Kochs E, Treede R D, Schulte am Esch J
Anaesthesist. 1986 Jun;35(6):359-64.
In 43 patients the time-dependent behaviour of somatosensory evoked potentials (SSEP) before and during induction of anesthesia with 0.3 mg/kg etomidate was studied. The SSEP components could be reliably recorded in one-minute intervals and the modulations of SSEP (early and middle latencies) following bolus injection with its pharmacokinetically non-stationary states could be quantified. The central conduction time (CCT) between the cervical N13- and the cortical N20-component was less prolonged (from 5.6 ms to 6.4 ms) than known from other anesthetics. Middle latency SSEP exhibited a more marked increase and were reduced in amplitude. All patients showed a 2- to 12-fold increase of the primary complex N20/P25 2-3 min after bolus injection. This amplification cannot be explained either by muscle artifacts nor exclusively by activation of muscle afferents. Myoclonia as a side effect of etomidate coincide with the increase of SSEP-components. The combination of myoclonia and SSEP-enhancement is known to be associated with the familial progressive myoclonus epilepsy. This observation therefore may indicate a cortical excitatory or disinhibitory effect, although no spike-wave complexes have been reported in the EEG after etomidate.
在43例患者中，研究了0.3mg/kg依托咪酯麻醉诱导前及诱导过程中体感诱发电位（SSEP）的时间依赖性变化。SSEP各成分能够以1分钟的间隔可靠记录，推注依托咪酯后，其药代动力学不稳定状态下SSEP（早、中潜伏期）的调制变化能够被量化。颈段N13成分与皮层N20成分之间的中枢传导时间（CCT）延长程度（从5.6ms至6.4ms）比其他麻醉药小。中潜伏期SSEP升高更为明显，波幅降低。所有患者在推注后2至3分钟时，主复合波N20/P25增大2至12倍。这种放大既不能用肌肉伪迹解释，也不能完全用肌肉传入神经激活来解释。依托咪酯的副作用肌阵挛与SSEP成分增加同时出现。肌阵挛与SSEP增强的组合已知与家族性进行性肌阵挛癫痫有关。因此，这一观察结果可能提示存在皮层兴奋或去抑制作用，尽管依托咪酯注射后脑电图中未报告棘波-慢波复合波。
