Urine therapy and polyneuropathy. Polyneuropathy (polyneuropathy). Treatment with goat milk

Polyneuropathy, or peripheral neuropathy, occurs as a result of damage to the peripheral nerves and often results in symptoms such as weakness, numbness and pain, usually in the arms and legs. But polyneuropathy can also affect other areas of the body. Peripheral neuropathy may develop in one nerve (mononeuropathy), two or more nerves in different areas, or may involve many nerves (polyneuropathy).

The peripheral nervous system transmits information from the brain and spinal cord (central nervous system) to the rest of the body. Peripheral neuropathy can result from traumatic injuries, infections, metabolic disorders, hereditary causes, and exposure to toxins. One of the most common causes of polyneuropathy is diabetes mellitus.

Patients with peripheral neuropathy typically describe pain as a tingling or burning sensation. In many cases, symptoms decrease if compensation occurs for the underlying disease.

Each nerve in the peripheral nervous system has a specific function, so symptoms depend on the type of nerve that is damaged. Nerves are divided into:

  • Sensory nerves that receive sensations from the skin, such as temperature, pain, vibration, or pressure
  • Motor (motor) nerves that control muscle movement
  • Autonomic nerves that control functions such as blood pressure, heart rate, digestion, and bladder function

Symptoms

Symptoms of polyneuropathy may include:

  • Gradual onset of numbness and tingling in the legs or arms that may spread up the arms and legs
  • Sharp stabbing or burning pain
  • Increased sensitivity to touch
  • Lack of coordination and falling
  • Muscle weakness or paralysis if motor nerves are damaged

If autonomic nerves are involved, symptoms may include:

  • Heat intolerance, as well as changes in sweating
  • Digestive, bladder, or bowel problems
  • Changes in blood pressure, which may cause dizziness

Reasons

A number of factors can lead to the development of neuropathy, including:

  • Alcoholism. A poor diet can lead to vitamin deficiencies.
  • Autoimmune diseases. These include diseases such as Sjögren's syndrome, systemic lupus erythematosus, rheumatoid arthritis, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy and necrotizing vasculitis.
  • Diabetes. More than half of people with diabetes develop some type of neuropathy.
  • Exposure to poisons. Toxic substances include heavy metals or chemicals.
  • Medicines. Some medications, especially those used to treat cancer (chemotherapy), can cause peripheral neuropathy.
  • Infections. These include some viral or bacterial infections, including Lyme disease, shingles, Epstein-Barr virus, hepatitis C, leprosy, diphtheria, and HIV.
  • Hereditary diseases. For example, a disease such as Charcot-Marie disease is a hereditary type of neuropathy.
  • Injury or compression on a nerve. Injuries such as car accidents, falls, or sports injuries can damage or even sever peripheral nerves. Nerve compression can occur when peripheral nerves are continuously impacted.
  • Tumors. Malignant and benign tumors can damage or put pressure on nerves.
  • Vitamin deficiency. B vitamins, including B-1, B-6 and B-12, vitamin E and niacin are important for nerves.
  • Bone marrow diseases. These include the presence of an abnormal protein in the blood (monoclonal gammopathies), multiple myeloma, lymphoma and amyloidosis.
  • Other diseases. These include kidney disease, liver disease, connective tissue disease and thyroid disease (hypothyroidism).

Complications of polyneuropathy may include

  • Burns and skin injuries. If there is numbness in parts of the body, the patient may not feel temperature changes or pain.
  • Infections. The legs and other areas of the body with reduced sensation may be unnoticed. It is necessary to monitor the integrity of the skin, especially if you have diabetes, since even minor damage to the skin can lead to tissue infection.

Diagnostics

When diagnosing polyneuropathy, a doctor may be primarily interested in answers to the following questions:

  • Does the patient have any medical conditions such as diabetes or kidney disease?
  • When did the symptoms start?
  • Were the symptoms constant or sporadic?
  • How severe are the symptoms?
  • What causes symptoms to increase or decrease?
  • Did anyone in the patient's family have similar symptoms?
  • The doctor needs a complete medical history. The doctor will review the patient's medical history, including symptoms, lifestyle, exposure to toxins, bad habits, and family history of neurological diseases.
  • During a neurological examination, the doctor can check tendon reflexes, muscle strength and tone, the ability to feel certain sensations, and coordination.

