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Evaluating regional blood spinal cord barrier dysfunction following spinal cord injury using longitudinal dynamic contrast-enhanced MRI.

Tatar I, Chou PC, Desouki MM, El Sayed H, Bilgen M - BMC Med Imaging (2009)

Bottom Line: At the injury sites, the damaged barriers occupied about 70% of the total cross section and 48% of the total volume on day 1, but the corresponding measurements were reduced to 55% and 25%, respectively on day 3.Diffusion computations included longitudinal and transverse diffusivities and fractional anisotropy index.This capability is expected to play an important role in characterizing the neurovascular changes and reorganization following SCI in longitudinal preclinical experiments, but with potential clinical implications.

View Article: PubMed Central - HTML - PubMed

Affiliation: Preclinical Imaging in Translational Research Laboratory, Radiology and Radiological Science, Medical University of South Carolina, 169 Ashley Avenue, Charleston, SC 29425, USA. ilkan@hacettepe.edu.tr

ABSTRACT

Background: In vivo preclinical imaging of spinal cord injury (SCI) in rodent models provides clinically relevant information in translational research. This paper uses multimodal magnetic resonance imaging (MRI) to investigate neurovascular pathology and changes in blood spinal cord barrier (BSCB) permeability following SCI in a mouse model of SCI.

Methods: C57BL/6 female mice (n = 5) were subjected to contusive injury at the thoracic T11 level and scanned on post injury days 1 and 3 using anatomical, dynamic contrast-enhanced (DCE-MRI) and diffusion tensor imaging (DTI). The injured cords were evaluated postmortem with histopathological stains specific to neurovascular changes. A computational model was implemented to map local changes in barrier function from the contrast enhancement. The area and volume of spinal cord tissue with dysfunctional barrier were determined using semi-automatic segmentation.

Results: Quantitative maps derived from the acquired DCE-MRI data depicted the degree of BSCB permeability variations in injured spinal cords. At the injury sites, the damaged barriers occupied about 70% of the total cross section and 48% of the total volume on day 1, but the corresponding measurements were reduced to 55% and 25%, respectively on day 3. These changes implied spatio-temporal remodeling of microvasculature and its architecture in injured SC. Diffusion computations included longitudinal and transverse diffusivities and fractional anisotropy index. Comparison of permeability and diffusion measurements indicated regions of injured cords with dysfunctional barriers had structural changes in the form of greater axonal loss and demyelination, as supported by histopathologic assessments.

Conclusion: The results from this study collectively demonstrated the feasibility of quantitatively mapping regional BSCB dysfunction in injured cord in mouse and obtaining complementary information about its structural integrity using in vivo DCE-MRI and DTI protocols. This capability is expected to play an important role in characterizing the neurovascular changes and reorganization following SCI in longitudinal preclinical experiments, but with potential clinical implications.

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Axial proton-density images of an injured mouse spinal cord. The serial images show normal caudal and rostral sections and injury epicenter on postinjury day 1. Arrows point to corticospinal tract (CST). In normal cord, the image intensity profile does not produce enough contrast to distinguish the CST from the surrounding white matter. Interestingly, in this injured SC, the CST at the rostral section, but not the caudal section, has been delineated by slight hyperintensity compared to the background white matter.
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Figure 1: Axial proton-density images of an injured mouse spinal cord. The serial images show normal caudal and rostral sections and injury epicenter on postinjury day 1. Arrows point to corticospinal tract (CST). In normal cord, the image intensity profile does not produce enough contrast to distinguish the CST from the surrounding white matter. Interestingly, in this injured SC, the CST at the rostral section, but not the caudal section, has been delineated by slight hyperintensity compared to the background white matter.

Mentions: Anatomical axial PD images acquired from one of the injured SC are shown in Figure 1. The intensity contrasts on these images from normal sections delineate gross anatomical details of the cord within the white matter (WM) and grey matter (GM) as well as the surrounding spinal structures. The lesion is depicted by an altered intensity contrast in the parenchyma below the laminectomy. The corticospinal tract in the mouse is anatomically located between the dorsal horns ventrally next to the central canal. In normal cords, the image intensity profile does not produce enough contrast to distinguish this tract from the surrounding WM and GM. In this particular injured SC, images from the rostral, but not the caudal, sections delineated the corticospinal tract with hyperintensity. The intensity change was indicative of alterations in the MR properties of the tract and of a pathological abnormality, which was likely associated with Wallerian degeneration [26].


