Covered with myelin. The myelin sheath of the nerve cell. The benefits of yoga and swimming

NERVE FIBERS

Nerve fibers are neuronal processes covered with glial membranes. There are two types of nerve fibers - myelin-free and myelin-free. Both types consist of a centrally lying process of a neuron (axial cylinder), surrounded by a sheath of oligodendroglial cells (in the PNS, they are called lemmocytes or Schwann cells).

Myelin-free nerve fibers in an adult, they are located mainly in the autonomic nervous system and are characterized by a relatively low speed of nerve impulses (0.5-2 m / s). They are formed by immersing an axial cylinder (axon) into the cytoplasm of lemmocytes, which are arranged in the form of strands. In this case, the plasmolemma of the lemmocyte bends, surrounding the axon, and forms a duplication - the mesaxon (Fig. 14-7). Often in the cytoplasm of one lemmocyte there can be up to 10-20 axial cylinders. This fiber resembles an electrical cable and is therefore called cable-type fiber. The surface of the fiber is covered with a basement membrane. In the central nervous system, especially during its development, myelin-free fibers are described, consisting of a "naked" axon, devoid of a membrane of lemmocytes.

Figure: 14-7. The formation of myelin (1-3) and myelin-free (4) nerve fibers in the peripheral nervous system... The nerve fiber is formed by immersing the axon (A) of the nerve cell into the cytoplasm of the lemmocyte (LC). When the myelin fiber is formed, the duplication of the LC plasmolemma - mesaxone (MA) - is wound around A, forming turns of the myelin sheath (MO). In the myelin-free fiber shown in the figure, several A ("cable" type fiber) are immersed in the cytoplasm of the LC. I am the core of the LC.

Myelinated nerve fibers are found in the central nervous system and PNS and are characterized by a high speed of nerve impulses (5-120 m / s). Myelin fibers are usually thicker than myelin fibers and contain larger axial cylinders. In the myelin fiber, the axial cylinder is directly surrounded by a special myelin sheath, around which a thin layer is located, including the cytoplasm and the lemmocyte nucleus - neurolemma (Fig. 14-8 and 14-9). Outside, the fiber is also covered with a basement membrane. The myelin sheath contains high concentrations of lipids and is intensely stained with osmic acid, having the appearance of a homogeneous layer under a light microscope, but under an electron microscope it is found that it arises from the fusion of numerous (up to 300) membrane loops (plates).

Figure: 14-8. The structure of the myelin nerve fiber. Myelin fiber consists of an axial cylinder, or axon (A), directly surrounded by the myelin sheath (MO) and the neurolemma (NL), which includes the cytoplasm (CL) and the lemmocyte nucleus (NL). Outside, the fiber is covered with a basement membrane (BM). Areas of MO, in which the gaps between the myelin loops, filled with CL and therefore not stained with osmium, are preserved, have the form of myelin notches (MN). MO is absent in the areas corresponding to the border of neighboring lemmocytes - nodal interceptions (NC).

Myelin sheath formation occurs when the axial cylinder and oligodendroglial cells interact with some differences in the PNS and CNS.

Myelin sheath formation in the PNS : immersion of the axial cylinder into the lemmocyte is accompanied by the formation of a long mesaxon, which begins to rotate around the axon, forming the first loosely located loops of the myelin sheath (see Fig. 14-7). As the number of turns (plates) increases in the process of myelin maturation, they are located more and more densely and partially merge; the gaps between them, filled with the cytoplasm of the lemmocyte, remain only in separate areas that are not stained with osmium - myelin notches (Schmidt-Lanterman). During the formation of the myelin sheath, the cytoplasm and the nucleus of the lemmocyte are pushed back to the periphery of the fiber, forming a neurolemma. The myelin sheath has an intermittent course along the length of the fiber.

Figure: 14-9. Ultrastructural organization of myelinated nerve fiber. Around the axon (A) are the loops of the myelin sheath (BMO), outside covered with neurolemma, and which includes the cytoplasm (CL) and the nucleus of the lemmocyte (YL). The fiber is surrounded on the outside by a basement membrane (BM). The CL, in addition to the neurolemma, forms an inner layer (VL) immediately adjacent to A (located between it and the IMO), it is also contained in the zone corresponding to the border of neighboring lemmocytes - nodal interception (NC), where the myelin sheath is absent, and in areas of loose packing WMO - myelin notches (MN).

Nodal Interceptions (Ranvier)- Areas in the region of the border of neighboring lemmocytes, in which the myelin sheath is absent, and the axon is covered only by interdigitating processes of neighboring lemmocytes (see Fig. 14-9). Nodal interceptions are repeated along the myelin fiber with an interval of, on average, 1-2 mm. In the area of \u200b\u200bthe nodal interception, the axon often expands, and its plasmolemma contains numerous sodium channels (which are absent outside the interceptions under the myelin sheath).

Spread of depolarization in myelin fiber carried out by jumps from interception to interception (saltatorial). Depolarization in the area of \u200b\u200bone nodal intercept is accompanied by its rapid passive propagation along the axon to the next intercept (since the current leakage in the inter-nodal region is minimal due to the high insulating properties of myelin). In the area of \u200b\u200bthe next interception, the pulse causes the existing ion channels to turn on and a new section of local depolarization appears, etc.

The formation of the myelin sheath in the central nervous system: the axial cylinder does not submerge into the cytoplasm of the oligodendrocyte, but is enveloped by its flat process, which subsequently rotates around it, losing the cytoplasm, and its coils turn into plates of the myelin

lobes (Fig. 14-10). In contrast to Schwann cells, one oligodendrocyte of the central nervous system with its processes can participate in the myelination of many (up to 40-50) nerve fibers. The sections of the axon in the area of \u200b\u200bRanvier's interceptions in the central nervous system are not covered by the cytoplasm of oligodendrocytes.