The doctor may order an examination

  • Imaging techniques CT or MRI can detect various diseases (including tumors).
  • Neurophysiology. Electromyography records electrical activity in muscles, which can help determine whether symptoms, including weakness, are caused by muscle tissue damage or nerve damage. ENMG checks the conduction of impulses along the nerves and allows you to determine the degree of damage to the nerve fibers. Neurophysiological studies of the autonomic nervous system may also be carried out - sensory tests that record how the patient feels touch, vibration, cold and heat.
  • Nerve biopsy. A doctor may recommend removing a small portion of a nerve, usually a sensory nerve, to examine morphological changes in the nerve to determine the cause of the nerve damage.
  • Skin biopsy. In this test, a small portion of skin is removed to examine the number of nerve endings. A decrease in the number of nerve endings indicates neuropathy.
  • Laboratory research methods are necessary to exclude various diseases, such as diabetes mellitus, autoimmune diseases, kidney disease, etc.

Treatment

The goal of treatment for polyneuropathy is to treat the underlying disease and minimize symptoms. If laboratory tests and other examinations indicate that there is no underlying disease, the doctor may recommend watchful waiting to see if the symptoms of neuropathy improve on their own. If there is exposure to toxins or alcohol, your doctor will recommend avoiding these substances.

Drug treatment

Medicines used to relieve pain from polyneuropathy include:

  • Painkillers such as paracetamol or NSAIDs reduce pain
  • Medicines containing opioids, such as tramadol (Conzip, Ultram ER and others) or oxycodone (Oxycontin, Roxicodone and others), can lead to dependence and addiction, so these drugs are generally prescribed only when other treatments have no effect.
  • Anticonvulsants. Medications such as gabapentin (Gralise, Neurontin) and pregabalin (Lyrica), developed to treat epilepsy, can significantly reduce the pain of neuropathy. Side effects of these drugs may include drowsiness and dizziness.
  • Capsaicin. A cream containing this substance (found naturally in hot peppers) can be used to provide some relief from the symptoms of neuropathy. But given the irritating effect of capsaicin on the skin, not all patients can tolerate the effects of capsaicin creams.
  • Antidepressants. Some tricyclic antidepressants, such as amitriptyline, doxepin, and nortriptyline (Pamelor), can be used to reduce neuropathy pain through their actions on the central nervous system.
  • The serotonin and norepinephrine reuptake inhibitor duloxetine (Cymbalta) and the antidepressant venlafaxine (Effexor XR) may also relieve pain from peripheral neuropathy caused by diabetes. Side effects may include dry mouth, nausea, drowsiness, dizziness, decreased appetite, and constipation.
  • Intravenous immunoglobulin is the mainstay of treatment for chronic inflammatory demyelinating polyneuropathy and other inflammatory neuropathies.
  • Alpha lipoic acid. Used to treat peripheral neuropathy in Europe for many years. This antioxidant helps reduce symptoms. You should discuss taking alpha lipoic acid with your doctor because it may affect your blood sugar levels. Other side effects may include stomach upset and skin rash.
  • Herbs. Some herbs, such as evening primrose oils, may help reduce neuropathic pain in patients with diabetes.
  • Amino acids. Amino acids such as acetyl-L-carnitine may help improve symptoms of peripheral neuropathy in patients undergoing chemotherapy and in patients with diabetes. Side effects may include nausea and vomiting.

In addition to drug treatment, other treatment methods may be used.

  • Myostimulation allows, to a certain extent, to restore the conduction of nerve impulses through the muscles.
  • Plasmapheresis and intravenous administration of immunoglobulin.
  • Exercise therapy. If you have muscle weakness, physical activity can improve muscle strength and tone. Regular exercise, such as walking three times a week, can reduce neuropathy pain, improve muscle strength, and help control blood sugar levels. Exercises such as yoga and tai chi can also be quite effective.
  • Acupuncture. Impact on biologically active points improves the sensitivity of nerve receptors and reduces pain.
  • It is necessary to take care of your feet, especially if you have diabetes. You should check your feet daily for blisters, cuts, or calluses. Soft, loose cotton socks and soft boots should be worn.
  • You need to quit smoking. Smoking can affect circulation in the extremities, increasing the risk of foot problems and other neuropathy complications.
  • Eat healthy. A healthy diet is especially important to ensure that the patient receives the necessary vitamins and minerals.
  • We must avoid drinking alcohol. Alcohol can worsen the symptoms of polyneuropathy.
  • Monitoring blood glucose levels in the presence of diabetes will help keep blood glucose levels under control and may help improve neuropathy.


