Materiały źródłowe

• #1 Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7589539/

  Spinal cord injury (SCI) is a destructive neurological and pathological state that causes major motor, sensory and autonomic dysfunctions. Its pathophysiology comprises acute and chronic phases and incorporates a cascade of destructive events such as ischemia, oxidative stress, inflammatory events, apoptotic pathways and locomotor dysfunctions. […] Understanding pathophysiology, phases and various wound recovery mechanisms associated with SCI is essential for the development of appropriate recovery treatments. […] The secondary injury phase reflects multi-featured pathological processes following the primary injury phase and lasts for several weeks. Clinical manifestation of secondary injury includes increased cell permeability, apoptotic signalling, ischemia, vascular damage, oedema, excitotoxicity, ionic deregulation, inflammation, lipid peroxidation, free radical formation, demyelination, Wallerian degeneration, fibroglial scar and cyst formation.

• #1 Spinal Cord Injuries – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK560721/

  Spinal cord injuries (SCIs) are complex medical conditions resulting from spinal cord damage, often caused by trauma, as in motor vehicular crashes and falls, and nontraumatic etiologies like malignancy and degeneration. […] The pathologic mechanisms causing SCIs are classified as either primary or secondary. Primary injury, often irreversible, arises from direct spinal cord damage. Secondary injury occurs as a consequence of the changes induced by a primary injury, such as inflammation. […] SCIs arise from complex mechanisms, producing varying degrees of neurologic deficits depending on the injury’s location and extent. The processes driving SCIs are classified as either primary or secondary. […] A primary SCI develops from mechanical forces directly damaging the cord. The most common primary SCI mechanism is direct cord trauma, followed by persistent compression from space-occupying pathologies like vertebral fractures, malignancies, hematomas, and abscesses.

• #1 An Audit of the Stages of Spinal Cord Injury Pathogenesis and their Relation to Secondary Medical Complications and Potential Chronicity in Patients | Esurgi

  https://myesurgi.com/an-audit-of-the-stages-of-spinal-cord-injury-pathogenesis-and-their-relation-to-secondary-medical-complications-and-potential-chronicity-in-patients/

  To understand the rationale of the recent therapeutic advances, it is first necessary to review the pathophysiology of spinal cord injury (SCI). There are four general types of SCI. The first is a cord maceration, in which the morphology of the cord is severely distorted. The second type is a cord laceration (gunshot or knife wounds). The third potential type is a contusion injury, in which damaged blood vessels leak into surrounding areas. Lastly, the fourth class is a solid cord injury, in which there is no central focus of hemorrhaging or an overt disruption in morphology. Of these four injury types, the contusion injury represents from 25 to 40% of the cases and is a progressive injury that enlarges over time. The most commonly used animal model in SCI research is patterned after the contusion injury. Within these four injury types, degree of completeness must be considered, as incomplete lesions will benefit more dramatically from experimental interventions than complete lesions in terms of degree of recovery that can be obtained. It is important to note that the clinical presentation of SCI is most often characterized as an anatomically incomplete lesion, irrespective of initial neurological presentation.

• #1 Acute spinal cord injury: Pathophysiology and pharmacological intervention (Review)

  https://www.spandidos-publications.com/10.3892/mmr.2021.12056?text=fulltext

  Spinal cord compression is the most frequent mechanism of SCI and can continue after the injury. Penetrating injuries and strain to the neural tissues or vascular structures are caused by dislocation, flexion, extension or distraction forces related to rotation. Other mechanical damage to bone structures and ligaments can result, or consequences related to compression can give rise to hematomas in the spinal cord channel. […] Secondary damage can be initiated by primary damage, whereas a number of pathophysiological mechanisms can come into play even hours and days after developing SCIs. The most notable mechanism is a lack of energy due to ischemia and impaired perfusion at the cellular level. Ischemia can result immediately after traumatic SCI and, if left untreated, additional damage may commence within the first 3 h and continue for at least 24 h.

• #1 Pathophysiology and Therapeutic Approaches for Spinal Cord Injury

  https://www.mdpi.com/1422-0067/23/22/13833

  Spinal cord injury (SCI) is a disabling condition that disrupts motor, sensory, and autonomic functions. […] The lack of effective therapeutic strategies for patients with SCI reflects its complex pathophysiology that leads to the point of no return in its function repair and regeneration capacity. […] SCI results from an insult that damages the spinal cord, which can be subdivided into non-traumatic and traumatic. Non-traumatic injury occurs when an acute or chronic disease, such as a tumor, infection, or degenerative disease, causes damage to the spinal cord. The traumatic and most common SCI results from a traumatic impact that fractures or dislocates vertebrae. The initial mechanical impact to the spinal cord at the time of injury is denominated primary injury. […] Following the primary injury, a derived degenerative process initiates within minutes and hours, which is proportional to the magnitude of the initial insult. This resultant process is commonly denominated by secondary injury. This comprises permeability and vascular alterations, ionic disruption and glutamate excitotoxicity, metabolic alterations, a dysfunctional inflammatory response, and initiation of glial scarring.

• #1

  https://www.orthobullets.com/spine/2006/spinal-cord-injuries

  Mechanism […] MVA causes 50% […] iatrogenic […] it is estimated that 3-25% of all spinal cord injuries occur after initial traumatic episode due to improper immobilization and transport […] Pathophysiology […] primary injury […] damage to neural tissue due to direct trauma […] irreversible […] secondary injury […] injury to adjacent tissue due to […] decreased perfusion […] lipid peroxidation […] free radical / cytokines […] cell apoptosis […] methylprednisolone used to prevent secondary injury by improving perfusion, inhibiting lipid peroxidation, and decreasing the release of free radicals […] Acute Phase Conditions […] Neurogenic shock […] mechanism […] circulatory collapse from loss of sympathetic tone […] disruption of autonomic pathway within the spinal cord leads to

• #1 Traumatic Spinal Cord Injury – TeachMeSurgery

  https://teachmesurgery.com/neurosurgery/traumatic-injuries/traumatic-spinal-cord-injury/

  A traumatic spinal cord injury (TSCI) is traumatic injury leading to damage of the spinal cord, resulting in temporary or permanent change to neurological function, including paralysis. […] Trauma causes injury to the spinal cord from (1) the initial acute impact, resulting in a concussion on the spinal cord (2) compression on the spinal cord from increased pressures from nearby rigid structures (such as vertebrae and discs) that may have been displaced by the injury. […] Based on pathophysiology, spinal cord injuries can be classified into primary or secondary injuries. Primary injury refers to the destructive forces that directly damage the neural structures, such as the shear forces tearing an axon or the direct compressive force occluding a blood vessel, resulting in ischaemia. Secondary injury refers to a cascade of vascular, cellular, and biochemical events which occur following the injury, which can worsen a concurrent primary injury.

• #1 Spinal Cord Injuries: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/793582-overview

  Spinal cord injury (SCI), as with acute stroke, is a dynamic process. In all acute cord syndromes, the full extent of injury may not be apparent initially. Incomplete cord lesions may evolve into more complete lesions. More commonly, the injury level rises 1 or 2 spinal levels during the hours to days after the initial event. A complex cascade of pathophysiologic events related to free radicals, vasogenic edema, and altered blood flow accounts for this clinical deterioration. Normal oxygenation, perfusion, and acid-base balance are required to prevent worsening of the SCI. […] SCI can be sustained through different mechanisms, with the following 3 common abnormalities leading to tissue damage: Destruction from direct trauma, Compression by bone fragments, hematoma, or disk material, Ischemia from damage or impingement on the spinal arteries.

• #1 Spinal Cord Injuries: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/793582-overview

  Neurogenic shock refers to the hemodynamic triad of hypotension, bradycardia, and peripheral vasodilation resulting from severe autonomic dysfunction and the interruption of sympathetic nervous system control in acute SCI. […] SCIs may be primary or secondary. Primary SCI arises from mechanical disruption, transection, or distraction of neural elements. Secondary SCIs are potentially modifiable injuries that occur hours to days after the initial trauma. These include such pathologies as hypotension, infection, and thromboembolism. Anoxic or hypoxic effects can compound the extent of SCI. […] Primary SCI usually occurs with fracture and/or dislocation of the spine. However, primary SCI may occur in the absence of spinal fracture or dislocation. Penetrating injuries due to bullets or weapons may also cause primary SCI through direct injury or propagation of a percussive wave. More commonly, displaced bony fragments cause penetrating spinal cord and/or segmental spinal nerve injuries.

• #1 Spinal Cord Injuries – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK560721/

  A secondary SCI emerges from a series of biological phenomena that begin within minutes of a primary injury and continue for weeks or months. The acute secondary injury phase encompasses vascular damage, ionic imbalances, free-radical formation, the initial inflammatory response, and neurotransmitter accumulation (excitotoxicity). […] Post-SCI neuroinflammation exhibits a dual nature, potentially causing both beneficial and deleterious outcomes, depending on the timing and immune cells present at the injury site. […] Spinal cord disruption leads to motor and sensory function deficits below the injury level. Disability patterns depend on the injury level and extent of spinal tract involvement.

