Diabetic polyneuropathy (DPN) is a lesion of the peripheral nervous system, one of the frequently identified complications of diabetes mellitus (DM). In 10% of people living with diabetes, symptoms of neuropathy are already present at the time of diagnosis of type 2 diabetes, and after 5-10 years the number of such cases increases to 50%. This is explained by the long asymptomatic period of the disease, when 5-7 years pass from the onset of carbohydrate metabolism disorders. All this time, the person remains in a state of chronically elevated blood glucose levels [1]. From the article you will learn the mechanism of development of diabetic neuropathy, its signs, diagnostic methods and approaches to prevention and treatment.
What is diabetic neuropathy
Diabetic neuropathy
is a combination of syndromes affecting various parts of the peripheral and autonomic nervous system, which occurs against the background of metabolic disorders in diabetes mellitus and complicates its course.
According to statistics, being one of the most common and serious complications of diabetes, various forms of diabetic neuropathy are diagnosed in almost half of all patients with diabetes.
Diabetic neuropathy is characterized by signs of impaired conduction of nerve impulses, sensitivity, as well as various disorders of the somatic and autonomic nervous systems that arose when other causes and factors of nervous system dysfunction (trauma, infections, etc.) were excluded. The clinical manifestations of the disease are very diverse, so most doctors with a narrow specialization encounter diabetic neuropathy - neurologists, urologists, endocrinologists, gastroenterologists, dermatologists, etc.
3.Symptoms
There are several clinical forms of diabetic polyneuropathy. In some cases, the syndrome manifests itself decades after the main diagnosis, in others, on the contrary, it turns out to be one of the first manifestations of diabetes mellitus.
With early onset of polyneuropathy, as a rule, sensitivity to vibration decreases and some reflexes are weakened. In the case of acute damage to the femoral, ulnar, trigeminal, sciatic and other nerves, disturbances in general tactile sensitivity develop, and partial paralysis is noted in the muscle groups associated with the affected nerve. The third, actually polyneuropathic option consists of multiple lesions of the nerves of the extremities, especially the lower ones, and is characterized by rest pain, a painfully aggravated reaction to heat, a tendency to mummification of the skin, the formation of trophic ulcers and gangrenous necrosis due to gross disturbances of tissue nutrition; Often there is concomitant inflammation and deformation of the joints (“diabetic foot”). Many patients describe, along with pain, itching or burning sensations, various kinds of paresthesia (illusory sensations, for example, “electrical discharges”), and muscle weakness.
As a rule, diabetic polyneuropathy occurs with a gradual worsening of symptoms. The most severe complications develop when the innervation system of internal organs, as well as the oculomotor nerve, is involved.
The diagnosis is established mainly clinically, using specially developed criteria and scales, reflexological research methods, analysis of anamnestic information and subjective complaints. Of the instrumental diagnostic methods, electroneuromyography, somatosensory evoked potentials, electrocardiography, etc. are of greatest importance.
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Causes and mechanisms of development of diabetic neuropathy
The main cause of diabetic neuropathy is chronically elevated blood glucose levels.
, ultimately leading to changes in the structure and functioning of nerve cells.
Due to impaired carbohydrate metabolism in diabetes mellitus, patients develop microangiopathies
- pathological changes in the vessels of the microvasculature, due to which the normal blood supply to the nerves is disrupted. As a result of multiple metabolic disorders, swelling of the nervous tissue develops, all metabolic processes in the nerve fibers are disrupted, the conduction of nerve impulses deteriorates, the antioxidant system is inhibited, leading to the accumulation of free radicals that have a detrimental effect on nerve cells, the production of autoimmune complexes begins, which ultimately can lead to atrophy of nerve fibers.
There are a number of factors that increase the risk of developing diabetic neuropathy:
- old age;
- long history of diabetes mellitus;
— decompression phase;
- increased blood pressure;
- overweight and obesity;
- smoking, drinking alcoholic beverages.
Modern approaches to the treatment of diabetic polyneuropathy
For citation. Umerova A.R., Dorfman I.P., Orlova E.A. Modern approaches to the treatment of diabetic polyneuropathy // RMJ. 2015. No. 26. pp. 1538–1542.
