Tsubokawa T, Katayama Y, Yamamoto T, Hirayama T, Koyama S
Department of Neurological Surgery, Nihon University School of Medicine, Tokyo, Japan.
J Neurosurg. 1993 Mar;78(3):393-401. doi: 10.3171/jns.1993.78.3.0393.
Analysis of the authors' experience over the last 10 years has indicated that excellent pain control has rarely been obtained by thalamic relay nucleus stimulation in patients with thalamic pain. In the present study, 11 patients with thalamic pain were treated by chronic stimulation of the precentral gyrus. In eight patients (73%), the stimulation system was internalized since excellent pain control was achieved during a 1-week test period of precentral gyrus stimulation. In contrast, no clear effect was noted or the original pain was even exacerbated by postcentral gyrus stimulation. The effect of precentral stimulation was unchanged in five patients (45%) for follow-up periods of more than 2 years. In the remaining three patients, the effect decreased gradually over several months. This outcome was significantly better than that obtained in an earlier series tested by the authors with thalamic relay nucleus stimulation (p < 0.05). The pain inhibition usually occurred at intensities below the threshold for production of muscle contraction (pulse duration 0.1 to 0.5 msec, intensity 3 to 8 V). When good pain inhibition was achieved, the patients reported a slight tingling or mild vibration sensation during stimulation projected in the same area of distribution as their pain. The authors discuss the possibility that, in deafferentation pain, sensory neurons below the level of deafferentation cannot exert their normal inhibitory influences toward deafferented nociceptive neurons because of the development of aberrant connections. Thus, while stimulation of the first- to third-order sensory neurons at the level of the thalamic relay nucleus or below cannot bring about good pain inhibition in patients with thalamic pain, activation of hypothetical fourth-order sensory neurons through precentral stimulation may be able to inhibit deafferented nociceptive neurons within the cortex. None of the patients developed either observable or electroencephalographic seizure activity.
对作者过去10年经验的分析表明，丘脑痛患者通过丘脑中继核刺激很少能获得良好的疼痛控制。在本研究中，11例丘脑痛患者接受了中央前回慢性刺激治疗。8例患者（73%）植入了刺激系统，因为在中央前回刺激的1周测试期内实现了良好的疼痛控制。相比之下，中央后回刺激未观察到明显效果，甚至原有疼痛加剧。5例患者（45%）在超过2年的随访期内中央前回刺激效果未变。其余3例患者，效果在几个月内逐渐下降。这一结果明显优于作者早期用丘脑中继核刺激测试的系列研究结果（p<0.05）。疼痛抑制通常发生在低于肌肉收缩阈值的强度时（脉冲持续时间0.1至0.5毫秒，强度3至8伏）。当实现良好的疼痛抑制时，患者在刺激期间报告在与疼痛相同的分布区域有轻微刺痛或轻度振动感。作者讨论了在去传入性疼痛中，由于异常连接的发展，低于去传入水平的感觉神经元无法对去传入的伤害性神经元施加正常抑制影响的可能性。因此，虽然在丘脑中继核或更低水平刺激第一至三级感觉神经元不能在丘脑痛患者中产生良好的疼痛抑制，但通过中央前回刺激激活假设的第四级感觉神经元可能能够抑制皮质内的去传入伤害性神经元。所有患者均未出现可观察到的或脑电图癫痫活动。