For quotation: Rachin A.P., Anisimova S.Yu. Polyneuropathy in the practice of a family medicine doctor: diagnosis and treatment // Breast Cancer. 2012. No. 29. S. 1470

The process of formation of polyneuropathy (PNP) is based on dystrophic, toxic, metabolic, ischemic and mechanical factors, leading to the development of changes in the connective tissue interstitium, myelin sheath and axial cylinder. Along with this, the involvement of peripheral nerves and spinal cord roots in the process indicates the development of polyradiculoneuropathy (PRNP).

Polyneuropathy is a neurological disorder that is characterized by a specific implementation of the pathological process at the level of the peripheral nervous system. Polyneuropathy is the most common cause of areflexia, while symmetrical loss of reflexes emphasizes the fact that the patient has or previously had damage to the peripheral nervous system.
Currently, about 150 etiological theories of the occurrence of polyneuropathy are known. This pathology is observed in a variety of intoxications: alcohol, industrial toxins (arsenic, lead, mercury, thallium), viral and bacterial infections, collagenoses, vitamin deficiencies, malignant neoplasms (cancer, lymphogranulomatosis, leukemia), diseases of internal organs (liver, kidneys, pancreas). ), endocrine glands (diabetes, hyperthyroidism, hypothyroidism, hypercortisolism), administration of serums and vaccines, a number of medications (treatment with emetine, bismuth, gold salts, sulfonamides, isoniazid, antibiotics) (Table 1).
Hereditary polyneuropathies
As with most genetic diseases, there are polyneuropathies with a known metabolic basis (hereditary amyloidoses, porphyrias, lipid metabolism diseases, diseases accompanied by impaired DNA repair) and polyneuropathies in which the etiology of the defect is unknown (hereditary motor-sensory, sensory and autonomic PSP, neuropathy with hereditary ataxias and mixed diseases). There are forms with both dominant and recessive types of inheritance.
Hereditary polyneuropathies can be considered as systemic diseases, which are characterized by damage to several organ systems. The presence of a metabolic defect has been identified in several hereditary polyneuropathies: metachromatic leukodystrophy (a disorder of the cellular metabolism of sulfatides, mainly in oligodendroglial cells of the central nervous system and Schwann cells of the PNS), Fabry disease (glycosphingolipidosis, a lipid accumulation disease), ataxic polyneuritis-like heredopathy - Refsum's disease (phytin storage disease). acids), Bassen-Kornzweig disease (low plasma cholesterol and complete absence of highly dispersed and dispersed lipoproteins). The group of peroneal muscular atrophies (Charcot-Marie-Tooth syndrome) also has a hereditary etiology.
Clinical manifestations of polyneuropathy depend on the degree of involvement of motor, sensory and autonomic fibers in the pathological process. Motor disorders are represented by muscle weakness, which is localized mainly in the distal parts, more manifested in the extensor muscles, accompanied by their atrophy, hypo- or areflexia. In severe cases, patients are unable to stand or move independently or hold any objects in their hands.
Sensory changes include positive (paresthesia, hyperpathia) and negative (loss of articular, muscle and tendon proprioception, leading to impaired stability when standing and walking; decreased skin tactile and pain sensitivity) symptoms.
Autonomic symptoms manifest themselves in the form of sympathalgia, vasomotor, trophic and secretory disorders (poorly localized pain of a burning, bursting nature, changes in sweating, swelling of the distal parts of the extremities, disruption of their normal color and temperature, trophic ulcers, changes in the muscles).
It should be noted that there are four types of polyneuropathy: acute (symptoms develop earlier than after 1 week), subacute (duration of symptoms develops no more than 1 month), chronic (duration of symptoms develops more than 1 month). The chronic type can be recurrent, when repeated exacerbations occur over many years, or progressive.
The diagnostic determination of peripheral polyneuropathy requires a complete neurological examination, including a medical history: symptoms of the disease, the patient’s profession, the presence of possible intoxications, infectious diseases and the presence of relatives with neuropathy. It is necessary to use additional laboratory and instrumental research methods to identify the cause of neuropathy and conduct examinations to determine the degree and type of nerve damage.
A general examination, tests, and laboratory techniques can help identify the presence of nerve damage due to systemic disease. Blood tests help diagnose diabetes, vitamin deficiencies, liver or kidney failure, other metabolic disorders, and signs of abnormal immune system activity.
Tests of muscle strength, muscle twitching, or fasciculations may indicate motor neuron damage. Assessing the patient's ability to perceive vibration, soft touch, temperature and pain sensitivity helps determine damage to sensory fibers. Based on the results of a neurological and physical examination and a detailed history of the disease, additional tests and examinations may be prescribed to clarify the diagnosis.
To assess the presence of changes in tactile sensitivity, a monofilament weighing 10 g is used; for pain - an injection of the back surface of the thumb with a special needle with a blunt end; temperature - by determining the difference in the sensations of heat and cold with a Tip-therm instrument, vibration - using a tuning fork or biothesiometer. To assess impaired motor function, the Achilles and knee reflexes are examined.