• #1 A comprehensive look at the psychoneuroimmunoendocrinology of spinal cord injury and its progression: mechanisms and clinical opportunities | Military Medical Research | Full Text

  https://mmrjournal.biomedcentral.com/articles/10.1186/s40779-023-00461-z

  Spinal cord injury (SCI) is a devastating and disabling medical condition generally caused by a traumatic event (primary injury). This initial trauma is accompanied by a set of biological mechanisms directed to ameliorate neural damage but also exacerbate initial damage (secondary injury). […] Understanding the pathogenesis and clinical impact of SCI requires its global consideration as a multiorgan process that affects and disrupts the function of different organs and systems. This global consideration of SCI is illuminated from the perspective of psychoneuroimmunoendocrinology (PNIE). […] The natural history of SCI includes two main phases: primary injury and secondary injury. Primary injury is due to the direct injurious effect of the etiological agent on the spinal cord, whereas secondary injury is due to the development of events following neural tissue damage and the infiltration of the injured tissue by cells of the immune inflammatory system.

• #1 A comprehensive look at the psychoneuroimmunoendocrinology of spinal cord injury and its progression: mechanisms and clinical opportunities | Military Medical Research | Full Text

  https://mmrjournal.biomedcentral.com/articles/10.1186/s40779-023-00461-z

  Research has shown that the beginning of secondary injury resides in the triggering of biochemical pathways in neural and vascular tissues. In this phase, inflammation becomes chronic and consequently erodes healthy tissue and surviving neurons. […] Previous works have noted that there are up to 25 described mechanisms of secondary damage after SCI. Here, we subdivide these mechanisms into 5 main groups: 1) vascular injury and ischemia, 2) exacerbated cell death, 3) OS, 4) immune infiltration and local inflammation, and 5) neuroglial disturbances. […] Vascular injury is a major mechanism of secondary damage in SCI. […] Exacerbated cell death events represent a critical mechanism of secondary injury in SCI, although two major forms of cell death should be distinguished here: programmed cell death (PCD) and necrosis.

• #1 Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7589539/

  The most vulnerable clinical manifestation immediately after injury is the interruption of spinal cord vascular supply and hypotension/hypo-perfusion, producing hypovolemia, neurogenic shock and bradycardia. […] Spinal cord ischemia causes cytotoxic, ionic and vasogenic oedemas. […] High levels of glutamate in necrotic cells alter the ionic flux by increasing intracellular Na+ and Ca2+ concentrations and decreasing intracellular K+ concentrations. […] Mitochondria are an integral component for cellular metabolism because they generate ATP (Adenosine triphosphate) molecules through phosphorylation. […] High ROS and reactive nitrogen species (RNS) generation induces various deleterious effects, including lipid peroxidation on different body organs. […] Apoptosis and necrosis are vital cell death processes in SCI.

• #1 Pathophysiology and Therapeutic Approaches for Spinal Cord Injury

  https://www.mdpi.com/1422-0067/23/22/13833

  The hemorrhage associated with the “primary injury,” coupled with systemic hypotension, culminates in a major reduction in the blood flow at the lesion site. […] After the insult, the homeostatic ionic balance is severely compromised. Membrane depolarization and ATPase disruption enhance neuronal and glial cell death by increasing intracellular calcium (Ca2+) levels. […] Inflammation is a major “secondary injury” event, and its dysregulated nature leads to more neuronal damage. […] The regeneration of CNS following injury is reduced due to multiple inhibitory factors at the injury site. […] The deposition of connective tissue and reactive gliosis creates a physical barrier, providing nonspecific topographical cues which affect cellular migration. […] The chronic phase is characterized by scar maturation, cystic cavitation, and axonal dieback. […] SCI pathophysiology involves many mechanistically distinct processes that interact in order to both limit and enhance recovery following injury.

• #1 Acute spinal cord injury: Pathophysiology and pharmacological intervention (Review)

  https://www.spandidos-publications.com/10.3892/mmr.2021.12056?text=fulltext

  Severe SCI causes a substantial decrease in blood supply, resulting in the initiation of ischemia following the trauma. […] Blocking potassium channels may be a potential therapeutic target for the treatment of SCI. […] The pathophysiological processes following SCI are highly complex and the extent of our knowledge concerning these processes is limited. This is evident from the slow advancement of currently available neuroprotective methods compared with rapid trauma revitalization and other clinical interventions. Emerging studies continue to be added to the existing literature, comprising studies on inflammation, dysregulation, lipid peroxidation and apoptosis, which may be considered while developing suitable pharmacological therapies.

• #1 Acute spinal cord injury: Pathophysiology and pharmacological intervention (Review)

  https://www.spandidos-publications.com/10.3892/mmr.2021.12056?text=fulltext

  High levels of glutamate can cause excitotoxicity, oxidative damage and ischemia, while Ca2+-dependent nitric oxide synthesis can cause secondary spinal cord damage. Following secondary injuries, increased free radical damage and lipid peroxidation in the cell membrane and secondary injury signaling cascades at the injured tissue areas can eventually lead to neuronal death. […] Nevertheless, extensive experiments show that the spinal cord has excellent healing properties. Proper blood flow is an essential factor in ensuring that progressive tissue damage precedes and promotes necrosis during the healing process. SCI is therefore regarded as a pathological condition involving injury to the nerve tissue. […] Systemic factors causing acute SCI include hypotension resulting from neurological shocks, minimized cardiac output and respiratory failure. In such cases, the supply of essential metabolites and oxygen to the nervous tissue is restricted.

• #1 Mechanism and prospects of mitochondrial transplantation for spinal cord injury treatment | Stem Cell Research & Therapy | Full Text

  https://stemcellres.biomedcentral.com/articles/10.1186/s13287-024-04077-5

  After SCI, the excessive production of intracellular free radicals overwhelms the antioxidant systems capacity to neutralize them, leading to oxidative stress damage. […] Following membrane damage, the activation of voltage-gated Ca2+ channels or calcium leakage leads to further increases in intracellular Ca2+ levels, which in turn enhances the release of the excitatory neurotransmitter glutamate, resulting in excitotoxic cell death. […] Simultaneously, mitochondrial dysfunction allows water and other small molecules to enter the mitochondrial matrix, causing matrix swelling and rupture of the outer membrane. […] This results in the release of large amounts of Ca2+, pro-apoptotic proteins, and ROS into the cytoplasm. […] Following SCI, oxidative stress within cells triggers a cascade of biochemical events.

• #1 Acute spinal cord injury: Pathophysiology and pharmacological intervention (Review)

  https://www.spandidos-publications.com/10.3892/mmr.2021.12056?text=fulltext

  Peripheral immune cells, including macrophages, neutrophils and T cells, can initiate an inflammatory response following SCI, which may gradually increase within a few days. Macrophages and neutrophils can cause the growth of lesions and lead to tissue damage. […] The generation of free radicals should be inhibited to maintain cell viability. The activity of the endogenous antioxidant system is reduced by aging and has a substantial impact on SCI. […] Apoptosis is activated following SCI due to the release of inflammatory cytokines and free radicals, which lead to inflammation and excitotoxicity. […] Opioid peptides are locally released during SCI. The hypothesis that endogenous opioids may have a significant role in the mechanism of secondary injury has been proven by previous studies that show that blocking the opiate receptors protects against cellular damage as well as preventing release of cellular contents.

• #1 A comprehensive look at the psychoneuroimmunoendocrinology of spinal cord injury and its progression: mechanisms and clinical opportunities | Military Medical Research | Full Text

  https://mmrjournal.biomedcentral.com/articles/10.1186/s40779-023-00461-z

  OS represents a state of imbalance in which pro-oxidative processes overwhelm cellular antioxidant defense due to the disruption of redox signaling and adaptation. […] Primary injury to the spinal cord triggers an inflammatory response orchestrated by the immune system. This inflammatory response plays a dual role. On the one hand, the inflammatory response is beneficial for the clearance of cellular debris and necrotic tissues. On the other hand, an aberrant inflammatory response is also considered a secondary mechanism of damage, exacerbating cell death and impairing axonal regeneration. […] Following primary SCI, in acute stages neurons and glial cells like oligodendrocytes (OLs) suffer from different types of cell death such as apoptosis or necrosis. This loss of OLs causes demyelination and impairs axon function and neuronal survival.

• #1 A comprehensive look at the psychoneuroimmunoendocrinology of spinal cord injury and its progression: mechanisms and clinical opportunities | Military Medical Research | Full Text

  https://mmrjournal.biomedcentral.com/articles/10.1186/s40779-023-00461-z

  The immune system plays a dual role by protecting or promoting secondary damage after SCI. […] Overall, the immune dysfunction occurred in patients with chronic SCI entails a huge complexity. […] The study of the peripheral immune cell populations in SCI patients has received growing attention in recent years, prominently because of their relevance to understanding immune dysfunction and the potential benefits that may arise from using them as biomarkers or therapeutic targets.

