• Ahmed Jorge, Tavis Taylor, Nitin Agarwal, and D Kojo Hamilton.
• Department of Neurological Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA.
• World Neurosurg. 2019 Dec 1; 132: 138-147.

BackgroundThe infliction of a traumatic spinal cord injury (SCI) propagates damage that occurs in 2 stages. The first phase of trauma develops from the initial mechanical insult. The second phase involves the degradation of nervous tissue but is likely not affected by the initial insult. Thus, therapeutic targets with a high specificity for these secondary injury processes have been of increasing interest. We reviewed the pathophysiologic cascades of inflammation after SCI and potential therapeutic targets.MethodsThe PubMed and EMBASE databases were queried using appropriate medical subject headings for studies involving tumor necrosis factor (TNF)-α), nuclear factor (NF)-κB, inducible nitric oxide synthase (iNOS), interleukin (IL)-1β, and/or Fas ligand (FasL) targets. The relevant studies found were graded into 3 levels (i.e., A, B, C) according to the quality of evidence.ResultsWe have summarized the basis of the neurological damage for TNF-α, NF-κB, iNOS, IL-1β, and FasL after SCI. A total of 17 studies were rated, each of which had reported histological, biochemical, physiological, and behavioral outcomes according to the treatment that had focused on TNF-α, NF-κB, iNOS, IL-1β, and FasL.ConclusionThe TNF-α, iNOS, NF-κB, IL-1β, and FasL will become active within minutes after SCI. The adverse effects from the activity of these receptors include inflammation and other important neurological damage. Each of these targets can be modulated by specific agents with differing degrees of efficacy according to the reported data.Copyright © 2019 Elsevier Inc. All rights reserved.

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