology at different levels of the neuraxis for dissimilar epilepsy models and upon which the sleep-waking state modulation of seizures is superimposed. Sleep deprivation may aggravate seizures in both models by nonspecific enhancement of thalamic and cortical excitability.
病理性躯体运动系统兴奋性和全身性癫痫发作在整个睡眠-觉醒周期中都会出现，但在杏仁核点燃模型和全身性青霉素癫痫模型中，其峰值出现在不同时间。睡眠剥夺会增加两种模型在所有清醒和睡眠状态下的癫痫发作活动，但不会改变睡眠-觉醒周期中癫痫易感性的时间。尽管睡眠剥夺诱发癫痫发作的机制尚不清楚，但我们认为睡眠剥夺会放大所有状态下的躯体运动系统过度兴奋模式，从而增加所有时间的癫痫易感性，尤其是在癫痫易发作的时间段。为了评估这一假设，在八只猫几乎完全睡眠剥夺前后，研究了整个睡眠-觉醒周期中以初级诱发电位幅度为指标的腹侧外侧丘脑和运动皮层兴奋性的时间。通过24小时暴露于改良的“花盆”程序诱导睡眠剥夺；对照程序包括24小时暴露于一个更大的基座上，该基座不会影响睡眠时间。研究结果证实了这一假设，如下：（i）睡眠剥夺非特异性地增加了腹侧外侧丘脑和运动皮层的兴奋性。（ii）运动皮层的过度兴奋与青霉素癫痫发作活动相关性最好；在睡眠剥夺前从慢波睡眠觉醒后的慢波睡眠和困倦状态下，两者均升高，且睡眠剥夺使其进一步增加。（iii）腹侧外侧丘脑的过度兴奋模式与点燃癫痫易感性的时间相关性最好；在睡眠剥夺前后，从慢波睡眠过渡到快速眼动睡眠期间，两者均达到峰值，但睡眠剥夺后达到最大值。（iv）睡眠剥夺在两种模型的稳定快速眼动睡眠期间增加了丘脑皮质兴奋性和癫痫易感性，但数值低于其他状态。这些结果表明，不同癫痫模型在神经轴的不同水平存在慢性神经病理学，癫痫发作的睡眠-觉醒状态调节叠加于此。睡眠剥夺可能通过非特异性增强丘脑和皮层兴奋性而加重两种模型中的癫痫发作。