• #1 Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7589539/

  Acute axonal degeneration (AAD) is another important clinical manifestation of early acute SCI phase. […] Demyelination occurs when myelin, the protective coating of nerve cells, is damaged. […] Glial scar formation (gliosis) is a reactive cellular mechanism that is facilitated by astrocytes and occurs during the chronic secondary phase of SCI. […] The continuous enlargement of lesion site and formation of the cyst is the hallmark feature of SCI. […] Multicellular interactions play an important role in developing effective neuroprotective and neurodegenerative strategies to overcome detrimental outcomes following SCI. […] Neuroprotection protects neuronal structure and function from further damage and is the relative preservation of the neurodegenerative effects of neurons and the maintenance of neuronal integrity to decrease neuronal lost ratio over time. […] Neuro-regeneration is the regrowth and repair of damaged nervous tissues (neurons, axons, synapses and glial cells) after injury.

• #1 Mechanism and prospects of mitochondrial transplantation for spinal cord injury treatment | Stem Cell Research & Therapy | Full Text

  https://stemcellres.biomedcentral.com/articles/10.1186/s13287-024-04077-5

  The interruption of anterograde transport in axons exacerbates local energy metabolism disorders at the injury site, and retrograde transport becomes impossible, preventing damaged mitochondria from fusing again to restore the respiratory chain and inhibit mitochondrial apoptosis. […] In this process, the synaptic protein Syntaphilin (Snph) plays a key role in the specific static anchoring of mitochondria within axons. […] Research by Zhou et al. has shown that the expression of Snph is elevated in mature neurons. […] However, it is crucial to clear these damaged mitochondria promptly after injury. […] By transplanting exogenous mitochondria to replace damaged mitochondria, it is possible to reduce the production of intracellular ROS, provide a new source of exogenous mitochondrial DNA, and enhance energy production and calcium buffering capacity.

• #1 Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

  https://www.mdpi.com/1422-0067/21/20/7533

  The available therapeutic approaches are broadly classified as neuroprotective, neuro-regenerative, and immune-modulating pathways that are briefly discussed in this section. […] Neuroprotection protects neuronal structure and function from further damage and is the relative preservation of the neurodegenerative effects of neurons and the maintenance of neuronal integrity to decrease neuronal lost ratio over time. […] The available strategies of neuroprotection can be divided into three main approaches, (i) pharmacological approaches, (ii) non-pharmacological approaches and (iii) cellular and genetic approaches. […] The apoptotic pathways are further divided into two major pathways, i.e., (i) the death receptor initiated (also called extrinsic) pathway and (ii) the mitochondrial (also called intrinsic or Bcl-2-regulated) pathway. […] Neuro-regeneration is the regrowth and repair of damaged nervous tissues (neurons, axons, synapses and glial cells) after injury. […] RhoA is a small GTPase protein belonging to the Rho GTPase family. RhoA downstream effector (ROCK) regulates the neuronal cytoskeleton.

• #1 Spinal Cord Injury: Time to Move? | Journal of Neuroscience

  https://www.jneurosci.org/content/27/44/11782

  The use of autologous macrophages was the first approach developed for clinical trial. […] The promising results of phase I encouraged the investigators to embark on phase II. […] Despite advances in medical and surgical treatment, current therapies for SCI are limited. […] However, the past 15 years has seen advances in biomedical research directed at minimizing the impact of secondary injury and promoting neural regeneration. […] The primary mechanical injury to the cord is amplified by a series of secondary injury mechanisms, which include compression and vertebral column instability, ischemia, glutamatergic excitotoxicity, derangements in ionic homeostasis, oxidative cell stress, inflammation, and apoptosis. […] Given the vulnerability of oligodendrocytes to secondary apoptotic death, coupled with a deficient expression of myelin-associated genes after SCI, demyelination of residual axons within the spinal cord white matter is an important contributor to the pathophysiology.

• #1 Spinal Cord Injury: Time to Move? | Journal of Neuroscience

  https://www.jneurosci.org/content/27/44/11782

  A novel Rho inhibitor recombinant protein (Cethrin) formulated with a fibrin sealant inhibits cell death, promotes neural regeneration, and improves locomotor recovery in transection and contusion animal models of SCI. […] The intensive biomedical research related to spinal cord injury over the past 15-20 years are now beginning to pay dividends with the translational of neuroprotective and regenerative approaches in clinical trials.

• #1 Spinal Cord Injury: Causes, Symptoms, Treatment & Types

  https://my.clevelandclinic.org/health/diseases/12098-spinal-cord-injury

  A spinal cord injury (SCI) happens when theres damage to your spinal cord, a thick bundle of nerve fibers that allows your brain to communicate with other nerves almost everywhere else in your body. […] SCIs also commonly involve multiple phases. The first phase is the initial injury. But in the following hours and days, a secondary injury can also develop, causing swelling and further damage to your spinal cord. […] The treatment for SCIs varies widely. The first distinction is whether or not its injury-related. A suspected trauma-related SCI is ALWAYS a medical emergency. SCIs due to certain other causes are also medical emergencies. Emergency causes include: […] Many methods can help, including: Surgery: The main priority of surgery is to relieve pressure on your spinal cord. It can also repair damage related to surrounding injuries pressing on your spinal cord. […] These are medications or treatment approaches that help damaged spinal cord or nerve tissue regenerate and repair itself.

• #1 Update on traumatic acute spinal cord injury. Part 1 | Medicina Intensiva

  https://www.medintensiva.org/en-update-on-traumatic-acute-spinal-articulo-S2173572717300681

  Current management includes surgical decompression, hemodynamic control, and methylprednisolone in selected cases. However, these early treatment measures are associated to only modest functional recovery. […] The search for an effective neuroprotective strategy capable of preventing secondary lesions in the context of acute traumatic SI remains a priority concern both in clinical practice and in basic research.

• #1 Spinal Cord Injury | Doctor

  https://patient.info/doctor/spinal-cord-injury

  A complete injury is indicated by a total lack of sensory and motor function below the level of injury. […] The prognosis is variable between almost complete recovery and complete paralysis. […] The spinal cord has very limited powers of regeneration. […] Patients with a complete cord injury have a very low chance of recovery, especially if paralysis persists for longer than 72 hours. […] The prognosis is much better for the incomplete cord syndromes. […] Prognosis for neurological deficit depends on the magnitude of the spinal cord damage present at the onset. […] Neurological deterioration is usually caused by secondary injury, resulting in oedema and/or haemorrhage.

• #1 Optimizing Hemodynamic Support of Acute Spinal Cord Injury Based on Injury Mechanism

  https://columbia.demo.elsevierpure.com/en/projects/optimizing-hemodynamic-support-of-acute-spinal-cord-injury-based-

  Using our large animal model of SCI, we hypothesize that well-intended increases in MAP will exacerbate a so-called 'reperfusion injury’ and ultimately have deleterious effects on regions of the spinal cord surrounding the injury site. […] Ultimately, a better understanding of how the spinal cord adjacent to the injury site responds to alterations in systemic blood pressure in the presence or absence of residual mechanical compression will help clinicians provide optimal hemodynamic management for patients with acute SCI and improve their chances of neurologic recovery.

• #1 Mechanism and prospects of mitochondrial transplantation for spinal cord injury treatment | Stem Cell Research & Therapy | Full Text

  https://stemcellres.biomedcentral.com/articles/10.1186/s13287-024-04077-5

  The results showed that exogenous mitochondria maintained energy supply to the injured spinal cord in a dose-dependent manner, significantly reducing the proportion of cells in the G1 phase. […] Additionally, they preserved the activity of antioxidants such as catalase and glutathione peroxidase in the damaged tissue, promoting oxidative phosphorylation function in the injured spinal cord to maintain at 90% of the sham-operated level. […] MT can also inhibit the expression of apoptosis-related proteins such as Grp78, Chop, and P-Akt, effectively reducing the number of apoptotic cells in the early stages of SCI and promoting cell survival. […] Furthermore, MT significantly decreases the formation of late-stage glial scars in the lesion area, reduces the size of the lesion cavity, and promotes myelin regeneration by increasing the number of cells expressing neurofilament.

• #1 Mechanism and prospects of mitochondrial transplantation for spinal cord injury treatment | Stem Cell Research & Therapy | Full Text

  https://stemcellres.biomedcentral.com/articles/10.1186/s13287-024-04077-5

  Additionally, studies have shown that during the process of MT, the levels of GAP-43, which is highly expressed in neuronal growth cones, are significantly elevated. […] Mitochondria delivered through MSC transplantation can fuse with neuronal mitochondrial membranes, restoring mitochondrial homeostasis. […] This process inhibits mitochondrial fission and mitophagy, ultimately alleviating neuronal ferroptosis and promoting functional recovery after SCI. […] After SCI, mitochondrial dysfunction leads to metabolic disturbances and cell death in spinal cord neurons. Transplanting exogenous mitochondria can correct this dysfunction, restore energy supply, and further regulate factors such as inflammation, apoptosis, and oxidative stress, demonstrating significant potential in the treatment of SCI.