Figure: 14-10. The formation of myelin fibers by oligodendrocytes in the central nervous system. 1 - the axon (A) of the neuron is covered by the flat process (PO) of the oligodendrocyte (ODC), the coils of which turn into the plates of the myelin sheath (MO). 2 - one ODC with its processes can participate in the myelination of many A. Areas A in the area of \u200b\u200bnodal interceptions (NC) are not covered by the cytoplasm of the ODC.

Disruption of formation and damage to the formed myelin underlie a number of serious diseases of the nervous system. Myelin in the central nervous system may be a target for autoimmune damage T-lymphocytes and macrophages with its destruction (demyelination). This process is actively proceeding with multiple sclerosis - serious illness unclear (probably viral) nature associated with a disorder of various functions, the development of paralysis, loss of sensitivity. The nature of neurological disorders is determined by the topography and size of the damaged areas. With some metabolic disorders, there are disorders in the formation of myelin - leukodystrophy, manifested in childhood by severe lesions of the nervous system.

Classification of nerve fibers

Classification of nerve fibersbased on the differences in their structure and function (speed of conduction of nerve impulses). There are three main types of nerve fibers:

1. Fibers of type A - thick, myelinated, with far-apart nodal interceptions. Conduct pulses at high speed

(15-120 m / s); are subdivided into 4 subtypes (α, β, γ, δ) with decreasing diameter and pulse conduction speed.

2. Type B fibers - medium thickness, myelinated, smaller diameter,

than type A fibers, with a thinner myelin sheath and a lower speed of nerve impulses (5-15 m / s).

3. Type C fibers - thin, myelin-free, conduct pulses at a relatively low speed (0.5-2 m / s).

Regeneration of nerve fibers in the PNS includes a naturally unfolding complex sequence of processes in the course of which the process of a neuron actively interacts with glial cells. The actual regeneration of fibers follows a series of reactive changes caused by their damage.

Reactive changes in a nerve fiber after cutting it. During the 1st week after the transection of the nerve fiber, an ascending degeneration of the proximal (closest to the neuron body) part of the axon develops, at the end of which an expansion (retraction bulb) is formed. The myelin sheath in the damaged area disintegrates, the neuron body swells, the nucleus shifts to the periphery, the chromatophilic substance dissolves (Fig. 14-11).

In the distal part of the fiber, after its cutting, there is a downward degeneration with complete destruction of the axon, disintegration of myelin, and subsequent phagocytosis of detritus by macrophages and glia.

Structural transformations during nerve fiber regeneration. After 4-6 weeks. the structure and function of the neuron are restored, thin branches (growth cones) begin to grow from the retraction bulb towards the distal part of the fiber. Schwann cells in the proximal part of the fiber proliferate, forming ribbons (Büngner) parallel to the course of the fiber. In the distal part of the fiber, Schwann cells are also preserved and mitotically divide, forming ribbons that connect with similar formations in the proximal part.

The regenerating axon grows distally at a rate of 3-4 mm / day. along the Bungner ribbons, which play a supporting and guiding role; Schwann cells form a new myelin sheath. Collaterals and axon terminals are restored within a few months.

Figure: 14-11. Regeneration of myelinated nerve fiber (according to R. Krstic, 1985, with changes). 1 - after cutting the nerve fiber, the proximal part of the axon (A) undergoes ascending degeneration, the myelin sheath (MO) in the damaged area disintegrates, the perikaryon (PC) of the neuron swells, the nucleus shifts to the periphery, the chromatophilic substance (CS) disintegrates (2). The distal part associated with the innervated organ (in the given example, the skeletal muscle) undergoes downward degeneration with complete destruction of A, disintegration of MO and phagocytosis of detritus by macrophages (MF) and glia. Lemmocytes (LC) are preserved and mitotically divide, forming cords - Büngner's ribbons (LB), connecting with similar formations in the proximal part of the fiber (thin arrows). After 4-6 weeks, the structure and function of the neuron are restored, thin branches grow distally from the proximal part A (bold arrow), growing along the LB (3). As a result of nerve fiber regeneration, the connection with the target organ (muscle) is restored and its atrophy caused by disturbed innervation regresses (4). In the event of an obstruction (P) in the path of regenerating A (for example, a connective tissue scar), the components of the nerve fiber

form a traumatic neuroma (TN), which consists of expanding branches A and LC (5).

Regeneration conditionsare: no damage to the neuron body, a small distance between the parts of the nerve fiber, the absence of connective tissue that can fill the gap between the parts of the fiber. When an obstacle arises in the path of the regenerating axon, a traumatic (amputation) neuroma is formed, which consists of the growing axon and Schwann cells, which are soldered into the connective tissue.

There is no regeneration of nerve fibers in the central nervous system : although the neurons of the central nervous system have the ability to restore their processes, this does not happen, apparently due to the adverse effects of the microenvironment. After neuron damage, microglia, astrocytes and hematogenous macrophages phagocytose detritus in the area of \u200b\u200bthe destroyed fiber, in its place, proliferating astrocytes form a dense glial scar.

NERVE ENDINGS

Nerve endings- terminal apparatus of nerve fibers. By function, they are divided into three groups:

1) interneuronal contacts (synapses)- provide a functional connection between neurons;

2) efferent (effector) endings- transmit signals from the nervous system to the executive organs (muscles, glands), are available on axons;

3) receptor (sensitive) endingsperceive irritations from the external and internal environment, are present on dendrites.

INTER-NEURAL CONTACTS (SYNAPSES)

Interneuronal contacts (synapses)are subdivided into electrical and chemical.

Electrical synapsesin the CNS of mammals are rare; they have a structure of gap junctions, in which the membranes of synaptically connected cells (pre- and postsynaptic) are separated by a gap 2 nm wide, penetrated by connexons. The latter are tubes formed by protein molecules and serve as water channels through which small molecules and ions can be transported from one cell to

another (see chapter 3). When an action potential propagating across the membrane of one cell reaches the gap junction, an electric current flows passively through the gap from one cell to another. The pulse can be transmitted in both directions and with little or no delay.

