Diabetic peripheral neuropathy (DPN) is a common complication of diabetes mellitus and one of the most important causes of peripheral neuropathy, seriously endangering human health.DPN is an insidiously progressive process that initiates pathophysiological pathways to foot ulcers and leads to amputation, is a major factor affecting patients’ quality of life, and places a heavy economic burden on society and families [1]. Early identification, education and appropriate foot care for individuals at risk can lead to a reduction in ulcers and consequent amputations, thereby reducing disability and mortality. Despite the increasing awareness of diabetes mellitus, not enough attention is paid to DPN, and there are still many misconceptions in the diagnosis and treatment, which should be fully understood. A. The prevalence of DPN should be understood objectively. When reviewing the literature, it is not difficult to find that the reports on the prevalence of DPN vary greatly from less than 10% in the low cases to more than 90% in the high cases. It seems puzzling. The statistical results of DPN prevalence are influenced by many other factors besides ethnic or geographical differences. First, there is no unified standard for the diagnosis of DPN in the world so far, so the statistics of DPN cases are not very consistent; second, the early stage of DPN is easily ignored by patients due to mild symptoms and few patients actively seek treatment, which makes the statistics of DPN easy to miss, resulting in underestimation of the prevalence; third, the onset of DPN increases with age and the duration of the disease, and the cases reported in the literature are different in terms of age range and duration of the disease. Lastly, the methods of detecting peripheral neuropathy differ, with some based only on clinical manifestations or (and) physical signs, and others on laboratory tests (e.g., nerve conduction velocity), which obviously differ in diagnostic sensitivity. Even if the same laboratory tests (e.g., nerve conduction velocity) are applied, the number of affected nerves and the threshold for slowing down the velocity required to determine neuropathy differ, and thus statistical differences are inevitable. It is clear that the differences in DPN prevalence are due to a variety of factors. Regardless of the statistical results, it is indisputable that DPN has a high prevalence. It has been reported that up to 10% of cases of type II diabetes are found to have DPN when the diagnosis is first established by careful examination [2]; the prevalence of DPN increases yearly with the duration of the disease, with an annual incidence of about 2% [3]; the total prevalence can be as high as 50% after 10 years of disease [4]. Therefore, DPN is a very common complication of diabetes mellitus and should be given sufficient attention, and every diabetic patient should be carefully screened to detect DPN. The symptoms of DPN are numerous and complicated, and can be acute or chronic, and may be focal or diffuse, involving sensory nerves, motor nerves and autonomic nerves, with chronic sensory-motor neuropathy being the most common. Motor neuropathy, especially distal polyneuropathy, is the most common. The symptoms are symmetrical and diffuse, involving sensory, motor, autonomic, and cerebral nerves. Sensory symptoms are mostly pain in the extremities and are more severe in the evening, but may also include numbness, nociceptive hypersensitivity, and hyperalgesia. Motor symptoms may include limb weakness, inflexible fine movements, and dragging or unstable gait. Because of the length-dependent pattern of DPN, the longer the axon, the more likely it is to be damaged, so the symptoms tend to be more severe in the distal extremities. Autonomic symptoms include excessive or excessive sweating, salivation, dizziness, tachycardia, postural hypotension, vomiting, diarrhea, urinary incontinence, and sexual dysfunction. Asymmetric DPN is less common and can manifest as a single or mostly mononeuropathy, such as elbow canal syndrome (ulnar neuropathy), carpal tunnel syndrome (median neuropathy), and cerebral neuropathy (mainly III, IV, VI, and VII pairs of cerebral nerves), often with an acute onset and inconsistent with blood glucose levels; it can also manifest as radicular plexopathy and diabetic myasthenia gravis [5]. For example, some patients may present to the clinic with significant pain but no objective signs on examination; conversely, other patients may have no complaints, but a careful physical examination reveals significant loss of sensation in the limbs and even foot ulceration. What’s more, in about 30% to 50% of cases, the symptoms can be completely absent in the early stage, which makes the diagnosis difficult. Therefore, DPN should never be limited to a few symptoms, and one should be vigilant to avoid considering “asymptomatic” as “no DPN”. Only after careful neurological examination, together with the necessary laboratory tests, comprehensive consideration and overall analysis, will the diagnosis not be missed. Moreover, even if DPN is ruled out, subsequent periodic examinations (at least one physical examination and necessary laboratory tests per year) are still indispensable to detect DPN in a timely manner [2]. Third, it should be realized that DPN and blood glucose levels are not identical Although the development of DPN is associated with hyperglycemia and its onset increases with poor glycemic control and prolonged disease duration in general, the specific pathogenesis of DPN is very complex and involves metabolism (enhanced polyol pathways, reduced inositol, non-enzymatic protein glycosylation, abnormal lipid metabolism, etc.), vascular (microvascular dysfunction, hypercoagulable blood. The severity of DPN is not completely consistent with blood glucose levels. It is generally accepted that type I diabetes usually develops neuropathy several years after the onset of the disease, but type II diabetes often starts soon after the onset of the disease or even at the beginning of the disease with neurological symptoms. The relationship between asymmetric DPN and blood glucose is even more inconsistent. Therefore, when first diagnosing diabetes mellitus, especially type II diabetes mellitus, it is important to be alert to the presence of concurrent DPN, and not to wait until obvious neurological symptoms appear before treating them accordingly. Although the clinical examination of DPN is in principle similar to the routine neurological examination, the focus is different, and familiarity with this can help detect minor neuropathy. For example, in terms of sensory examination, in addition to pinprick sensation, temperature sensory examination is indispensable; while toe tuning fork vibration sensory (deep sensory) examination is important to detect minor neuropathy; the application of 10g single nylon wire for light touch examination of the foot is very sensitive according to the cloud and has been recommended as a routine diagnostic method for DPN [6]. Of course, it is worth noting that the results of sensory examination are closely related to the correct response of the patient and require close cooperation of the patient. In terms of movement, in addition to the routine examination, the focus should be on checking the tendon reflexes, especially the Achilles reflex, whose disappearance is an early and sensitive sign of impaired movement. In addition, attention should be paid to checking for foot ulcers, hard skin nodules or deformities. Measurement of postural blood pressure and Valsalva test can help to detect autonomic neuropathy. V. It is important to conduct relevant laboratory tests in time. The damage of hyperglycemia to blood vessels or nerves is often insidious, so the early symptoms of DPN are often mild and clinically undetectable, and sometimes even a comprehensive clinical examination is not helpful. The timely detection of DPN is crucial to actively intervene and stop further progression of the disease. Fortunately, DPN may have electrophysiological changes in its early stages before the clinical signs and symptoms become apparent [5]. Therefore, in addition to being alert to the development of DPN and performing careful clinical examinations in diabetic patients, it is important to perform timely laboratory tests to detect subclinical DPN as early as possible. There are many relevant laboratory tests, and nerve conduction velocity (NCV) is particularly sensitive (showing slowed conduction velocity, decreased wave amplitude, and prolonged latency) and is now used as an important tool for the diagnosis of DPN. Secondly, electrocardiogram (may show tachycardia or prolonged QT interval), ultrasound (shows enlarged gallbladder with poor systolic function, often accompanied by gallstones; increased bladder residual urine volume, late urinary retention), blood gas analysis (shows hypoxemia) and other tests are also important and can be applied as appropriate. In difficult cases, skin or peroneal nerve biopsy for pathological examination can help to confirm the diagnosis, such as light microscopy reveals axonal degeneration and reduction of myelinated nerve fibers; electron microscopy reveals mitochondrial enlargement within the axon and myelin degeneration with nerve fiber regeneration. Of course, the test is invasive and should be strictly controlled for indications. As mentioned above, DPN is the most common complication of diabetes mellitus and one of the most important causes of peripheral neuropathy, so once a diabetic patient develops peripheral neuropathy, there is no doubt that the possibility of DPN should be considered first. However, diabetic patients are often accompanied by many other diseases, some of which are likely