Clinic Barmelweid, Aargau, Switzerland.
Sci Rep. 2016 Jul 22;6:29671. doi: 10.1038/srep29671.
The integration of near-infrared spectroscopy and electroencephalography measures presents an ideal method to study the haemodynamics of sleep. While the cortical dynamics and neuro-modulating influences affecting the transition from wakefulness to sleep is well researched, the assumption has been that individual slow waves, the hallmark of deep sleep, are spontaneously occurring cortical events. By creating event-related potentials from the NIRS recording, time-locked to the onset of thousands of individual slow waves, we show the onset of slow waves is phase-locked to an ongoing oscillation in the NIRS recording. This oscillation stems from the moment to moment fluctuations of light absorption caused by arterial pulsations driven by the heart beat. The same oscillating signal can be detected if the electrocardiogram is time-locked to the onset of the slow wave. The ongoing NIRS oscillation suggests that individual slow wave initiation is dependent on that signal, and not the other way round. However, the precise causal links remain speculative. We propose several potential mechanisms: that the heart-beat or arterial pulsation acts as a stimulus which evokes a down-state; local fluctuations in energy supply may lead to a network effect of hyperpolarization; that the arterial pulsations lead to corresponding changes in the cerebral-spinal-fluid which evokes the slow wave; or that a third neural generator, regulating heart rate and slow waves may be involved.
近红外光谱和脑电图测量的整合提供了一种研究睡眠血液动力学的理想方法。虽然已经对影响从清醒到睡眠过渡的皮质动力学和神经调节影响进行了深入研究，但假设个体慢波（深度睡眠的标志）是自发发生的皮质事件。通过从 NIRS 记录中创建与数千个个体慢波起始时间锁定的事件相关电位，我们表明慢波的起始与 NIRS 记录中正在进行的振荡锁相。这种振荡源于由心跳驱动的动脉搏动引起的光吸收的瞬间波动。如果心电图与慢波的起始时间锁定，也可以检测到相同的振荡信号。持续的 NIRS 振荡表明个体慢波的起始取决于该信号，而不是相反。然而，确切的因果关系仍在推测之中。我们提出了几种潜在的机制：心跳或动脉搏动作为引发去极化状态的刺激；能量供应的局部波动可能导致超极化的网络效应；动脉搏动导致脑脊液相应变化，从而引发慢波；或者涉及调节心率和慢波的第三个神经发生器。
