Rehabilitation of diabetic peripheral neuropathy

  Diabetic peripheral neuropathy is one of the most common microvascular complications of diabetes mellitus. According to statistics, the prevalence of diabetic peripheral neuropathy is more than 32% among diabetic patients over 40 years of age, and increases significantly with the duration of diabetes. Diabetic peripheral neuropathy has a variety of manifestations, the most common being symmetrical peripheral neuropathy, which can involve sensory, motor and autonomic nerves, mostly with sensory nerve involvement, and can manifest as severe symmetrical sensory numbness, such as wearing gloves and socks, limb pain, severe skin breakdown, infection, long-lasting wound healing, and the formation of diabetic foot, which may eventually lead to amputation.  Scientists have discovered that oxidative damage plays a key role in the pathogenesis of diabetic peripheral neuropathy. What is oxidation? It is not new to us. We live in oxygen-rich air. Iron rusts, copper turns green, and paper turns yellow and brittle, all as a result of oxidation, and the substances generated by rusting are oxidative products. It has been suggested that although oxygen is the source of sustaining human life, it is sometimes a “mystery killer” that damages healthy cells and even “kills” people. In fact, this “mysterious killer” is not oxygen itself, but the oxygen radicals produced by it, also known as reactive oxygen species. The vast majority of oxygen inhaled into the body through the role of oxidative enzymes, to oxidize sugar, fat, protein, to maintain the energy required for life, and then generate carbon dioxide and water, while it will produce some reactive oxygen species. Under normal circumstances, the body will be removed through a series of antioxidant mechanisms. However, if the body produces too much reactive oxygen species for various reasons, the reactive oxygen species that are not cleared in time will cause damage to the structure of cells and cause extensive cellular damage, leading to various diseases.  In recent years, scientists have found that type 2 diabetic patients are vulnerable to free radicals. In addition, the presence of various metabolites of sugar in the body of type 2 diabetic patients often leads to oxidative stress, which increases reactive oxygen species. The result causes extensive damage to the body and injury to the vascular endothelium, which can lead to the development of diabetic microvascular complications, and the pathogenesis of diabetic peripheral neuropathy is closely related to this. Reactive oxygen can also directly damage cells and tissues. Reactive oxygen is present for a very short period of time and the damage to the tissue is limited to the surrounding area where it is located. This explains why many diabetic patients with excellent glycemic control still have diabetic peripheral neuropathy, suggesting that oxidative damage to neurons occurs immediately upon elevation of blood glucose. Therefore, antioxidants and free radical scavenging are important in the treatment of diabetic peripheral neuropathy.  The treatment of diabetic peripheral neuropathy starts with blood glucose control, which is the root of all diabetic complications. However, compared with general glucose-lowering therapy, strict glycemic control alone can only partially delay the process of diabetic peripheral neuropathy but cannot completely prevent it from occurring.  At the same time, we should also pay attention to symptomatic treatment, which is very important in the treatment of diabetic peripheral neuropathy. Pain is the most common complaint of these patients, and it seriously affects their quality of life. The most common complaint of these patients is pain, which seriously affects their quality of life. At present, it is mostly advocated that the maximum dose of analgesic therapy should be given according to the individual patient’s condition based on blood glucose control and antioxidant therapy, i.e. stepwise therapy. However, analgesic treatment has no effect on the development of diabetic peripheral neuropathy.  The last thing we would like to emphasize is antioxidant therapy, which is currently the main treatment for diabetic peripheral neuropathy. Traditional drug therapy is often administered intravenously or orally, but oxygen radicals are extremely unstable by nature and have an extremely short survival time, and their direct damage to the surrounding tissues is more obvious after they are produced. Therefore, our antioxidant therapy should also take into account local antioxidant therapy in addition to systemic medication. Compared with the traditional intravenous and oral drug therapy, the traditional Chinese medicine of acupuncture point injection therapy provides us with a new way of local antioxidant treatment, which is proven to be effective and immediate in clinical practice. Acupoint injection therapy with antioxidant and neurotrophic drugs improves the local peroxidative environment and nutrient metabolism of the injured nerve, creating conditions for the repair of peripheral nerves; at the same time, it is combined with motor function exercise and sensory re-education to facilitate the overall improvement of nerve function, allowing the injured nerve to return to its optimal functional state.