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

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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.


Sample histological data for NeuN-positive quantification. (A) Acquired images at 20× magnification. (B) Manually identified regions of interest of ventral horns. (C) Sample NeuN-positive neurons with nucleoli presenting as a darkened center of the cell nucleus. NeuN, neuronal nuclei.
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f3: Sample histological data for NeuN-positive quantification. (A) Acquired images at 20× magnification. (B) Manually identified regions of interest of ventral horns. (C) Sample NeuN-positive neurons with nucleoli presenting as a darkened center of the cell nucleus. NeuN, neuronal nuclei.

Mentions: For each transverse image (Fig. 3A), an ROI was manually drawn around the left and right ventral horns (Fig. 3B), according to the previously outlined protocol for identifying GM.


Relating Histopathology and Mechanical Strain in Experimental Contusion Spinal Cord Injury in a Rat Model
Sample histological data for NeuN-positive quantification. (A) Acquired images at 20× magnification. (B) Manually identified regions of interest of ventral horns. (C) Sample NeuN-positive neurons with nucleoli presenting as a darkened center of the cell nucleus. NeuN, neuronal nuclei.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f3: Sample histological data for NeuN-positive quantification. (A) Acquired images at 20× magnification. (B) Manually identified regions of interest of ventral horns. (C) Sample NeuN-positive neurons with nucleoli presenting as a darkened center of the cell nucleus. NeuN, neuronal nuclei.
Mentions: For each transverse image (Fig. 3A), an ROI was manually drawn around the left and right ventral horns (Fig. 3B), according to the previously outlined protocol for identifying GM.

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.