• #1 Study documents safety, improvements from stem cell therapy after spinal cord injury – Mayo Clinic News Network

  https://newsnetwork.mayoclinic.org/discussion/study-documents-safety-improvements-from-stem-cell-therapy-after-spinal-cord-injury/

  ROCHESTER, Minn. — A Mayo Clinic study shows stem cells derived from patients’ own fat are safe and may improve sensation and movement after traumatic spinal cord injuries. […] Although it is understood that stem cells move toward areas of inflammation — in this case the location of the spinal cord injury — the cells’ mechanism of interacting with the spinal cord is not fully understood, Dr. Bydon says. […] The spinal cord has limited ability to repair its cells or make new ones. […] Based on researchers’ understanding of traumatic thoracic spinal cord injury, only 5% of people with a complete injury would be expected to regain any feeling or movement. […] „In spinal cord injury, even a mild improvement can make a significant difference in that patient’s quality of life,” Dr. Bydon says.

• #1 Study documents safety, improvements from stem cell therapy after spinal cord injury – Mayo Clinic News Network

  https://newsnetwork.mayoclinic.org/discussion/study-documents-safety-improvements-from-stem-cell-therapy-after-spinal-cord-injury/

  An important next step is assessing the effectiveness of stem cell therapies and subsets of patients who would most benefit, Dr. Bydon says. […] „For years, treatment of spinal cord injury has been limited to supportive care, more specifically stabilization surgery and physical therapy,” Dr. Bydon says. „Many historical textbooks state that this condition does not improve. In recent years, we have seen findings from the medical and scientific community that challenge prior assumptions. This research is a step forward toward the ultimate goal of improving treatments for patients.”

• #2 Pathogenesis of spinal cord injuries and mechanisms of repair induced by olfactory ensheathing cells

  https://www.imrpress.com/journal/RN/56/10/10.33588/rn.5610.2013109

  Pathogenesis of spinal cord injuries and mechanisms of repair induced by olfactory ensheathing cells. […] Spinal cord injury is a catastrophic event with permanent consequences during the all life. […] AIM Detailed account of spinal cord injury pathogeny, primary and secondary, and the OEC mechanisms for the regeneration effects that have been described in the literature. […] After the trauma, spinal cord injury develops in two phases, the primary injury with characteristics compression lesions, and the secondary produce for several factors that occur in parallel and include: vascular, cellular and molecular factors, and glial scar formation. […] The most of spinal cord models and OEC transplants have been reported functional recovery, remielinization and axonal regeneration. […] These cells exert their action in a direct way by producing grow factors and in an indirect way inducing directly neuronal an axonal regeneration and remielinization. […] OEC are a therapeutic option in patients with spinal cord injury, because they induce in a direct or indirect way, neuronal and axonal regeneration, remielinization, decrease the glial scar and produce other effects that conduce a functional recovery.

• #2 Spinal Cord Injuries – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK560721/

  Spinal cord injuries (SCIs) are complex medical conditions resulting from spinal cord damage, often caused by trauma, as in motor vehicular crashes and falls, and nontraumatic etiologies like malignancy and degeneration. […] The pathologic mechanisms causing SCIs are classified as either primary or secondary. Primary injury, often irreversible, arises from direct spinal cord damage. Secondary injury occurs as a consequence of the changes induced by a primary injury, such as inflammation. […] SCIs arise from complex mechanisms, producing varying degrees of neurologic deficits depending on the injury’s location and extent. The processes driving SCIs are classified as either primary or secondary. […] A primary SCI develops from mechanical forces directly damaging the cord. The most common primary SCI mechanism is direct cord trauma, followed by persistent compression from space-occupying pathologies like vertebral fractures, malignancies, hematomas, and abscesses.

• #2 An Audit of the Stages of Spinal Cord Injury Pathogenesis and their Relation to Secondary Medical Complications and Potential Chronicity in Patients | Esurgi

  https://myesurgi.com/an-audit-of-the-stages-of-spinal-cord-injury-pathogenesis-and-their-relation-to-secondary-medical-complications-and-potential-chronicity-in-patients/

  To understand the rationale of the recent therapeutic advances, it is first necessary to review the pathophysiology of spinal cord injury (SCI). There are four general types of SCI. The first is a cord maceration, in which the morphology of the cord is severely distorted. The second type is a cord laceration (gunshot or knife wounds). The third potential type is a contusion injury, in which damaged blood vessels leak into surrounding areas. Lastly, the fourth class is a solid cord injury, in which there is no central focus of hemorrhaging or an overt disruption in morphology. Of these four injury types, the contusion injury represents from 25 to 40% of the cases and is a progressive injury that enlarges over time. The most commonly used animal model in SCI research is patterned after the contusion injury. Within these four injury types, degree of completeness must be considered, as incomplete lesions will benefit more dramatically from experimental interventions than complete lesions in terms of degree of recovery that can be obtained. It is important to note that the clinical presentation of SCI is most often characterized as an anatomically incomplete lesion, irrespective of initial neurological presentation.

• #2 Acute spinal cord injury: Pathophysiology and pharmacological intervention (Review)

  https://www.spandidos-publications.com/10.3892/mmr.2021.12056?text=fulltext

  Spinal cord compression is the most frequent mechanism of SCI and can continue after the injury. Penetrating injuries and strain to the neural tissues or vascular structures are caused by dislocation, flexion, extension or distraction forces related to rotation. Other mechanical damage to bone structures and ligaments can result, or consequences related to compression can give rise to hematomas in the spinal cord channel. […] Secondary damage can be initiated by primary damage, whereas a number of pathophysiological mechanisms can come into play even hours and days after developing SCIs. The most notable mechanism is a lack of energy due to ischemia and impaired perfusion at the cellular level. Ischemia can result immediately after traumatic SCI and, if left untreated, additional damage may commence within the first 3 h and continue for at least 24 h.

• #2 Traumatic Spinal Cord Injury – TeachMeSurgery

  https://teachmesurgery.com/neurosurgery/traumatic-injuries/traumatic-spinal-cord-injury/

  A traumatic spinal cord injury (TSCI) is traumatic injury leading to damage of the spinal cord, resulting in temporary or permanent change to neurological function, including paralysis. […] Trauma causes injury to the spinal cord from (1) the initial acute impact, resulting in a concussion on the spinal cord (2) compression on the spinal cord from increased pressures from nearby rigid structures (such as vertebrae and discs) that may have been displaced by the injury. […] Based on pathophysiology, spinal cord injuries can be classified into primary or secondary injuries. Primary injury refers to the destructive forces that directly damage the neural structures, such as the shear forces tearing an axon or the direct compressive force occluding a blood vessel, resulting in ischaemia. Secondary injury refers to a cascade of vascular, cellular, and biochemical events which occur following the injury, which can worsen a concurrent primary injury.

• #2 Spinal Cord Injuries – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK560721/

  A secondary SCI emerges from a series of biological phenomena that begin within minutes of a primary injury and continue for weeks or months. The acute secondary injury phase encompasses vascular damage, ionic imbalances, free-radical formation, the initial inflammatory response, and neurotransmitter accumulation (excitotoxicity). […] Post-SCI neuroinflammation exhibits a dual nature, potentially causing both beneficial and deleterious outcomes, depending on the timing and immune cells present at the injury site. […] Spinal cord disruption leads to motor and sensory function deficits below the injury level. Disability patterns depend on the injury level and extent of spinal tract involvement.

• #2 Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7589539/

  The most vulnerable clinical manifestation immediately after injury is the interruption of spinal cord vascular supply and hypotension/hypo-perfusion, producing hypovolemia, neurogenic shock and bradycardia. […] Spinal cord ischemia causes cytotoxic, ionic and vasogenic oedemas. […] High levels of glutamate in necrotic cells alter the ionic flux by increasing intracellular Na+ and Ca2+ concentrations and decreasing intracellular K+ concentrations. […] Mitochondria are an integral component for cellular metabolism because they generate ATP (Adenosine triphosphate) molecules through phosphorylation. […] High ROS and reactive nitrogen species (RNS) generation induces various deleterious effects, including lipid peroxidation on different body organs. […] Apoptosis and necrosis are vital cell death processes in SCI.

• #2 A comprehensive look at the psychoneuroimmunoendocrinology of spinal cord injury and its progression: mechanisms and clinical opportunities | Military Medical Research | Full Text

  https://mmrjournal.biomedcentral.com/articles/10.1186/s40779-023-00461-z

  Research has shown that the beginning of secondary injury resides in the triggering of biochemical pathways in neural and vascular tissues. In this phase, inflammation becomes chronic and consequently erodes healthy tissue and surviving neurons. […] Previous works have noted that there are up to 25 described mechanisms of secondary damage after SCI. Here, we subdivide these mechanisms into 5 main groups: 1) vascular injury and ischemia, 2) exacerbated cell death, 3) OS, 4) immune infiltration and local inflammation, and 5) neuroglial disturbances. […] Vascular injury is a major mechanism of secondary damage in SCI. […] Exacerbated cell death events represent a critical mechanism of secondary injury in SCI, although two major forms of cell death should be distinguished here: programmed cell death (PCD) and necrosis.

