Hosobuchi Y
Acta Neurochir Suppl (Wien). 1980;30:219-27. doi: 10.1007/978-3-7091-8592-6_27.
This paper reviews the author's nine years of experience in analgesic brain stimulation. During this time, of 22 patients with pain of peripheral origin who were treated with periaqueductal gray (PAG), stimulation 16 achieved successful control of pain. Of 40 patients who presented with deafferentation pain, 16 were able to control their dysesthesia by brain stimulation of the subcortical somatosensory region alone; follow-up was over a long period. The mechanism of deafferentation pain is poorly understood and the effectiveness of subcortical somatosensory electrical stimulation to relieve such pain is based on empirical observation. The analgesia produced by PAG stimulation appears to be mediated by the release of beta-endorphin from the anterior hypothalamus. The released beta-endorphin binds to the opiate receptors in the PAG and activates the descending pain-inhibitory pathway. However, the repetitive stimulation of this serotonergic system produces tolerance to its analgesic effect, due to a decreased rate of serotonin turnover. Loading of the serotonin precursor by dietary supplementation of the essential amino acid L-tryptophan reverses this tolerance.
本文回顾了作者在镇痛性脑刺激方面九年的经验。在此期间,22例外周性疼痛患者接受了中脑导水管周围灰质(PAG)刺激治疗,其中16例疼痛得到成功控制。40例传入神经阻滞性疼痛患者中,16例仅通过刺激皮质下体感区就能控制感觉异常;随访时间很长。传入神经阻滞性疼痛的机制尚不清楚,皮质下体感电刺激缓解此类疼痛的有效性是基于经验观察。PAG刺激产生的镇痛作用似乎是由下丘脑前部释放β-内啡肽介导的。释放的β-内啡肽与PAG中的阿片受体结合,激活下行性疼痛抑制通路。然而,由于血清素周转率降低,对该5-羟色胺能系统的重复刺激会产生对其镇痛作用的耐受性。通过饮食补充必需氨基酸L-色氨酸来加载血清素前体可逆转这种耐受性。