Propofol-induced Changes in α-β Sensorimotor Cortical Connectivity.
Propofol-induced Changes in α-β Sensorimotor Cortical Connectivity.
复制标题
丙泊酚诱导的α-β感觉运动皮质连通性的变化。
DOI：
10.1097/aln.0000000000001940
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发表时间：
2018-03
期刊：
影响因子：
8.8
通讯作者：
Pouratian N
中科院分区：
文献类型：
--
作者：
Malekmohammadi M;AuYong N;Price CM;Tsolaki E;Hudson AE;Pouratian N
麻醉剂被认为会改变大脑区域的功能连接。然而，麻醉的网络水平分析，特别是在人类中是稀疏的。我们假设丙泊酚引起的意识丧失导致人类感觉运动皮层功能性断开，而这种断开是意志运动反应丧失的基础。我们记录了接受脑深部电刺激手术的帕金森病（N = 12）和特发性震颤（N = 7）患者在丙泊酚诱导的意识丧失前后感觉运动皮层的局部场电位。局部光谱功率和区域间的连接性（相干性和虚相干性）分别在两个人群的条件下进行了评估。丙泊酚麻醉导致感觉运动皮层2 - 100 Hz之间频率的功率增加，α和β频率的主要频谱峰向较低频率移动（中位± SD峰频率：帕金森病为24.5 ± 2.6 Hz至12.8 ± 2.3 Hz，特发性震颤为13.8 ± 2.1 Hz至12.1 ± 1.0 Hz）。尽管局部功率增加，但两个队列中的感觉运动皮层相干性均受到丙泊酚抑制，特别是帕金森病的β频率（18 - 29 Hz）和特发性震颤的α和β（10 - 48 Hz）。尽管局部谱功率增加，但感觉和运动皮层之间的功能连接性降低，这表明丙泊酚导致皮层功能断开，皮层区域内自主活动增加。这种模式发生在评估的疾病中，表明这些可能是丙泊酚在运动障碍及其他疾病患者中的普遍作用。感觉神经网络中断可能是麻醉诱导的意志控制丧失的基础。
Anesthetics are believed to alter functional connectivity across brain regions. However, network level analyses of anesthesia, particularly in humans are sparse. We hypothesized that propofol-induced loss of consciousness results in functional disconnection of human sensorimotor cortices underlying the loss of volitional motor responses. We recorded local field potentials from sensorimotor cortices in patients with Parkinson disease (N =12) and essential tremor (N =7) undergoing deep brain stimulation surgery, before and after propofol-induced loss of consciousness. Local spectral power and inter-regional connectivity (coherence and imaginary coherence) were evaluated across conditions for the two populations separately. Propofol anesthesia caused power increase for frequencies between 2–100 Hz across the sensorimotor cortices and a shift of the dominant spectral peak in α and β frequencies toward lower frequencies (Median ±SD peak frequency: 24.5 ±2.6 Hz to 12.8 ±2.3 Hz in Parkinson disease and 13.8 ±2.1 Hz to 12.1 ±1.0 Hz in essential tremor). Despite local increases in power, sensorimotor cortical coherence was suppressed with propofol in both cohorts, specifically in β frequencies (18–29 Hz) for Parkinson disease and α and β (10–48 Hz) in essential tremor. The decrease in functional connectivity between sensory and motor cortices despite an increase in local spectral power suggests propofol causes a functional disconnection of cortices with increases in autonomous activity within cortical regions. This pattern occurs across diseases evaluated, suggesting these may be generalizable effects of propofol in patients with movement disorders and beyond. Sensoriomotor network disruption may underlie anesthetic-induced loss of volitional control.