Tsubokawa Takashi, Yamamoto Takamitsu, Katayama Yoichi, Hirayama Teruyasu, Sibuya Haruo
Department of Neurological Surgery, Nihon University, Tokyo, Japan National Center for Nervous, Mental and Muscular Disorders, Tokyo, Japan.
Pain. 1984 Feb;18(2):115-126. doi: 10.1016/0304-3959(84)90879-0.
Deep brain stimulation (thalamic relay nucleus, periaqueductal gray and internal capsule) was applied to various cases of intractable pain, and the resulting degree of pain reduction and alteration in beta-endorphin immunoreactivity in the cerebrospinal fluid (CSF) were compared. The following results were obtained. (1) The studies on intractable pain revealed that the levels of beta-endorphin immunoreactivity in the CSF were lower than those in the control group. (2) Thalamic relay nucleus stimulation proved effective not only for deafferentiation pain, but also for somatogenic pain. No relationship was, however, noted between pain reduction and the rate of increase of beta-endorphin immunoreactivity in the CSF. (3) The incidence of stimulation tolerance following prolonged stimulation of the thalamic relay nucleus can be reduced to a minimum by administration of L-DOPA. It is concluded that the increase in beta-endorphin in the CSF is not the direct and major cause of pain reduction during treatment by thalamic relay nucleus stimulation. It may be assumed that neuronal facilitation on the monoaminergic descending pain inhibitory system plays a role in reducing pain.
对各种顽固性疼痛病例进行了深部脑刺激（丘脑中继核、导水管周围灰质和内囊），并比较了由此产生的疼痛减轻程度以及脑脊液（CSF）中β-内啡肽免疫反应性的变化。得到了以下结果。（1）对顽固性疼痛的研究表明，脑脊液中β-内啡肽免疫反应性水平低于对照组。（2）丘脑中继核刺激不仅对去传入性疼痛有效，对躯体性疼痛也有效。然而，疼痛减轻与脑脊液中β-内啡肽免疫反应性的增加率之间没有关系。（3）通过给予左旋多巴，长期刺激丘脑中继核后刺激耐受性的发生率可降至最低。得出的结论是，脑脊液中β-内啡肽的增加不是丘脑中继核刺激治疗期间疼痛减轻的直接和主要原因。可以假定单胺能下行疼痛抑制系统上的神经元易化在减轻疼痛中起作用。