Peripheral neuropathy is characterized by diffuse damage to peripheral nerve fibers. The most common cause of this pathology is diabetes mellitus (DM). Thus, 30–90% of patients with diabetes have this complication [22, 30]. With newly diagnosed type 2 diabetes, diabetic neuropathy is diagnosed in 14–20% of patients, and with diabetes duration of more than 15 years – in 50–70% of cases [14]. Sensorimotor diabetic polyneuropathy is the most common type of diabetic neuropathy and has the greatest medical and social significance. In the population of patients with diabetes living in Moscow, it is observed in more than 50% [4]. 16–34% of patients with diabetes complain of symptoms of neuropathic pain, most often these are patients with type 2 diabetes, women and residents of South Asia [16, 30, 32]. Symptoms of painful diabetic neuropathy can be distressing, cause sleep disturbances, anxiety, and disrupt the patient's normal lifestyle [24]. Diabetic neuropathy significantly reduces the quality of life of patients and is one of the main causes of disability in patients, thereby leading to increased healthcare costs [30]. It has been established that from 40 to 70% of all non-traumatic amputations occur in patients with diabetes, so it is extremely important to diagnose neuropathy in a timely manner and take appropriate preventive and treatment measures [3]. Treatment of patients with diabetic polyneuropathy is based on 3 main principles: control of glucose levels, other metabolic disorders and correction of risk factors, pathogenetic therapy and symptomatic treatment. Pathogenetic therapy targets the underlying pathophysiological processes to prevent damage to nerve fibers and slow the progression of diabetic polyneuropathy. Symptomatic treatment is used to relieve pain and normalize physical and psychological condition [1, 30]. The pathogenesis of diabetic polyneuropathy is complex and is the result of the interaction of many factors, which include various metabolic, vascular, autoimmune, genetic and other disorders [8]. Currently, the model for the development of diabetic neuropathy is a multi-stage process, including a whole cascade of pathogenetic mechanisms: 1. Activation of the polyol pathway of glucose conversion using the enzyme aldose reductase, decrease in Na+/K+-ATPase activity. An increase in aldose reductase activity is accompanied by an increase in the formation and accumulation in the cell of osmotically active substrates, such as sorbitol and fructose [5, 14]. The polyol pathway is activated only under hyperglycemic conditions. Sorbitol, being a powerful osmoregulator, accumulates in tissues, including Schwann cells, causing their edema, swelling and death. Activation of the polyol pathway of glucose transformation can affect the state of intraneural blood flow, leading to its decrease, the development of chronic hypoxia and, as a consequence, structural changes in the nerves, which leads to disruption of neuronal functions [8]. The accumulation of sorbitol also leads to a decrease in the content of myo-inositol and thiamine in the nerve and a decrease in the activity of membrane Na+/K+-ATPase [4]. Decreased Na+/K+-ATPase activity causes sodium and fluid retention, myelin sheath swelling, decreased numbers of axonal glial cells, and peripheral nerve degeneration. A decrease in the level of myo-inositol leads to a decrease in the synthesis of phosphoinositol (a component of nerve cell membranes), which ultimately contributes to a decrease in energy metabolism and disruption of the conduction of nerve impulses [10, 11]. Increasing the activity of aldose reductase prevents the formation of NO, which leads to disruption of the blood supply to the nerves. In addition to sorbitol and nitric oxide, prostaglandins are involved in the development of diabetic neuropathy, the metabolism of which causes an increase in tissue hypoxia. A decrease in the synthesis of prostaglandins, which are strong vasodilators, leads to a narrowing of intraneural vessels, platelet aggregation, an increase in microvascular ischemia and endoneurial hypoxia. In addition, some prostaglandins reduce the nociceptive threshold and are involved in the generation of pain impulses [8]. 2. Non-enzymatic glycation of proteins. This theory of the pathogenesis of diabetic neuropathy is based on the ability of glucose, fructose and galactose to enter into glycosylation reactions with amino groups of proteins, lipid structures and nucleic acids [14]. This interaction leads to the formation of advanced glycation end products (AGEs). A key characteristic of AGEs is their ability to interact with proteins of the neuronal cytoskeleton, basement membranes, myelin and a number of other cellular structures, which leads to demyelination, endoneurial hypoxia, impaired neuronal regeneration, axonal atrophy, impaired axonal transport and, finally, neuronal degeneration. It should be noted that an increase in the level of advanced glycation end products occurs exogenously and endogenously. In the first case, with food that has undergone high-temperature cooking, as well as due to smoking. The endogenous pathway of AGEs formation is associated with hyperglycemia [4]. 3. Disorders of fatty acid metabolism. Characterized by a disturbance in the metabolism of gamma-linolenic and arachidonic acids and, as a consequence, a change in the metabolism of vasoactive substances, leading to a decrease in endoneurial blood flow. 4. Neurotrophic disorders. Impaired synthesis of neurotrophic factors and/or their receptors [14]. 