Jiang Li, Ji Yadong, Voulalas Pamela J, Keaser Michael, Xu Su, Gullapalli Rao P, Greenspan Joel, Masri Radi
Department of Endodontics, Prosthodontics and Operative Dentistry, University of Maryland School of Dentistry, Baltimore, MD 21201, USA; Program in Neuroscience, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Department of Endodontics, Prosthodontics and Operative Dentistry, University of Maryland School of Dentistry, Baltimore, MD 21201, USA.
Brain Stimul. 2014 Mar-Apr;7(2):182-9. doi: 10.1016/j.brs.2013.12.013. Epub 2013 Dec 27.
Motor cortex stimulation (MCS) is a potentially effective treatment for chronic neuropathic pain. The neural mechanisms underlying the reduction of hyperalgesia and allodynia after MCS are not completely understood.
To investigate the neural mechanisms responsible for analgesic effects after MCS. We test the hypothesis that MCS attenuates evoked blood oxygen-level dependent signals in cortical areas involved in nociceptive processing in an animal model of chronic neuropathic pain.
We used adult female Sprague-Dawley rats (n = 10) that received unilateral electrolytic lesions of the right spinal cord at the level of C6 (SCL animals). In these animals, we performed magnetic resonance imaging (fMRI) experiments to study the analgesic effects of MCS. On the day of fMRI experiment, 14 days after spinal cord lesion, the animals were anesthetized and epidural bipolar platinum electrodes were placed above the left primary motor cortex. Two 10-min sessions of fMRI were performed before and after a session of MCS (50 μA, 50 Hz, 300 μs, for 30 min). During each fMRI session, the right hindpaw was electrically stimulated (noxious stimulation: 5 mA, 5 Hz, 3 ms) using a block design of 20 s stimulation off and 20 s stimulation on. A general linear model-based statistical parametric analysis was used to analyze whole brain activation maps. Region of interest (ROI) analysis and paired t-test were used to compare changes in activation before and after MCS in these ROI.
MCS suppressed evoked blood oxygen dependent signals significantly (Family-wise error corrected P < 0.05) and bilaterally in 2 areas heavily implicated in nociceptive processing. These areas consisted of the primary somatosensory cortex and the prefrontal cortex.
These findings suggest that, in animals with SCL, MCS attenuates hypersensitivity by suppressing activity in the primary somatosensory cortex and prefrontal cortex.
运动皮层刺激（MCS）是治疗慢性神经性疼痛的一种潜在有效方法。MCS后痛觉过敏和异常性疼痛减轻的神经机制尚未完全明确。
研究MCS后镇痛作用的神经机制。我们检验了这样一个假设，即在慢性神经性疼痛动物模型中，MCS可减弱参与伤害性处理的皮层区域中诱发的血氧水平依赖信号。
我们使用成年雌性Sprague-Dawley大鼠（n = 10），这些大鼠在C6水平接受右侧脊髓单侧电解损伤（SCL动物）。在这些动物中，我们进行了磁共振成像（fMRI）实验以研究MCS的镇痛作用。在fMRI实验当天，即脊髓损伤后14天，将动物麻醉并在左侧初级运动皮层上方放置硬膜外双极铂电极。在MCS（50 μA，50 Hz，300 μs，持续30分钟）前后分别进行两个10分钟的fMRI会话。在每个fMRI会话期间，使用20秒刺激关闭和20秒刺激开启的组块设计对右后爪进行电刺激（伤害性刺激：5 mA，5 Hz，3 ms）。使用基于一般线性模型的统计参数分析来分析全脑激活图。采用感兴趣区域（ROI）分析和配对t检验来比较这些ROI中MCS前后激活的变化。
MCS显著抑制了诱发的血氧依赖信号（家族性错误校正P < 0.05），并且在两个与伤害性处理密切相关的区域呈双侧抑制。这些区域包括初级体感皮层和前额叶皮层。
这些发现表明，在SCL动物中，MCS通过抑制初级体感皮层和前额叶皮层的活动来减轻超敏反应。
