Nerve injury is an injury to the neural network. There is no single classification system that can describe all the many variations of nerve injury. In 1941, Seddon introduced a classification of nerve injury based on three major types of nerve fiber injury and whether there was nerve continuity. Usually, however, (peripheral) nerve injury is classified in five stages, based on the degree of damage to the nerves and surrounding connective tissues, as it supports glial cells may be involved. Unlike in the central nervous system, neuroregeneration in the peripheral nervous system may be. The processes that occur in peripheral regeneration can be divided into the following major events: Wallerian degeneration, regeneration/growth of axons, and neural reinnervation. The incidence occurring in peripheral regeneration occurs with respect to the axis of the nerve injury. The proximal stump refers to the end of the injured neuron still attached to the body of the neuron; it is the part that regenerates. The distal stump refers to the end of the injured neuron still attached to the axon end; it is a part of the neurons that will degenerate but remain in the area that becomes the growth axis of regeneration. The study of peripheral nerve injuries started during the American Civil War and has been greatly developed to use molecules that promote growth.
Video Nerve injury
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Neuropraxia
This is the mildest form of nerve injury, with total recovery. In this case, the axon remains intact, but there is damage to myelin which causes impulse conduction disturbance down the nerve fibers. Most commonly, this involves nerve compression or disorders of the blood supply (ischemia). There is a temporary loss of functionality that can be recovered within hours until the injury months (average is 6-9 weeks). Wallerian degeneration does not occur, so recovery does not involve actual regeneration. Often there is greater motor involvement than sensory functions with autonomous functions maintained. In electrodiagnostic testing with a neural conduction study, there is a motion of motility action of the distal normal compound to the lesion on day 10, and this indicates the diagnosis of mild neuropracia rather than axonotmesis or neurotmesis.
Axonotmesis
This is a more severe neurological injury with neuronal axon disorders, but with the maintenance of epineurium. This type of nerve damage can cause motor, sensory, and autonomic disabilities. Especially seen in crush injuries.
If forces that create nerve damage are removed in a timely manner, axons can regenerate, leading to recovery. Electronically, the nerve exhibits rapid and complete degeneration, with the loss of voluntary motor units. Regeneration of the motor end plate will occur, as long as the endoneural tubules are intact.
Axonotmesis involves axon disorder and myelin cover but preservation of the skeleton of neural connective tissue (encapsulating tissue, epineurium and perineurium, preserved). Since the axons continuity is lost, the degrees of Wallerian occur. Electromyography (EMG) performed 2 to 4 weeks later shows fibrillation and the potential for denervation in the distal muscles to the site of injury. Loss on motor and sensory thorns is more complete with axonotmesis than neurapraxia, and recovery occurs only through axon regeneration, a process that takes time.
Axonotmesis is usually the result of a crush or bruise that is more severe than neurapraxia, but can also occur when the nerves stretch (without damaging epineurium). There is usually a proximal retrograde element of axon degeneration, and for regeneration to occur, this loss must first be resolved. Regenerating fibers should traverse the site of injury and regeneration through the proximal or retrograde areas of degeneration may take several weeks. Then the tip of the neuritis continues to the bottom, such as the wrist or hand. The proximal lesions can grow distally as fast as 2 to 3 mm per day and distal lesions as late as 1.5 mm per day. Regeneration occurs from week to year.
Neurotmesis
Neurotmesis is the most severe lesion without full recovery potential. This occurs in severe bruising, stretching, laceration, or local anesthetic poisoning. The axon and the connective tissue encapsulation lose its continuity. The last (extreme) level of neurotherapy is transsection, but most neurotmic injuries do not result in permanent loss of nerve continuity but an internal disturbance of the neural architecture sufficient to involve the perineurium and endoneurium as well as the axons and closures. The Denervation changes recorded by EMG are similar to those seen with axonotmetic injuries. There is a loss of motor function, sensory, and autonomous. If the nerve has been completely divided, axonal regeneration causes the neuroma to form in the proximal stump. For neurothermesis, it is better to use a new, more complete classification called the Sunderland System.