5. Oxidative stress. The state of chronic hyperglycemia leads to excessive formation of free radicals, damage to the protein and lipid structures of neurons, disruption of neuronal energy metabolism, development of chronic endoneurial hypoxia and decreased conductivity. Excessive formation of peroxidation products has a damaging effect at the neuronal level directly or indirectly through disruption of intraneural blood flow, since the vascular endothelium is especially sensitive to their action. An increase in the production of free radicals is accompanied by a decrease in the effectiveness of endogenous antioxidant defense systems. Pathological disorders form a vicious circle. Endoneural microangiopathy and axonal hypoxia lead to increased oxidative stress, which in turn can induce neurovascular defects. Conditions for excessive formation of free radicals are: hypoxia, decreased antioxidant protection, autoxidation of glucose, activation of the polyol shunt [14, 15]. Emerging metabolic disorders lead to functional changes and neurophysiological abnormalities. The progress of the process is expressed in the development of structural changes in neurons and neuronal apoptosis [5]. The multifactorial nature of the pathogenesis of diabetic neuropathy makes different approaches to the treatment of this pathology justified. The main manifestation of diabetes is chronic hyperglycemia, which induces a chain of metabolic disorders in organs and tissues, therefore, correction of carbohydrate metabolism is of paramount importance in the treatment of complications of diabetes, including diabetic neuropathy. In cases of acute hyperglycemic painful polyneuropathy, restoration of the euglycemic state led to regression of neurological symptoms [8]. An association between chronic hyperglycemia and diabetic neuropathy has been established in several observational studies [29, 30]. The results of a multicenter randomized trial (Diabetes Control and Complications Trial - DCCT), as well as a prospective study of patients with diabetes in the UK (United Kingdom Prospective Diabetes Study, UKPDS) showed the role of chronic hyperglycemia in the development of late complications of this disease. According to DCCT, intensive insulin therapy reduces the risk of developing clinical manifestations of neuropathy in patients with type 1 diabetes by 64% after 5 years from the start of strict metabolic control [8]. Similarly, Epidemiology of Diabetes Interventions and Complications demonstrated a reduction in the incidence of neuropathy in patients with type 1 diabetes treated with intensive insulin therapy [17, 30]. In patients with type 2 diabetes, the role of promoting glycemic control in the prevention and treatment of diabetic neuropathy is less clear, as studies show conflicting results. A recent meta-analysis of randomized controlled trials did not find a significant benefit of intensive glycemic control in reducing neuropathy in patients with type 2 diabetes [20, 30]. This conclusion was supported by data from a Cochrane review, which showed no significant improvement in neuropathy in patients with type 2 diabetes with intensive glycemic control [23, 30]. However, most studies conducted in patients with type 2 diabetes were not specifically designed to investigate the effect of intensive glycemic control on diabetic polyneuropathy and included only basic assessment of neuropathy [30]. It is not always possible to achieve and maintain glycemic targets. Strict control of carbohydrate metabolism in many patients is unattainable, since it is accompanied by an increase in the frequency of hypoglycemic conditions, which, in turn, can cause the development of neuropathy. Therefore, correction of pathobiochemical processes induced by hyperglycemia is also necessary [4, 8]. Taking into account the importance of activation of the polyol pathway for glucose conversion using the enzyme aldose reductase in the pathogenesis of diabetic neuropathy, inhibitors of this enzyme have been proposed to prevent this complication. A number of these drugs have been studied, but most have shown significant side effects and limited effectiveness [19, 28]. The aldose reductase inhibitor epalrestat has been shown to improve neuropathic symptoms in patients with an acceptable safety profile. A three-year randomized trial confirmed the preventive role of epalrestat in the development of diabetic neuropathy [26, 30]. Recently, much evidence has been accumulated on the important role of AGEs in the etiology of diabetic peripheral neuropathy. Under conditions of hyperglycemia, advanced glycation end products accumulate in the peripheral nerves of patients with diabetes. The use of drugs that help reduce the formation of AGEs improves nerve conduction and restores neuronal blood supply. It has been proven that the formation of AGEs is prevented by the thiamine-dependent enzyme transketolase, an enzyme that reduces the pentose phosphate pathway of glucose metabolism. The introduction of thiamine can significantly increase the activity of this enzyme and direct glucose along the pentose phosphate pathway, thereby preventing its entry into alternative metabolism pathways and, therefore, avoiding neuronal damage [4, 7, 12]. In addition, thiamine (vitamin B1), in the human body, as a result of phosphorylation processes, transforms into cocarboxylase, which is a coenzyme, participates in many enzymatic reactions, plays an important role in carbohydrate, protein and fat metabolism, and is actively involved in the processes of nerve excitation in synapses. [eleven]. Thiamine reduces degenerative processes in nerve fiber, improves blood flow in tissues, and increases the amount of ATP [2]. In addition to thiamine, other vitamins are also used to treat diabetic polyneuropathy. Diabetics have a much higher risk of developing hypovitaminosis than people without this disease. The reason for this is the control of blood glucose levels, which requires constant strict adherence to the diet, which can lead to an unbalanced supply of vitamins [5]. In diabetes, there is a deficiency of many vitamins and