Objective: The present study aimed to investigate the analgesic effect of electroacupuncture (EA) in neuropathic pain due to brachial plexus avulsion injury (BPAI) and related changes in the metabolic brain connectivity. Methods: Neuropathic pain model due to BPAI was established in adult female Sprague-Dawley rats. EA stimulations (2/15 Hz, 30 min/day, 5-day intervention followed by 2-day rest in each session) were applied to the fifth-seventh cervical "Jiaji" acupoints on the noninjured side from 1st to 12th weeks following BPAI (EA group, n = 8). Three control groups included sham EA (nonelectrical acupuncture applied to 3 mm lateral to the real "Jiaji" acupoints), BPAI-only, and normal rats (no particular intervention; eight rats in each group). Thermal withdrawal latency (TWL) of the noninjured forepaw was regularly tested to evaluate the threshold of thermalgesia. Small animal [fluorine-18]-fluoro-2-deoxy-D-glucose (18F-FDG) PET/CT scans of brain were conducted at the end of 4th, 12th, and 16th weeks to explore metabolic alterations of brain. Results: In the EA group, the TWL of the noninjured forepaw significantly decreased following BPAI and then increased following EA stimulation, compared with sham EA (P < 0.001). The metabolic brain connectivity among somatosensory cortex (SC), motor cortex (MC), caudate putamen (Cpu), and dorsolateral thalamus (DLT) in bilateral hemispheres decreased throughout the 16 weeks' observation in the BPAI-only group, compared with the normal rats (P < 0.05). In the EA group, the strength of connectivity among the above regions were found to be increased at the end of 4th week following BPAI modeling, decreased at 12th week, and then increased again at 16th week (P < 0.05). The changes in metabolic connectivity were uncharacteristic and dispersed in the sham EA group. Conclusion: The study revealed long-term and extensive changes of metabolic brain connectivity in EA-treated BPAI-induced neuropathic pain rats. Bilateral sensorimotor and pain-related brain regions were mainly involved in this process. It indicated that modulation of brain metabolic connectivity might be an important mechanism of analgesic effect in EA stimulation for the treatment of neuropathic pain.

中文翻译：

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大鼠臂丛撕脱伤所致神经性疼痛中与电针相关的代谢性大脑连通性。

目的：本研究旨在探讨电针（EA）对臂丛神经撕脱伤（BPAI）引起的神经性疼痛的镇痛作用以及代谢性脑连通性的相关变化。方法：建立成年雌性Sprague-Dawley大鼠的BPAI引起的神经性疼痛模型。在BPAI后第1周至第12周，对未受伤的第五至第七个颈椎“ Jiaji”穴位进行EA刺激（2/15 Hz，每天30分钟/天，每天进行5天干预，然后休息2天） （EA组，n = 8）。三个对照组包括假EA（非电针刺于真正的“ Jiaji”穴位侧面3 mm），仅BPAI和正常大鼠（无特殊干预；每组八只大鼠）。定期测试未受伤前爪的退热潜伏期（TWL），以评估热痛阈。在第4周，第12周和第16周结束时进行了小动物大脑的[氟18]-氟-2-脱氧-D-葡萄糖（18F-FDG）PET / CT扫描，以研究大脑的代谢变化。结果：与假EA相比，在EA组中，未受伤的前爪的TWL在BPAI后显着降低，然后在EA刺激后升高（P <0.001）。在仅BPAI的组中观察了16周，与正常人相比，双侧半球体感皮层（SC），运动皮层（MC），尾状壳核（Cpu）和背外侧丘脑（DLT）之间的代谢性大脑连通性降低了大鼠（P <0.05）。在EA组中，在BPAI建模后的第4周末，上述区域之间的连通性强度增加，在第12周时降低，然后在第16周时再次增加（P <0.05）。假性EA组的代谢连通性变化不典型且分散。结论：该研究揭示了EA治疗的BPAI引起的神经性疼痛大鼠的代谢性脑连接的长期和广泛变化。双侧感觉运动和疼痛相关的大脑区域主要参与此过程。这表明调节脑代谢连通性可能是EA刺激镇痛作用的重要机制，可用于治疗神经性疼痛。假性EA组的代谢连通性变化不典型且分散。结论：该研究揭示了EA治疗的BPAI引起的神经性疼痛大鼠的代谢性脑连接的长期和广泛变化。双侧感觉运动和疼痛相关的大脑区域主要参与此过程。这表明调节脑代谢连通性可能是EA刺激镇痛作用的重要机制，可用于治疗神经性疼痛。假性EA组的代谢连通性变化不典型且分散。结论：该研究揭示了EA治疗的BPAI引起的神经性疼痛大鼠的代谢性脑连接的长期和广泛变化。双侧感觉运动和疼痛相关的大脑区域主要参与此过程。这表明调节脑代谢连通性可能是EA刺激镇痛作用的重要机制，可用于治疗神经性疼痛。