Evaluation of Delayed Neuronal and Axonal Damage Secondary to Moderate and Severe Traumatic Brain Injury Using Quantitative MR Imaging Techniques

Abstract

BACKGROUND AND PURPOSE: Traumatic brain injury (TBI) is a classic model of monophasic neuronal and axonal injury, in which tissue damage mainly occurs at the moment of trauma. There is some evidence of delayed progression of the neuronal and axonal loss. Our purpose was to test the hypothesis that quantitative MR imaging techniques can estimate the biologic changes secondary to delayed neuronal and axonal loss after TBI.

Transplantation of Marrow Stromal Cells Restores Cerebral Blood Flow and Reduces Cerebral Atrophy in Rats with Traumatic Brain Injury: In vivo MRI Study

“…Volumetric studies demonstrate that regional and global cerebral atrophy is related to unfavorable functional outcomes Blatter et al, 1997;Sidaros et al, 2009), whereas more tissue preservation is associated with better recovery (Wilde et al, 2005). Mechanisms that may account for cerebral tissue shrinkage after TBI include progressive neuronal loss (Immonen et al, 2009a;Smith et al, 1997) and diffuse axonal injury (Bigler, 1987;Ding et al, 2008;Mamere et al, 2009;Sidaros et al, 2009). As found in the present study, MSCs diminish hemodynamic abnormalities (Fig.…”

“…To date, however, the management of patients with TBI has generally concentrated on the prevention or amelioration of such devastating secondary Although mechanisms responsible for the observed therapeutic potential of MSCs remain to be explored, it is suggested that the beneficial effects are owed to the ability of MSCs to secrete an array of cytokines and trophic factors that activate endogenous restorative and regenerative processes, e.g., angiogenesis, synaptogenesis, gliogenesis, and neurogenesis (Chopp and Li, 2006;Mahmood et al, 2004aMahmood et al, , 2004b. Treatment of TBI with transplantation of MSCs may also moderate post-TBI hypoperfusion that results from impaired vasculature or disturbed hemodynamics (Hofman et al, 2001) and may reduce cerebral atrophy that occurs concomitantly with progressive neuronal loss (Immonen et al, 2009a;Smith et al, 1997) and diffuse axonal injury (Bigler, 1987;Ding et al, 2008;Mamere et al, 2009;Sidaros et al, 2009). To our knowledge, however, little is known about the dynamic effect of grafted MSCs on post-TBI hemodynamic and atrophic progression.…”

“…Extensive axonal degeneration (Bigler, 1987;Ding et al, 2008;Mamere et al, 2009) and generalized cerebral atrophy (MacKenzie et al, 2002;Sidaros et al, 2009;Trivedi et al, 2007) associated with poor functional outcomes are the common sequelae. TBI-induced hypoperfusion, which could occur beyond the site of primary injury (Bonne et al, 2003;Hofman et al, 2001;Pasco et al, 2007), aggravates this trauma-triggered brain damage.…”

Emerging Imaging Tools for Use with Traumatic Brain Injury Research

“…Studies have shown decreased MTR in white matter regions of patients with TBI McGowan et al, 2000) even when there was no observable pathology on conventional imaging (Duckworth and Stevens, 2010;Kimura et al, 1996;Mamere et al, 2009;Sinson et al, 2001). Furthermore, MTI has proven sensitive in detecting changes in patients with even mild brain injury .…”

Early Microstructural and Metabolic Changes following Controlled Cortical Impact Injury in Rat: A Magnetic Resonance Imaging and Spectroscopy Study

“…Axial diffusivity is believed to be sensitive to axonal integrity and radial diffusivity reflects myelin integrity (Song et al, 2002(Song et al, , 2003. Previous TBI studies on both humans and animals have shown altered MD (Alsop et al, 1996;Huisman et al, 2003;Liu et al, 1999;Mamere et al, 2009), and FA in white matter regions (Arfanakis et al, 2002;Bazarian et al, 2007;Huisman et al, 2004;Mac Donald et al, 2007a,b;Mayer et al, 2010;Wilde et al, 2006;Wozniak et al, 2007) anywhere from 24 h to several days after injury.…”