Focal brain injury and its effects on cerebral mantle, neurons, and fiber tracks

Matthews, Murray A.; Carey, Michael E.; Soblosky, Joseph S.; Davidson, June F.; Tabor, Stacy L.

doi:10.1016/s0006-8993(98)00107-3

Cited by 26 publications

(14 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Disconnection is more likely, because the injured ipsilesional cortex can, in fact, be locally activated by direct stimulation after fluid percussion injury. 33 Ongoing intra-and intercortical and corticothalamic denervation has been shown to be rather more widespread than merely affecting the contused region after rodent CCI injury, 34,35 and axonal damage and disconnection underlying the contusion and mid-line region is evident at this level of injury in this model. 22 Even after more mild CCI injury, there is a persistent reduction in both callosal, 36 as well corticospinal, fiber tracks, as assessed by diffusion tensor imaging, 37 suggesting that ongoing inactivation of gray matter is consistent with deficits in connectivity to other relay centers within the central nervous system (CNS).…”

Section: Ipsilesional M1/s1hl Cortical Activation Is Depressed Acutelymentioning

confidence: 79%

Cortical Reorganization after Experimental Traumatic Brain Injury: A Functional Autoradiography Study

Harris

Chen

Pickard

2013

Journal of Neurotrauma

View full text Add to dashboard Cite

Cortical sensorimotor (SM) maps are a useful readout for providing a global view of the underlying status of evoked brain function, as well as a gross overview of ongoing mechanisms of plasticity. Recent evidence in the rat controlled cortical impact (CCI) injury model shows that the ipsilesional (injured) hemisphere is temporarily permissive for axon sprouting. This would predict that size and spatial alterations in cortical maps may occur much earlier than previously tested and that they might be useful as potential markers of the postinjury plasticity period as well as indicators of outcome. We investigated the evolution of changes in brain activation evoked by affected hindlimb electrical stimulation at 4, 7, and 30 days following CCI or sham injury over the hindlimb cortical region of adult rats. [(14)C]-iodoantipyrine autoradiography was used to quantitatively examine the local cerebral blood flow changes in response to hindlimb stimulation as a marker for neuronal activity. The results show that although ipsilesional hindlimb SM activity was persistently depressed from 4 days, additional novel regions of ipsilesional activity appeared concurrently within SM barrel and S2 regions as well as posterior auditory cortex. Simultaneously with this was the appearance of evoked activity within the intact, contralesional cortex that was maximal at 4 and 7 days, compared to stimulated sham-injured rats, where activation was solely unilateral. By 30 days, however, contralesional activation had greatly subsided and existing ipsilesional activity was enhanced within the same novel cortical regions that were identified acutely. These data indicate that significant reorganization of the cortical SM maps occurs after injury that evolves with a particular postinjury time course. We discuss these data in terms of the known mechanisms of plasticity that are likely to underlie these map changes, with particular reference to the differences and similarities that exist between rodent models of stroke and traumatic brain injury.

show abstract

Section: Ipsilesional M1/s1hl Cortical Activation Is Depressed Acutelymentioning

confidence: 79%

Cortical Reorganization after Experimental Traumatic Brain Injury: A Functional Autoradiography Study

Harris

Chen

Pickard

2013

Journal of Neurotrauma

View full text Add to dashboard Cite

show abstract

“…As whole brain analysis is used routinely in clinical studies, such a study may also uncover greater similarities to clinical data. In the controlled cortical impact injury (CCI) model of TBI, contrary to current dogma on the focal nature of the injury, there is in fact widespread axonal degeneration both bilaterally as well as caudally in the forebrain after CCI injury, as indicated by silver staining data (Hall et al, 2008, 2005; Matthews et al, 1998). We hypothesize that a whole brain approach to rodent DTI analysis would yield a better approximation to the total amount of axonal damage present after CCI injury as reflected in those studies.…”

Section: Introductionmentioning

confidence: 89%

Bi-directional changes in fractional anisotropy after experiment TBI: Disorganization and reorganization?

et al. 2016

View full text Add to dashboard Cite

The current dogma to explain the extent of injury related changes following rodent controlled cortical impact (CCI) injury is a focal injury with limited axonal pathology. However, there is in fact good, published histologic evidence to suggest that axonal injury is far more widespread in this model than generally thought. One possibility that might help to explain this is the often-used region-of-interest data analysis approach taken by experimental traumatic brain injury (TBI) diffusion tensor imaging (DTI) or histologic studies that might miss more widespread damage, when compared to the whole brain, statistically robust method of tract based analysis used more routinely in clinical research. To determine the extent of DTI changes in this model, we acquired in vivo DTI data before and at 1 and 4 weeks after CCI injury in 17 adult, male rats and analyzed parametric maps of fractional anisotropy (FA), axial, radial and mean diffusivity (AD, RD, MD), tensor mode (MO), and fiber tract density (FTD) using tract based spatial statistics. Contusion volume was used as a surrogate marker of injury severity and as a covariate for investigating severity dependence of the data. Mean fiber tract length was also computed from seeds in the cortical spinal tract regions. In parallel experiments (n=3–5/group) we investigated corpus callosum neurofilaments and demyelination using immunohistochemistry (IHC) at 3 days and 6 weeks, callosal tract patency using dual-label retrograde tract-tracing at 5 weeks, and the contribution of gliosis to DTI parameter maps using GFAP IHC at 4 weeks post-injury. The data show widespread ipsilateral regions of significantly reduced FA at 1 week post-injury, driven by temporally changing values of AD, RD and MD that persist to 4 weeks. Demyelination, retrograde label tract loss, and reductions in MO (tract degeneration) and FTD were shown to underpin these data. Significant FA increases occurred in subcortical and corticospinal tract regions that were spatially distinct from regions of FA decrease, grossly affected gliotic areas and from MO changes. However, there was good spatial correspondence between regions of increased FA and areas of increased FTD and mean fiber length. We discuss these widespread changes in DTI parameters in terms of axonal degeneration and potential reorganization, with reference to a resting state fMRI companion paper (Harris et al, 2016, Exp. Neurol.227:124–138) that demonstrated altered functional connectivity data acquired from the same rats used in this study.

show abstract

“…Darkened neurons or axonal processes due to silver impregnation staining indicate damage (chromatolysis) (Matthews et al, 1998). Neurodegenrative index of post-TBI brains, as evaluated by DeOlmos Silver Stain for degenerating neurons, showed very interesting results (Fig.…”

Section: Deolmos Silver Stainmentioning

confidence: 98%

Neuroanatomical correlation of behavioral deficits in the CCI model of TBI

Chauhan

Gatto

Chauhan

2010

Journal of Neuroscience Methods

View full text Add to dashboard Cite

Focal brain injury and its effects on cerebral mantle, neurons, and fiber tracks

Cited by 26 publications

References 42 publications

Cortical Reorganization after Experimental Traumatic Brain Injury: A Functional Autoradiography Study

Cortical Reorganization after Experimental Traumatic Brain Injury: A Functional Autoradiography Study

Bi-directional changes in fractional anisotropy after experiment TBI: Disorganization and reorganization?

Neuroanatomical correlation of behavioral deficits in the CCI model of TBI

Contact Info

Product

Resources

About