Abstract
Diabetic neuropathy is one of the most common complications of diabetes. Its exact prevalence is not known but is supposed to range between 25% and 90%.
The etiology of diabetic neuropathy is multifactorial, with a dominant role played by hyperglycemia or length of exposure to hyperglycemia. The basic symptom of diabetic peripheral sensitive neuropathy is represented by paresthesias.
Clinical symptoms and signs of cardiac autonomic neuropathy are scarce (orthostatic hypotension, reduced exercise tolerance). While resting tachycardia is a typical sign, malignant arrhythmia is a severe complication.
Evaluation of RR interval variability may be helpful. The mainstay of diabetic neuropathy treatment and prevention of its development are both based on intensification of diabetes therapy, aiming at its optimal compensation.
Most of the current pharmacotherapy is just symptomatic, alleviating the patient's subjective complaints. This therapy has to be rational, given the high prevalence of pharmacotherapy side effects.
Thioctic acid is the only available drug which clearly influences the pathophysiological processes behind diabetic neuropathy.