ABSTRACT
The pathophysiology of diabetic neuropathy is multifactorial, and a comprehensive theory is still lacking. Chronic hyperglycemia is the most common pathway for diabetic neuropathy and tissue damage. Several factors have been recognized to play a role in the pathogenesis of diabetic neuropathy, such as metabolism, vascular insufficiency, autoimmune destruction of small unmyelinated nerves in a visceral and cutaneous distribution, oxidative stress, and inflammation. Cardiac autonomic neuropathy results from the impairment of cardiac-vagal innervation affecting beat-to-beat heart-rate regulation and cardiac reflexes. Distal length-dependent loss of sweating is an early feature of diabetic autonomic neuropathy. Distal loss of sweating typically affects the feet and manifests more proximally with progression of neuropathy. Diabetic polyneuropathy is a distal symmetric axonal polyneuropathy. It is the most common form of neuropathy in diabetes and affects sensory, motor, and autonomic nerves. Cranial neuropathies usually accompany diabetic polyneuropathy and rarely can be the initial manifestation of diabetic neuropathy.