Chemical synapses- the most common type in mammals. Their action is based on the conversion of an electrical signal into a chemical signal, which is then converted back into an electrical one. The chemical synapse consists of three components: the presynaptic part, the postsynaptic part, and the synaptic cleft (Fig. 14-12). The presynaptic part contains a (neuro) mediator, which, under the influence of a nerve impulse, is released into the synaptic cleft and, by binding to receptors in the postsynaptic part, causes changes in the ionic permeability of its membrane, which leads to its depolarization (in excitatory synapses) or hyperpolarization (in inhibitory synapses ). Chemical synapses differ from electrical one-way conduction of impulses, a delay in their transmission (synaptic delay of 0.2-0.5 ms duration), providing both excitation and inhibition of the postsynaptic neuron.

Figure: 14-12. The structure of the chemical synapse. The presynaptic part (PRSP) has the form of a terminal bud (CB) and includes: synaptic vesicles (SP), mitochondria (MTX), neurotubules (NT), neurofilaments (NF), presynaptic membrane (PRSM) with presynaptic compaction (PRSU). The postsynaptic part (POSC) includes the postsynaptic membrane (POSM) with postsynaptic consolidation (POSM). Intrasynaptic filaments (ISF) are located in the synaptic cleft (SS).

1. Presynaptic partformed by an axon along its course (passing synapse) or is an extended terminal part of an axon (terminal bud). It contains mitochondria, aEPS, neurofilaments, neurotubules and synaptic vesicles with a diameter of 20-65 nm, which contain a neurotransmitter. The shape and nature of the contents of the vesicles depend on the neurotransmitters located in them. Round light vesicles usually contain acetylcholine, vesicles with a compact dense center - norepinephrine, large dense vesicles with a light submembrane rim - peptides. Neurotransmitters are produced in the body of the neuron and are transported by the mechanism of rapid transport to the endings of the axon, where they are deposited. Partially synaptic vesicles are formed in the synapse itself by cleavage of the aEPS from the cisterns. On the inner side of the plasmolemma, facing the synaptic cleft (presynaptic membrane), there is a presynaptic seal formed by a fibrillar hexagonal protein network, the cells of which contribute to the uniform distribution of synaptic vesicles over the membrane surface.

2. Postsynaptic partit is represented by a postsynaptic membrane containing special complexes of integral proteins - synaptic receptors that bind to a neurotransmitter. The membrane is thickened due to the accumulation of dense filamentous protein material under it (postsynaptic compaction). Depending on whether the postsynaptic part of the interneuronal synapse is a dendrite, the body of a neuron, or (less often) its axon, synapses are subdivided into axo-dendritic, axosomatic, and axo-axonal, respectively.

3. Synaptic cleft20-30 nm wide sometimes contains transversely located glycoprotein intrasynaptic filaments 5 nm thick, which are elements of a specialized glycocalyx that provide adhesive bonds of the pre- and post-synatic parts, as well as directed diffusion of the mediator.

The mechanism of transmission of a nerve impulse in a chemical synapse. Under the influence of a nerve impulse, voltage-gated calcium channels of the presynaptic membrane are activated; Ca2+ rushes into the axon, membranes of synaptic vesicles in the presence of Ca2 + merge with the presynaptic membrane, and their contents (mediator) are released into the synaptic cleft by the mechanism of exocytosis. By acting on the receptors of the postsynaptic membrane, the mediator causes either its depolarization, the emergence of a postsynaptic action potential and the formation of a nerve impulse, or its hyper-

larization, causing the inhibition reaction. Arousal mediators, for example, are acetylcholine and glutamate, and inhibition is mediated by GABA and glycine.

After the termination of the interaction of the mediator with the receptors of the postsynaptic membrane, most of its endocytosis is captured by the presynaptic part, the smaller part is scattered in space and captured by the surrounding glial cells. Some neurotransmitters (for example, acetylcholine) are broken down by enzymes into components, which are then captured by the presynaptic part. The membranes of synaptic vesicles, embedded in the presynaptic membrane, are subsequently incorporated into the endocytic bordered vesicles and are reused to form new synaptic vesicles.

In the absence of a nerve impulse, the presynaptic part secretes individual small portions of the neurotransmitter, causing spontaneous miniature potentials in the postsynaptic membrane.

EFFECTIVE (EFFECTIVE) NERVOUS ENDINGS

Efferent (effector) nerve endings depending on the nature of the innervated organ, they are subdivided into motor and secretory. Motor endings are found in striated and smooth muscles, secretory - in the glands.

Neuromuscular endings (neuromuscular synapse, motor plaque) - the motor end of the motor neuron axon on the fibers of striated somatic muscles - consists of the terminal branching of the axon forming the presynaptic part, a specialized area on the muscle fiber corresponding to the postsynaptic part, and the synaptic cleft separating them (Fig. 14-13).

In large muscles that develop significant strength, one axon, branching out, innervates a large number (hundreds and thousands) of muscle fibers. In contrast, in small muscles that perform fine movements (for example, the external muscles of the eye), each fiber or a small group of them is innervated by a separate axon. One motoneuron, together with the muscle fibers innervated by it, forms a motor unit.

Presynaptic part.Near the muscle fiber, the axon loses the myelin sheath and gives off several branches, which

The nervous system performs essential functions in the body. She is responsible for all actions and thoughts of a person, forms his personality. But all this hard work would be impossible without one component - myelin.

Myelin is a substance that forms the myelin (pulp) membrane, which is responsible for the electrical insulation of nerve fibers and the speed of transmission of electrical impulses.

Myelin anatomy in the structure of the nerve

The main cell of the nervous system is a neuron. The body of the neuron is called the soma. Inside it is the core. The body of the neuron is surrounded by short processes called dendrites. They are responsible for communication with other neurons. One long process, the axon, departs from the soma. It carries an impulse from a neuron to other cells. Most often, at the end, it connects with the dendrites of other nerve cells.