• #2 Pathophysiology and Therapeutic Approaches for Spinal Cord Injury

  https://www.mdpi.com/1422-0067/23/22/13833

  The hemorrhage associated with the “primary injury,” coupled with systemic hypotension, culminates in a major reduction in the blood flow at the lesion site. […] After the insult, the homeostatic ionic balance is severely compromised. Membrane depolarization and ATPase disruption enhance neuronal and glial cell death by increasing intracellular calcium (Ca2+) levels. […] Inflammation is a major “secondary injury” event, and its dysregulated nature leads to more neuronal damage. […] The regeneration of CNS following injury is reduced due to multiple inhibitory factors at the injury site. […] The deposition of connective tissue and reactive gliosis creates a physical barrier, providing nonspecific topographical cues which affect cellular migration. […] The chronic phase is characterized by scar maturation, cystic cavitation, and axonal dieback. […] SCI pathophysiology involves many mechanistically distinct processes that interact in order to both limit and enhance recovery following injury.

• #2 Mechanism and prospects of mitochondrial transplantation for spinal cord injury treatment | Stem Cell Research & Therapy | Full Text

  https://stemcellres.biomedcentral.com/articles/10.1186/s13287-024-04077-5

  After SCI, the excessive production of intracellular free radicals overwhelms the antioxidant systems capacity to neutralize them, leading to oxidative stress damage. […] Following membrane damage, the activation of voltage-gated Ca2+ channels or calcium leakage leads to further increases in intracellular Ca2+ levels, which in turn enhances the release of the excitatory neurotransmitter glutamate, resulting in excitotoxic cell death. […] Simultaneously, mitochondrial dysfunction allows water and other small molecules to enter the mitochondrial matrix, causing matrix swelling and rupture of the outer membrane. […] This results in the release of large amounts of Ca2+, pro-apoptotic proteins, and ROS into the cytoplasm. […] Following SCI, oxidative stress within cells triggers a cascade of biochemical events.

• #2 Acute spinal cord injury: Pathophysiology and pharmacological intervention (Review)

  https://www.spandidos-publications.com/10.3892/mmr.2021.12056?text=fulltext

  High levels of glutamate can cause excitotoxicity, oxidative damage and ischemia, while Ca2+-dependent nitric oxide synthesis can cause secondary spinal cord damage. Following secondary injuries, increased free radical damage and lipid peroxidation in the cell membrane and secondary injury signaling cascades at the injured tissue areas can eventually lead to neuronal death. […] Nevertheless, extensive experiments show that the spinal cord has excellent healing properties. Proper blood flow is an essential factor in ensuring that progressive tissue damage precedes and promotes necrosis during the healing process. SCI is therefore regarded as a pathological condition involving injury to the nerve tissue. […] Systemic factors causing acute SCI include hypotension resulting from neurological shocks, minimized cardiac output and respiratory failure. In such cases, the supply of essential metabolites and oxygen to the nervous tissue is restricted.

• #2 Acute spinal cord injury: Pathophysiology and pharmacological intervention (Review)

  https://www.spandidos-publications.com/10.3892/mmr.2021.12056?text=fulltext

  Peripheral immune cells, including macrophages, neutrophils and T cells, can initiate an inflammatory response following SCI, which may gradually increase within a few days. Macrophages and neutrophils can cause the growth of lesions and lead to tissue damage. […] The generation of free radicals should be inhibited to maintain cell viability. The activity of the endogenous antioxidant system is reduced by aging and has a substantial impact on SCI. […] Apoptosis is activated following SCI due to the release of inflammatory cytokines and free radicals, which lead to inflammation and excitotoxicity. […] Opioid peptides are locally released during SCI. The hypothesis that endogenous opioids may have a significant role in the mechanism of secondary injury has been proven by previous studies that show that blocking the opiate receptors protects against cellular damage as well as preventing release of cellular contents.

• #2 Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7589539/

  Acute axonal degeneration (AAD) is another important clinical manifestation of early acute SCI phase. […] Demyelination occurs when myelin, the protective coating of nerve cells, is damaged. […] Glial scar formation (gliosis) is a reactive cellular mechanism that is facilitated by astrocytes and occurs during the chronic secondary phase of SCI. […] The continuous enlargement of lesion site and formation of the cyst is the hallmark feature of SCI. […] Multicellular interactions play an important role in developing effective neuroprotective and neurodegenerative strategies to overcome detrimental outcomes following SCI. […] Neuroprotection protects neuronal structure and function from further damage and is the relative preservation of the neurodegenerative effects of neurons and the maintenance of neuronal integrity to decrease neuronal lost ratio over time. […] Neuro-regeneration is the regrowth and repair of damaged nervous tissues (neurons, axons, synapses and glial cells) after injury.

• #2 A comprehensive look at the psychoneuroimmunoendocrinology of spinal cord injury and its progression: mechanisms and clinical opportunities | Military Medical Research | Full Text

  https://mmrjournal.biomedcentral.com/articles/10.1186/s40779-023-00461-z

  OS represents a state of imbalance in which pro-oxidative processes overwhelm cellular antioxidant defense due to the disruption of redox signaling and adaptation. […] Primary injury to the spinal cord triggers an inflammatory response orchestrated by the immune system. This inflammatory response plays a dual role. On the one hand, the inflammatory response is beneficial for the clearance of cellular debris and necrotic tissues. On the other hand, an aberrant inflammatory response is also considered a secondary mechanism of damage, exacerbating cell death and impairing axonal regeneration. […] Following primary SCI, in acute stages neurons and glial cells like oligodendrocytes (OLs) suffer from different types of cell death such as apoptosis or necrosis. This loss of OLs causes demyelination and impairs axon function and neuronal survival.

• #2 Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

  https://www.mdpi.com/1422-0067/21/20/7533

  The available therapeutic approaches are broadly classified as neuroprotective, neuro-regenerative, and immune-modulating pathways that are briefly discussed in this section. […] Neuroprotection protects neuronal structure and function from further damage and is the relative preservation of the neurodegenerative effects of neurons and the maintenance of neuronal integrity to decrease neuronal lost ratio over time. […] The available strategies of neuroprotection can be divided into three main approaches, (i) pharmacological approaches, (ii) non-pharmacological approaches and (iii) cellular and genetic approaches. […] The apoptotic pathways are further divided into two major pathways, i.e., (i) the death receptor initiated (also called extrinsic) pathway and (ii) the mitochondrial (also called intrinsic or Bcl-2-regulated) pathway. […] Neuro-regeneration is the regrowth and repair of damaged nervous tissues (neurons, axons, synapses and glial cells) after injury. […] RhoA is a small GTPase protein belonging to the Rho GTPase family. RhoA downstream effector (ROCK) regulates the neuronal cytoskeleton.

• #2 Update on traumatic acute spinal cord injury. Part 1 | Medicina Intensiva

  https://www.medintensiva.org/en-update-on-traumatic-acute-spinal-articulo-S2173572717300681

  Current management includes surgical decompression, hemodynamic control, and methylprednisolone in selected cases. However, these early treatment measures are associated to only modest functional recovery. […] The search for an effective neuroprotective strategy capable of preventing secondary lesions in the context of acute traumatic SI remains a priority concern both in clinical practice and in basic research.

• #2 Spinal Cord Injury: Causes, Symptoms, Treatment & Types

  https://my.clevelandclinic.org/health/diseases/12098-spinal-cord-injury

  A spinal cord injury (SCI) happens when theres damage to your spinal cord, a thick bundle of nerve fibers that allows your brain to communicate with other nerves almost everywhere else in your body. […] SCIs also commonly involve multiple phases. The first phase is the initial injury. But in the following hours and days, a secondary injury can also develop, causing swelling and further damage to your spinal cord. […] The treatment for SCIs varies widely. The first distinction is whether or not its injury-related. A suspected trauma-related SCI is ALWAYS a medical emergency. SCIs due to certain other causes are also medical emergencies. Emergency causes include: […] Many methods can help, including: Surgery: The main priority of surgery is to relieve pressure on your spinal cord. It can also repair damage related to surrounding injuries pressing on your spinal cord. […] These are medications or treatment approaches that help damaged spinal cord or nerve tissue regenerate and repair itself.

• #2 Spinal Cord Injury | Doctor

  https://patient.info/doctor/spinal-cord-injury

  A complete injury is indicated by a total lack of sensory and motor function below the level of injury. […] The prognosis is variable between almost complete recovery and complete paralysis. […] The spinal cord has very limited powers of regeneration. […] Patients with a complete cord injury have a very low chance of recovery, especially if paralysis persists for longer than 72 hours. […] The prognosis is much better for the incomplete cord syndromes. […] Prognosis for neurological deficit depends on the magnitude of the spinal cord damage present at the onset. […] Neurological deterioration is usually caused by secondary injury, resulting in oedema and/or haemorrhage.

