Abstract
To investigate the mechanisms underlying the efficacy of surgical treatment for painful diabetic peripheral neuropathy. Rats were initially divided into 3 groups (I, control rats, II, streptozotocin-induced diabetic rats, III, streptozotocin-induced diabetic rats with latex tube encircling the sciatic nerve without compression). When mechanical allodynia (MA) became stable in the third week, one third of group III rats were sacrificed and the remainder were further divided into subgroups depending on whether the latex tube was removed. Except for some rats in group III, all rats were sacrificed in the fifth week. Morphometric analysis of nerve fibers was performed. Expression level of GABAB receptor protein in spinal dorsal horn was determined. Changes of GABAB receptor within areas of primary afferents central terminal were identified. Chronic nerve compression caused by the interaction of diabetic nerves swelling and the encircling latex tube increased the incidence of MA in diabetic rats, and nerve decompression could ameliorate MA. In diabetic rats with MA, demyelination of myelinated fibers was noted and reduction of GABAB receptor was mainly detected in the area of myelinated afferent central terminals. MA in DPN should be partially attributed to compression impairment of myelinated afferents, supporting the rationale for surgical decompression.
Highlights
As a hallmark of neuropathic pain, mechanical allodynia (MA) is not uncommon in patients with painful diabetic peripheral neuropathy (DPN) [1], posing multidisciplinary therapeutic challenges
Since peripheral nerves in diabetes are proven to be susceptible to mechanical compression [19], a modified rat model of chronic nerve compression, in which the diabetic sciatic nerve distal to the ischial notch was surrounded by a 1.5-cm length of latex tube [20, 21], was used for this study
In the present study we have found that chronic nerve compression increases the incidence of MA in diabetic rats
Summary
As a hallmark of neuropathic pain, mechanical allodynia (MA) is not uncommon in patients with painful diabetic peripheral neuropathy (DPN) [1], posing multidisciplinary therapeutic challenges. It is well accepted that diabetic neuropathic pain is caused by peripheral neuropathy [7] and a series of peripheral mechanisms were reported to underlie the development of painful DPN. The effect of surgical decompression of peripheral nerves has been challenged and the mechanisms underlying the efficacy of surgical treatment for painful DPN remained uncertain and controversial. Both peripheral (input) and central (transmission) mechanisms should be considered together to provide a comprehensive understanding of underlying pathological processes and to develop better therapeutic strategies
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