Maps Nerve injury
Event summary in peripheral regeneration
Wallerian degeneration is a process that occurs prior to nerve regeneration and can be described as a cleansing or cleaning process that essentially prepares distal stumps for reinvestment. Schwann cells are the glial cells in the peripheral nervous system that support neurons by forming myelin that encloses the nerves. During the degeneration of Wallerian, Schwann cells and macrophages interact to remove debris, especially damaged myelin and axon, from the site of injury in the distal. (Medscape) Calcium has a role in degeneration of axon destruction. BÃÆ'¼ngner bands are formed when unsupervised Schwann cells proliferate and the rest of the base membrane of the connective tissue forms an endoneurial pipe. BÃÆ'¼ngner bands are important to guide the growing axons.
In nerve cell cells, a process called chromatolysis occurs where the nucleus migrates to the periphery of the cell body and the endoplasmic reticulum ruptures and spreads. Nerve damage causes cell metabolic functions to change from those that produce molecules for synaptic transmission to those that produce molecules for growth and repair. These factors include GAP-43, tubulin and actin. Chromatolysis is reversed when cells are prepared for axon regeneration.
The regeneration of axon is characterized by the formation of growth cones. The growth cones have the ability to produce proteases that digest any material or debris that remains in its regeneration path to the distal site. The growth cones respond to molecules produced by Schwann cells such as laminin and fibronectin.
Schwann cell role
Schwann cells are active in the degrees of Wallerian. They not only have a role in myelin phagocytosis, but they also have a role in macrophage recruitment to continue myelin phagocytosis. The role of Schwann cell phagocytosis has been studied by studying the expression of molecules in Schwann cells that are usually specific to inflammatory macrophages. The expression of a single molecule like MAC-2, a specific galactose lectin, is observed not only in the macrophage-rich degeneration nerve but also macrophage-rare macular degeneration and the rich Schwann cells. Furthermore, the effects of MAC-2 in nerve degeneration are associated with myelin fagocytosis. There is a positive correlation between the number of MAC-2 expression and the level of myelin phagocytosis. Lack of MAC-2 expression can even lead to inhibition of myelin removal from the injury site.
Schwann cells are active in wounded nerve demylenation before macrophages are even present at the site of nerve injury. Electron microscopy and immunohistochemical staining analysis of the teasing nerve fibers shows that before macrophages arrive at the site of injury, myelin is fragmented and myelin debris and lipid droplets are found in the Schwann cell cytoplasm, suggesting phagocytic activity before macrophages arrive.
Schwann cell activity includes the recruitment of macrophages to the site of injury. Monocyte chemoattractant protein (MCP-1) plays a role in recruiting monocytes/macrophages. In demumenation triggered by eye eggs without axon degeneration, a nerve crush with axon degeneration, and nerve transection with axon degeneration occurs an increase in MCP-1 mRNA expression followed by an increase in macrophage recruitment. In addition, different levels of MCP-1 mRNA expression also have an effect. Increased MCP-1 mRNA levels correlated positively with increased macrophage recruitment. Furthermore, in situ hybridization determines that the cellular source of MCP-1 is Schwann cells.
Schwann cells play an important role in not only producing neurotropic factors such as neurotrophic growth factors (NGF) and ciliary neurotrophic factors (CNTF), which promote growth, both damaged nerves and support Schwann cells, but also produce neurite support factors, which guide axons that are growing, both are discussed below.
The role of macrophages
The main role of macrophages in peripheral regeneration is demylenation during the degeneration of Wallerian. Immunohistochemical analysis showed that in tellumium eggs disseminated, crushed, and cut, the expression of lysozyme, which is a marker for myelin phagocytosis, and ED1, which is a marker of macrophages, occurs in the same region. Lysozyme is also investigated in connection with the temporal development of myelin phagocytosis by macrophages in nerve injury. Northern blotting shows that the peak expression of lysozyme mRNA occurs at the right time with respect to the temporal model of myelin phagocytosis. Macrophages do not phagocytosis all cellular debris at the site of nerve injury; they are selective and will save certain factors. Macrophages produce apolipoprotien E which is involved in saving cholesterol on damaged nerves. In the same investigation, the temporal level of expression of apolipoprotein E mRNA in three models for demylenation and consistent nerve damage with respect to models for rescuing cholesterol on nerve injury. Macrophages play a role in saving cholesterol during nerve injury.
Macrophages also play a role in inducing the proliferation of Schwann cells that occur during the degeneration of Wallerian. The supernatant has been collected from the medium where macrophages are active in myelin fagocytosis in which the lysosome process of myelin occurs within the macrophages. The supernatant contains mitogenic factors, a mitotic propulsion factor, characterized by heat and trypsin sensitivity, both characterized as peptides. The treatment of Schwann cells with the collected supernatant suggests that it is a mitogenic factor and thus plays an important role in Schwann cell proliferation.