• #2 Mechanism and prospects of mitochondrial transplantation for spinal cord injury treatment | Stem Cell Research & Therapy | Full Text

  https://stemcellres.biomedcentral.com/articles/10.1186/s13287-024-04077-5

  The interruption of anterograde transport in axons exacerbates local energy metabolism disorders at the injury site, and retrograde transport becomes impossible, preventing damaged mitochondria from fusing again to restore the respiratory chain and inhibit mitochondrial apoptosis. […] In this process, the synaptic protein Syntaphilin (Snph) plays a key role in the specific static anchoring of mitochondria within axons. […] Research by Zhou et al. has shown that the expression of Snph is elevated in mature neurons. […] However, it is crucial to clear these damaged mitochondria promptly after injury. […] By transplanting exogenous mitochondria to replace damaged mitochondria, it is possible to reduce the production of intracellular ROS, provide a new source of exogenous mitochondrial DNA, and enhance energy production and calcium buffering capacity.

• #2 Mechanism and prospects of mitochondrial transplantation for spinal cord injury treatment | Stem Cell Research & Therapy | Full Text

  https://stemcellres.biomedcentral.com/articles/10.1186/s13287-024-04077-5

  The results showed that exogenous mitochondria maintained energy supply to the injured spinal cord in a dose-dependent manner, significantly reducing the proportion of cells in the G1 phase. […] Additionally, they preserved the activity of antioxidants such as catalase and glutathione peroxidase in the damaged tissue, promoting oxidative phosphorylation function in the injured spinal cord to maintain at 90% of the sham-operated level. […] MT can also inhibit the expression of apoptosis-related proteins such as Grp78, Chop, and P-Akt, effectively reducing the number of apoptotic cells in the early stages of SCI and promoting cell survival. […] Furthermore, MT significantly decreases the formation of late-stage glial scars in the lesion area, reduces the size of the lesion cavity, and promotes myelin regeneration by increasing the number of cells expressing neurofilament.

• #2 Spinal Cord Injury: Time to Move? | Journal of Neuroscience

  https://www.jneurosci.org/content/27/44/11782

  The use of autologous macrophages was the first approach developed for clinical trial. […] The promising results of phase I encouraged the investigators to embark on phase II. […] Despite advances in medical and surgical treatment, current therapies for SCI are limited. […] However, the past 15 years has seen advances in biomedical research directed at minimizing the impact of secondary injury and promoting neural regeneration. […] The primary mechanical injury to the cord is amplified by a series of secondary injury mechanisms, which include compression and vertebral column instability, ischemia, glutamatergic excitotoxicity, derangements in ionic homeostasis, oxidative cell stress, inflammation, and apoptosis. […] Given the vulnerability of oligodendrocytes to secondary apoptotic death, coupled with a deficient expression of myelin-associated genes after SCI, demyelination of residual axons within the spinal cord white matter is an important contributor to the pathophysiology.

• #2 Study documents safety, improvements from stem cell therapy after spinal cord injury – Mayo Clinic News Network

  https://newsnetwork.mayoclinic.org/discussion/study-documents-safety-improvements-from-stem-cell-therapy-after-spinal-cord-injury/

  ROCHESTER, Minn. — A Mayo Clinic study shows stem cells derived from patients’ own fat are safe and may improve sensation and movement after traumatic spinal cord injuries. […] Although it is understood that stem cells move toward areas of inflammation — in this case the location of the spinal cord injury — the cells’ mechanism of interacting with the spinal cord is not fully understood, Dr. Bydon says. […] The spinal cord has limited ability to repair its cells or make new ones. […] Based on researchers’ understanding of traumatic thoracic spinal cord injury, only 5% of people with a complete injury would be expected to regain any feeling or movement. […] „In spinal cord injury, even a mild improvement can make a significant difference in that patient’s quality of life,” Dr. Bydon says.

• #3 Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7589539/

  Spinal cord injury (SCI) is a destructive neurological and pathological state that causes major motor, sensory and autonomic dysfunctions. Its pathophysiology comprises acute and chronic phases and incorporates a cascade of destructive events such as ischemia, oxidative stress, inflammatory events, apoptotic pathways and locomotor dysfunctions. […] Understanding pathophysiology, phases and various wound recovery mechanisms associated with SCI is essential for the development of appropriate recovery treatments. […] The secondary injury phase reflects multi-featured pathological processes following the primary injury phase and lasts for several weeks. Clinical manifestation of secondary injury includes increased cell permeability, apoptotic signalling, ischemia, vascular damage, oedema, excitotoxicity, ionic deregulation, inflammation, lipid peroxidation, free radical formation, demyelination, Wallerian degeneration, fibroglial scar and cyst formation.

• #3 Spinal Cord Injuries – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK560721/

  Spinal cord injuries (SCIs) are complex medical conditions resulting from spinal cord damage, often caused by trauma, as in motor vehicular crashes and falls, and nontraumatic etiologies like malignancy and degeneration. […] The pathologic mechanisms causing SCIs are classified as either primary or secondary. Primary injury, often irreversible, arises from direct spinal cord damage. Secondary injury occurs as a consequence of the changes induced by a primary injury, such as inflammation. […] SCIs arise from complex mechanisms, producing varying degrees of neurologic deficits depending on the injury’s location and extent. The processes driving SCIs are classified as either primary or secondary. […] A primary SCI develops from mechanical forces directly damaging the cord. The most common primary SCI mechanism is direct cord trauma, followed by persistent compression from space-occupying pathologies like vertebral fractures, malignancies, hematomas, and abscesses.

• #3 Pathogenesis of spinal cord injuries and mechanisms of repair induced by olfactory ensheathing cells

  https://www.imrpress.com/journal/RN/56/10/10.33588/rn.5610.2013109

  Pathogenesis of spinal cord injuries and mechanisms of repair induced by olfactory ensheathing cells. […] Spinal cord injury is a catastrophic event with permanent consequences during the all life. […] AIM Detailed account of spinal cord injury pathogeny, primary and secondary, and the OEC mechanisms for the regeneration effects that have been described in the literature. […] After the trauma, spinal cord injury develops in two phases, the primary injury with characteristics compression lesions, and the secondary produce for several factors that occur in parallel and include: vascular, cellular and molecular factors, and glial scar formation. […] The most of spinal cord models and OEC transplants have been reported functional recovery, remielinization and axonal regeneration. […] These cells exert their action in a direct way by producing grow factors and in an indirect way inducing directly neuronal an axonal regeneration and remielinization. […] OEC are a therapeutic option in patients with spinal cord injury, because they induce in a direct or indirect way, neuronal and axonal regeneration, remielinization, decrease the glial scar and produce other effects that conduce a functional recovery.

• #3 Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7589539/

  The most vulnerable clinical manifestation immediately after injury is the interruption of spinal cord vascular supply and hypotension/hypo-perfusion, producing hypovolemia, neurogenic shock and bradycardia. […] Spinal cord ischemia causes cytotoxic, ionic and vasogenic oedemas. […] High levels of glutamate in necrotic cells alter the ionic flux by increasing intracellular Na+ and Ca2+ concentrations and decreasing intracellular K+ concentrations. […] Mitochondria are an integral component for cellular metabolism because they generate ATP (Adenosine triphosphate) molecules through phosphorylation. […] High ROS and reactive nitrogen species (RNS) generation induces various deleterious effects, including lipid peroxidation on different body organs. […] Apoptosis and necrosis are vital cell death processes in SCI.

• #3 Pathophysiology and Therapeutic Approaches for Spinal Cord Injury

  https://www.mdpi.com/1422-0067/23/22/13833

  The hemorrhage associated with the “primary injury,” coupled with systemic hypotension, culminates in a major reduction in the blood flow at the lesion site. […] After the insult, the homeostatic ionic balance is severely compromised. Membrane depolarization and ATPase disruption enhance neuronal and glial cell death by increasing intracellular calcium (Ca2+) levels. […] Inflammation is a major “secondary injury” event, and its dysregulated nature leads to more neuronal damage. […] The regeneration of CNS following injury is reduced due to multiple inhibitory factors at the injury site. […] The deposition of connective tissue and reactive gliosis creates a physical barrier, providing nonspecific topographical cues which affect cellular migration. […] The chronic phase is characterized by scar maturation, cystic cavitation, and axonal dieback. […] SCI pathophysiology involves many mechanistically distinct processes that interact in order to both limit and enhance recovery following injury.

• #3 Acute spinal cord injury: Pathophysiology and pharmacological intervention (Review)

  https://www.spandidos-publications.com/10.3892/mmr.2021.12056?text=fulltext

  Peripheral immune cells, including macrophages, neutrophils and T cells, can initiate an inflammatory response following SCI, which may gradually increase within a few days. Macrophages and neutrophils can cause the growth of lesions and lead to tissue damage. […] The generation of free radicals should be inhibited to maintain cell viability. The activity of the endogenous antioxidant system is reduced by aging and has a substantial impact on SCI. […] Apoptosis is activated following SCI due to the release of inflammatory cytokines and free radicals, which lead to inflammation and excitotoxicity. […] Opioid peptides are locally released during SCI. The hypothesis that endogenous opioids may have a significant role in the mechanism of secondary injury has been proven by previous studies that show that blocking the opiate receptors protects against cellular damage as well as preventing release of cellular contents.

