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Relating Histopathology and Mechanical Strain in Experimental Contusion Spinal Cord Injury in a Rat Model

View Article: PubMed Central - PubMed

ABSTRACT

During traumatic spinal cord injury (SCI), the spinal cord is subject to external displacements that result in damage of neural tissues. These displacements produce complex internal deformations, or strains, of the spinal cord parenchyma. The aim of this study is to determine a relationship between these internal strains during SCI and primary damage to spinal cord gray matter (GM) in an in vivo rat contusion model. Using magnetic resonance imaging and novel image registration methods, we measured three-dimensional (3D) mechanical strain in in vivo rat cervical spinal cord (n = 12) during an imposed contusion injury. We then assessed expression of the neuronal transcription factor, neuronal nuclei (NeuN), in ventral horns of GM (at the epicenter of injury as well as at intervals cranially and caudally), immediately post-injury. We found that minimum principal strain was most strongly correlated with loss of NeuN stain across all animals (R2 = 0.19), but varied in strength between individual animals (R2 = 0.06–0.52). Craniocaudal distribution of anatomical damage was similar to measured strain distribution. A Monte Carlo simulation was used to assess strain field error, and minimum principal strain (which ranged from 8% to 36% in GM ventral horns) exhibited a standard deviation of 2.6% attributed to the simulated error. This study is the first to measure 3D deformation of the spinal cord and relate it to patterns of ensuing tissue damage in an in vivo model. It provides a platform on which to build future studies addressing the tolerance of spinal cord tissue to mechanical deformation.

No MeSH data available.


Related in: MedlinePlus

Linear regression of NeuN-positive density against transverse-plane strain types for individual animal data (IV 1–4). Scatter plots with trendlines and calculated R2 values are shown for each transverse-plane strain: lateral normal strain (eXX-blue); transverse-plane shear strain (eXY-green); dorsoventral normal strain (eYY-red); minimum principal strain (emin-black); and maximum principal strain (emax-purple). Asterisk (*) indicates a significant relationship at α = 0.05. NeuN, neuronal nuclei.
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f6: Linear regression of NeuN-positive density against transverse-plane strain types for individual animal data (IV 1–4). Scatter plots with trendlines and calculated R2 values are shown for each transverse-plane strain: lateral normal strain (eXX-blue); transverse-plane shear strain (eXY-green); dorsoventral normal strain (eYY-red); minimum principal strain (emin-black); and maximum principal strain (emax-purple). Asterisk (*) indicates a significant relationship at α = 0.05. NeuN, neuronal nuclei.

Mentions: Linear regression analyses for each strain type, for each individual animal, were plotted (Figs. 6A and 6B). R2 values (and associated p values) from these analyses of NeuN-positive density against the various strain types are summarized in Table 3. The minimum principal strain and NeuN-positive density for both the left and right ventral horns, for each animal, were plotted over the craniocaudal region of interest (Fig. 7). NeuN-positve density noninjury thresholds exhibited similar variation throughout the craniocaudal ROI. In all animals, there appeared to be greater strain in the right ventral horn, compared to the left ventral horn. In both NeuN-positive density and strain data, lower values were generally observed at the epicenter of injury and increased at greater craniocaudal distances. In animals that received a mid-line impact (IV 1, IV 9, and IV 12), increased compressive strains were observed in both ventral horns as well as decreased NeuN-positive density values closer to the epicenter of injury (with the exception of IV 12, which did not have epicenter histological data available). However, in some animals that received a lateral-right impact, similar decreases in NeuN-positive density closer to the epicenter were observed in both left and right ventral horns, whereas larger strains were only observed in the right ventral horn (IV 2–4). Some animals exhibited local minima of NeuN-positive density at the epicenter and also further away, craniocaudally (IV 10–11).


Relating Histopathology and Mechanical Strain in Experimental Contusion Spinal Cord Injury in a Rat Model
Linear regression of NeuN-positive density against transverse-plane strain types for individual animal data (IV 1–4). Scatter plots with trendlines and calculated R2 values are shown for each transverse-plane strain: lateral normal strain (eXX-blue); transverse-plane shear strain (eXY-green); dorsoventral normal strain (eYY-red); minimum principal strain (emin-black); and maximum principal strain (emax-purple). Asterisk (*) indicates a significant relationship at α = 0.05. NeuN, neuronal nuclei.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5035832&req=5

f6: Linear regression of NeuN-positive density against transverse-plane strain types for individual animal data (IV 1–4). Scatter plots with trendlines and calculated R2 values are shown for each transverse-plane strain: lateral normal strain (eXX-blue); transverse-plane shear strain (eXY-green); dorsoventral normal strain (eYY-red); minimum principal strain (emin-black); and maximum principal strain (emax-purple). Asterisk (*) indicates a significant relationship at α = 0.05. NeuN, neuronal nuclei.
Mentions: Linear regression analyses for each strain type, for each individual animal, were plotted (Figs. 6A and 6B). R2 values (and associated p values) from these analyses of NeuN-positive density against the various strain types are summarized in Table 3. The minimum principal strain and NeuN-positive density for both the left and right ventral horns, for each animal, were plotted over the craniocaudal region of interest (Fig. 7). NeuN-positve density noninjury thresholds exhibited similar variation throughout the craniocaudal ROI. In all animals, there appeared to be greater strain in the right ventral horn, compared to the left ventral horn. In both NeuN-positive density and strain data, lower values were generally observed at the epicenter of injury and increased at greater craniocaudal distances. In animals that received a mid-line impact (IV 1, IV 9, and IV 12), increased compressive strains were observed in both ventral horns as well as decreased NeuN-positive density values closer to the epicenter of injury (with the exception of IV 12, which did not have epicenter histological data available). However, in some animals that received a lateral-right impact, similar decreases in NeuN-positive density closer to the epicenter were observed in both left and right ventral horns, whereas larger strains were only observed in the right ventral horn (IV 2–4). Some animals exhibited local minima of NeuN-positive density at the epicenter and also further away, craniocaudally (IV 10–11).

View Article: PubMed Central - PubMed

ABSTRACT

During traumatic spinal cord injury (SCI), the spinal cord is subject to external displacements that result in damage of neural tissues. These displacements produce complex internal deformations, or strains, of the spinal cord parenchyma. The aim of this study is to determine a relationship between these internal strains during SCI and primary damage to spinal cord gray matter (GM) in an in vivo rat contusion model. Using magnetic resonance imaging and novel image registration methods, we measured three-dimensional (3D) mechanical strain in in vivo rat cervical spinal cord (n = 12) during an imposed contusion injury. We then assessed expression of the neuronal transcription factor, neuronal nuclei (NeuN), in ventral horns of GM (at the epicenter of injury as well as at intervals cranially and caudally), immediately post-injury. We found that minimum principal strain was most strongly correlated with loss of NeuN stain across all animals (R2 = 0.19), but varied in strength between individual animals (R2 = 0.06–0.52). Craniocaudal distribution of anatomical damage was similar to measured strain distribution. A Monte Carlo simulation was used to assess strain field error, and minimum principal strain (which ranged from 8% to 36% in GM ventral horns) exhibited a standard deviation of 2.6% attributed to the simulated error. This study is the first to measure 3D deformation of the spinal cord and relate it to patterns of ensuing tissue damage in an in vivo model. It provides a platform on which to build future studies addressing the tolerance of spinal cord tissue to mechanical deformation.

No MeSH data available.


Related in: MedlinePlus