## 1 Introduction  
Worldwide, diabetic neuropathy is the most common complication of diabetes and the most common cause of hospitalization and non-traumatic amputations among diabetic complications. Diabetic neuropathy can occur at any time in its course and affects between 50 and 75% of patients with diabetes [1]. Diabetic neuropathy (DN) is defined as the totality of anatomical, clinical, neurological, and metabolic disorders occurring during the course of diabetes mellitus, after the exclusion of other neurological manifestations belonging to diabetes mellitus-associated or other causes (hereditary, traumatic, neoplastic, infectious, compressive, metabolic, autoimmune) or secondary to other systemic conditions. Its frequency increases with disease duration, patient age, abdominal circumference, ethanol, and neurotoxic consumption. After 20 years of progression, two-thirds of people with diabetes will have at least one clinical or subclinical manifestation of neuropathy. Distal symmetric polyneuropathy and diabetic autonomic neuropathy, especially cardiovascular neuropathy, are the most prevalent and studied clinical forms [2]. In recent years, different non-invasive techniques have been implemented for the early detection and treatment of DN. Among these, infrared thermography has shown promise as a diagnostic technique for this disease. Recent studies [3; 4; 5] have shown that infrared thermal imaging can identify early indicators of neuropathy by studying heat patterns in the skin.These techniques also provide important new insights into vascular and neuronal alterations related to diabetic neuropathy. However, in order to provide a comprehensive assessment of neuropathic problems in diabetic patients, our study is based on another non-invasive technique, which is Sudoscan. The manifestation of autonomic neuropathy with peripheral consequences is sudomotor neuropathy; thus, sweat glands are sympathetically innervated and the touching of postganglionic fibers is manifested by reduced secretion of these glands, resulting in an-hidrosis and dry, cracked skin, with trophic disorders in advanced stages, but also disorders of adaptation to temperature changes (frequently heat intolerance) [6; 7]. Reduced/absent sweating correlates with other signs and symptoms of autonomic neuropathy, especially orthostatic hypotension, but also with other cardiovascular changes (loss of heart rate variability). The association between the existence of non-physiological pressure points and hyposudoration, anhidrosis, and dry skin will lead, over time, through repeated mechanical overstrain, to the appearance of calluses, cracks, or other areas of continuity which are real entry points for various pathogens [8]. Assessment of peripheral autonomic neuropathy can be performed by the sympathetic skin reaction: an examination of sympathetic efferent using sweating produced by tension changes (\"galvanic skin reflex\"). This analysis can be performed with Sudoscan, equipment also used in this study to assess sudomotor dysfunction by measuring skin conductance, providing valuable information on DAN risk. This medical device provides a non-invasive assessment of sweat gland function on the palms and soles of the feet, areas with the highest density of sweat glands. The reliability and validity of Sudoscan have been demonstrated in several articles [9], e.g., [PERSON] demonstrated the correlation between electrochemical skin conductance (ESC) and clinical, somatic, and autonomic measures of neuropathy [10], [PERSON] et al. showed that it is a test that promises to diagnose DAN with similar intraepidermal nerve fiber density performances, but cannot replace the diagnosis made with electromyography [11]. [PERSON] et al. emphasized the importance of examining patients with Sudoscan to improve individualized management of diabetics through early detection and intervention [12]. Thus, early recognition of DAN symptoms is essential for the management of diabetes and related complications.