The entire surface of the axon is covered by the myelin sheath, which is a process of the Schwann cell, devoid of cytoplasm. Essentially, these are several layers of cell membrane wrapped around an axon.

The Schwann cells enveloping the axon are separated by Ranvier interceptions, which lack myelin.

Functions

The main functions of the myelin sheath are:

• isolation of the axon;
• acceleration of impulse conduction;
• energy savings due to the conservation of ion flows;
• support of the nerve fiber;
• axon nutrition.

How impulses work

Nerve cells are isolated due to their membranes, but nevertheless they are interconnected. The areas where the cells meet are called synapses. This is where the axon of one cell meets the soma or dendrite of another.

An electrical impulse can be transmitted within a single cell or from neuron to neuron. This is a complex electrochemical process that is based on the movement of ions through the membrane of the nerve cell.

In a calm state, only potassium ions enter the neuron, while sodium ions remain outside. At the moment of arousal, they begin to change places. The axon is positively charged from within. Then sodium ceases to flow through the membrane, and the outflow of potassium does not stop.

The change in voltage due to the movement of potassium and sodium ions is called the "action potential". It spreads slowly, but the myelin sheath surrounding the axon accelerates this process by preventing the outflow and influx of potassium and sodium ions from the axon body.

Passing through the interception of Ranvier, the impulse jumps from one section of the axon to another, which allows him to move faster.

After the action potential crosses the gap in myelin, the impulse stops and the resting state returns.

This method of energy transfer is characteristic of the central nervous system. As far as the autonomic nervous system is concerned, there are often axons covered with little or no myelin. There are no jumps between Schwann cells, and the impulse passes much more slowly.

Composition

The myelin layer consists of two layers of lipids and three layers of protein. It contains much more lipids (70-75%):

• phospholipids (up to 50%);
• cholesterol (25%);
• glactocerebroside (20%), etc.

Protein layers are thinner than lipid layers. Protein content in myelin - 25-30%:

• proteolipid (35-50%);
• myelin basic protein (30%);
• wolfram proteins (20%).

There are simple and complex proteins in the nervous tissue.

The role of lipids in the structure of the membrane

Lipids play a key role in the structure of the pulp. They are the structural material of nerve tissue and protect the axon from energy loss and ion currents. Lipid molecules have the ability to repair brain tissue after damage. Myelin lipids are responsible for the adaptation of the mature nervous system. They act as hormone receptors and communicate between cells.

The role of proteins

Protein molecules are of great importance in the structure of the myelin layer. They, along with lipids, act as a building material for nervous tissue. Their main task is to transport nutrients to the axon. They also decode the signals entering the nerve cell and speed up the reactions in it. Participation in metabolism is an important function of the myelin sheath protein molecules.

Myelination defects

The destruction of the myelin layer of the nervous system is a very serious pathology, due to which there is a violation of the transmission of a nerve impulse. It causes dangerous diseases, often incompatible with life. There are two types of factors that influence the onset of demyelination:

• genetic predisposition to myelin destruction;
• the impact on myelin of internal or external factors.
• Demyelization is divided into three types:
• sharp;
• remitting;
• acute monophasic.

Why is destruction happening

Most frequent reasons destruction of the pulp are:

• rheumatic diseases;
• a significant predominance of proteins and fats in the diet;
• genetic predisposition;
• bacterial infections;
• heavy metal poisoning;
• tumors and metastases;
• prolonged severe stress;
• bad ecology;
• pathology of the immune system;
• long-term use of neuroleptics.

Diseases due to demyelination

Demyelinating diseases of the central nervous system:

1. Canavan's disease - a genetic disease that occurs at an early age. It is characterized by blindness, problems with swallowing and eating, impaired motor skills and development. Epilepsy, macrocephaly and muscle hypotension are also a consequence of this disease.
2. Binswanger's disease. Most often caused by arterial hypertension. Patients expect thought disorders, dementia, as well as impaired walking and pelvic organ functions.
3. . May cause damage to several parts of the central nervous system. It is accompanied by paresis, paralysis, convulsions, and motor impairment. Also, the symptoms of multiple sclerosis are behavioral disorders, weakening of the facial muscles and vocal cords, impaired sensitivity. Vision is impaired, the perception of color and brightness changes. Multiple sclerosis is also characterized by disorders of the pelvic organs and dystrophy of the brainstem, cerebellum, and cranial nerves.
4. Devik's disease - demyelination in the optic nerve and spinal cord. The disease is characterized by impaired coordination, sensitivity and functions of the pelvic organs. She is distinguished by severe visual impairment and even blindness. In the clinical picture, paresis, muscle weakness, and autonomic dysfunction are also observed.
5. Osmotic demyelination syndrome... It occurs due to a lack of sodium in the cells. Symptoms are seizures, personality disorders, loss of consciousness, up to coma and death. The consequence of the disease is cerebral edema, hypothalamic infarction and hernia of the brain stem.
6. Myelopathy - various dystrophic changes in the spinal cord. They are characterized by muscle disorders, sensory disorders and pelvic dysfunction.
7. Leukoencephalopathy - destruction of the myelin sheath in the subcortex of the brain. Patients suffer from constant headache and epileptic seizures. Impaired vision, speech, coordination and walking are also observed. Sensitivity decreases, personality and consciousness disorders are observed, dementia progresses.
8. Leukodystrophy - a genetic metabolic disorder that causes the destruction of myelin. The course of the disease is accompanied by muscle and movement disorders, paralysis, visual and hearing impairment, and progressive dementia.

Demyelinating diseases of the peripheral nervous system:

1. Guillain-Barré syndrome is an acute inflammatory demyelination. It is characterized by muscle and movement disorders, respiratory failure, partial or complete absence of tendon reflexes. Patients suffer from heart disease, disruption of the digestive system and pelvic organs. Paresis and sensory disturbances are also signs of this syndrome.
2. Charcot-Marie-Tooth neural amyotrophy is a hereditary pathology of the myelin sheath. It is distinguished by sensory disturbances, dystrophy of the limbs, spinal deformity and tremor.

