Diabetic neuropathy is a type of nerve damage that can occur if you have diabetes. Peripheral neuropathy is the most common type of diabetic neuropathy. It can affect nerves in the feet, legs, hands, and arms. It often starts in the feet and usually affects both feet at the same time. Most often, the symptoms of peripheral neuropathy affect both sides of the body.
DPN is a common and annoying complication of diabetes mellitus. Diabetes is manifested in a variety of case-specific signs and symptoms and is associated with complex biochemical, functional and structural anomalies of the peripheral nervous system. Although the obvious hyperglycemia present in diabetes may explain the appearance of these anomalies, data suggest that other factors may also contribute. We have analyzed the evidence of insulinopenia in type 1 diabetes or insulin resistance in type 2 diabetes as causal factors in the development of DPN.
We have suggested that these two cases actually represent a single cause of impaired insulin signaling. A more comprehensive analysis of the role of insulin signaling in DPN more fully explains changes in nerve function in prediabetic or early-diabetic patients and in animal models. This does not exclude that hyperglycemia is also a factor in PND, but it allows obtaining a more complete picture of the pathological process (figure 1). In addition to insulin signaling, there is also some evidence to show that IGF and C-peptide act as mediators of DPN.
The pathogenesis of DPN is obviously multifactorial and, despite long-standing efforts, remains poorly understood. This work has also suggested that insulin signaling has effects that occur with different levels of receptor occupancy. Therefore, the action of insulin on nerve function requires a higher level of receptor occupancy than the action of insulin on glycemic control. This could be explained by the different levels of attachment of receptors to the second messenger signaling pathways in the nerve, compared to the liver or muscle.
Future studies should elucidate these mechanisms in order to obtain a clearer picture of DPN, especially in prediabetes, where early detection could improve therapeutic outcomes. As the first phase of diabetic neuropathy, prediabetic neuropathy refers to nerve damage that occurs in people who have not yet been diagnosed with diabetes but who have higher than normal blood sugar levels. This condition can be a warning sign of the development of diabetes and should not be ignored. The main symptom is nerve pain that starts in the upper thigh of one leg and can affect the hips and lower back.
Weight loss is a symptom in approximately 35% of patients with proximal neuropathy, and around 18% experience weakness in the affected area in addition to pain. Rarely, proximal neuropathy may occur in the arm. Diabetic neuropathy most commonly affects the sensory and motor nerves in the legs and feet. This is known as peripheral neuropathy.
DSPN is the most common form of diabetic neuropathy. Clinically, it is primarily sensory neuropathy that depends on length, and significant distal weakness is rare. However, as with cryptogenic distal sensory neuropathy (CSPN), there is usually electrophysiological evidence of subclinical motor impairment. In fact, the clinical and electrophysiological findings in cryptogenic and diabetic distal sensory and sensorimotor neuropathy are very similar 84. However, since diabetic patients are often closely monitored before they develop symptoms of neuropathy, the first signs of neuropathy may be a decrease in distal vibration, touch and pain, and a loss of the ankle reflex during the exam. The first symptoms are usually a decrease in sensation or tingling in the toes.
Dysesthesia, usually burning pain, may occur, although most diabetic patients with distal sensory neuropathy do not complain of significant discomfort. In a population of 382 diabetic subjects treated with insulin, 41 (10.7%) had painful symptoms 85 In a two-phase cross-sectional descriptive study of patients with type 2 diabetes (postal survey followed by history and neurological examination), up to 27% of diabetics experienced neuropathic pain or mixed pain that had a significant negative effect on quality of life 86 Sensory symptoms may eventually progress to the ankles and knees and reach the fingers, hands and forearms. If the sensory loss extends to the elbows, patients may develop a symmetric midline zone of sensory loss in the shape of a trunk wedge, 87. The effect of intensive diabetes treatment on the development and progression of long-term complications in insulin-dependent diabetes mellitus. Diabetic polyneuropathy (DPN) affects multiple peripheral sensory and motor nerves that branch from the spinal cord to the arms, hands, legs and feet. It is important to establish the correct lower limit for the diagnosis of prediabetes because it determines if clinical tests should be performed to detect complications and recommendations should be provided to patients on how to modify lifestyle and diet.
The presence of symmetric proximal or trunk dysesthesia associated with profound weight loss should be a clinical sign that supports the diagnosis of diabetic neuropathic cachexia, rather than the most common neuropathic neuropathic disorder of diabetes. The wide variability of data on the symmetric prevalence of diabetic polyneuropathy is due to the lack of coherent diagnostic criteria, to the varying methods of selecting patients for study and to the different evaluation techniques. The impact of the early stages of diabetic neuropathy on daily life can be significant and influence several aspects of your well-being. Once a person has neuropathy, symptoms will persist indefinitely, but most people with diabetic neuropathy can lead active and full lives.
Efficacy of the Nav1.7 blocker PF-05089771 in a double-blind, randomized, placebo-controlled clinical study in subjects with painful diabetic peripheral neuropathy. Diabetic neuropathy can cause chronic pain and complications, such as gastrointestinal problems, dizziness and weakness, and urinary or sexual problems. The most commonly used oral drugs for the symptomatic treatment of diabetic and non-diabetic painful neuropathy are tricyclic antidepressants, carbamazepine, gabapentin, mexiletene and, more recently, pregabalin and cymbalta. Several consensus panels recommend the inclusion of electrophysiological tests in the evaluation of diabetic neuropathy.
In the Rochester diabetic neuropathy study, none of the 380 diabetics had disabling polyneuropathy, even after follow-up for many years.
