A comparison of propofol- and dexmedetomidine-induced electroencephalogram dynamics using spectral and coherence analysis.
A comparison of propofol- and dexmedetomidine-induced electroencephalogram dynamics using spectral and coherence analysis.
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DOI：
10.1097/aln.0000000000000419
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发表时间：
2014-11
期刊：
影响因子：
8.8
通讯作者：
Purdon PL
中科院分区：
文献类型：
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作者：
Akeju O;Pavone KJ;Westover MB;Vazquez R;Prerau MJ;Harrell PG;Hartnack KE;Rhee J;Sampson AL;Habeeb K;Gao L;Pierce ET;Walsh JL;Brown EN;Purdon PL
在右美托咪定镇静期间观察到的脑电模式与异丙酚全麻时观察到的脑电模式相似。这一点在慢(0.1-1赫兹)、德尔塔(1-4赫兹)、异丙酚诱导的阿尔法(8-12赫兹)和右美托咪定诱导的纺锤波(12-16赫兹)的振荡中表现得很明显。然而，这些药物具有不同的分子机制和行为特性，并可能伴随着区分神经回路的动力学。我们测量了18-36岁健康志愿者在右旋美托咪定(n=9)和异丙酚(n=8)作用下的通道脑电。我们在10分钟内以1mcg/kg的负荷量给予右美托咪定，然后以0.7mcg/kg/小时输注。对于异丙酚，我们使用计算机控制输注来靶向效应点浓度，从0微克/毫升到5微克/毫升。志愿者听听觉刺激，并通过按下按钮来做出反应，以确定无意识。我们用多锥谱和相干分析对脑电进行了分析。右美托咪定的特征是纺锤波在~13 Hz处具有最大的功率和相干(平均±标准差；功率，−10.8dB±3.6；相干，0.8±0.08)，而异丙酚的特征是额部α振荡，峰值频率在~11 Hz(功率，1.1dB±4.5；相干，0.9±0.05)。值得注意的是，异丙酚麻醉状态下的慢振荡功率(功率，13.2dB±2.4)明显大于镇静状态下的慢振荡功率(功率，−，2.5分贝±3.5)和右美托咪定(功率，−，0.4分贝±3.1)。我们的结果表明，右旋美托咪定和异丙酚将患者置于不同的大脑状态，并表明异丙酚通过诱导大幅度的缓慢振荡而使患者进入更深层次的无意识状态，从而导致神经元长时间沉默。
Electroencephalogram patterns observed during sedation with dexmedetomidine appear similar to those observed during general anesthesia with propofol. This is evident with the occurrence of slow (0.1–1 Hz), delta (1–4 Hz), propofol-induced alpha (8–12 Hz), and dexmedetomidine-induced spindle (12–16 Hz) oscillations. However, these drugs have different molecular mechanisms and behavioral properties, and are likely accompanied by distinguishing neural circuit dynamics. We measured 64-channel electroencephalogram under dexmedetomidine (n = 9) and propofol (n = 8) in healthy volunteers, 18–36 years of age. We administered dexmedetomidine with a 1mcg/kg loading bolus over 10 minutes, followed by a 0.7mcg/kg/hr infusion. For propofol, we used a computer controlled infusion to target the effect-site concentration gradually from and 0 µg/mL to 5 µg/mL. Volunteers listened to auditory stimuli and responded by button-press to determine unconsciousness. We analyzed the electroencephalogram using multitaper spectral and coherence analysis. Dexmedetomidine was characterized by spindles with maximum power and coherence at ~13 Hz, (mean±std; power, −10.8dB±3.6; coherence, 0.8±0.08), while propofol was characterized with frontal alpha oscillations with peak frequency at ~11 Hz (power, 1.1dB±4.5; coherence, 0.9±0.05). Notably, slow oscillation power during a general anesthetic state under propofol (power, 13.2dB±2.4) was much larger than during sedative states under both propofol (power, −2.5dB±3.5) and dexmedetomidine (power, −0.4dB±3.1). Our results indicate that dexmedetomidine and propofol place patients into different brain states, and suggests that propofol enables a deeper state of unconsciousness by inducing large amplitude slow oscillations that produce prolonged states of neuronal silence.