This is just a part of the diseases arising from the destruction of the myelin layer. The symptoms are similar in most cases. Accurate diagnosis can be delivered only after a computed or magnetic resonance imaging. The level of qualification of the doctor plays an important role in making the diagnosis.

Treatment principles for shell defects

Diseases associated with the destruction of the pulp are very difficult to treat. Therapy is aimed mainly at relieving symptoms and stopping the destruction processes. The earlier the disease is diagnosed, the more chances to stop its course.

Myelin recovery options

Thanks to timely treatment, the myelin recovery process can be started. However, the new myelin sheath will not function as well. In addition, the disease can go into a chronic stage, and the symptoms persist, only slightly subside. But even a slight remyelination can stop the course of the disease and partially restore the lost functions.

Modern drugs aimed at myelin regeneration are more effective, but they are very expensive.

Therapy

For the treatment of diseases caused by the destruction of the myelin sheath, the following drugs and procedures are used:

• beta-interferons (stop the course of the disease, reduce the risk of relapse and disability);
• immunomodulators (affect the activity of the immune system);
• muscle relaxants (help restore motor functions);

• nootropics (restore conductive activity);
• anti-inflammatory (relieve the inflammatory process that caused the destruction of myelin);
• (prevent damage to brain neurons);
• pain relievers and anticonvulsants;
• vitamins and antidepressants;
• filtration of cerebrospinal fluid (a procedure aimed at cleansing cerebrospinal fluid).

Disease prognosis

Currently, the treatment of demyelination does not give one hundred percent result, but scientists are actively developing drugs aimed at restoring the pulp. Research is carried out in the following areas:

1. Stimulation of oligodendrocytes... These are the cells that make myelin. In a demyelinated organism, they do not work. Artificial stimulation of these cells will help start the process of repairing damaged areas of the myelin sheath.
2. Stem cell stimulation... Stem cells can be transformed into complete tissue. There is a possibility that they can also fill the pulp.
3. Regeneration of the blood-brain barrier... With demyelination, this barrier is destroyed and allows lymphocytes to negatively affect myelin. Its restoration protects the myelin layer from the attack of the immune system.

Perhaps, soon the diseases associated with the destruction of myelin will cease to be incurable.

Systemic damage to peripheral nerves (polyneuropathy) and damage to individual nerve trunks (neuropathy) constitute a large group of diseases of the peripheral nervous system of various etiologies and complex pathogenesis, leading to the destruction of nerve fibers or their membranes. The prevalence of pathological processes occurring with damage to peripheral nerves is so great that most of the patients' visits to a neurologist are associated with them.

The International Statistical Classification of Diseases (ICD-10) contains a huge section (G 50 - 64), which includes the whole variety of clinical variants of neuropathies: from damage to individual nerves, roots and plexuses to systemic polyneuropathies.

Damage to peripheral nerves can be caused by metabolic disorders, ischemia, blood diseases, intoxication, alimentary factors, trauma, allergic reactions, inflammatory processes and other reasons.

Sufferings of formations of the peripheral nervous system act as an independent disease or clinical syndrome and are so common in the practice of a doctor that no specialist, both therapeutic and surgical, can ignore this problem.

The peripheral nervous system includes the posterior and anterior roots of the spinal cord, intervertebral spinal ganglia, spinal nerves, their plexuses, peripheral nerves, as well as the roots and ganglia of the cranial nerves and the cranial nerves.

The formation of a peripheral nerve is as follows. Following to the periphery from the spinal cord (or from the cranial cavity), spinal nerves (or cranial nerves), consisting of portions of motor, sensory fibers, form a peripheral nerve. Peripheral nerves are mostly mixed and consist of motor fibers of the anterior roots (axons of the cells of the anterior horns), sensory fibers (dendrites of the cells of the intervertebral nodes) and vasomotor-secretory-trophic fibers (sympathetic and parasympathetic) from the corresponding cells of the gray matter of the lateral horns of the spinal cord and ganglia of the sympathetic borderline trunk.

The nerve fiber, which is part of the peripheral nerve, consists of an axial cylinder located in the center of the fiber, the myelin sheath that covers the axial cylinder and the Schwann sheath. The large nerve trunks are composed of 800,000 to 1,000,000 nerve fibers, which provide a significant functional margin for the peripheral nervous system. It is believed that the function of the nerve trunk is disturbed only if half of the nerve fibers die.

The myelin sheath of the nerve fiber is interrupted in places, forming the so-called Ravnier interceptions. For many years, it was believed that the myelin sheath provides the role of an electrical insulator in the process of conducting excitation along the nerve fiber. However, the role of the myelin sheath is probably more significant - it is directly involved in the formation of the electrical potential of the nerve fiber. Undoubtedly, its participation in the metabolic processes of the nerve cell is extremely large - the function of the nerve fiber is disrupted when the myelin sheath is damaged. Connective tissue in the peripheral nerves it is represented by the sheaths that dress the nerve trunk (epineurium), its individual bundles (perineurium) and nerve fibers (endoneurium). The vessels that feed the nerve pass in the membranes. The myelin sheath makes up the bulk of the peripheral nerve.

Myelin - a substance consisting of cholesterol, phospholipids and proteins - is the result of folate-dependent synthesis, which occurs with the direct participation of the enzyme methylenetetrahydrofolate reductase (MTHFR) and coenzymes (folic acid and B vitamins).

The myelin sheath is the most vulnerable part of the peripheral nerve. She suffers as a result of destruction (toxic, immune mechanisms) or insufficient synthesis of myelin constituents (metabolic disorders, lack of vitamins). In any case, the synthesis of myelin requires significant tension of numerous enzyme systems, since the total mass of this substance in the body exceeds 200 grams.