• #3 A comprehensive look at the psychoneuroimmunoendocrinology of spinal cord injury and its progression: mechanisms and clinical opportunities | Military Medical Research | Full Text

  https://mmrjournal.biomedcentral.com/articles/10.1186/s40779-023-00461-z

  Research has shown that the beginning of secondary injury resides in the triggering of biochemical pathways in neural and vascular tissues. In this phase, inflammation becomes chronic and consequently erodes healthy tissue and surviving neurons. […] Previous works have noted that there are up to 25 described mechanisms of secondary damage after SCI. Here, we subdivide these mechanisms into 5 main groups: 1) vascular injury and ischemia, 2) exacerbated cell death, 3) OS, 4) immune infiltration and local inflammation, and 5) neuroglial disturbances. […] Vascular injury is a major mechanism of secondary damage in SCI. […] Exacerbated cell death events represent a critical mechanism of secondary injury in SCI, although two major forms of cell death should be distinguished here: programmed cell death (PCD) and necrosis.

• #3 Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7589539/

  Acute axonal degeneration (AAD) is another important clinical manifestation of early acute SCI phase. […] Demyelination occurs when myelin, the protective coating of nerve cells, is damaged. […] Glial scar formation (gliosis) is a reactive cellular mechanism that is facilitated by astrocytes and occurs during the chronic secondary phase of SCI. […] The continuous enlargement of lesion site and formation of the cyst is the hallmark feature of SCI. […] Multicellular interactions play an important role in developing effective neuroprotective and neurodegenerative strategies to overcome detrimental outcomes following SCI. […] Neuroprotection protects neuronal structure and function from further damage and is the relative preservation of the neurodegenerative effects of neurons and the maintenance of neuronal integrity to decrease neuronal lost ratio over time. […] Neuro-regeneration is the regrowth and repair of damaged nervous tissues (neurons, axons, synapses and glial cells) after injury.

• #3 Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

  https://www.mdpi.com/1422-0067/21/20/7533

  Spinal cord injury (SCI) is a destructive neurological and pathological state that causes major motor, sensory and autonomic dysfunctions. Its pathophysiology comprises acute and chronic phases and incorporates a cascade of destructive events such as ischemia, oxidative stress, inflammatory events, apoptotic pathways and locomotor dysfunctions. […] Understanding pathophysiology, phases and various wound recovery mechanisms associated with SCI is essential for the development of appropriate recovery treatments. […] Normal spinal cord physiology involves interactions among many cell types such as astrocytes, neurons, microglia and oligodendrocytes. After a spinal injury, these multicellular interactions are interrupted and disorganised, leading to an impaired spinal recovery. […] The secondary injury phase reflects multi-featured pathological processes following the primary injury phase and lasts for several weeks.

• #3 Mechanism and prospects of mitochondrial transplantation for spinal cord injury treatment | Stem Cell Research & Therapy | Full Text

  https://stemcellres.biomedcentral.com/articles/10.1186/s13287-024-04077-5

  After SCI, the excessive production of intracellular free radicals overwhelms the antioxidant systems capacity to neutralize them, leading to oxidative stress damage. […] Following membrane damage, the activation of voltage-gated Ca2+ channels or calcium leakage leads to further increases in intracellular Ca2+ levels, which in turn enhances the release of the excitatory neurotransmitter glutamate, resulting in excitotoxic cell death. […] Simultaneously, mitochondrial dysfunction allows water and other small molecules to enter the mitochondrial matrix, causing matrix swelling and rupture of the outer membrane. […] This results in the release of large amounts of Ca2+, pro-apoptotic proteins, and ROS into the cytoplasm. […] Following SCI, oxidative stress within cells triggers a cascade of biochemical events.

• #3 Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

  https://www.mdpi.com/1422-0067/21/20/7533

  The available therapeutic approaches are broadly classified as neuroprotective, neuro-regenerative, and immune-modulating pathways that are briefly discussed in this section. […] Neuroprotection protects neuronal structure and function from further damage and is the relative preservation of the neurodegenerative effects of neurons and the maintenance of neuronal integrity to decrease neuronal lost ratio over time. […] The available strategies of neuroprotection can be divided into three main approaches, (i) pharmacological approaches, (ii) non-pharmacological approaches and (iii) cellular and genetic approaches. […] The apoptotic pathways are further divided into two major pathways, i.e., (i) the death receptor initiated (also called extrinsic) pathway and (ii) the mitochondrial (also called intrinsic or Bcl-2-regulated) pathway. […] Neuro-regeneration is the regrowth and repair of damaged nervous tissues (neurons, axons, synapses and glial cells) after injury. […] RhoA is a small GTPase protein belonging to the Rho GTPase family. RhoA downstream effector (ROCK) regulates the neuronal cytoskeleton.

• #3 Acute spinal cord injury: Pathophysiology and pharmacological intervention (Review)

  https://www.spandidos-publications.com/10.3892/mmr.2021.12056

  Peripheral immune cells, including macrophages, neutrophils and T cells, can initiate an inflammatory response following SCI, which may gradually increase within a few days. Macrophages and neutrophils can cause the growth of lesions and lead to tissue damage. […] The generation of free radicals should be inhibited to maintain cell viability. The activity of the endogenous antioxidant system is reduced by aging and has a substantial impact on SCI. […] There is a direct influence of the excitatory neurotransmitter in the spinal cord by N-methyl-D-aspartate (NMDA) receptors. Studies reveal that blocking the NMDA receptor results in protection from secondary damage due to trauma and ischemia in animal models. […] Apoptosis is activated following SCI due to the release of inflammatory cytokines and free radicals, which lead to inflammation and excitotoxicity.

• #3 Spinal Cord Injuries – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK560721/

  A secondary SCI emerges from a series of biological phenomena that begin within minutes of a primary injury and continue for weeks or months. The acute secondary injury phase encompasses vascular damage, ionic imbalances, free-radical formation, the initial inflammatory response, and neurotransmitter accumulation (excitotoxicity). […] Post-SCI neuroinflammation exhibits a dual nature, potentially causing both beneficial and deleterious outcomes, depending on the timing and immune cells present at the injury site. […] Spinal cord disruption leads to motor and sensory function deficits below the injury level. Disability patterns depend on the injury level and extent of spinal tract involvement.

• #4 Spinal Cord Injuries – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK560721/

  Spinal cord injuries (SCIs) are complex medical conditions resulting from spinal cord damage, often caused by trauma, as in motor vehicular crashes and falls, and nontraumatic etiologies like malignancy and degeneration. […] The pathologic mechanisms causing SCIs are classified as either primary or secondary. Primary injury, often irreversible, arises from direct spinal cord damage. Secondary injury occurs as a consequence of the changes induced by a primary injury, such as inflammation. […] SCIs arise from complex mechanisms, producing varying degrees of neurologic deficits depending on the injury’s location and extent. The processes driving SCIs are classified as either primary or secondary. […] A primary SCI develops from mechanical forces directly damaging the cord. The most common primary SCI mechanism is direct cord trauma, followed by persistent compression from space-occupying pathologies like vertebral fractures, malignancies, hematomas, and abscesses.

• #4 Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7589539/

  Spinal cord injury (SCI) is a destructive neurological and pathological state that causes major motor, sensory and autonomic dysfunctions. Its pathophysiology comprises acute and chronic phases and incorporates a cascade of destructive events such as ischemia, oxidative stress, inflammatory events, apoptotic pathways and locomotor dysfunctions. […] Understanding pathophysiology, phases and various wound recovery mechanisms associated with SCI is essential for the development of appropriate recovery treatments. […] The secondary injury phase reflects multi-featured pathological processes following the primary injury phase and lasts for several weeks. Clinical manifestation of secondary injury includes increased cell permeability, apoptotic signalling, ischemia, vascular damage, oedema, excitotoxicity, ionic deregulation, inflammation, lipid peroxidation, free radical formation, demyelination, Wallerian degeneration, fibroglial scar and cyst formation.

• #4 Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7589539/

  The most vulnerable clinical manifestation immediately after injury is the interruption of spinal cord vascular supply and hypotension/hypo-perfusion, producing hypovolemia, neurogenic shock and bradycardia. […] Spinal cord ischemia causes cytotoxic, ionic and vasogenic oedemas. […] High levels of glutamate in necrotic cells alter the ionic flux by increasing intracellular Na+ and Ca2+ concentrations and decreasing intracellular K+ concentrations. […] Mitochondria are an integral component for cellular metabolism because they generate ATP (Adenosine triphosphate) molecules through phosphorylation. […] High ROS and reactive nitrogen species (RNS) generation induces various deleterious effects, including lipid peroxidation on different body organs. […] Apoptosis and necrosis are vital cell death processes in SCI.

