【罂粟摘要】硬膜外应用罗哌卡因降低经颅电刺激运动诱发电位的振幅:一项双盲、随机、对照试验
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贵州医科大学 高鸿教授课题组
翻译：潘志军 修改/编辑：佟睿 审校：曹莹
硬膜外局部麻醉药主要作用于硬膜外神经根，并可通过硬脊膜直接作用于脊髓。我们假设硬膜外给予罗哌卡因会通过阻断脊髓神经传导来降低经颅电刺激运动诱发电位的振幅。因此，我们进行了一项双盲、随机、对照试验。
根据罗哌卡因硬膜外使用浓度将30名接受肺部手术的成年患者随机分为3组：0.2%组、0.375%组和0.75%组。盲法的实施为：主治麻醉医生、负责神经生理学监测的医生和患者均不知道相应分组。T5–6或T6–7间隙旁正中入路置入硬膜外导管，用生理盐水阻力消失法来确定硬膜外间隙。使用丙泊酚和瑞芬太尼诱导并维持全身麻醉。在胫骨前肌记录经颅电刺激运动诱发电位，恒定电压刺激器以2ms的时间间隔通过5个脉冲序列激发。在腘窝处通过胫神经电刺激记录体感诱发电位(SSEPs)。测量两种诱发电位基线值后，硬膜外腔分别注射0.2%、0.375%或0.75%罗哌卡因10ml。将在给予罗哌卡因之前记录的基线振幅和潜伏期设定为100%。我们主要目的是监测硬膜外给予不同浓度罗哌卡因60分钟后运动诱发电位的相对振幅。研究使用Kruskal-Wallis测试分析了这些诱发电位的振幅和潜伏期，并使用Dunn多重比较测试作为统计分析的事后检验。
数据以中位数(四分位间距)表示。硬膜外注射罗哌卡因60分钟后，0.75%组(7%[3%–18%]，组间差异P <0 .001)和0.375%组(52%[43%–59%])的运动诱发电位振幅低于0.2%组(96%[89%–105%])。与0.2%组相比，0.75%组的SSEP潜伏期更长，但振幅不受影响。
与低剂量组相比，硬膜外给予高浓度罗哌卡因降低了运动诱发电位的振幅，延长了运动诱发电位和SSEPs的发作潜伏期。高浓度罗哌卡因可通过硬脑膜作用于运动通路。
Kenta Furutani, Toshiyuki Tobita, Hideaki Ishii, et al. Epidural Administration of Ropivacaine Reduces the Amplitude of Transcranial Electrical Motor–Evoked Potentials: A Double-Blinded, Randomized, Controlled Trial.[J]. (Anesth Analg 2021 04 01;132(4)).
Epidural Administration of Ropivacaine Reduces the Amplitude of Transcranial Electrical Motor–Evoked Potentials: A Double-Blinded, Randomized, Controlled Trial
ABSTRACT
Background: An epidurally administered local anesthetic acts primarily on the epidural nerve roots and can act directly on the spinal cord through the dural sleeve. We hypothesized that epidurally administered ropivacaine would reduce the amplitude of transcranial electrical motor-evoked potentials by blocking nerve conduction in the spinal cord. Therefore, we conducted a double-blind, randomized, controlled trial.
Methods: Thirty adult patients who underwent lung surgery were randomly allocated to 1 of 3 groups, based on the ropivacaine concentration: the 0.2% group, the 0.375% group, and the 0.75% group. The attending anesthesiologists, neurophysiologists, and patients were blinded to the allocation. The epidural catheter was inserted at the T5–6 or T6–7 interspace by a paramedian approach, using the loss of resistance technique with normal saline. General anesthesia was induced and maintained using propofol and remifentanil. Transcranial electrical motor-evoked potentials were elicited by a train of 5 pulses with an interstimulus interval of 2 milliseconds by using a constant-voltage stimulator and were recorded from the tibialis anterior muscle. Somatosensory-evoked potentials (SSEPs) were evoked by electrical tibial nerve stimulation at the popliteal fossa. After measuring the baseline values of these evoked potentials, 10 mL of epidural ropivacaine was administered at the 0.2%, 0.375%, or 0.75% concentration. The baseline amplitudes and latencies recorded before administering ropivacaine were defined as 100%. Our primary end point was the relative amplitude of the motor-evoked potentials at 60 minutes after the epidural administration of ropivacaine. We analyzed the amplitudes and latencies of these evoked potentials by using the Kruskal-Wallis test and used the Dunn multiple comparison test as the post hoc test for statistical analysis.
Results: The data are expressed as the median (interquartile range). Sixty minutes after epidurally administering ropivacaine, the motor-evoked potential amplitude was lower in the 0.75% group (7% [3%–18%], between-group difference P < 0.001) and in the 0.375% group (52% [43%–59%]) compared to that in the 0.2% group (96% [89%–105%]). The latency of SSEP was longer in the 0.75% group compared to that in the 0.2% group, but the amplitude was unaffected.
Conclusions: Epidurally administered high-dose ropivacaine lowered the amplitude of motor-evoked potentials and prolonged the onset latencies of motor-evoked potentials and SSEPs compared to those in the low-dose group. High-dose ropivacaine can act on the motor pathway through the dura mater .
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