Electromyography (EMG) involves inserting a thin needle into a muscle to measure its electrical activity at rest and during contraction. Based on the EMG results, it is possible to differentiate damage to the muscle itself and nerve fibers. Nerve conduction speed can help pinpoint the extent of damage in nerve fibers, clearly indicating whether symptoms are due to myelin sheath or axon degeneration. During this study, electrical stimulation of the fiber is performed, in response to which a response impulse appears in the nerve. An electrode placed further along the nerve measures the speed of impulse transmission along the axon. Slow transmission rates and impulse blocking typically indicate damage to the myelin sheath, while decreased impulse levels are a sign of axonal degeneration.
In doubtful cases, a biopsy of the nerves can help - there are no histological changes in them with progressive muscular dystrophy.
Currently, it is accepted to divide all polyneuropathies into axonopathies, the pathogenesis of which is based on primary damage to the axial cylinders of the nerves, and myelinopathies, characterized by impaired conduction function due to damage to the myelin sheaths. However, such a division is possible only in the early stages of the pathological process, because As the disease progresses, combined damage to both the axial cylinders and the myelin sheaths of the nerves develops.
Currently, thioctic (α-lipoic) acid, in particular Thiogamma, is one of the important drugs in the treatment of peripheral polyneuropathy, which has been confirmed by large-scale multicenter long-term studies, such as the ALADIN Study (Alpha-Lipoic Acid in Diabetic Neuropathy).
Thioctic acid, accumulating in nerve fibers:
- reduces the content of free radicals;
- increases endoneurial blood flow;
- normalizes the content of NO, a regulator of relaxation of the vascular wall (if there is a lot of it, as in diabetes mellitus, then it begins to act as a free radical);
- improves endothelial function;
- reduces the level of total cholesterol, increases the level of the antiatherogenic fraction of lipoproteins (HDL).
Thioctic acid is a coenzyme of key enzymes in the Krebs cycle, which explains its effectiveness. An additional advantage in the mechanism of action of thioctic acid is its clearly documented effect of glucose utilization.
Studies have shown that the use of intravenous infusions of 600 mg α-lipoic acid for 3 weeks. is accompanied by a significant regression of neurological symptoms in patients with a painful form of DP.
The main mechanisms of the pharmacodynamics of thioctic acid are to suppress the formation of free radicals, optimize the energy metabolism of neurons, and restore impaired endoneurial blood flow. The result of this action is improved conduction along sensory and motor nerve fibers. This is confirmed by the results of the multicenter DEKAN study. Thus, during long-term observation of 73 patients, it was noted that oral therapy with thioctic acid daily for 4 months. significantly improved the functional parameters of the cardiac nervous system. The results of the ALADIN II study (1999) demonstrated that long-term oral therapy with thioctic acid statistically significantly improves neurophysiological parameters, increasing the conduction velocity of sensory and motor fibers. Against the background of the use of thioctic acid, stabilization of carbohydrate metabolism indicators also occurs. In addition, a positive effect of the drug on liver cells was noted - a decrease in the severity of the morphological manifestations of fatty hepatosis and normalization of biochemical parameters. A course of therapy with thioctic acid must necessarily include 10-15 intravenous drip infusions of 50 ml of 1.2% solution of meglumine salt of thioctic acid (600 mg of thioctic acid) followed by taking the tablet form (1-3 tablets in the morning on an empty stomach for at least 1 month ).
Thiogamma, an effective dosage form of thioctic acid, is widely used in clinical practice. It is available in the form of tablets containing 600 mg of the drug, a solution for intravenous infusion in bottles containing 600 mg of the drug in the form of meglumine salt, and ampoules. When treating polyneuropathy, you should start with intravenous administration of Thiogamma solution at 600 mg/day. for 1-2, and sometimes 3 weeks. (especially when it comes to complicated forms of diabetes). And only then do oral doses begin in a daily dose of 600 to 1800 mg for 2-4 months. The duration of the course of therapy is selected individually depending on the severity of the clinical manifestations of the disease and the effectiveness of the initial therapy. Considering the chronic nature of the underlying pathological process, it is advisable to carry out repeated courses of drug administration.
The drug Tiogamma is well tolerated. The frequency of side effects when using it does not exceed that when taking placebo. These disorders are usually moderate and do not require discontinuation of the drug. Thiogamma can be prescribed simultaneously with other medications. No convincing information about the occurrence of drug interactions was provided. The good tolerability of Thiogamma is an important incentive for the patient to choose this particular medicine for the treatment of polyneuropathies.
Thus, the available data indicate the advisability of using the drug Thiogamma by general practitioners in the treatment of patients with neuropathy of somatogenic origin. Timely identification of patients with damage to the nervous system and their systematic treatment significantly increase the effectiveness of therapeutic measures.
For hereditary polyneuropathies, treatment is symptomatic. For autoimmune polyneuropathies, the goal of treatment is to achieve remission; and in Guillain-Barré syndrome, supporting vital functions is of fundamental importance. For diabetic, uremic, alcoholic and other chronic progressive polyneuropathies, treatment is reduced to reducing the severity of symptoms (including pain) and slowing down the process.
One of the important aspects of treatment is physical therapy aimed at maintaining muscle tone and preventing contractures. In case of development of respiratory disorders in Guillain-Barre syndrome and diphtheria polyneuropathy, mechanical ventilation may be required.
Thus, in modern conditions in outpatient practice, the doctor has every opportunity for timely diagnosis and effective treatment of peripheral polyneuropathy.

