Danziger Nicolas, Fournier Emmanuel, Bouhassira Didier, Michaud Didier, De Broucker Thomas, Santarcangelo Erica, Carli Giancarlo, Chertock Léon, Willer Jean Claude
Laboratoire de Neurophysiologie, Faculté de Médecine, Pitié-Salpêtrière, 91, Bd. de l'Hôpital, 75013 Paris, France Institut d'Hypnose Larochefoucault, Siena, Italy Laboratoire de Physiologie Humaine, Siena, Italy.
Pain. 1998 Mar;75(1):85-92. doi: 10.1016/S0304-3959(97)00208-X.
Nociceptive electrical stimuli were applied to the sural nerve during hypnotically-suggested analgesia in the left lower limb of 18 highly susceptible subjects. During this procedure, the verbally reported pain threshold, the nociceptive flexion (RIII) reflex and late somatosensory evoked potentials were investigated in parallel with autonomic responses and the spontaneous electroencephalogram (EEG). The hypnotic suggestion of analgesia induced a significant increase in pain threshold in all the selected subjects. All the subjects showed large changes (i.e., by 20% or more) in the amplitudes of their RIII reflexes during hypnotic analgesia by comparison with control conditions. Although the extent of the increase in pain threshold was similar in all the subjects, two distinct patterns of modulation of the RIII reflex were observed during the hypnotic analgesia: in 11 subjects (subgroup 1), a strong inhibition of the reflex was observed whereas in the other seven subjects (subgroup 2) there was a strong facilitation of the reflex. All the subjects in both subgroups displayed similar decreases in the amplitude of late somatosensory evoked cerebral potentials during the hypnotic analgesia. No modification in the autonomic parameters or the EEG was observed. These data suggest that different strategies of modulation can be operative during effective hypnotic analgesia and that these are subject-dependent. Although all subjects may shift their attention away from the painful stimulus (which could explain the decrease of the late somatosensory evoked potentials), some of them inhibit their motor reaction to the stimulus at the spinal level, while in others, in contrast, this reaction is facilitated.
在18名高度敏感受试者的左下肢进行催眠暗示镇痛期间，对腓肠神经施加伤害性电刺激。在此过程中，同时研究了口头报告的疼痛阈值、伤害性屈曲（RIII）反射和晚期体感诱发电位，并与自主反应和自发脑电图（EEG）进行了对比。镇痛的催眠暗示使所有选定受试者的疼痛阈值显著提高。与对照条件相比，所有受试者在催眠镇痛期间的RIII反射幅度均出现了大幅变化（即变化20%或更多）。尽管所有受试者的疼痛阈值升高程度相似，但在催眠镇痛期间观察到了两种不同的RIII反射调节模式：11名受试者（第1亚组）表现出反射的强烈抑制，而其他7名受试者（第2亚组）则表现出反射的强烈易化。两个亚组中的所有受试者在催眠镇痛期间晚期体感诱发脑电位的幅度均出现了类似程度的下降。未观察到自主参数或脑电图的改变。这些数据表明，在有效的催眠镇痛过程中可能存在不同的调节策略，且这些策略因个体而异。尽管所有受试者可能会将注意力从疼痛刺激上转移开（这可以解释晚期体感诱发电位的下降），但其中一些人在脊髓水平抑制了对刺激的运动反应，而另一些人则相反，这种反应得到了促进。
