Polyneuropathy is a disorder in which the peripheral nerves are damaged, causing various disturbances of sensation, movement, and autonomic functions.
Main causes of polyneuropathy
Diabetes: Diabetic polyneuropathy is one of the most common forms. Chronically high blood sugar causes nerve damage, most often in the legs and arms.
Infectious diseases: Polyneuropathy can develop with viral and bacterial infections, such as the human immunodeficiency virus (HIV), Epstein-Barr virus, and Lyme disease.
Toxic effects: Certain medications, especially chemotherapy drugs, as well as exposure to alcohol and toxins (such as lead or mercury) can damage nerve tissue.
Autoimmune diseases: Diseases in which the immune system attacks its own tissues (such as Guillain-Barr syndrome) can cause inflammation and nerve damage.
Vitamin Deficiencies: Deficiencies in vitamins B1, B6, and B12 can cause nerve damage, as these vitamins are important for nerve health and function.
Symptoms and Features of polyneuropathy:
Polyneuropathy typically begins with numbness, tingling, and pain in the extremities. The following symptoms may gradually develop:
Loss of sensation: This may manifest as a lack of sensation in the skin, or an inability to feel heat, cold, or touch.
Soreness and burning: Often, a burning pain and a “pins and needles” sensation occurs in the legs and arms.
Muscle weakness: Muscle cramps and weakness may develop, making it difficult to walk and perform normal movements.Coordination problems: Nerve damage can lead to poor coordination, falls, and instability.
Autonomic dysfunction: Polyneuropathy can cause changes in internal organs, such as increased sweating, changes in blood pressure, and problems with urination.
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Why does polyneuropathy occur in diabetes mellitus
Polyneuropathy in diabetes mellitus (diabetic polyneuropathy) occurs as a result of chronically high blood sugar levels, which damage nerves, especially in the legs and arms. The main mechanisms that lead to the development of diabetic polyneuropathy include:
Glucotoxicity: When glucose levels are elevated in the blood, toxic substances (such as advanced glycation end products) accumulate, causing inflammation and damage to nerve cells. These substances destroy the structure and function of nerve fibers, leading to decreased nerve conduction.
Oxidative stress: High sugar levels increase the production of free radicals, which causes oxidative stress. Free radicals destroy cellular structures, including nerve cells, disrupting their functioning.
Microvascular disorders: Increased sugar levels negatively affect the small vessels that feed the nerves, which leads to ischemia (lack of oxygen and nutrients). Impaired blood supply impairs the restoration and nutrition of nerve cells, which leads to their gradual degeneration.
Inflammation: Chronic hyperglycemia causes inflammation in the nervous system. Inflammation disrupts the normal transmission of signals between nerve cells, which manifests itself in the form of pain, numbness, and other symptoms.
Together, these factors lead to progressive nerve damage, which ultimately causes polyneuropathy in patients with diabetes.
Why does polyneuropathy occur in toxic poisoning of the body
Polyneuropathy in toxic poisoning occurs due to the effect of toxic substances on nerve cells, such as heavy metals (lead, mercury), alcohol, drugs (e.g., chemotherapy drugs), insecticides, solvents, and other chemicals. These toxins disrupt the metabolism of nerve cells and their structure, which leads to their damage and deterioration of the transmission of nerve impulses.
Main mechanisms of toxic polyneuropathy development
Metabolic disorders and energy deficiency: Toxic substances can disrupt metabolic processes inside neurons, blocking the normal functioning of mitochondria (cell energy sources). Energy deficiency leads to degeneration of nerve fibers and deterioration of nerve function.
Oxidative stress and cell damage: Many toxins cause the formation of free radicals, which damage cellular structures. This oxidative stress disrupts the functions of cell membranes and causes the death of nerve cells.
Inflammatory process: Some toxins can stimulate inflammatory reactions in the nervous system.Inflammation damages the myelin sheaths of nerve fibers, slowing down signal transmission and impairing sensitivity.
Alteration of protein structure and function: Some toxic substances disrupt the synthesis and function of proteins that are important for the functioning of neurons and maintaining their integrity. This leads to destabilization of neural structures and gradual damage to nerve cells.
Thus, toxic poisoning of the body has a complex effect on nerve cells, which leads to their damage, death and the development of polyneuropathy. Treatment of toxic polyneuropathy often requires eliminating the effects of toxins, the use of antioxidants, vitamins (especially group B), as well as detoxification measures to restore nerve function
Why does polyneuropathy occur in autoimmune diseases
Polyneuropathy in autoimmune diseases occurs as a result of a pathological reaction of the immune system, which attacks its own peripheral nerves. Autoimmune diseases such as Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), and systemic lupus erythematosus can trigger inflammation and destruction of nerve cells and their sheaths.