microelements, but for the treatment of diabetic polyneuropathy, the most important role is played by eliminating the deficiency of B vitamins, which are also called neurotropic. These vitamins are coenzymes involved in various biochemical processes, improve the energy of the nerve cell, and prevent the formation of end products of protein glycation [11]. In addition to thiamine, neurotropic vitamins also include pyridoxine and cyanocobalamin. Pyridoxine (vitamin B6) is necessary for the normal functioning of the central and peripheral nervous system. It is a cofactor for more than 100 enzymes, and thanks to its ability to regulate the metabolism of amino acids, it normalizes protein metabolism, has an antioxidant effect, increases intracellular reserves of magnesium, which also plays an important role in the metabolic processes of the nervous system, and supports the synthesis of transport proteins in the axial cylinders. Also involved in the biosynthesis of many neurotransmitters, such as dopamine, norepinephrine, adrenaline, histamine and γ-aminobutyric acid. Pyridoxine deficiency leads to the development of distal symmetrical, predominantly sensory, polyneuropathy, manifested by a feeling of numbness and paresthesia in the form of “pins and needles” [11, 12]. Cyanocobalamin (vitamin B12) is necessary for normal hematopoiesis and maturation of red blood cells, and is also involved in a number of biochemical reactions that ensure the vital functions of the body: in the transfer of methyl groups (and other one-carbon fragments), in the synthesis of nucleic acids, proteins, in the metabolism of amino acids, carbohydrates, lipids. It has a beneficial effect on processes in the nervous system (synthesis of nucleic acids and lipid composition of cerebrosides and phospholipids). Coenzyme forms of cyanocobalamin - methylcobalamin and adenosylcobalamin are necessary for cell replication and growth [11]. In the process of prevention and treatment of diabetic polyneuropathy, it is also important to take into account the features (pharmacological properties and side effects) of the main therapy of diabetes. Thus, against the background of long-term use of metformin in the case of treatment of type 2 diabetes, it is important to remember the possibility of developing B12 hypovitaminosis, which determines the validity of the prevention of B12 deficiency using cyanocobalamin in therapeutic doses [6]. To achieve a better therapeutic effect in patients with diabetes, it is advisable to use long-term vitamin therapy. It is necessary that vitamin therapy be comprehensive and take into account as much as possible the peculiarities of the interaction of all vitamins [5]. However, the separate use of each B vitamin adds several more injections or tablets to the treatment, which is extremely inconvenient for patients and reduces their compliance [11]. In this regard, it is advisable to use balanced multivitamin complexes, which take into account the rational interactions of vitamins. One of these multivitamin preparations for injection is Vitaxon. The drug is available in injection form (solution for intramuscular injection in ampoules of 2 ml, in packs of 5 or 10 pieces). 1 ml of solution contains thiamine hydrochloride - 50 mg, pyridoxine hydrochloride - 50 mg, cyanocobalamin - 0.5 mg. Once again, it is necessary to emphasize that all the vitamins included in this drug are neurotropic, provide the physiological structure and function of nerve cells and prevent their damage in somatic diseases, including diabetes. They also have an additional analgesic effect. According to E.V. Shikh, the neurotropic complex is effective in diabetic neuropathy in relation not only to symptoms, but also to the functional state of nerve fibers [9,15]. Thus, Vitaxon is an effective combination of B vitamins and can be used for the prevention and treatment of diabetic polyneuropathy. The drug is administered following standard recommendations for intramuscular injections. In order to quickly achieve high plasma concentrations in severe and acute pain conditions, 2 ml is administered 1 r./day during the first days. In mild forms of the pathology or after pain has decreased, the drug intake can be reduced to 2 ml, administered intramuscularly 2–3 times/week. [9,15]. Another important link in the pathogenesis of diabetic polyneuropathy is oxidative stress. Therefore, the administration of drugs with antioxidant properties is necessary for the treatment of such patients. They reduce the production of free radicals, thereby limiting their damaging effects and preventing the development of a pathological cascade of reactions [15]. The drugs used for this purpose primarily include alpha-lipoic acid (ALA). ALC, when administered intravenously, is the only pathogenetic therapy with proven effectiveness in several randomized controlled trials and in a meta-analysis (recommendation level A) [13]. ALA, also known as thioctic acid, is a naturally occurring substance essential for the function of various enzymes in oxidative metabolism. ALA was discovered in 1937 by Snell, but was isolated only in 1951 by Reed. The first clinical use of ALA was described in Germany in 1959 for the treatment of acute poisoning by toadstool. Shortly thereafter, the same authors (Bock E., Schneeweiss J.) described a positive result from the use of ALA in the treatment of neuropathy [25]. In addition to the antioxidant effect of the ALK or its restored form - digidolipoic acid has the following biological properties: - improvement of transmembrane glucose transport with activation of glucose oxidation processes; - decrease in the intensity of protein glycosylation processes; - decrease in the concentration of fatty acids in plasma; - a decrease in the content of total cholesterol and its esters in the blood; - increasing cell