Spinal cord injury

dc.authorscopusid6505539592
dc.authorscopusid35240222100
dc.authorscopusid15765190000
dc.contributor.authorKerimo?lu M.
dc.contributor.authorHanci V.
dc.contributor.authorKerimo?lu A.
dc.date.accessioned2024-06-12T10:28:13Z
dc.date.available2024-06-12T10:28:13Z
dc.date.issued2006
dc.description.abstractTraumatic injury to the spinal cord typically results in axonal damage and cell death and leaves individuals with varying degrees of functional impairments. Damage arising from acute Spinal Cord Injury is generally described as two distinct pathophysiological events. The damage incurred at the time of injury is termed primary injury and typically results from direct mechanical disruption of cord integrity. Secondary injury occurs in a delayed yet progressive fashion and involves cellular and biochemical events that initiate cascades culminating in tissue damage and cell death. Secondary injury spreads away from the injury epicenter, incorporating tissue both rostral and caudal to the primary lesion with increasing functional deficits. The pathophysiological events contributing to secondary injury are thought to involve free radical production, lipid peroxidation, eicosanoid and prostaglandin production, protease activity, excitotoxic molecules such as glutamate, and intracellular increases in Ca2+. Neuroprotective strategies aimed at preventing damage arising from secondary injury processes provide some hope for tissue sparing and improved functional outcome. To date, methylprednisolone is the only drug currently approved for use in the treatment of acute Spinal Cord Injury. However, the use of high-dose methylprednisolone in acute Spinal Cord Injury has become largely risk and serious adverse effects, in This conjunction with the fact that current treatment options are need to find novel therapeutic agents. In this article, pathophysiologia and effect on therapy of secondary celluler injury after spinal cord injury have been reviewed.en_US
dc.identifier.endpage32en_US
dc.identifier.issn1016-5134
dc.identifier.issue12en_US
dc.identifier.scopus2-s2.0-33846205052en_US
dc.identifier.scopusqualityN/Aen_US
dc.identifier.startpage26en_US
dc.identifier.urihttps://hdl.handle.net/20.500.14551/17148
dc.identifier.volume18en_US
dc.indekslendigikaynakScopusen_US
dc.language.isotren_US
dc.relation.ispartofSENDROMen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectDizocilpine; Ganglioside Gm1; Icosanoid; Methylprednisolone; N Methyl Dextro Aspartic Acid Receptor; Prostaglandin; Proteinase; Axonal Injury; Cell Death; Clinical Trial; Enzyme Activity; Human; Lipid Peroxidation; Review; Risk Factor; Spinal Cord Injury; Tissue Injuryen_US
dc.titleSpinal cord injuryen_US
dc.title.alternativeSpinal hasarlanmalaren_US
dc.typeReview Articleen_US

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