Lorenz J, Beck H, Bromm B
Institute of Physiology, University Hospital Eppendorf, Hamburg, Germany.
Electroencephalogr Clin Neurophysiol. 1997 Nov;104(6):514-21. doi: 10.1016/s0168-5597(97)00064-6.
The present study investigates the differential behavior of laser evoked brain potentials (LEPs), late auditory evoked potentials (AEP) and the endogenous P300 in response to morphine treatment, examined in 6 chronic pain patients. The main result was that in parallel with marked clinical pain relief, amplitudes of the long latency LEP positivity (P400) were significantly reduced under morphine. One patient suffering from extremely painful osteoporosis for 20 years exhibited a large middle latency component (N170) which was prominently attenuated by morphine. In contrast to LEP amplitude reductions, auditory N1 and P2 potentials appeared either unchanged or even enlarged during morphine treatment. Also P300 amplitude was slightly increased under morphine. Reaction time and mood scales also failed to indicate any sedation. Obviously, LEPs reflected specifically the analgesic morphine effect in this study, while stability or enhancement of AEPs and P300 during morphine treatment indicated lack of sedation or even improved perception and concentration due to the removal of persistent pain as a disruptive perceptual-cognitive stressor.
本研究调查了6例慢性疼痛患者在接受吗啡治疗时，激光诱发脑电位（LEP）、晚期听觉诱发电位（AEP）和内源性P300的差异行为。主要结果是，随着临床疼痛显著缓解，吗啡作用下长潜伏期LEP阳性波（P400）的波幅显著降低。一名患有极度疼痛的骨质疏松症20年的患者表现出一个大的中潜伏期成分（N170），吗啡使其明显减弱。与LEP波幅降低相反，在吗啡治疗期间，听觉N1和P2电位要么未改变，甚至增大。吗啡作用下P300波幅也略有增加。反应时间和情绪量表也未显示任何镇静作用。显然，在本研究中LEP特别反映了吗啡的镇痛作用，而吗啡治疗期间AEP和P300的稳定性或增强表明没有镇静作用，甚至由于消除了作为干扰性感知-认知应激源的持续性疼痛，感知和注意力得到改善。
