Kochs E, Scharein E, Möllenberg O, Bromm B, Schulte am Esch J
Department of Anesthesiology, Klinikum rechts der Isar, Technische Universität München, Germany.
Anesthesiology. 1996 Aug;85(2):304-14. doi: 10.1097/00000542-199608000-00012.
Low-dose ketamine has been shown to exert analgesic effects. Whether ketamine-induced pain relief may be quantitated by somatosensory evoked cerebral potentials has not been established.
Thirty healthy volunteers were assigned randomly to one of three groups. Subjects of group 1 (n = 10, control) were given saline as placebo. In groups 2 (n = 10) and 3 (n = 10), intravenous ketamine (0.25 mg. kg-1 and 0.50 mg. kg-1, respectively) was administered. The following variables were recorded at baseline and for 50 min after drug administration: electroencephalographic (EEG) data, somatosensory-evoked late cortical responses (SEP) elicited by intracutaneous stimulation of the fingertip (2-3 fold pain threshold), heart rate, mean arterial blood pressure, and end-tidal PETCO2 via a tight-fitting mask. Electroencephalographic spectral power in selected frequency bands and frequency percentiles were calculated from the spontaneous EEG segment preceding each somatosensory stimulus. Somatosensory-evoked late cortical response parameters were calculated from the respective poststimulus EEG segments. After recording of each EEG response, subjects were asked to rate the individual pain sensation.
In group 1, all variables did not change over time. Ketamine administration resulted in dose-dependent decreases in alpha-activity and increases in theta power (group 2: 190%, group 3: 440%). Electroencephalographic changes were not related to changes in pain perception. For the first 30 min after ketamine injection, a dose-dependent decrease of the long-latency N150-P250 somatosensory-evoked late cortical response component was observed (group 2: 15-20%; group 3: 25-30%). Subjective pain ratings were also different between groups, with a higher degree of pain relief in group 3 for the first 30 min. At the end of the observation period, pain relief and the N150-P250 amplitude were comparable in both ketamine groups.
These data indicate that pain relief induced by low-dose ketamine is dose-dependent for the first 30 min after bolus injection. Changes in pain perception may be quantitated by somatosensory-evoked cortical responses. Also, EEG changes are not specific for changes in nociception, but the increase in theta power may reflect the hypnotic effect of low-dose ketamine.
低剂量氯胺酮已被证明具有镇痛作用。氯胺酮诱导的疼痛缓解是否可以通过体感诱发电位来量化尚未确定。
30名健康志愿者被随机分配到三组中的一组。第1组（n = 10，对照组）给予生理盐水作为安慰剂。第2组（n = 10）和第3组（n = 10）分别静脉注射氯胺酮（0.25 mg·kg-1和0.50 mg·kg-1）。在基线和给药后50分钟记录以下变量：脑电图（EEG）数据、通过皮内刺激指尖（2 - 3倍疼痛阈值）诱发的体感诱发电位晚期皮层反应（SEP）、心率、平均动脉血压以及通过紧密贴合面罩测得的呼气末二氧化碳分压（PETCO2）。从每个体感刺激之前的自发脑电图段计算选定频段和频率百分位数的脑电图频谱功率。从各自的刺激后脑电图段计算体感诱发电位晚期皮层反应参数。在记录每个脑电图反应后，要求受试者对个体疼痛感觉进行评分。
在第1组中，所有变量随时间均无变化。氯胺酮给药导致α活动剂量依赖性降低，θ功率增加（第2组：190%，第3组：440%）。脑电图变化与疼痛感知变化无关。在氯胺酮注射后的前30分钟，观察到长潜伏期N150 - P250体感诱发电位晚期皮层反应成分剂量依赖性降低（第2组：15 - 20%；第3组：25 - 30%）。各组之间主观疼痛评分也不同，第3组在前30分钟疼痛缓解程度更高。在观察期结束时，两个氯胺酮组的疼痛缓解和N150 - P250波幅相当。
这些数据表明，静脉推注后最初30分钟内，低剂量氯胺酮诱导的疼痛缓解呈剂量依赖性。疼痛感知的变化可以通过体感诱发电位皮层反应来量化。此外，并脑电图变化并非伤害感受变化所特有，但θ功率增加可能反映了低剂量氯胺酮的催眠作用。