Clinical syndrome of peripheral nerve damage is most often associated with segmental demyelination of nerve fibers. Segmental demyelination (myelinopathy) means damage to the myelin sheaths while the axons are intact. The most significant functional manifestation of demyelination is conduction blockade. Functional impairment in a blocked axon manifests itself in the same way as when crossing an axon. Despite the fact that nerve transection and conduction blockade during demyelination show similarities in the severity of the development of motor and sensory disorders, there are differences between them. Thus, in demyelinating neuropathies, the blockage of conduction is often transient and remyelination can proceed quickly within days or weeks, often ending in recovery (4). Thus, with this process, the prognosis is more favorable and recovery is faster than the course. The most important clinical sign of segmental demyelination is a distal-peripheral type of dysfunction - the greater the length of the peripheral nerve, the more noticeable conduction disturbances become. First of all, this is manifested by sensory disorders in the distal extremities.

So, folate-dependent synthesis of myelin is impossible without vitamins of group B. Meanwhile, the lack of thiamine (vitamin B1) is considered one of the characteristic features of typical diseases of civilization (5). Changes in the nature of nutrition with an increase in the proportion of refined carbohydrates, significant acidification of the internal environment due to changes in the structure of food products - do not contribute to the assimilation of thiamine, even if it is present in sufficient quantities in food. Meanwhile, B1 takes part in protein synthesis, regulation of fat and water-salt metabolism. Numerous studies have established that thiamine has antioxidant, immunomodulatory properties, is involved in the metabolism of the most important neurotransmitters - serotonin and gamma-aminobutyric acid, acetylcholine. Being the main coenzyme of MTHFR, it is directly involved in the synthesis of myelin.

Vitamin B6 - pyridoxine is a coenzyme of more than 100 enzymes, takes part in the synthesis of neurotransmitters (tryptophan, glycine, serotonin, dopamine, norepinephrine, adrenaline, histamine). It lowers cholesterol, homocysteine \u200b\u200blevels in the blood. Vitamin B6 controls erythropoiesis and is involved in the formation of the immune response. There is a strong correlation between a decrease in the level of pyridoxine in the blood and the clinical manifestations of polyneuropathies.

Vitamin B12 (cyanocobalamin) is the main source of cobalt, which is essential for protein synthesis. B12 is directly involved in the synthesis of methionine and nucleic acids. It activates all types of metabolism: protein, fat and carbohydrate. It has been established that high concentrations of cyanocobalamin are necessary to prevent cognitive impairment (senile dementia) and depression. The participation of B12 in the synthesis of myelin is its most important function. Complex vitamin preparations are widely used in the treatment of patients with various diseases and pathological processes. But the most significant is their use in diseases of the nervous system. It is no coincidence that B vitamins have taken a central place in the treatment of diseases of the peripheral nervous system. Among the numerous diseases of the nervous system, the most significant are the indications for vitamin preparations for polyneuropathies of various origins (1 - 3). Although the etiology of polyneuropathies is extremely diverse, a lack of B vitamins unites most of the clinical variants of this neurological syndrome. According to literature data, polyneuropathies resulting from complications of diabetes mellitus or alcohol intoxication account for more than two thirds of all cases of polyneuropathies (1). Modern research shows that in patients with diabetes mellitus, thiamine deficiency develops due to its increased excretion by the kidneys. Replenishing thiamine for diabetic patients is a daily practice. It has been established that the administration of thiamine in a dose of about 300 mg per day in combination with vitamins B6 and B12 significantly reduces or eliminates the manifestations of polyneuropathy, primarily, reducing neuropathic pain (2). In addition to reducing the manifestations of sensitivity disorders, vitamins in polyneuropathy have a significant effect on the manifestations of vegetative-trophic disorders in the neuropathic form of diabetic foot syndrome.

Systemic metabolic disorders occurring with obesity, in last years attract more and more attention of doctors. Operative treatment morbid obesity is becoming an increasingly common practice. Operational reconstruction gastrointestinal tract often saves patients from a number of fatal complications. However, subsequently, as a result of a disturbance in the assimilation of biologically important substances, patients often suffer from disorders of the peripheral nervous system. Patients, after surgery for morbid obesity, require compensatory treatment with the obligatory inclusion of B vitamins during the entire period of rehabilitation. The main purpose of prescribing vitamin preparations in this case is to prevent dysmetabolic polyneuropathies.

Acute inflammatory demyelinating polyneuropathies require parenteral administration of B vitamins in both acute and recovery period... Moreover, to activate the synthesis of myelin, a combination of B vitamins with folic acid is required (4).

Lack of B vitamins in alcoholic polyneuropathy is due to at least three factors. Ethyl alcohol inhibits the phosphorylation of thiamine. Alcohol interferes with the absorption of all vitamins in the intestines and decreases liver thiamine stores. Vitamin deficiency in alcoholics is associated with an alimentary factor - insufficiently varied diet. In alcoholic patients, medications containing vitamins are an essential part of treatment. In this case, long-term administration of drugs containing thiamine and pyridoxine is necessary. An open prospective study by E.A. Anisimova (2001) studied the efficacy of bentiamine in men suffering from chronic alcoholism... Against the background of monotherapy with benfotiamine, a decrease in pain syndrome, a reduction in sensory, autonomic and movement disorders was noted. An increase in the speed of conduction along the nerve fiber was found.

An unconditional indication for the appointment of vitamin preparations should be considered lesions of the cranial nerves of various etiologies. In clinical practice, complex therapy most often requires sensorineural hearing loss, acoustic neuritis, facial nerve neuropathy, and optic neuropathy. In most cases, vascular factors play a significant role in the pathogenesis of cranial nerve neuropathies. Restoration of conduction along the nerve trunks in these cases is possible with the restoration of microcirculation and long-term treatment with B vitamins.

Relatively short courses of vitamin therapy require radiculopathy associated with vertebrogenic factors. After eliminating the causes of root compression, B vitamins are prescribed for 2 - 3 weeks, which significantly speeds up the rehabilitation process.