stability to hypoxia; - prevention of inhibiting of activity No; - reduction of oxidized forms of other antioxidants, such as vitamins C, E and glutathione; - reduction of endothelial dysfunction [8, 25]. Thanks to the indicated effects, the ALK can simultaneously affect several links in the pathogenesis of diabetic polyneuropathy [8]. The results of large multi-centered randomized doubles of placebo-controlled studies conducted in Europe and the USA showed high efficiency of Alk [27]. A major study by Sydney demonstrated the effectiveness of the ALK with V/in the introduction: patients with diabetic polyneuropathy noted a rapid and significant decrease in the severity of neuropathic symptoms [6, 18]. Intravenous ALK therapy promotes not only the regression of clinical symptoms, but also improves objective indicators of the function of the peripheral nervous system [13]. A number of studies have demonstrated an improvement in antioxidant status when adding Alc to the treatment of diabetes even in patients with unsatisfactory control of glycemia [6]. One of the representatives of the ALK is the drug Neurolipin. The drug is administered in/V slowly at a dose of 600 mg, mixed with 50-250 ml of a 0.9% sodium chloride solution, 1 p./Day. In severe cases, you can enter up to 1200 mg. Infusion solutions should be protected from light, covering them with light -protective screens (a light filter is included in the neurolipon configuration)) of treatment - from 2 to 4 weeks. After that, they switch to supporting therapy with drug forms for oral administration for 1-3 months. [9]. With oral therapy for diabetic neuropathy, various schemes and prescription modes of the ALK are used. In most cases, the oral daily dose of the ALK is 600–1800 mg. Usually patients tolerate Alc drugs well. Nevertheless, some patients may have various undesirable phenomena that make it difficult to comply with the prescribed treatment regimen (heartburn, nausea). More often, unwanted adverse reactions are observed with a single reception of large doses of Alk. In a similar situation, to improve the tolerance of Alk, the daily dose of the drug is usually divided into 2-3 doses [13]. To consolidate the effect of treatment, the ALK therapy course is recommended to be carried out 2 p./Year. To increase the effectiveness of the therapy, Alc drugs can be combined with neurotropic vitamins, which also effectively eliminate oxidative stress [9]. Alk and vitamins of group B, when using them in therapeutic doses, taking into account the described mechanisms of action, experimental data and the results of clinical observations, can be used in the treatment of polyneuropathies, as in the composition of pathogenetic therapy aimed at correcting the main mechanisms leading to the development of the disease and in composition of symptomatic and restorative therapy. The inclusion of these drugs in the therapy of polyneuropathy helps to increase the effectiveness and safety of the treatment [15]. As a symptomatic therapy for the treatment of pain form of diabetic polyneuropathy, [6, 21, 31]: 1. Anticonvulsants: pregabalin (level of evidence a), gabapentin, sodium valproate (level of evidence B). The role of topiramate continues to be discussed, because there are not enough data confirming its effectiveness. 2. Antidepressants: tricyclic antidepressant - amitriptylin, inhibitors of the reverse capture of serotonin and norepinephrine - Wenlafaxin and dulceset (level of evidence B). The use of amitriptyline can be limited in connection with its possible side effects. It is recommended to carry out a gradual titration of the dose of amitriptyline to reduce the likelihood of developing side effects. The effectiveness of selective inhibitors of the reverse capture of serotonin is discussed. Based on the results of a number of studies of paroxetine and cityloprams, it can be effective in relief of pain. Fluoxetine did not show its effectiveness in the treatment of pain diabetic polyneuropathy. 3. Opioid tramadol (level of evidence B). 4. Non -steroidal anti -inflammatory drugs (level of evidence B). 5. Topic drugs: capsaicin, lidocaine [6, 30]. Monotherapy with anticonvulsants and antidepressants should be considered as the first line therapy, and with insufficient effectiveness it is possible to prescribe their combinations or a combination with second -line drugs (tramadol, a patch with lidocaine, etc.) [13]. The purpose of opiates with neuropathic pains and today remains the subject of discussion. In some patients with such pains, the use of opiates can provide an optimal ratio of analgesic activity and side effects of therapy. For example, elderly patients transfer opiates better than tricyclic antidepressants and many anti -ilsants. However, in the treatment of neuropathic pain, opiates cannot be the first choice; If there are indications, only tramadol can be temporarily recommended [14]. Local forms of capsaicin or lidocaine can also be used for the treatment of pain syndrome. Capsaicin is an active substance contained in the red burning Chilean pepper, which depletes reserves of substance P in the terminals of sensory fibers. It is used locally in the form of creams and gels containing a number of additional components (extractor pepper extract, cooling additives), 3-4 rubles/day. Against the background of the use of capsaicin, it is possible to temporarily increase pain symptoms with a gradual weakening by the end of 2-3 weeks. treatment. In addition to capsaicin, 2.5% and 5% gels of lidocaine can be used [14]. When drawing conclusions, we can say that only comprehensive treatment, which includes control of metabolic disorders, pathogenetic therapy and symptomatic therapy of pain, will contribute to the slowdown of the progression of diabetic polyneuropathy and improve the quality of life of patients.