The main mechanisms of polyneuropathy development in autoimmune diseases
An attack of immune cells on the myelin sheaths of nerves: In some cases, the immune system begins to perceive myelin, the protective sheath covering nerve fibers, as a foreign agent. Antibodies and immune cells attack myelin, which leads to demyelination.This disrupts the transmission of electrical signals along the nerves, causing numbness, pain and muscle weakness.
Destruction of axons: In some autoimmune diseases, antibodies attack not only the myelin but also the nerve fibers (axons) themselves, causing them to be damaged or even die. This causes loss of nerve function, which is manifested by impaired sensitivity and motor function.
Inflammatory processes: Autoimmune diseases are often accompanied by inflammation, which causes damage to the vessels that supply the nerves and the surrounding tissue. This inflammation disrupts the nutrition of nerve cells and causes their degeneration.
Production of cytokines and autoantibodies: Immune cells produce molecules (cytokines) and autoantibodies that trigger inflammatory reactions. These molecules can destroy nerve cells and cause conduction disturbances in nerve impulses.
Treatment of polyneuropathy in autoimmune diseases is aimed at suppressing the activity of the immune system. This may include immunosuppressants, corticosteroids and plasmapheresis, as well as medications to control symptoms, such as painkillers and vitamins.
Treatment of polyneuropathy with neural stem cells (NSC) is considered a promising method due to the ability of these cells to restore damaged nerves and stimulate regenerative processes in the peripheral nervous system. Neural stem cells are able to transform into various types of nerve cells and provide them with support and nutrition, which is especially important in polyneuropathy, where nerve fibers are damaged and their function is impaired.
More information you can find here:Peripheral Neuropathy Therapy With Stem Cells
Main mechanisms of action of neural stem cells
Regulation of inflammation: Neural stem cells can reduce inflammation by secreting anti-inflammatory molecules, which protects nerves from further damage. This is especially important in autoimmune and inflammatory forms of polyneuropathy, where inflammation destroys nerve cells.
Secretion of neurotrophic factors: NSCs secrete neurotrophic factors (such as BDNF and GDNF) that support the survival and growth of nerve cells and improve signal transmission along nerve fibers. These factors help to repair damaged nerve endings and improve sensation and muscle function.
Myelin regeneration: NSCs can help restore the myelin sheath that is damaged in polyneuropathy. This improves the conduction of nerve impulses and reduces symptoms such as numbness, pain, and muscle weakness.
Migration to damaged areas: Once introduced into the body, neural stem cells can migrate to damaged areas, providing local regeneration of nerve tissue.
MORE INFORMATION ABOUT NEUROPATHY TREATMENT Treatment, Safety and Clinical Insights
Neural stem cells (NSCs) can be obtained from several sources, each with its own characteristics and potential applications:
Embryonic stem cells (ESCs): These cells are obtained from early embryos (5-7 days after fertilization). ESCs have a high capacity for differentiation into any type of cell, including neural cells. However, the use of embryonic cells raises ethical issues, and there are restrictions on their use in medicine.
Induced pluripotent stem cells (iPSCs): iPSCs are derived from adult somatic cells (such as skin cells) through gene reprogramming. iPSCs can be converted into neural cells, avoiding the ethical issues associated with using embryos. These cells are widely used in research and show great potential for therapies targeting the nervous system, including the treatment of polyneuropathy.
Adult Brain-Derived Neural Stem Cells: Some areas of the adult brain, such as the hippocampus and olfactory bulbs, retain their own neural stem cells. These cells are involved in the natural regeneration and repair of neural tissue, but their numbers are limited and their isolation for therapeutic purposes is difficult.
Umbilical Cord Blood Stem Cells: Cells derived from the umbilical cord of newborns contain neural precursors and have a lower risk of rejection during transplantation. They have great potential for regenerative medicine, although research in this area is still in its early stages.
Mesenchymal stem cells (MSCs): Although MSCs are not originally neural stem cells, they can differentiate into neuronal-like cells and provide support to neuronal tissue by secreting growth factors and anti-inflammatory molecules. MSCs are often derived from bone marrow or adipose tissue.
In our treatment protocols we use multipotent neural stem cells from MSCs and umbilical cord blood, unipotent from embryonic material.
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