Preparations containing vitamins in the required proportions are widely represented in the products of such large manufacturers as a corporation. All essential vitamins contains. The high content of B vitamins distinguishes the composition. The multivitamin complex is suitable both for the prevention of lesions of the nervous system and for treatment programs. From medicines in clinical practice such drugs as Milgamma, neuromultivitis have found application.

Thus, treatment with vitamins in the complex therapy of diseases of the peripheral nervous system not only has not lost its importance, but has received a deeper justification. Should be considered an unconditional indication the appointment of B vitamins in all cases of damage to the nervous system, which are based on the processes of demyelination or impaired remyelination. Modern correction of myelinopathies as systemic metabolic disorders is impossible without timely and adequate treatment with drugs containing thiamine, pyridoxine and cyanocobalamin. In diseases occurring with disorders of carbohydrate, fat and protein metabolism (diabetes mellitus), systematic treatment with vitamin preparations is necessary to activate metabolic processes, restore the synthesis of protein compounds. Preparations containing vitamins are absolutely necessary for patients suffering from disorders of absorption of essential coenzymes (alcoholism, patients who have undergone complex reconstructive surgery on the organs of the gastrointestinal tract).

Literature

1. Anisimova E.I. The effectiveness of benfotiamine in the treatment of alcoholic polyneuropathy. Journal of Neurology and Psychiatry. S. S. Korsakov. 2001. T 12.No. 101. S. 32-36.

2. Antsiferov M.B., Volkova A.K. Diagnostics and treatment of diabetic distal polyneuropathy in patients with diabetes mellitus in outpatient practice. Breast cancer. 2008. T. 16.No.15. S. 12. - 15.

3. Zinovieva O.E. Alpha-lipoic acid preparations in the treatment of diabetic polyneuropathy. Neurology, psychiatry, neurosomatics. 2009. No. 1. S. 58 - 62.

5. Mooney S., Leudorf J.E. Vitamin B6: a long known compound of surprising complexity. Molecules. 2009. V.14. p. 329 - 51.

According to Californian experts, the body of every person, regardless of gender, weight and lifestyle, begins to deteriorate at the same time - after 39 years. At the same time, sports activities, verified nutrition, etc. give those who have reached this mark, only a feeling of vigor, while upon reaching a "critical" age, aging of cells cannot stop even the most careful observance of the rules healthy way life.

The researchers came to this conclusion, calculating that upon reaching 39 years of age, the human body stops producing myelin... This chemical compound coats the nerve cells in the brain, protecting them from external factors, and is also responsible for the general condition of blood vessels, muscles and skeleton.

« With a lack of myelin, unprotected cells die, as a result of which there is a gradual extinction of mental abilities and impairment of musculoskeletal functions, that is, an irreversible aging process starts ", - the teaching is noted. The defeat of the myelin sheath can lead to numerous injuries, multiple sclerosis and even heart failure, American experts say. True, many of their colleagues working on the same problem do not think so. On the contrary, they are convinced that the theory of the Californian researchers requires careful refinement, as it contradicts the results of earlier studies, which say that the aging process cannot be tied to a certain age.

Neuron and its myelin sheath

However, there are natural ways to restore myelin in the body.... The myelin sheath helps nerves transmit signals. If it is damaged, memory problems arise, often a person has specific movements and functional disorders. Certain autoimmune diseases and external chemicals, such as pesticides in food, can damage the myelin sheath. But there are a number of ways, including vitamins and food, that can help regenerate this nerve coating: you need specific minerals and fats, preferably from a nutritious diet. This is all the more required if you suffer from a disease like multiple sclerosis: usually the body is able to repair the damaged myelin sheath with some help from you, but if sclerosis manifests itself, treatment can become very difficult. So, here are the remedies that will help support the recovery and regeneration of the myelin sheath, as well as prevent sclerosis.

You will need:
- folic acid;
- vitamin B12;
- essential fatty acids;
- vitamin C;
- vitamin D;
- green tea;
- martinia;
- white willow;
- boswellia;
- olive oil;
- fish;
- nuts;
- cocoa;
- avocado;
- whole grains;
- legumes;
- spinach.

1. Provide Yourself with Folic Acid and Vitamin B12 Supplements... The body requires these two substances to protect the nervous system and to competently "repair" the myelin sheaths. In a study published in the Russian medical journal Vrachebnoe Delo in the 1990s, researchers found that patients with multiple sclerosis who were treated with folic acid showed significant improvement in symptomatology and in myelin recovery. Both folic acid and B12 can both help prevent myelin breakdown and regenerate myelin damage.

2.Reduce inflammation in the body to protect the myelin sheaths from damage... Anti-inflammatory therapy is currently the mainstay of treatment for multiple sclerosis and in addition to taking prescribed medications, patients can also try dietary and herbal anti-inflammatory drugs. Among the natural remedies are essential fatty acids, vitamin C, vitamin D, green tea, martinia, white willow and boswellia.

3. Consume essential fatty acids daily. The myelin sheath is mainly composed of essential fatty acids: oleic acid, omega-6, found in fish, olives, chicken, nuts and seeds. Plus, eating deep sea fish will provide you with a good amount of omega-3s to improve mood, learning, memory and overall brain health. Omega-3 fatty acids reduce inflammation in the body and help protect the myelin sheaths. Fatty acids can also be found in flaxseed, fish oil, salmon, avocado, walnuts and beans.

4. Support the immune system. Inflammation, which causes damage to the myelin sheaths, is caused by immune cells and autoimmune diseases in the body. Nutrients that help immunity include: vitamin C, zinc, vitamin A, vitamin D, and vitamin B complex. In a 2006 study published in The Journal of the American Medical Association, vitamin D has been named as an agent that significantly helps reduce the risk of demyelination and the manifestation of multiple sclerosis.

