Different mechanisms of electroacupuncture and pregabalin in neuropathic pain-induced ultrastructure damage in a rat model of brachial plexus neuralgia

Brachial plexus neuralgia (BPN) can result from injury, trauma, or cancer, and it significantly impacts the patient’s quality of life. This study investigated electroacupuncture (EA) vs. pregabalin on the structural changes in the peripheral nervous system (PNS) and central nervous system (CNS) in rats with BPN. Male Sprague-Dawley rats were randomized to the sham-operated (Con), BPN (using cobra venom), BPN+EA (EA), and BPN+pregabalin (PGB) groups (<i>n</i> = 8/group). EA or pregabalin was given from postoperative day (POD)14 to POD35. Structural alterations were determined by transmission electron microscopy in the primary sensory cortex, forelimb region (S1FL), anterior cingulate cortex (ACC), hippocampus, thalamus, cervical, thoracic, and lumbar spinal cords on POD40, and in the bilateral brachial plexus and dorsal root ganglions (DRG) at the cervical, thoracic and lumbar levels. Compared with the CON group, BPN rats exhibited significant changes in mechanical withdrawal threshold (MWT) (<i>p</i> &lt; 0.05). The MWT showed a significant increase compared with the BNP group after EA or pregabalin (<i>p</i> &lt; 0.05), but the long-term analgesic effects of EA appeared superior to pregabalin (<i>p</i> &lt; 0.05). Furthermore, EA alleviated myelin sheath damage at the spinal cord levels. Damage, including demyelination, was limited to the ipsilateral DRG at the corresponding segment and bilateral CNS. Neuropathic pain-induced damage is limited to the ipsilateral DRG at corresponding segment and bilateral CNS pain centers. EA and pregabalin each partially attenuate neuropathic pain and alleviate neuronal damage in BPN, but EA has a longer-term analgesic effect.