Neurology and Neurophysiology Unit, Neuroscience Department, Azienda Ospedaliera Universitaria Integrata, Verona, Italy.
Department of Neurological, Neuropsychological, Morphological and Motor Sciences, University of Verona, Verona, Italy.
Eur J Pain. 2021 Mar;25(3):550-557. doi: 10.1002/ejp.1693. Epub 2020 Nov 28.
The 'pain-inhibits-pain' effect stems from neurophysiological mechanisms involving endogenous modulatory systems termed diffuse noxious inhibitory controls (DNIC) or conditioned pain modulation (CPM). Laser-evoked potentials (LEPs) components, the N2/P2 complex, and the N1 wave, reflect the medial and lateral pain pathway, respectively: anatomically, the lateral thalamic nuclei (LT) project mainly to the somatosensory cortex (N1 generator), while the medial thalamic nuclei (MT) are bound to the limbic cortices (N2/P2 generators).
We applied a CPM protocol in which the test stimulus was laser stimulation and the conditioning stimulus was a cold pressor test. LEPs recordings were obtained from 15 healthy subjects in three different conditions: baseline, during heterotopic noxious conditioning stimulation (HNCS) and post-HNCS.
We observed a significant reduction in N2/P2 amplitude during HNCS and a return to pre-test amplitude post-HNCS, whereas the N1 wave remained unchanged during and post-HNCS.
Our results indicate that CPM affects only the medial pain system. The spinothalamic tract (STT) transmits to both the LT and the MT, while the spinoreticulothalamic (SRT) projects only to the MT. The reduction in the amplitude of the N2/P2 complex and the absence of change in the N1 wave suggest that DNIC inhibition on the dorsal horn neurons affects only pain transmission via the SRT, while the neurons that give rise to the STT are not involved. The N1 wave can be a reliable neurophysiological parameter for assessment of STT function in clinical practice, as it does not seem to be influenced by CPM.
No reports have described the effect of DNIC on lateral and medial pain pathways. We studied the N1 wave and the N2/P2 complex to detect changes during a CPM protocol. We found a reduction in the amplitude of the N2/P2 complex and no change in the N1 wave. This suggests that the DNIC inhibitory effect on dorsal horns neurons affects only pain transmission via the SRT, whereas the neurons that give rise to the STT are not involved.
“疼痛抑制疼痛”效应源自涉及内源性调节系统的神经生理机制，这些系统被称为弥散性伤害性抑制控制（DNIC）或条件性疼痛调制（CPM）。激光诱发电位（LEP）的成分，N2/P2 复合体和 N1 波，分别反映了内侧和外侧疼痛通路：解剖学上，外侧丘脑核（LT）主要投射到体感皮层（N1 发生器），而内侧丘脑核（MT）与边缘皮质有关（N2/P2 发生器）。
我们应用了 CPM 方案，其中测试刺激是激光刺激，条件刺激是冷压测试。在三种不同的条件下，从 15 名健康受试者中获得了 LEP 记录：基线、异源性伤害性条件刺激（HNCS）期间和 HNCS 后。
我们观察到 HNCS 期间 N2/P2 幅度显著降低，HNCS 后恢复到测试前幅度，而 N1 波在 HNCS 期间和之后保持不变。
我们的结果表明，CPM 仅影响内侧疼痛系统。脊髓丘脑束（STT）既传递到 LT 又传递到 MT，而脊髓网状丘脑束（SRT）仅传递到 MT。N2/P2 复合体幅度的降低和 N1 波没有变化表明，背角神经元的 DNIC 抑制仅影响通过 SRT 的疼痛传递，而不涉及产生 STT 的神经元。N1 波可以成为评估临床实践中 STT 功能的可靠神经生理学参数，因为它似乎不受 CPM 的影响。
没有报道描述 DNIC 对内侧和外侧疼痛通路的影响。我们研究了 N1 波和 N2/P2 复合体，以检测 CPM 方案期间的变化。我们发现 N2/P2 复合体幅度降低，N1 波没有变化。这表明，DNIC 对背角神经元的抑制作用仅影响通过 SRT 的疼痛传递，而不涉及产生 STT 的神经元。
