Diabetic neuropathy involves damage to the central and peripheral nervous system in diabetes mellitus.
There is the following classification.
1. Sensomotor neuropathy:
2) focal (mononeuropathy) or polyfocal (cranial, proximal motor, mononeuropathy of the limbs and torso).
2. Autonomic (vegetative) neuropathy:
1) cardiovascular (orthostatic hypotension, cardiac denervation syndrome);
2) gastrointestinal (atony of the stomach), biliary dyskinesia, diabetic enteropathy);
3) urogenital (with impaired function of the urinary bubble, with impaired sexual function);
4) violation of the patient’s ability to recognize goggles;
5) violation of the pupil;
6) violation of the function of the glands (distal anhydrosis, hyperhidrosis when eating).
A key element in the pathogenesis of this complication is chronic hyperglycemia. There are three theories of the development of diabetic neuropathy.
Polyol-myo-inositol theory. According to it, as a result of hyperglycemia inside the nerve, a significant increase in glucose concentration occurs. Since excess glucose does not undergo complete metabolism, this contributes to the formation of sorbitol. This substance is osmotically active. As a result of an increase in the concentration of sorbitol intravenously, the activity of sodium potassium ATPТase decreases. This fact causes swelling of axons, as well as other structures of the neuron of a progressive nature.
Theory of endoneural microangiopathy. It consists in the fact that as a result of microangiopathy of the vessels of the nerves, axon hypoxia develops, which, in turn, leads to impaired metabolism and the occurrence of microchromosomes.
The manifestation of diabetic neuropathy depends on its type by classification.
In sensory neuropathy, a disturbance in vibration sensitivity is initially noted. This violation is detected using a graduated tuning fork, which is mounted on the head of the first tarsal bone. Diagnosis is based on the sensation of the patient’s vibration of the car tone. The most common symptom of the distal form of this complication of diabetes mellitus is the appearance of numbness and paresthesia in the lower extremities. Ordinary sting Bats are cold sensations in the legs, which are warm during palpation. For sensorimotor neuropathy, the appearance of restless legs syndrome is characteristic. This syndrome is associated with a combination of hypersensitivity with the appearance of paresthesias at night. Pain in the legs often appear at night.
As pathology progresses, these sensations appear in the hands, as well as in the chest and abdomen. With a long course of the disease, the death of small painful nerve fibers occurs, which is manifested by the spontaneous cessation of pain in the extremities. Sensomotor neuropathy may be accompanied by hypoesthesia, manifestations of which are loss of sensation of the “stocking and glove” type. In case of violation of proprioceptive sensitivity, the development of sensory ataxia is noted, which consists in impeding movement and movement coordination problems. Since pain sensitivity is impaired, patients often do not notice minor damage to the feet, which subsequently undergo easy infection. In the case of mononeuropathy, in most cases, the facial, abdominal and sciatic nerves are affected.
Cardiovascular form. In autonomic neuropathy, the vagus nerve is the first to be affected, which leads to an increase in sympathetic effects on the heart. These changes explain the development of resting tachycardia. The progression of the process leads to the defeat of the sympathetic nervous system, which is manifested by a slight decrease in tachycardia. All these changes in the innervation of the heart muscle lead to a violation of its adaptation to physical exertion.
The gastrointestinal form of diabetic neuropathy develops as a result of insufficient cholinergic regulation of the gastrointestinal tract function. Clinically, this form is manifested by the atony of the esophagus, the development of reflux esophagitis, and gastric paresis occurs, which can cause both slowing down and accelerating its emptying. As a result of intestinal motility disorders, there is an alternation of diarrhea and constipation. In addition, there is a violation of the exocrine function of the pancreatic gland. Salivation often develops, as well as biliary dyskinesia, which increases the tendency to form stones.
The urogenital form is a consequence of the spread of the pathological process to the sacral plexus. In this case, the regulation of the function of the urogenital tract is violated. Clinically, this form of diabetic neuropathy may manifest as an atony of the ureters of the bladder, reflux or stagnation of urine, an increase in a tendency to infection of the urinary system. In 50% of men, the appearance of erectile dysfunction, retrograde ejaculation is noted, and a violation of testicular pain innervation is also observed.
Women may have a violation of wetting of the shag.
Impaired ability to recognize hypoglycemia. Normally, hypoglycemia causes an emergency release of glucagon into the bloodstream. Its initial release occurs as a result of parasympathetic stimulation of pancreatic islets. Subsequently, glucagon is released due to mechanisms of humoral regulation. With the development of diabetic neuropathy, glucagon is released due to the first mechanism. Symptoms that are harbingers of hypoglycemia are also found to disappear. All these disorders lead to the fact that the patient loses the ability to recognize approaching hypoglycemia.
Diabetic neuropathy is accompanied by impaired pupil function, which is manifested by Argyll-Robertson syndrome or impaired vision adaptation in the dark.
Impaired function of the sweat glands develops as a result of a violation of the trophic skin innervation. As the function of the sweat glands falls, the skin becomes dry – anhidrosis occurs.
Treatment of this complication is carried out in three stages. The first stage is to achieve compensation of metabolic processes in diabetes mellitus. For this purpose, intensive insulin therapy. The second stage of treatment is to stimulate the regeneration of damaged nerve fibers. For this purpose, lipoic acid preparations and vitamins of group B are used.
Under the influence of lipoic acid preparations, the energy balance in nerve formations is restored, and their further damage is prevented. Originally the drug is administered intravenously at a dose of 300-600 mg / day. The duration of such therapy is 2-4 weeks. After a lapse of this time, they switch to a tablet form of the drug at a dose of 600 mg / day for 3-6 months. The third stage is to conduct symptomatic therapy, which depends on the form of diabetic neuropathy.