title: Secondary injury mechanisms in traumatic spinal cord injury: a nugget of this multiply cascade.
abstract: The pathophysiology of acute spinal cord injury (SCI) involves primary and secondary mechanisms of injury. Though both mechanisms are involved in the neurological dysfunction in SCI most research however has focused on understanding the pathophysiology of the secondary damage and reducing the amount of delayed cell loss following SCI. Research has revealed extensive therapeutic windows in secondary injury mechanisms that could be manipulated by appropriate exogenous interventions. In contrast, primary injury to the cord happens unexpectedly, and it is associated with inevitable delays; ranging from several hours to days before care intervention is administered. Therefore, apart from achieving patient's stabilization, the therapeutic window in the primary phase of injury is essentially obliterated, and consequently inaccessible for specialized. Coupled to this, the exacerbating effect of secondary injury mechanisms has generally commenced before the specialist intervention. Hence, knowledge of secondary injury mechanisms and their intricacies are invaluable requisite for any tailored therapeutic strategy in the persistent search for a cure of SCI. There are about 25 well-established secondary injury mechanisms in SCI, and are found in bits or clusters in literature. A vast number of these articles are not open access. Besides, articles with a comprehensive catalog of these mechanisms are not readily available. This article has cataloged over twenty five identified secondary mechanisms of injury in the spinal cord in an open access portal, and is particularly versatile for starters in spinal cord injury research.
authors: Department of Human Anatomy, Faculty of Basic Medical Sciences, College of Health Sciences, Niger Delta University, Wilberforce Island, Bayelsa State, Nigeria. charlesoyinbo@gmail.com.
authors: Charles Aidemise
authors: CA
authors: Oyinbo
mesh_terms: D017209:Apoptosis / Q000187:drug effects / Q000502:physiology; D002118:Calcium / Q000378:metabolism; D018450:Disease Progression; D018698:Glutamic Acid / Q000633:toxicity; D006801:Humans; D007154:Immune System Diseases / Q000188:drug therapy / Q000209:etiology; D015227:Lipid Peroxidation; D009410:Nerve Degeneration / Q000188:drug therapy / Q000209:etiology; D009422:Nervous System Diseases / Q000188:drug therapy* / Q000209:etiology*; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D013119:Spinal Cord Injuries / Q000150:complications* / Q000188:drug therapy*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D018696:Neuroprotective Agents; D014409:Tumor Necrosis Factor-alpha; D018698:Glutamic Acid; D002118:Calcium