Kale Bülent, Yüksel Fuat, Celiköz Bahattin, Sirvanci Serap, Ergün Ozge, Arbak Serap
Department of Plastic and Reconstructive Surgery, Gülhane Military Medical Academy, Haydarpasa Hospital, Istanbul, Turkey.
Plast Reconstr Surg. 2003 Jun;111(7):2265-72. doi: 10.1097/01.PRS.0000060100.80687.D9.
It is known that diabetic neuropathy is the result of endoneurial edema caused by various biochemical reactions triggered by hyperglycemia. This sequence of events can cause cessation of circulation at the perineurial level, or the tough layer, which is not resilient enough to spread intraneural pressure. Internal and external limiting structures create a double crush phenomenon to the nerve structure. Decompression of the nerve trunk at separate levels is one of the adjuncts to the overall treatment plan for diabetic neuropathy. In this study, the right sciatic nerves of 30 rats with streptozotocin-induced diabetes were used; three groups were created. In the control group, the sciatic nerves were explored and dissected only. In group II, tarsal tunnel release was performed and accompanied by epineurotomy of the sciatic nerve and its peroneal and tibial extensions. In group III, in addition to the procedures performed in group II, perineural sheaths, exposed through the epineurotomy sites at both the peroneal and tibial nerves, were incised for decompression of the fascicles. Improvement in diabetic neuropathy was evaluated by using footprint parameters. The last print length values, estimated according to the 38-month measurements, were 26.1 +/- 0.12 mm in the control group, 23.2 +/- 0.07 mm in group II, and 22.2 +/- 0.1 mm in group III. The toe spread and intermediate toe spread values of the groups were parallel to improvements in print lengths throughout the study. The best improvement was observed in the perineurotomy group. Finally, an electron microscopic study revealed variable degenerative changes in all groups, but they were milder in groups II and III. This experimental study reveals that adding internal decompression to external release doubled the effect in reducing derangement in the sciatic nerves of the rats and, in the authors' opinion, offers cause for further optimism in the treatment of diabetic neuropathy.
已知糖尿病性神经病变是由高血糖引发的各种生化反应导致神经内膜水肿的结果。这一系列事件可导致神经束膜水平（即坚韧层，其弹性不足以分散神经内压力）的循环停止。内部和外部限制结构对神经结构造成双重挤压现象。在不同层面进行神经干减压是糖尿病性神经病变整体治疗方案的辅助手段之一。在本研究中，使用链脲佐菌素诱导糖尿病的30只大鼠的右侧坐骨神经；分为三组。对照组仅对坐骨神经进行探查和解剖。第二组进行跗管松解，并伴有坐骨神经及其腓总神经和胫神经分支的神经外膜切开术。第三组除了进行第二组的操作外，还切开通过腓总神经和胫神经神经外膜切开部位暴露的神经束膜以进行束膜减压。通过足迹参数评估糖尿病性神经病变的改善情况。根据38个月的测量估计，对照组的末次足迹长度值为26.1±0.12毫米，第二组为23.2±0.07毫米，第三组为22.2±0.1毫米。在整个研究过程中，各组的趾展和中间趾展值与足迹长度的改善情况平行。神经外膜切开术组观察到的改善最佳。最后，电子显微镜研究显示所有组均有不同程度的退行性改变，但第二组和第三组的改变较轻。这项实验研究表明，在外部松解的基础上增加内部减压可使大鼠坐骨神经紊乱的减少效果加倍，并且在作者看来，为糖尿病性神经病变的治疗带来了进一步乐观的理由。
