Naprapathy attenuates neuropathic pain after brachial plexus injury

This study was to explore the potential mechanism of naprapathy in treating neuropathic pain (NP) after brachial plexus injury (BPI).

Totally 72 rats were randomly divided into normal group, model control group, and naprapathy group (n=24 per group). A right upper-limb chronic NP model was established, and naprapathy was administered at C5-T1 Jiaji Points on 4th day after modeling. Naprapathy was performed for 15 min once daily with a frequency of 60 per minute. The treatment was applied for altogether 28 days. Cold pain threshold and mechanical pain threshold were measured 1 day before modeling, 3 days after modeling, and 7, 14, 21 and 28 days after naprapathy; 7, 14, 21 and 28 days after naprapathy, rats were killed and the β-endorphin expression and γ-aminobutyric acid (GABA) content were detected in the thalamus.

After 14-day treatment, there was significant difference of mechanical pain threshold between the naprapathy group and the normal group (P<0.05); after treatment for 21 and 28 days, there was no significant difference between the naprapathy group and the normal group (P>0.05); after 28-day naprapathy, there was significant difference of β-EP expression between the normal group and the naprapathy group (P<0.05), while the difference between model control group and naprapathy group was statistically significant (P<0.05). After 14-day treatment, there was significant difference of GABA content between the model control group and the naprapathy group (P<0.05). After 28-day treatment, significant difference was also found between the model control group and the naprapathy group (P<0.05).

After naprapathy, chronic NP is attenuated in rats with BPI, which might be ascribed to the upregulation of β-endorphin and GABA.