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Updated: Jun 23, 2026

A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation
Published on: June 10, 2020
Pro-inflammatory and pro-apoptotic elements of the neuroinflammatory response are activated in traumatic brain injury
J C Goodman1, M Van, S P Gopinath
1Department of Neurosurgery, Baylor College of Medicine, One Baylor Plaza MS:BCM650, Houston, TX 77030, USA. jgoodman@bcm.tmc.edu
Background:
The inflammatory response may contribute to cerebral edema, increased intracranial pressure and cellular loss in traumatic brain injury (TBI). Cytokines are biomarkers of this inflammatory response and new methods allow simultaneous measurement of multiple cytokines.
Methods:
We examined the IL-1beta, IL-6, IL-8 and IL-12, TNFalpha, and IL-10 in arterial and jugular blood as well as cerebrospinal fluid in patients with severe traumatic brain injury.
Findings:
Multiple cytokines, particularly pro-inflammatory cytokines, are up-regulated following TBI. Cerebrospinal fluid and arteriovenous differences of some of the cytokines suggest production within the central nervous system. Antiinflammatory cytokines are not up-regulated.
Conclusions:
Cytokine up-regulation may contribute to the neuroinflammatory reaction that follows traumatic brain injury and may contribute to secondary injury.
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