Diabetic neuropathy - symptoms, syndromes, types
Diabetic neuropathy is classified in several ways. A number of authors distinguish four main types of diabetic neuropathy:
— peripheral neuropathy
- one of the most common types, in which there is damage to the nerve fibers of the extremities, and the lower extremities are affected more often;
— autonomic neuropathy
- in which the functioning of many internal organs is disrupted - the heart, stomach, intestines, and sexual dysfunction develops;
— proximal neuropathy
- characterized by severe pain in the thighs, buttocks and hip joints;
— focal neuropathy
- in which local damage to individual nerve fibers occurs.
There is a classification of diabetic neuropathy, which is based on the principle of identifying syndromes with characteristic clinical manifestations and course. According to it, diffuse neuropathy
(affecting all nerve fibers) and
focal neuropathy
(affecting certain areas of the human body).
The prevalence of diffuse neuropathy is much higher, it progresses rapidly and is often asymptomatic. It includes autonomic diabetic neuropathy
and
distal symmetric sensorimotor diabetic polyneuropathy
.
Focal neuropathy is less common and occurs acutely, losing its clinical manifestations over time. It includes cranial neuropathy, radiculopathy, plexopathy, mononeuropathy.
Folk remedies
Treatment of polyneuropathy with folk remedies has a good effect and is possible only as part of complex therapy.
Blue or green clay (50–100g) is mixed with water and brought to a mushy state. Used as a compress, applied and left until completely dry. The procedures continue for 2 weeks, after a 10-day break the treatment is repeated. This method restores nerve fibers and increases the functionality of receptors.
To treat diabetic polyneuropathy, lemon peel is used, which is applied to the foot at night, bandaged, and a sock is put on top. The course of treatment is from 2 to 3 weeks. The procedure stimulates the nervous system and promotes the renewal of nerve fibers.
Stinging nettle and chamomile are mixed in equal proportions. Two teaspoons of the mixture are poured into a glass of water. And kept in a water bath for a quarter of an hour. Cool for 30 minutes, strain. Use three times a day in equal parts. The course lasts 2–3 months.
The decoction reduces sugar levels and improves nutrition of nerve cells
Peripheral neuropathy
Peripheral diabetic neuropathy occurs predominantly in the lower extremities and is characterized by burning and painful sensations in the legs, often occurring at night, a feeling of sudden heat or cold, and pins and needles in the legs. Patients are very sensitive to touch, sometimes it is even painful. Deformations of the muscles of the limbs may be observed. Any damage. violating the integrity of the skin of the extremities become wounds that do not heal over a long period.
Diagnostics
Timely treatment of diabetic polyneuropathy improves quality of life and prevents disability. Therefore, early diagnosis of the disease is very important.
Diagnostic methods include electroneuromyography - a comprehensive assessment of the electrical activity of nerve fibers and muscles. The results of the study reveal damage to the sensory and motor nerves in the end parts of the legs. An orthostatic test or quantitative autonomic and sensory testing is useful to detect small fiber pathology.
To objectively assess peripheral nerve function, the TSS (Total Symptom Score) and NISS-LL (Neuropathy Score in the Lower Extremities) scales are used. The TSS evaluates symptoms such as pain, burning, numbness, and tingling, while the NISS-LL provides insight into muscle strength in the feet, the integrity of the Achilles reflex, and pain sensitivity. The scales are easy to use; their filling time does not exceed several minutes [4].
Autonomic neuropathy
Autonomic diabetic neuropathy is characterized by damage to the autonomic nervous system, which controls and coordinates the functioning of internal organs. In this case, violations of most organs and systems may be observed.
In particular, when the nerve fibers responsible for the functioning of the digestive system are damaged, patients complain of nausea, heartburn, a feeling of heaviness in the stomach even with a small amount of food consumed, flatulence, diarrhea or constipation. These symptoms may indicate the development of gastroparesis, a dysfunction of the stomach. At the same time, there is a slowdown in the evacuation of food from the stomach to the intestines. If the process involves the nerves that control the small intestine, nocturnal diarrhea develops.
If the nerve fibers responsible for the functioning of the genitourinary system are damaged, bladder paresis may develop, while urine is not evacuated from the bladder in a timely manner due to the lack of urge to urinate, thereby increasing the risk of a genitourinary tract infection. Patients complain of frequent, infrequent or involuntary urination.
In addition, due to the negative impact on the nerves responsible for the occurrence and maintenance of an erection in men during sexual arousal, autonomic neuropathy can lead to erectile dysfunction while maintaining sexual desire in the patient. Female patients may complain of decreased arousal and excessive dryness in the vagina, which occurs due to a decrease in the amount of vaginal secretion during sexual intercourse.
