Abstract
Diabetic neuropathy is one of the most frequent complications of diabetes. Precise prevalence is not known; the range of 25-90% is reported.
Etiology is multifactorial with the dominant influence of hyperglycemia, or rather the length of exposure to hyperglycemia. The primary symptom of diabetic peripheral sensory neuropathy is paresthesia.
Clinical signs of cardiac autonomic neuropathy are sparse (orthostatic hypotension, lowered tolerance to strain). Typical manifestation is tachycardia at rest, and malignant arrhythmia is a severe complication.
Examination of R-R interval variability helps in the process of diagnostics. Symptoms of sudomotor dysfunction (bouts of hyperhidrosis due to failing thermoregulation) are the most bothersome symptoms.
The basis of therapy and prevention of the development of diabetic neuropathy is an intensification of diabetic treatment with the best compensation possible. Most of the current drug therapy is only symptomatic, focusing on reducing subjective problems.
With regards to a high occurrence of adverse effects, it is necessary to proceed rationally during treatment. Thioctic acid is the only currently available substance with proven influence on pathophysiological processes that lead to diabetic neuropathy.