![]() 4Ī large number of neuroanatomical, neurophysiologic, and neurochemical mechanisms are thought to contribute to the development and maintenance of DPN. An improved therapeutic approach may include using protective and regenerative factors to enhance the action to insulin-regulated genes in the endothelial cells to promote antioxidant and anti-inflammatory factors. Expanding knowledge of central and peripheral nervous system processes may help identify therapeutic methods that effectively target the underlying mechanisms of pathogenesis. The impaired vascular supply to the nerves ultimately plays a role in DPN.Ģ) Advanced glycation end products (hemoglobin, plasma albumin, lipoproteins, fibrin, and collagen) cause tissue damage.ģ) Oxidative stress is the main pathological process that induces nerve damage by a direct toxic effect or by inhibition of nitric oxide production, thereby leading to nerve ischemia.Ĥ) Intracellular glucose activates protein kinase C, decreases nerve growth factor, and decreases gamma-linolenic acid (subsequently reducing prostacyclin, a vasodilator), which is necessary for ensuring blood flow.Ĭurrently, strict glycemic control is the most tangible treatment for DPN. ![]() It also reduces nicotinamide adenine dinucleotide phosphate, which leads to impairment of the primary vasodilatory system. Hyperglycemia, paramount to the pathogenesis of DPN, plays a central role in the cascade of nerve damage, which is described below: 1ġ) Increased intracellular glucose and nerve and vascular tissue increases sorbitol and fructose and decreases myo-inositol. Pathophysiologically, DPN involves metabolic and vascular dysfunction. Up to half of these patients, however, may be asymptomatic, and an incidental finding of a painless foot ulceration can confirm the diagnosis. 2 The symptoms frequently affect patients’ ability to perform daily activities. Sensorimotor neuropathy presents with pain, paresthesia, and sensory loss, while autonomic neuropathy can contribute to myocardial infarction, malignant arrhythmia, and sudden death.ĭistal sensory diabetic polyneuropathy affects up to 50% of patients. Sensorimotor and autonomic neuropathies are the most common diabetic neuropathies. 1 Patients may also experience cold or numb sensations. The presentation of diabetic neuropathy characteristically involves a burning or tingling sensation, hyperesthesia, sensory loss in the feet or hands, or combinations of these factors. 1,2 The landmark Diabetes Control and Complication Trial demonstrated that proper glycemic control can reduce the development and progression of neuropathy significantly, by 64%. 2 Several risks factors are associated with DPN, including hyperglycemia, older age, tobacco use, hypertension, obesity, alcohol consumption, and taller height. 1 Neuropathy is a common complication of type 1 and type 2 diabetes, with a prevalence of nearly 8% in newly diagnosed patients with diabetes and more than 50% in patients with long-standing disease. In 1864, Marchel de Calvi described diabetic peripheral neuropathy (DPN) as a consequence rather than a cause of diabetes. The dramatic rise in the incidence of diabetes worldwide can be attributed to human behavior and lifestyle changes over the last century. Strict glycemic control is the most reliable treatment for diabetic peripheral neuropathy, but expanding knowledge of central and peripheral nervous system processes may help identify therapeutic methods that can effectively target the underlying mechanisms of pathogenesis.īy Sarnarendra Miranpuri, DPM, MD Kush Patel Gurwattan Miranpuri, PhD Abhishek Chopra and Ravinderjit Singh
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