With autonomic neuropathy due to damage to the cardiovascular system, symptoms such as dizziness and causeless loss of consciousness, increased heart rate, painless angina, etc. may occur.
On the skin side, patients note excessive dryness of the extremities, profuse sweating or its complete absence.
Symptoms
The most common form of the disease is chronic sensorimotor neuropathy [5]. Polyneuropathy of the lower extremities begins from the end parts of the legs and spreads towards the trunk [2]. Thin sensitive fibers are affected first. This is manifested by pain, unpleasant burning and tingling sensations, and numbness. Symptoms of DPN, especially neuropathic pain, can appear suddenly and be quite severe, which can reduce the quality of life of patients, create difficulties in movement, cause low mood and social maladjustment [2].
Along with this, impaired reflexes and a decrease in superficial (pain and temperature) and deep (vibration) sensitivity appear. Motor disturbances (weakness and thinning of the muscles of the feet and legs) are noted in later stages of the disease. The sensitivity disorder in the arms and legs with DPN has the appearance of “gloves” and “stockings”. People with damage to thick myelin fibers complain of numbness, tingling, and pain. Unsteadiness of gait is common, especially in the dark or when walking on uneven surfaces. Individuals with this type of polyneuropathy are at high risk of developing ulcerative lesions, which can ultimately lead to amputation.
In a minority of patients with DPN, thin myelin fibers are predominantly affected. Clinically, this is manifested by a decrease in temperature and pain sensitivity with relatively preserved vibration and muscle senses. Quite often, neuropathic pain develops, which patients describe as burning, stinging, pulling, like “needles” [2].
Another form of the disease is autonomic polyneuropathy. It is manifested by disorders of the autonomic nervous system, occurs quite often and occurs under various clinical masks [6]. Complaints vary depending on which organ system is affected [5]:
- cardiovascular - dizziness, fainting;
- gastrointestinal - swallowing disorder, nausea, vomiting, constipation/diarrhea, bedwetting;
- genitourinary - the need to wake up several times at night to urinate, a feeling of incomplete emptying of the bladder, erectile dysfunction, vaginal dryness.
Autonomic polyneuropathy is also characterized by impaired sweating (absence or sweat during meals), disorder of pupil adaptation to light, and “silent” myocardial ischemia [5].
There is evidence that a patient with DPN, while driving a vehicle, can pose a threat to himself and others. People with lower extremity neuropathy have a slower braking response, which increases the likelihood of an accident.
Impaired pupillary reactions are expressed in a paradoxical decrease in pupil diameter during adaptation to darkness in the early stages and the absence or very slow and incomplete dilation of the pupil in the future. This feature manifests itself as difficulty driving at night [2].
Focal neuropathy
This type of neuropathy usually occurs suddenly, affecting the nerve fibers of the head, torso, and limbs. It is characterized by pain of varying strength and muscle weakness. In addition to these signs, Bell's palsy, which affects one side of the face, double vision, and pain in the chest or abdomen, which is often mistaken for a heart attack or appendicitis, may occur.
If one or a complex of the above symptoms are detected, patients suffering from diabetes should consult a specialist for differential diagnosis of diabetic neuropathy with other diseases with similar symptoms, such as alcoholic neuropathy, neuropathy that occurs while taking neurotoxic drugs or exposure to toxic chemicals (solvents, heavy metal compounds, etc.).
A set of methods for diagnosing diabetic neuropathy
The list of diagnostic methods for diabetic neuropathy is directly related to the form of neuropathy the patient presented with. Therefore, at the initial consultation, anamnesis and complaints are carefully collected, based on which the endocrinologist or diabetologist involves other specialists in the study.
All patients need to determine the level of sugar, insulin and glycosylated hemoglobin in the blood; examination of the legs is mandatory to identify wounds, trophic ulcers, fungal infections, calluses, etc.
Neurological examination of patients with diabetic neuropathy includes electromyography and electroneurography, assessment of reflexes and the level of perception of all senses.
If there are symptoms of damage to the digestive tract, it would not be superfluous to do an ultrasound examination of the abdominal organs, radiography of the stomach, and esophagogastroduodenoscopy. If the patient has complaints from the genitourinary system, it is necessary to conduct a general urine test, ultrasound of the kidneys and bladder with determination of residual urine volume, cystoscopy and urography.