to complicate peripheral neuropathy and should be identified in order to facilitate proper treatment. According to statistics, about 5-10% of diabetic peripheral neuropathy is not due to diabetes itself, but is associated with other diseases. For example, vitamin B12 deficiency, alcoholism, hypothyroidism, and renal dysfunction are common in diabetes, and they can all complicate peripheral neuropathy. The incidence of diabetes complicated by chronic inflammatory demyelinating polyneuropathy (CIDP) is also high, and its older age of onset, more severe axonal damage, and poorer treatment outcome, combined with increased cerebrospinal fluid protein levels, suggest the possibility of CIDP compared to classical CIDP. In addition, the possibility of carcinomatous neuropathy needs to be guarded against [2,5]. In conclusion, when diagnosing and treating DPN, attention must be paid to making appropriate examinations to detect or exclude non-diabetic neuropathy. VII. To treat DPN scientifically and rationally It used to be thought that once a diabetic patient had DPN as a complication, the lesion was irreversible and there was little hope for treatment. This pessimistic view should be discarded. Although the prevention and treatment of DPN needs to be further deepened and improved, but practice has proved that DPN can be prevented and treated. High blood sugar plays a key role in the development of DPN, regardless of the mechanism, it is related to the increase of blood sugar and the decrease of glucose tolerance. Data show that early and strict control of blood glucose can reduce the occurrence of DPN or delay its development, so blood glucose control should be the key step in the treatment of DPN. The internationally renowned Diabetes Control and Complications Trial (DCCT) has fully demonstrated that intensive treatment of diabetes can significantly reduce the incidence of neuropathy [7]. 2, not to ignore the etiological treatment Theoretically, it is very important to treat DPN for its pathogenesis, and there are many studies about it, and certain efficacy has been achieved. For example, aldose reductase inhibitors (such as epalrestat), supplementation with inositol, neurotrophic factors, antioxidants, protein kinase C inhibitors, and linolenic acid are used to enhance the polyol pathway, although the efficacy is limited and far from a cure, the appropriate application of several drugs for comprehensive treatment is still an option [2,5]. 3. Appropriate symptomatic treatment is very important The symptoms of DPN, especially limb pain, cause great pain to patients and seriously interfere with their normal life, and appropriate symptomatic treatment should be performed to relieve the symptoms and thus improve the quality of life of patients. Oral tricyclic or SSRI antidepressants or antiepileptic drugs such as carbamazepine and local application of capsaicin cream can significantly reduce pain symptoms [8]. Injection of methylcobalamin helps to improve symptoms such as limb numbness. Those with autonomic dysfunction can be treated accordingly, such as oral gastrofacial, morpholine or cisapride for mild gastroparesis; α2 adrenergic agonist colistin, simethicone, compound phenylephrine or bismuth subcarbonate for intractable diarrhea, and antibiotics should be given for those with intestinal infections. Those with neurogenic bladder should avoid continued expansion of bladder volume, timely prevention and control of infection, encourage patients to urinate regularly, use suprapubic massage with pressure to assist urination, dextran and gastrodia help improve contractile function of the detrusor muscle, and self-intermittent catheterization is feasible when necessary. Physiotherapy can promote the recovery of nerve function. Acupuncture and laser treatment can improve the ischemic and hypoxic state of nerves, reduce tissue edema and increase the conduction speed of nerves, which can be used as appropriate. Paying attention to the comfort of shoes and socks can reduce the formation of diabetic foot. In summary, all diabetic patients should be alert to the possibility of DPN and undergo timely and meticulous physical and laboratory examinations for early detection of DPN. all diabetic patients should be screened annually for DPN by examining distal bunion pinprick sensation, temperature sensation, vibration sensation, pressure sensation and ankle reflex, foot ulcers, skin hardness and deformities should be examined, and footwear should also be examined regularly; quantitative electrophysiology, sensory and autonomic function tests can be used to , sensory and autonomic function tests to confirm the diagnosis. Once the diagnosis of DPN is confirmed, appropriate causal and symptomatic treatment should be carried out on the basis of strict glycemic control to enable effective symptom control and delay the progression of the disease.