• #4 Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7589539/

  Acute axonal degeneration (AAD) is another important clinical manifestation of early acute SCI phase. […] Demyelination occurs when myelin, the protective coating of nerve cells, is damaged. […] Glial scar formation (gliosis) is a reactive cellular mechanism that is facilitated by astrocytes and occurs during the chronic secondary phase of SCI. […] The continuous enlargement of lesion site and formation of the cyst is the hallmark feature of SCI. […] Multicellular interactions play an important role in developing effective neuroprotective and neurodegenerative strategies to overcome detrimental outcomes following SCI. […] Neuroprotection protects neuronal structure and function from further damage and is the relative preservation of the neurodegenerative effects of neurons and the maintenance of neuronal integrity to decrease neuronal lost ratio over time. […] Neuro-regeneration is the regrowth and repair of damaged nervous tissues (neurons, axons, synapses and glial cells) after injury.

• #4 Pathophysiology and Therapeutic Approaches for Spinal Cord Injury

  https://www.mdpi.com/1422-0067/23/22/13833

  The hemorrhage associated with the “primary injury,” coupled with systemic hypotension, culminates in a major reduction in the blood flow at the lesion site. […] After the insult, the homeostatic ionic balance is severely compromised. Membrane depolarization and ATPase disruption enhance neuronal and glial cell death by increasing intracellular calcium (Ca2+) levels. […] Inflammation is a major “secondary injury” event, and its dysregulated nature leads to more neuronal damage. […] The regeneration of CNS following injury is reduced due to multiple inhibitory factors at the injury site. […] The deposition of connective tissue and reactive gliosis creates a physical barrier, providing nonspecific topographical cues which affect cellular migration. […] The chronic phase is characterized by scar maturation, cystic cavitation, and axonal dieback. […] SCI pathophysiology involves many mechanistically distinct processes that interact in order to both limit and enhance recovery following injury.

• #4 Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

  https://www.mdpi.com/1422-0067/21/20/7533

  The available therapeutic approaches are broadly classified as neuroprotective, neuro-regenerative, and immune-modulating pathways that are briefly discussed in this section. […] Neuroprotection protects neuronal structure and function from further damage and is the relative preservation of the neurodegenerative effects of neurons and the maintenance of neuronal integrity to decrease neuronal lost ratio over time. […] The available strategies of neuroprotection can be divided into three main approaches, (i) pharmacological approaches, (ii) non-pharmacological approaches and (iii) cellular and genetic approaches. […] The apoptotic pathways are further divided into two major pathways, i.e., (i) the death receptor initiated (also called extrinsic) pathway and (ii) the mitochondrial (also called intrinsic or Bcl-2-regulated) pathway. […] Neuro-regeneration is the regrowth and repair of damaged nervous tissues (neurons, axons, synapses and glial cells) after injury. […] RhoA is a small GTPase protein belonging to the Rho GTPase family. RhoA downstream effector (ROCK) regulates the neuronal cytoskeleton.

• #5 Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7589539/

  The most vulnerable clinical manifestation immediately after injury is the interruption of spinal cord vascular supply and hypotension/hypo-perfusion, producing hypovolemia, neurogenic shock and bradycardia. […] Spinal cord ischemia causes cytotoxic, ionic and vasogenic oedemas. […] High levels of glutamate in necrotic cells alter the ionic flux by increasing intracellular Na+ and Ca2+ concentrations and decreasing intracellular K+ concentrations. […] Mitochondria are an integral component for cellular metabolism because they generate ATP (Adenosine triphosphate) molecules through phosphorylation. […] High ROS and reactive nitrogen species (RNS) generation induces various deleterious effects, including lipid peroxidation on different body organs. […] Apoptosis and necrosis are vital cell death processes in SCI.

• #5 Pathophysiology and Therapeutic Approaches for Spinal Cord Injury

  https://www.mdpi.com/1422-0067/23/22/13833

  The hemorrhage associated with the “primary injury,” coupled with systemic hypotension, culminates in a major reduction in the blood flow at the lesion site. […] After the insult, the homeostatic ionic balance is severely compromised. Membrane depolarization and ATPase disruption enhance neuronal and glial cell death by increasing intracellular calcium (Ca2+) levels. […] Inflammation is a major “secondary injury” event, and its dysregulated nature leads to more neuronal damage. […] The regeneration of CNS following injury is reduced due to multiple inhibitory factors at the injury site. […] The deposition of connective tissue and reactive gliosis creates a physical barrier, providing nonspecific topographical cues which affect cellular migration. […] The chronic phase is characterized by scar maturation, cystic cavitation, and axonal dieback. […] SCI pathophysiology involves many mechanistically distinct processes that interact in order to both limit and enhance recovery following injury.

• #5 Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7589539/

  Acute axonal degeneration (AAD) is another important clinical manifestation of early acute SCI phase. […] Demyelination occurs when myelin, the protective coating of nerve cells, is damaged. […] Glial scar formation (gliosis) is a reactive cellular mechanism that is facilitated by astrocytes and occurs during the chronic secondary phase of SCI. […] The continuous enlargement of lesion site and formation of the cyst is the hallmark feature of SCI. […] Multicellular interactions play an important role in developing effective neuroprotective and neurodegenerative strategies to overcome detrimental outcomes following SCI. […] Neuroprotection protects neuronal structure and function from further damage and is the relative preservation of the neurodegenerative effects of neurons and the maintenance of neuronal integrity to decrease neuronal lost ratio over time. […] Neuro-regeneration is the regrowth and repair of damaged nervous tissues (neurons, axons, synapses and glial cells) after injury.

• #5 Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

  https://www.mdpi.com/1422-0067/21/20/7533

  The available therapeutic approaches are broadly classified as neuroprotective, neuro-regenerative, and immune-modulating pathways that are briefly discussed in this section. […] Neuroprotection protects neuronal structure and function from further damage and is the relative preservation of the neurodegenerative effects of neurons and the maintenance of neuronal integrity to decrease neuronal lost ratio over time. […] The available strategies of neuroprotection can be divided into three main approaches, (i) pharmacological approaches, (ii) non-pharmacological approaches and (iii) cellular and genetic approaches. […] The apoptotic pathways are further divided into two major pathways, i.e., (i) the death receptor initiated (also called extrinsic) pathway and (ii) the mitochondrial (also called intrinsic or Bcl-2-regulated) pathway. […] Neuro-regeneration is the regrowth and repair of damaged nervous tissues (neurons, axons, synapses and glial cells) after injury. […] RhoA is a small GTPase protein belonging to the Rho GTPase family. RhoA downstream effector (ROCK) regulates the neuronal cytoskeleton.

• #6 Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7589539/

  The most vulnerable clinical manifestation immediately after injury is the interruption of spinal cord vascular supply and hypotension/hypo-perfusion, producing hypovolemia, neurogenic shock and bradycardia. […] Spinal cord ischemia causes cytotoxic, ionic and vasogenic oedemas. […] High levels of glutamate in necrotic cells alter the ionic flux by increasing intracellular Na+ and Ca2+ concentrations and decreasing intracellular K+ concentrations. […] Mitochondria are an integral component for cellular metabolism because they generate ATP (Adenosine triphosphate) molecules through phosphorylation. […] High ROS and reactive nitrogen species (RNS) generation induces various deleterious effects, including lipid peroxidation on different body organs. […] Apoptosis and necrosis are vital cell death processes in SCI.

• #6 Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7589539/

  Acute axonal degeneration (AAD) is another important clinical manifestation of early acute SCI phase. […] Demyelination occurs when myelin, the protective coating of nerve cells, is damaged. […] Glial scar formation (gliosis) is a reactive cellular mechanism that is facilitated by astrocytes and occurs during the chronic secondary phase of SCI. […] The continuous enlargement of lesion site and formation of the cyst is the hallmark feature of SCI. […] Multicellular interactions play an important role in developing effective neuroprotective and neurodegenerative strategies to overcome detrimental outcomes following SCI. […] Neuroprotection protects neuronal structure and function from further damage and is the relative preservation of the neurodegenerative effects of neurons and the maintenance of neuronal integrity to decrease neuronal lost ratio over time. […] Neuro-regeneration is the regrowth and repair of damaged nervous tissues (neurons, axons, synapses and glial cells) after injury.

• #7 Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms

  https://pmc.ncbi.nlm.nih.gov/articles/PMC7589539/

  Acute axonal degeneration (AAD) is another important clinical manifestation of early acute SCI phase. […] Demyelination occurs when myelin, the protective coating of nerve cells, is damaged. […] Glial scar formation (gliosis) is a reactive cellular mechanism that is facilitated by astrocytes and occurs during the chronic secondary phase of SCI. […] The continuous enlargement of lesion site and formation of the cyst is the hallmark feature of SCI. […] Multicellular interactions play an important role in developing effective neuroprotective and neurodegenerative strategies to overcome detrimental outcomes following SCI. […] Neuroprotection protects neuronal structure and function from further damage and is the relative preservation of the neurodegenerative effects of neurons and the maintenance of neuronal integrity to decrease neuronal lost ratio over time. […] Neuro-regeneration is the regrowth and repair of damaged nervous tissues (neurons, axons, synapses and glial cells) after injury.

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