Abstract
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.
Highlights
Brachial plexus avulsion injury (BPAI), which is often caused by motorcycle accident, is one of the most devastating peripheral nerve injuries
All rats were in good condition and active after BPAI modeling
BPAI is a specific type of brachial plexus injury that causes preganglionic disruption of nerve roots from the spinal cord (Murphey et al, 1947)
Summary
Brachial plexus avulsion injury (BPAI), which is often caused by motorcycle accident, is one of the most devastating peripheral nerve injuries. Partial or global BPAI would lead to sensory and motor dysfunction Neuropathic pain is another intractable problem caused by BPAI. It is reported that 70–90% BPAI patients suffer from persistent neuropathic pain (Teixeira et al, 2015). Functional and structural changes in the nervous system involve the peripheral nerve fibers, spine, brain, and several pain pathways (Teixeira et al, 2015). These factors would contribute to both development and maintenance of neuropathic pain (Gierthmühlen and Baron, 2016; Zilliox, 2017). Investigation on the mechanisms underlying neuropathic pain due to BPAI would be necessary for seeking the solve for neuropathic pain
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