Ries C R, Scoates P J, Puil E
Department of Anaesthesia, University of British Columbia, Vancouver.
Can J Anaesth. 1994 May;41(5 Pt 1):414-9. doi: 10.1007/BF03009864.
In this report of opisthotonos during recovery from propofol anaesthesia, we relate clinical observations with scientific considerations, and propose a strategy for treatment of this rare side effect. Following a brief operative procedure, a healthy 29-yr-old woman developed recurrent opisthotonos while recovering from anaesthesia with alfentanil, propofol, and nitrous oxide. In contrast to accumulating reports, the patient remained conscious during each episode of back extension and retrocollis. The preservation of consciousness and similarities to strychnine-induced opisthotonos suggest to us that the mechanism may have a brainstem and spinal origin. Recent investigations show that propofol potentiates the inhibitory transmitters glycine and gamma-aminobutyric acid (GABA) which would enhance spinal inhibition during anaesthesia. Postanaesthetic opisthotonos, however, may be due to a propofol-induced tolerance to inhibitory transmitters. This rebound phenomenon would lead to an acute, enduring refractoriness in inhibitory pathways of the brainstem and spinal cord, resulting in increased activity of extensor motoneurons. We recommend a therapeutic strategy that restores inhibition by glycine and GABA at multiple sites; the preferred therapeutic agents would be diazepam and physostigmine. The episodes are usually short-lived, but two of the reviewed 17 patients developed recurrent retrocollis for four and 23 days following antiepileptic drug therapy. Since high doses of phenytoin and carbamazepine can result in opisthotonos, we recommend that anticonvulsants be reserved for postanaesthetic patients with electroencephalographic evidence of seizure activity.
在这份关于丙泊酚麻醉恢复过程中出现角弓反张的报告中,我们将临床观察与科学考量相结合,并提出了针对这种罕见副作用的治疗策略。在一次简短的手术操作后,一名29岁的健康女性在从阿芬太尼、丙泊酚和氧化亚氮麻醉中恢复时出现了反复的角弓反张。与越来越多的报告不同,该患者在每次背部伸展和头后仰发作期间仍保持清醒。意识的保留以及与士的宁诱导的角弓反张的相似性向我们表明,其机制可能起源于脑干和脊髓。最近的研究表明,丙泊酚可增强抑制性递质甘氨酸和γ-氨基丁酸(GABA),这会在麻醉期间增强脊髓抑制作用。然而,麻醉后角弓反张可能是由于丙泊酚诱导的对抑制性递质的耐受性。这种反弹现象会导致脑干和脊髓抑制通路出现急性、持久的不应性,从而导致伸肌运动神经元活动增加。我们推荐一种在多个部位恢复甘氨酸和GABA抑制作用的治疗策略;首选的治疗药物是地西泮和毒扁豆碱。这些发作通常持续时间较短,但在17例接受审查的患者中,有2例在抗癫痫药物治疗后出现了持续4天和23天的反复头后仰。由于高剂量的苯妥英钠和卡马西平可导致角弓反张,我们建议仅在有脑电图癫痫活动证据的麻醉后患者中使用抗惊厥药物。