García-Larrea L, Peyron R, Mertens P, Gregoire M C, Lavenne F, Le Bars D, Convers P, Mauguière F, Sindou M, Laurent B
Functional Neurology Unit, UPRES-EA 1880, Claude Bernard University, and Institut Fédératif de Neurosciences of Lyon (IFNL), Lyon, France.
Pain. 1999 Nov;83(2):259-73. doi: 10.1016/s0304-3959(99)00114-1.
Although electrical stimulation of the precentral gyrus (MCS) is emerging as a promising technique for pain control, its mechanisms of action remain obscure, and its application largely empirical. Using positron emission tomography (PET) we studied regional changes in cerebral flood flow (rCBF) in 10 patients undergoing motor cortex stimulation for pain control, seven of whom also underwent somatosensory evoked potentials and nociceptive spinal reflex recordings. The most significant MCS-related increase in rCBF concerned the ventral-lateral thalamus, probably reflecting cortico-thalamic connections from motor areas. CBF increases were also observed in medial thalamus, anterior cingulate/orbitofrontal cortex, anterior insula and upper brainstem; conversely, no significant CBF changes appeared in motor areas beneath the stimulating electrode. Somatosensory evoked potentials from SI remained stable during MCS, and no rCBF changes were observed in somatosensory cortex during the procedure. Our results suggest that descending axons, rather than apical dendrites, are primarily activated by MCS, and highlight the thalamus as the key structure mediating functional MCS effects. A model of MCS action is proposed, whereby activation of thalamic nuclei directly connected with motor and premotor cortices would entail a cascade of synaptic events in pain-related structures receiving afferents from these nuclei, including the medial thalamus, anterior cingulate and upper brainstem. MCS could influence the affective-emotional component of chronic pain by way of cingulate/orbitofrontal activation, and lead to descending inhibition of pain impulses by activation of the brainstem, also suggested by attenuation of spinal flexion reflexes. In contrast, the hypothesis of somatosensory cortex activation by MCS could not be confirmed by our results.
尽管对中央前回(运动皮层刺激)进行电刺激正成为一种很有前景的疼痛控制技术,但其作用机制仍不清楚,应用也大多基于经验。我们使用正电子发射断层扫描(PET)研究了10例接受运动皮层刺激以控制疼痛的患者的脑血流区域变化(rCBF),其中7例还进行了体感诱发电位和伤害性脊髓反射记录。与运动皮层刺激最相关的rCBF显著增加涉及腹外侧丘脑,这可能反映了来自运动区域的皮质-丘脑连接。在内侧丘脑、前扣带回/眶额皮质、前岛叶和脑桥上段也观察到CBF增加;相反,在刺激电极下方的运动区域未出现明显的CBF变化。在运动皮层刺激期间,来自初级体感皮层(SI)的体感诱发电位保持稳定,在此过程中体感皮层未观察到rCBF变化。我们的结果表明,运动皮层刺激主要激活的是下行轴突,而非顶端树突,并突出了丘脑作为介导运动皮层刺激功能效应的关键结构。我们提出了一个运动皮层刺激作用模型,即与运动和运动前皮层直接相连的丘脑核团的激活将在接受来自这些核团传入的疼痛相关结构中引发一系列突触事件,这些结构包括内侧丘脑、前扣带回和脑桥上段。运动皮层刺激可能通过激活扣带回/眶额皮质来影响慢性疼痛的情感-情绪成分,并通过激活脑干导致疼痛冲动的下行抑制,脊髓屈曲反射的减弱也表明了这一点。相比之下,我们的结果无法证实运动皮层刺激激活体感皮层的假说。