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How difficult it is to care for a paralyzed patient is difficult to imagine for a person who is unfamiliar with such a disease as polyneuropathy. It is characterized by multiple lesions of nerve fibers and the development of incomplete paralysis, with the nerves of the extremities first affected, then gradually spreading from the peripheral nervous system to the internal organs and brain.

The death of the patient can occur due to cardiac arrest or suffocation caused by paralysis of the intercostal muscles. But more often, patients die due to concomitant diseases that are caused by limited mobility.

Symptoms in patients with polyneuropathy

The disease develops gradually, first, damage to nerve cells is manifested by symptoms that occur when the nerve is irritated. Such patients experience tremor (shaking), convulsions, and muscle pain. Tissue sensitivity is impaired, a feeling of numbness and goosebumps appear. General disorders of the heart, kidneys and other organs with autonomic innervation appear.

After some time, the symptoms of irritation of nerve cells disappear, and they are replaced by symptoms, which can be considered the initial stage. The patient complains of weakness and decreased muscle tone. Weakness does not develop in all muscles of the extremities, but can usually be diagnosed in symmetrical distal muscles. For example, on the legs, the muscles of the lower leg are the first to be affected. Weakness first occurs in the anterior muscles that flex the foot forward. The patient cannot stand on his heels. Then muscle weakness spreads to the calf muscles and then the patient can no longer stand on his toes.

