Onishi Okihiro, Ikoma Kazuya, Oda Ryo, Yamazaki Tetsuro, Fujiwara Hiroyoshi, Yamada Shunji, Tanaka Masaki, Kubo Toshikazu
Department of Orthopaedics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, 602-8566 465, Kajiicho, Kamigyo-ku Kyoto-shi, Kyoto, Japan.
Department of Anatomy and Neurobiology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, 602-8566 465, Kajiicho, Kamigyo-ku Kyoto-shi, Kyoto, Japan.
Neurosci Lett. 2018 Apr 23;673:150-156. doi: 10.1016/j.neulet.2018.03.003. Epub 2018 Mar 7.
Although treatment protocols are available, patients experience both acute neuropathic pain and chronic neuropathic pain, hyperalgesia, and allodynia after peripheral nerve injury. The purpose of this study was to identify the brain regions activated after peripheral nerve injury using functional magnetic resonance imaging (fMRI) sequentially and assess the relevance of the imaging results using histological findings. To model peripheral nerve injury in male Sprague-Dawley rats, the right sciatic nerve was crushed using an aneurysm clip, under general anesthesia. We used a 7.04T MRI system. T weighted image, coronal slice, repetition time, 7 ms; echo time, 3.3 ms; field of view, 30 mm × 30 mm; pixel matrix, 64 × 64 by zero-filling; slice thickness, 2 mm; numbers of slices, 9; numbers of average, 2; and flip angle, 8°. fMR images were acquired during electrical stimulation to the rat's foot sole; after 90 min, c-Fos immunohistochemical staining of the brain was performed in rats with induced peripheral nerve injury for 3, 6, and 9 weeks. Data were pre-processed by realignment in the Statistical Parametric Mapping 8 software. A General Linear Model first level analysis was used to obtain T-values. One week after the injury, significant changes were detected in the cingulate cortex, insular cortex, amygdala, and basal ganglia; at 6 weeks, the brain regions with significant changes in signal density were contracted; at 9 weeks, the amygdala and hippocampus showed activation. Histological findings of the rat brain supported the fMRI findings. We detected sequential activation in the rat brain using fMRI after sciatic nerve injury. Many brain regions were activated during the acute stage of peripheral nerve injury. Conversely, during the chronic stage, activation of the amygdala and hippocampus may be related to chronic-stage hyperalgesia, allodynia, and chronic neuropathic pain.
尽管有治疗方案,但患者在周围神经损伤后会经历急性神经性疼痛和慢性神经性疼痛、痛觉过敏和异常性疼痛。本研究的目的是使用功能磁共振成像(fMRI)依次识别周围神经损伤后激活的脑区,并使用组织学结果评估成像结果的相关性。为了在雄性Sprague-Dawley大鼠中模拟周围神经损伤,在全身麻醉下用动脉瘤夹夹闭右侧坐骨神经。我们使用了一台7.04T MRI系统。T加权图像,冠状切片,重复时间7毫秒;回波时间3.3毫秒;视野30毫米×30毫米;像素矩阵,通过零填充为64×64;切片厚度2毫米;切片数量9;平均次数2;翻转角8°。在对大鼠足底进行电刺激期间采集fMR图像;90分钟后,对诱导周围神经损伤3周、6周和9周的大鼠进行脑c-Fos免疫组织化学染色。数据在统计参数映射8软件中通过重新对齐进行预处理。使用一般线性模型一级分析来获得T值。损伤后1周,在扣带回皮质、岛叶皮质、杏仁核和基底神经节中检测到显著变化;6周时,信号密度有显著变化的脑区缩小;9周时,杏仁核和海马体显示激活。大鼠脑的组织学结果支持了fMRI的结果。坐骨神经损伤后,我们使用fMRI检测到大鼠脑中的依次激活。在周围神经损伤的急性期,许多脑区被激活。相反,在慢性期,杏仁核和海马体的激活可能与慢性期痛觉过敏、异常性疼痛和慢性神经性疼痛有关。