Macrophages are also involved in secretion factors that promote nerve regeneration. Macrophages secrete not only interleukin-1, a cytokine that induces expression of nerve growth factor (NGF) in Schwann cells but also interleukin-1 receptor antagonists (IL-1ra). IL-1ra expression in mice with transitional sciatic nerve through tubular implantation releasing IL-1ra showed less myocardial aquiline and myelin reconstitution. The secretion of interleukin-1 macrophages is involved in the stimulation of nerve regeneration.
The role of neurotropic factors
Neurotropic factors are factors that promote the survival and growth of neurons. Trophic factors can be described as factors associated with the provision of food to allow for growth. In general they are protein ligands for tyrosine kinase receptors; binding to specific receptors results in autophosphorylation and subsequent phosphorylation of tyrosine residues in proteins that participate in further downstream signaling to activate proteins and genes involved in growth and proliferation. Neurotropic factors act through retrograde transport in neurons, where they are picked up by the cone of growth of a wounded neuron and transported back into the body cell.
Nerve growth factor (NGF) typically has low levels of expression in healthy nerves and does not grow or develop, but in response to NGF expression with increased nerve injury in Schwann cells. This is a mechanism to increase Schwann cell growth and proliferation in distal stumps to prepare for regeneration axons acceptance. NGF not only has a trophic role but also a tropical role or a guide. Schwann cells forming Bungner bands at distal wound locations express NGF receptors as a guiding factor for the injured neuronal regeneration axons. NGF bound to receptors in Schwann cells provides a growing neuron that is contacted by trophic factors to promote growth and further regeneration.
Ciliary neurotropic factors (CNTF) typically have high levels of expression in Schwann cells associated with healthy nerves, but in response to nerve injury CNTF expression decreases in Schwann cells located near the site of injury and remains relatively low unless the injured axon begins to grow back. CNTF has many trophic roles in motor neurons in the peripheral nervous system including the prevention of hardened tissue atrophy and the prevention of degeneration and death of motor neurons after nerve injury. (Frostick) In sciatic motor neurons both CNTF mRNA receptor expression and CNTF receptors increase after injury for long periods of time compared to short time frames in the central nervous system indicating the role of CNTF in nerve regeneration.
Insulin-like growth factors (IGFs) have been shown to increase the regeneration rate of axonal peripheral nervous system. IGF-I and IGF-II mRNA levels were significantly increased in the distal to the site of scab wounds on rat's sciatic nerve. In place of neuronal repair, locally transmitted IGF-I can significantly increase axon regeneration rates in a neural graft and help speed up functional recovery of a paralyzed muscle.
The role of the neurite trigger factor
The neurite driving factors include many of the extracellular matrix proteins produced by Schwann cells in distal stumps including fibronectin and laminin. Fibronectin is a component of the basal lamina and promotes neurite growth and growth cones adhesion to basal laminae. In the regeneration of nerve cells, neurite support factors play a role in axon adhesion and include nerve cell adhesion molecules (N-CAM) and N-cadherin.
Nerve regeneration therapy
Electrical stimulation can increase nerve regeneration. The frequency of stimulation is an important factor in the successful quality and quantity of axon regeneration as well as the growth of myelin and surrounding blood vessels that support axons. Histologic analysis and regeneration measurements showed that low-frequency stimulation had a more successful outcome than high-frequency stimulation of sciatic nerve regeneration.
Surgery can be done if the nerve has been cut or divided. Recovery of nerves after surgical repair mainly depends on the age of the patient. Young children can restore nerve function from close to normal. Conversely, patients over the age of 60 with nerve cuts in hand will hope to recover only a protective sensation, ie the ability to distinguish hot/cold or sharp/dull. Many other factors also affect nerve recovery. The use of autologous nervous transplant procedures that involves redirecting the regenerative donor nerve fibers into the graft channel has successfully restored the target muscle function. The local release of dissolved neurotrophic factors may help promote the axon regeneration rate observed in this graft channel.
The expansion of nerve regeneration research areas is concerned with the development of scaffolding and bio-conduits. Scaffolding developed from biomaterials will be useful in nerve regeneration if they succeed in showing a role that is essentially the same as the endoneurial tubes and Schwann cells in guiding the growing axons.
See also
- Brain injury
References
Source of the article : Wikipedia
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