Muscle weakness leads to poor coordination when walking and atrophy. It is difficult for the patient to walk several steps with his eyes closed, since the muscles do not “listen” to him. Subsequently, this is accompanied by deformations of small, then large joints of the arms and legs. These symptoms are caused by polyneuropathy of the extremities.

Further sensitivity is also observed; the patient does not feel heat, cold, or touch with sharp objects. The nerve endings of the feet and hands are primarily affected. This is the so-called “socks and gloves” symptom.

General changes in the body are characterized by dizziness and nausea. Sometimes orthostatic collapse may occur. This is due to a decrease in the innervation of small vessels of the extremities. If normally they contract and blood enters the general bloodstream, then with polyneuropathy, when a person tries to stand up, blood is retained in the small vessels of the extremities, which causes a decrease in blood supply to the brain and the patient may lose consciousness. Other symptoms of polyneuropathy include dry skin, constipation, and a stable, unchanging pulse. These symptoms are also caused by problems in the nerve tissue that carries impulses from the brain to the gut, skin and heart.

Causes of the disease

The main causes of polyneuropathy are:

  • Autoimmune diseases, including systemic diseases. They occur when a person's immune system malfunctions and, instead of attacking microorganisms or abnormally developing tumor cells, it attacks normal cells and tissues, causing inflammation in them. The inflammatory process enhances the formation of connective tissue, disrupts microcirculation, and impairs the supply of nutrients.
  • Poisoning with substances toxic to the body. These can be salts of heavy metals (mercury or lead poisoning), chemical solvents (gasoline acetone), medications (in case of suicide or overdose). Polyneuropathy is very common in alcoholism. These are toxic polyneuropathy.
  • Infectious diseases accompanied by a toxic-allergic reaction. Of these, polyneuropathy is especially often caused by AIDS and diphtheria.
  • Endocrine diseases. They cause metabolic disorders that adversely affect nerve cells. For example, with diabetes mellitus, diabetic polyneuropathy develops.
  • Malignant neoplasms. Polyneuropathies that occur against the background of tumors are called paraneoplastic.
  • Hereditary predisposition or disorder in the genotype.

Types of polyneuropathy

Depending on what disorders are expressed in the patient, the following are distinguished:

  • Sensory polyneuropathy. Patients complain more about impaired sensitivity and paresthesia (numbness, crawling sensations).
  • Motor polyneuropathy and it is called polyneuropathy of the extremities. With it, muscle weakness and atrophy prevail.
  • Autonomic polyneuropathy. This form is characterized by damage to the nerves that regulate the functioning of internal organs (heart, intestines).
  • Mixed polyneuropathy. There may be signs of disruption of all types of impulses. There is a sensory-muscular polyneuropathy, in which disorders of the skin and muscle tissue are expressed.

Depending on the type of damage to nerve fibers, polyneuropathy is divided into:

Axonal. Associated with damage to the nerve cell process, through which impulses from the central system are transmitted to the tissues and back.

Neuropathic. Usually occur when neuron cell bodies are damaged.

Particularly noteworthy is demyelinating polyneuropathy, which occurs due to the destruction of the myelin sheath covering nerve cells. It responds better to treatment.

Diagnostics

The diagnosis of polyneuropathy is made after a thorough examination of the patient. In addition to examination by a neurologist and collecting an anamnesis (history of the disease), patients are prescribed additional tests that help identify the cause of the disease. At the same time, to determine the depth of the disturbances, electroneuromyography is performed, which helps determine the speed of impulse transmission to the tissues from the nervous system.

In some cases, they resort to histological examination of tissue under a microscope; this is carried out after sampling the nerve tissue by biopsy.

Treatment of polyneuropathy

Treatment methods for polyneuropathy are aimed at eliminating the cause that caused it and restoring damaged cells. To eliminate the cause of the disease in diabetes mellitus, it is necessary to monitor the patient’s blood glucose level and take blood sugar-lowering medications on time. In case of toxic polyneuropathies, it is necessary to exclude further exposure of the patient to the toxic agent. Poisoning with heavy metal salts often occurs in industrial enterprises, so monitoring the level of a toxic substance can reduce the incidence of illness within this organization.