Evaluating regional blood spinal cord barrier dysfunction following spinal cord injury using longitudinal dynamic contrast-enhanced MRI.

Tatar I, Chou PC, Desouki MM, El Sayed H, Bilgen M - BMC Med Imaging (2009)

Axial proton-density images of an injured mouse spinal cord. The serial images show normal caudal and rostral sections and injury epicenter on postinjury day 1. Arrows point to corticospinal tract (CST). In normal cord, the image intensity profile does not produce enough contrast to distinguish the CST from the surrounding white matter. Interestingly, in this injured SC, the CST at the rostral section, but not the caudal section, has been delineated by slight hyperintensity compared to the background white matter.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2714086&req=5

Figure 1: Axial proton-density images of an injured mouse spinal cord. The serial images show normal caudal and rostral sections and injury epicenter on postinjury day 1. Arrows point to corticospinal tract (CST). In normal cord, the image intensity profile does not produce enough contrast to distinguish the CST from the surrounding white matter. Interestingly, in this injured SC, the CST at the rostral section, but not the caudal section, has been delineated by slight hyperintensity compared to the background white matter.
Mentions: Anatomical axial PD images acquired from one of the injured SC are shown in Figure 1. The intensity contrasts on these images from normal sections delineate gross anatomical details of the cord within the white matter (WM) and grey matter (GM) as well as the surrounding spinal structures. The lesion is depicted by an altered intensity contrast in the parenchyma below the laminectomy. The corticospinal tract in the mouse is anatomically located between the dorsal horns ventrally next to the central canal. In normal cords, the image intensity profile does not produce enough contrast to distinguish this tract from the surrounding WM and GM. In this particular injured SC, images from the rostral, but not the caudal, sections delineated the corticospinal tract with hyperintensity. The intensity change was indicative of alterations in the MR properties of the tract and of a pathological abnormality, which was likely associated with Wallerian degeneration [26].

Bottom Line: At the injury sites, the damaged barriers occupied about 70% of the total cross section and 48% of the total volume on day 1, but the corresponding measurements were reduced to 55% and 25%, respectively on day 3.Diffusion computations included longitudinal and transverse diffusivities and fractional anisotropy index.This capability is expected to play an important role in characterizing the neurovascular changes and reorganization following SCI in longitudinal preclinical experiments, but with potential clinical implications.

View Article: PubMed Central - HTML - PubMed

Affiliation: Preclinical Imaging in Translational Research Laboratory, Radiology and Radiological Science, Medical University of South Carolina, 169 Ashley Avenue, Charleston, SC 29425, USA. ilkan@hacettepe.edu.tr

ABSTRACT

Background: In vivo preclinical imaging of spinal cord injury (SCI) in rodent models provides clinically relevant information in translational research. This paper uses multimodal magnetic resonance imaging (MRI) to investigate neurovascular pathology and changes in blood spinal cord barrier (BSCB) permeability following SCI in a mouse model of SCI.

Methods: C57BL/6 female mice (n = 5) were subjected to contusive injury at the thoracic T11 level and scanned on post injury days 1 and 3 using anatomical, dynamic contrast-enhanced (DCE-MRI) and diffusion tensor imaging (DTI). The injured cords were evaluated postmortem with histopathological stains specific to neurovascular changes. A computational model was implemented to map local changes in barrier function from the contrast enhancement. The area and volume of spinal cord tissue with dysfunctional barrier were determined using semi-automatic segmentation.

Results: Quantitative maps derived from the acquired DCE-MRI data depicted the degree of BSCB permeability variations in injured spinal cords. At the injury sites, the damaged barriers occupied about 70% of the total cross section and 48% of the total volume on day 1, but the corresponding measurements were reduced to 55% and 25%, respectively on day 3. These changes implied spatio-temporal remodeling of microvasculature and its architecture in injured SC. Diffusion computations included longitudinal and transverse diffusivities and fractional anisotropy index. Comparison of permeability and diffusion measurements indicated regions of injured cords with dysfunctional barriers had structural changes in the form of greater axonal loss and demyelination, as supported by histopathologic assessments.

Conclusion: The results from this study collectively demonstrated the feasibility of quantitatively mapping regional BSCB dysfunction in injured cord in mouse and obtaining complementary information about its structural integrity using in vivo DCE-MRI and DTI protocols. This capability is expected to play an important role in characterizing the neurovascular changes and reorganization following SCI in longitudinal preclinical experiments, but with potential clinical implications.

Show MeSH
Related in: MedlinePlus