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Diabetic Neuropathy - Information Overview
Last reviewed: 12.07.2025

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Diabetic neuropathy is a pathogenetically associated with diabetes mellitus combination of syndromes of damage to the nervous system, classified depending on the predominant involvement in the process of the spinal nerves (distal, or peripheral, diabetic neuropathy) and (or) the autonomic nervous system (visceral, or autonomic, diabetic neuropathy with the exclusion of other causes of their damage.
According to this definition, only that type of damage to the peripheral nervous system can be considered diabetic in which other etiological factors for the development of polyneuropathy are excluded, for example, toxic etiology (alcoholic) or other diseases of the endocrine system (hypothyroidism).
Causes and pathogenesis of diabetic neuropathy
The pathogenesis of diabetic neuropathy is not fully understood. The main initial pathogenetic factor of diabetic neuropathy is chronic hyperglycemia, which ultimately leads to changes in the structure and function of nerve cells. Probably, the most important role is played by microangiopathy (changes in vasa nervorum with impaired blood supply to nerve fibers) and metabolic disorders, which include:
- activation of the polyol shunt (fructose metabolism disorder) - an alternative pathway of glucose metabolism, as a result of which it is converted into sorbitol under the action of aldose reductase, then into fructose, the accumulation of sorbitol and fructose leads to hyperosmolarity of the intercellular space and swelling of the nervous tissue;
- reduction of the synthesis of components of the membranes of nerve cells, leading to disruption of the conduction of nerve impulses. In this regard, the use of cyanocobalamin, which is involved in the synthesis of the myelin sheath of the nerve, reduces pain associated with damage to the peripheral nervous system, and stimulates nucleic acid metabolism through the activation of folic acid, seems to be effective in diabetic neuropathy;
Symptoms of diabetic neuropathy
There are no clinical manifestations of diabetic neuropathy in the initial stages. Neuropathy is detected only with the help of special research methods. In this case, it is possible:
- changes in electrodiagnostic test results:
- decreased conductivity of nerve impulses in sensory and motor peripheral nerves;
- decrease in the amplitude of induced neuromuscular potentials,
- changes in sensitivity test results;
- vibration;
- tactile;
- temperature;
Diagnosis of diabetic neuropathy
The diagnosis of diabetic neuropathy is made on the basis of relevant complaints, a history of type 1 or type 2 diabetes mellitus, data from a standardized clinical examination and instrumental research methods (including quantitative sensory, electrophysiological (electromyography) and autofunctional tests).
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Complaints and standardized clinical examination
To quantitatively assess the intensity of pain, special scales are used (TSS - General Symptom Scale, VAS - Visual Analogue Scale, McGill scale, HPAL - Hamburg Pain Questionnaire).
Diagnosis of diabetic neuropathy
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How to examine?
What tests are needed?
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Treatment of diabetic neuropathy
The main measure for the prevention and treatment of diabetic neuropathy is achieving and maintaining target glycemic values.
Recommendations for pathogenetic therapy of diabetic neuropathy (benfotiamine, aldolase reductase inhibitors, thioctic acid, nerve growth factor, aminoguanidine, protein kinase C inhibitor) are in the development stage. In some cases, these drugs relieve neuropathic pain. Treatment of diffuse and focal neuropathies is mainly symptomatic.
Thioctic acid - intravenously by drip (over 30 minutes) 600 mg in 100-250 ml of 0.9% sodium chloride solution once a day, course 10-12 injections, then orally 600-1800 mg/day, in 1-3 doses, 2-3 months.