Diabetic neuropathy

Diabetic neuropathies usually develop with long-term diabetes, but do not depend on its severity. Some forms (for example, damage to the oculomotor nerve) occur, as a rule, only in patients older than 50-60 years. In old age, even with mild diabetes, senile and atherosclerotic neuropathies often develop . They are naturally not diabetic. This also applies to the radiculo – and plexopathies and mononeuritis of the sciatic, femoral, external cutaneous and other nerves and, apparently, proximal amyotrophy, which are often described in patients with diabetes . Pathomorphological changes begin even in the preclinical period, focusing at first in the end plates, as well as in motor sub-terminals , then moving to fibers, initially vegetative (poor in myelin), and later on to thicker ones. First, Schwann cells are affected , and then the myelin sheaths and then axial cylinders. Axoplasm is compacted, neurofibrils stick together and partially dissolve. The neuropathies of various neurons exhibit various features. So, in the oculomotor nerve, there is a thickening of the nerve vessels and ischemic disorders with necrosis in the center of the nerve, the destruction of myelin and axial cylinders and the proliferation of connective tissue elements, spindle-shaped thickening of the retrobulbar part of the nerve. The role of microangiopathy is also very significant in case of retro-labyrinth lesion of the vestibular nerve; with intra-maze damage to the nerve, cerebral atherosclerosis plays the main role. In the auditory nerves, pronounced degenerative changes are found without noticeable vascular changes. Thus, angiopathies , which are an essential factor in polyneuropathy ( especially in the elderly), do not exhaust the pathogenesis of these diabetes complications . There is no parallelism between the severity of limb ischemia and the severity of angiopathy of its nerve trunks. Hypoxia is only one of the links in the pathogenetic chain that unfolds in connection with the main factor – metabolic disorders. The effect of metabolic disorders is very complex. Due to the lack of insulin, the use of glucose by peripheral nerves is impaired. Glycolysis is disturbed in the nerve, an excess of pyruvic and lactic acids occurs, the process of thiamine phosphorylation , in particular thiamine pyrophosphate ( cocarboxylase ) , is disturbed . Concomitant secondary changes in water-electrolyte metabolism lead to nerve dehydration with loss of intracellular potassium, an increase in the content of intracellular sodium, and disruption of the potassium-sodium pump. Energy deficiency develops, acetylcholine synthesis decreases and degeneration occurs. An important role is played, apparently, by existing disorders of other types of metabolism in diabetes – fat and protein. 

Diabetic polyneuropathies are characterized by bilateral (somewhat asymmetric) lesions, usually of the lower extremities. In less than half of the observations, neuropathy of the upper extremities also joins . Patients complain of dull or pulling pain, usually in the distal parts of the extremities, aggravating more often at rest, and at night – tingling, crawling, chills or burning sensations, as well as crumps . In the distal parts of the legs (less often than the hands), sensory disturbances are revealed, first of the type hyper – and later hypesthesia (on average in 1/3 of patients). Deep sensitivity is rarely severely affected, vibrational – in 80% of cases. Flaccid paresis is recorded infrequently. Muscle atrophies are noted, sometimes their compaction and significant soreness. In most cases, tendon hyporeflexia is present . Although clear motor defects are infrequent, EMG and a study of the rate of conduct establish an early and gross involvement of motor fibers. Autonomic pathology, noted on average in 20% of cases, is manifested by sympathalgia , soreness along the vessels, changes in pilomotor reflexes, sweating, skin temperature, skin trophic disorders, osteoarthropathy . Visceral diabetic neuropathies ( vagal and sympathetic) are manifested by pain and a feeling of heaviness in the epigastric region, flatulence, gastroparesis and often an increase in colon tone, diarrhea. In other patients, constipation predominates. In parallel with gastric hypokinesia, disorders of the exocrine pancreatic function also develop. In diabetic polyneuropathy , orthostatic hypotension occurs due to the loss of a sympathetic vasodilating reflex for the legs, impaired innervation of the heart, impotence, intermittent urinary retention, loss of sensation of filling the bladder, and sometimes urinary and fecal incontinence.

local_offerevent_note September 30, 2019

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