5. Eat foods high in choline (vitamin D) and inositol (inositol; B8). These amino acids are critical for the repair of the myelin sheaths. Choline is found in eggs, beef, beans, and some nuts. It helps prevent fat storage. Inositol supports the health of the nervous system by assisting in the creation of serotonin. Nuts, vegetables and bananas contain inositol. Two amino acids combine to produce lecithin, which reduces the amount of bad fats in the bloodstream. Well, cholesterol and similar fats are known for their property to inhibit the restoration of the myelin sheaths.

6. Eat foods rich in B vitamins... Vitamin B-1, also called thiamine, and B-12 are physical components of the myelin sheath. B-1 is found in rice, spinach, pork. Vitamin B-5 can be found in yogurt and tuna. Whole grains and dairy products are rich in all B vitamins and can also be found in whole grain breads. These nutrients enhance the body's fat-burning metabolism and transport oxygen.

7. You also need food containing copper. Lipids can only be created using copper-dependent enzymes. Without this help, other nutrients cannot do their job. Copper is found in lentils, almonds, pumpkin seeds, sesame seeds, and semi-sweet chocolate. Liver and seafood can also contain copper in lower doses. Dry herbs like oregano and thyme are an easy way to add this mineral to your diet.

Demyelination Demyelination is a disease caused by selective damage to the myelin sheath around nerve fibers

Demyelination - a pathological process in which myelinated nerve fibers lose their insulating myelin layer. Myelin phagocytosed by microglia and macrophages, and subsequently by astrocytes, is replaced by fibrous tissue (plaques). Demyelination disrupts impulse conduction along the white matter pathways of the brain and spinal cord; peripheral nerves are not affected.

DEMYELINIZATION - destruction of the myelin sheath of nerve fibers as a result of inflammation, ischemia, trauma, toxic-metabolic or other disorders.

Demyelination (Demyelination) - a disease caused by selective damage to the myelin sheath, which runs around the nerve fibers of the central or peripheral nervous system. This, in turn, leads to dysfunction of the myelin nerve fibers. Demyelination can be primary (for example, in multiple sclerosis), or develops after a skull injury.

DEMYELINIZING DISEASES

Diseases, one of the main manifestations of which is the destruction of myelin, is one of the most urgent problems clinical medicine, mainly neurology. In recent years, there has been a clear increase in the number of cases of diseases accompanied by myelin damage.

Myelin - a special type of cell membrane surrounding the processes of nerve cells, mainly axons, in the central (CNS) and peripheral nervous system (PNS).

The main functions of myelin:
axon nutrition
isolation and acceleration of nerve impulse conduction
supporting
barrier function.

By chemical composition myelinis a lipoprotein membrane, consisting of a biomolecular lipid layer located between monomolecular layers of proteins, spirally twisted around the internodal segment of the nerve fiber.

Myelin lipids are represented by phospholipids, glycolipids and steroids. All these lipids are built according to a single plan and necessarily have a hydrophobic component ("tail") and a hydrophilic group ("head").

Proteins make up up to 20% of the dry weight of myelin. They are of two types: proteins located on the surface and proteins immersed in lipid layers or penetrating the membrane through and through. In total, more than 29 myelin proteins have been described. Myelin basic protein (MBP), proteolipid protein (PLP), myelin-associated glycoprotin (MAG) make up 80% of the protein mass. They perform structural, stabilizing, transport functions, have pronounced immunogenic and encephalitogenic properties. Among small myelin proteins, myelin-oligodendrocyte glycoprotein (MOG) and myelin enzymes, which are of great importance in maintaining structural and functional relationships in myelin, deserve special attention.

Myelins of the CNS and PNS differ in their chemical composition
in the PNS, myelin is synthesized by Schwann cells, with several cells synthesizing myelin for one axon. One Schwann cell produces myelin for only one segment between areas without myelin (Ranvier interceptions). The myelin of the PNS is noticeably thicker than that of the central nervous system. All peripheral and cranial nerves have such myelin; only short proximal segments of the cranial nerves and spinal roots contain CNS myelin. The optic and olfactory nerves contain predominantly central myelin
in the central nervous system, myelin is synthesized by oligodendrocytes, and one cell takes part in the myelination of several fibers.

Myelin breakdown is a universal mechanism for the response of nerve tissue to damage.

Myelin diseases are classified into two main groups
myelinopathies - associated with a biochemical defect in the structure of myelin, usually genetically determined

Myelinoclastic - myelinoclastic (or demyelinating) diseases are based on the destruction of normally synthesized myelin under the influence of various influences, both external and internal.

The division into these two groups is rather arbitrary, since the first clinical manifestations myelinopathies can be associated with the influence of various external factors, and myelinoclasts are most likely to develop in predisposed individuals.

The most common disease of the entire group of myelin diseases is multiple sclerosis. It is with this disease that differential diagnostics have to be carried out most often.

Hereditary myelinopathies

The clinical manifestations of most of these diseases are more often noted already in childhood... At the same time, there are a number of diseases that can begin at a later age.

Adrenoleukodystrophy (ALD) associated with insufficient function of the adrenal cortex and are characterized by active diffuse demyelination of various parts of both the central nervous system and the PNS. The main genetic defect in ALD is associated with a locus on the X chromosome - Xq28, whose genetic product (ALD-P protein) is a peroxisomal membrane protein. The type of inheritance is typically recessive, sex-dependent. To date, more than 20 mutations have been described at different loci associated with different clinical variants of ALD.

The main metabolic defect in this disease is an increase in the content of long-chain saturated fatty acids (especially C-26) in tissues, which leads to gross violations of the structure and functions of myelin. Along with the degenerative process in the pathogenesis of the disease, chronic inflammation in the brain tissue associated with increased production of tumor necrosis factor alpha (TNF-a) is essential. The ALD phenotype is determined by the activity of this inflammatory process and is most likely due to both a different set of mutations on the X chromosome and an autosomal modification of the influence of a defective genetic product, i.e. a combination of the main genetic defect in the sex X chromosome with a peculiar set of genes on other chromosomes.