Treatment at the Energy of Health clinic
Neurologists at the Energy of Health clinic will provide assistance with any form of polyneuropathy. Specialists will conduct a full diagnosis to accurately identify the extent and location of the lesion, and then prescribe treatment and rehabilitation in accordance with the individual characteristics of the body. We use comprehensive methods that include:
- drug therapy in accordance with indications and modern recommendations for the treatment of polyneuropathy, including courses of infusions;
- various types of physiotherapy: magnetic therapy, laser and ultrasound exposure, phonophoresis and electrophoresis;
- physical therapy under the supervision of an experienced instructor, training in exercises to restore limb function at home;
- massotherapy;
- sessions with a psychotherapist if you have depression, insomnia, or increased anxiety;
- organization of sanatorium-resort treatment for complete rehabilitation.
How to treat diabetic neuropathy
In the treatment of diabetic neuropathy, consistency and phasing are important. Since the disease is concomitant with the main one - diabetes mellitus of the first and second types, first of all it is necessary to transfer diabetes mellitus to the stage of compensation. Correction of blood glucose levels is carried out by an endocrinologist or diabetologist by prescribing insulin or antidiabetic drugs. Regular monitoring of blood sugar levels is necessary. In addition, for complex treatment of the patient, a special diet must be developed and a physical activity regimen must be determined. If the patient is obese, it is necessary to develop a program to reduce excess weight. Monitoring blood pressure levels is no less important.
Symptomatic treatment depends on the type of diabetic neuropathy and consists of taking B vitamins that have a neurotropic effect, antioxidants, magnesium and zinc. When diabetic neuropathy is accompanied by severe pain, they resort to prescribing painkillers and anticonvulsants.
Specialists widely use physiotherapeutic methods of treatment in the treatment of diabetic neuropathy of the legs, such as electrical nerve stimulation, magnetic therapy, laser therapy, acupuncture, and physical therapy. Patients with predominant lesions of the feet are recommended to carefully care for the feet, moisturize them and wear comfortable shoes to prevent the formation of calluses and corns.
Treatment
For effective treatment of diabetic polyneuropathy, it is important to lose weight, stop smoking, and control blood pressure and blood lipids [2]. It is useful to adhere to a diet, maintain physical activity and engage in therapeutic exercises [4]. The main method of treating the disease is to achieve and long-term maintenance of optimal glycemic control [2].
Drug therapy for DPN is divided into pathogenetic and symptomatic.
Pathogenetic treatment is aimed at reducing neurological symptoms and improving nerve function. It includes the prescription of antioxidants, combination preparations of B vitamins and hemoderivative-based products.
Symptomatic therapy is aimed at eliminating the main manifestations of polyneuropathy; analgesics are most often prescribed to relieve neuropathic pain [1]. However, it should be borne in mind that, while reducing the intensity of pain, these drugs do not slow down the progression of DPN [4]:
- anticonvulsants;
- antidepressants;
- opioids.
Anxiety or depressive disorder is diagnosed in 2/3 of people with a painful form of DPN, and 95% have sleep disorders, so such patients require psychological or psychotherapeutic help [4].
Prevention and Treatment – Differences in Effectiveness
The likelihood of developing and the severity of complications of diabetes mellitus directly depends on the fullness of compensation for carbohydrate metabolism, as well as on the implementation of a set of preventive measures. Every patient with diabetes should undergo a course of vascular therapy at least once every 6 months, aimed at preventing the development of complications, including diabetic neuropathy.
Unfortunately, it is often quite difficult to convince patients with diabetes mellitus of the need for preventive courses of treatment, since in the initial stages of the disease nothing bothers patients, and the person usually ignores elevated glucose levels altogether. At the same time, the effectiveness of treatment measures directly depends on how early they are started and how regularly they are carried out.
After complications become visible to the naked eye (at this point the quality of life of patients begins to rapidly decline), almost all patients begin to undergo active treatment. Unfortunately, in the later stages of the disease, the effectiveness of vascular therapy is no longer as high as at the beginning of the disease. Therefore, it should be recognized as absolutely proven that the prevention of the development of neuropathy and other complications of diabetes mellitus should begin immediately after diabetes is diagnosed and continue throughout the entire period of its treatment.
Causes
Damage to peripheral nerves can occur due to the following conditions:
- diabetes mellitus: the most common cause of polyneuropathy, resulting from metabolic disorders in the myelin sheath of nerve fibers; mainly the lower extremities are affected;
- severe and prolonged deficiency of B vitamins necessary for the full functioning of the nervous system;
- infectious diseases: HIV, tick-borne borelliosis, leprosy;
- renal failure;
- alcohol abuse;
- acute and chronic intoxication, including drugs;
- autoimmune diseases: damage occurs against the background of a malfunction of the immune system; the most common are chronic and acute inflammatory polyneuropathy (Guillain-Barré syndrome);
- long stay in intensive care, for example, with extensive injuries or serious illness;
- exposure to ionizing radiation;
- pregnancy: carrying a child can cause vitamin deficiency and autoimmune lesions.
In addition, there are hereditary forms of the disease, transmitted from relatives, as well as idiopathic polyneuropathy, the cause of which cannot be determined.