Polyneuropathy caused by drugs, suicide or overdose, is often manifested by impaired functioning of the kidneys and liver; it is the restoration of their functionality that helps reduce the severity of the symptoms of the disease.

For polyneuropathy that develops against the background of alcoholism, it is necessary to treat the underlying disease, namely, eliminate alcohol. Infectious polyneuropathies are treated in traditional ways, by treating the infection. Intravenous administration of large quantities of solutions, which flushes out toxins from the body, helps reduce the concentration of toxic substances in the patient’s body; methods of hemosorption, lymphosorption, and hemodialysis are also used.

Malignant tumors are treated by surgical removal, chemotherapy and the administration of cytotoxic drugs.

Symptomatic treatments and therapies to improve nerve cell recovery include:

  • Vitamin therapy. Treatment with B vitamins, which restore the membrane of nerve cells, is indicated. That is, they promote the formation of myelin. It is this effect that gives good results in the demyelinating form of the disease, when only the neuron membrane is damaged.
  • Prescription of drugs that improve metabolic processes in tissues and their blood supply (microcirculation).
  • Painkillers. They are indicated for severe pain.
  • Symptomatic treatment. It is carried out for concomitant diseases.
  • Depending on the rate of development of disorders of the nervous system, acute, subacute and chronic polyneuropathy can be distinguished. In the acute stage, treatment is aimed at eliminating the toxic effects on the human body. The chronic course of the disease includes physiotherapeutic procedures and massage for polyneuropathy.
  • The complex effect can improve the patient’s condition, but, unfortunately, patients with polyneuropathy of the extremities are rarely able to fully recover.

Complications

Patients with this disease may develop both local and general complications. Disruption of the innervation of internal organs, in particular the heart, can lead to sudden death of the patient from cardiac arrest or suffocation if paralysis of the respiratory muscles occurs.

Muscle weakness makes it difficult to move the limbs. The patient cannot move independently and provide for himself. He needs constant care and help. In addition, treatment is required over a long period of time. Along with taking medications, you need to carry out reflexology and massage, they will reduce the rate of muscle atrophy and improve tissue trophism.

Forecast

The prognosis of the disease often depends on the speed of development of disorders and timely, adequate treatment. Some types of polyneuropathy can be cured. Movement in the patient's limbs is gradually restored, but this requires time and great patience on the part of the relatives caring for him.

Caring for patients with polyneuropathy

If complex treatment of such patients is not carried out, they often become disabled and move in a wheelchair, since the leg muscles and deformation of the joints of the feet do not allow the patient to walk calmly. Over time, the muscles atrophy, become thinner, and then the patient not only does not walk, but cannot even stand on his own.

Damage to the nerve cells that provide sensitivity and contraction of the arm muscles causes motor impairment. Patients become completely dependent on their caregivers. They cannot cook their own food, wash their clothes or clean up after themselves. The further the disorders develop, the more problems arise when caring for the patient.

It becomes difficult for patients to hold cutlery in their hands and they have to feed them. As for hygiene, even more difficulties arise. It is difficult to take a person who does not go to the toilet. To correct physiological needs, a duck, a vessel and other devices are used. This is not only inconvenient, but can also cause additional trophic disorders in the tissues. So, in patients who constantly wear diapers, they develop, they become inflamed, fester and can lead to general blood poisoning (sepsis).

Caring for such patients is similar to and often requires a professional medical approach. It is difficult to treat such a sick person at home. If you live in an apartment, then problems may arise with moving around it in a wheelchair, then the patient almost constantly lies or sits in bed. Forced immobility causes even greater disturbances on the part of organs and systems. Such patients may develop congestive pneumonia, bedsores, and trophic ulcers. When an infection occurs, the patient's condition worsens, which can lead to death.

It is impossible not to mention the problems associated with physiotherapeutic treatment and manual therapy. It is necessary to transport the patient to procedures every day, but the house is not equipped with ramps, or there is no suitable vehicle, then this becomes torment for the patient’s relatives.

Constant care for such a patient requires time and effort, so they often invite a nurse or call a massage therapist at home. You can place a patient with polyneuropathy in a special one, in which he will be provided with proper care and medical assistance.