Abstract

ABSTRACT The objective of the paper is to analyze the frequency and efficacy of experimental studies with antioxidant therapy. A search was conducted in the pubmed.gov database using the keywords "antioxidants" AND "spinal cord injury", from January 2000 to December 2015, resulting in 686 articles. Studies of non-traumatic injuries, non-antioxidant therapies, absence of neurological and functional evaluation, and non-experimental studies were excluded, leaving a total of 43 articles. The most used therapies were melatonin (16.2%), quercetin (9.3%), epigallocatechin and edaravone (6.9%). The most frequent route of administration was intraperitoneal (72.09%). The dose and mode of administration varied greatly, with a single dose being the most commonly used (39.53%). The time elapsed from trauma to treatment was 0-15 minutes (41.8%), 15-60 minutes (30%) and over 60 minutes (10.6%). Histological analysis was performed in 32 studies (74.41%). The BBB scale was the main functional measure applied (55.8%), followed by the inclined plane test (16.2%) and the Tarlov scale (13.9%). Positive outcomes were observed in 37 studies (86.04%). The heterogeneity of antioxidant therapy, with different types, doses, and measurements observed, limits the comparison of efficacy. Standardized protocols are required to make clinical translation possible.

Highlights

  • Spinal cord injury (SCI) can occur by traumatic or ischemic event

  • After SCI, the inflammatory response occurs by cellular activation in order to reorganize the damaged tissue

  • Antioxidant therapy seeks to minimize the cellular effects of hypoxia and ischemia, leading to a better functional outcome after trauma.[1,2,3,4]

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Summary

Introduction

Cellular necrosis and tissue degeneration are the secondary events, caused mainly by hypoxia and ischemia.[1,2] A reduction in blood flow and microvascular abnormalities were demonstrated, leading to an increase in intracellular free radical species.[3,4] Lipid peroxidation of the cell membrane has a novel role in the pathophysiology of neuronal lesion.[2]. There is no effective treatment to prevent the secondary damage caused by SCI.[5] Corticosteroids were used to reduce edema formation and inflammatory events, with controversial results.[3,6,7,8,9] Investigations to find a specific therapy to control the formation of free radicals are ongoing.[10] The role of antioxidant drugs and hyperbaric oxygenic therapy is being discussed.[11,12]

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