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Review
. 2011 Apr;28(4):675-88.
doi: 10.1089/neu.2010.1645. Epub 2011 Mar 25.

Naturally occurring disk herniation in dogs: an opportunity for pre-clinical spinal cord injury research

Affiliations
Review

Naturally occurring disk herniation in dogs: an opportunity for pre-clinical spinal cord injury research

Jonathan M Levine et al. J Neurotrauma. 2011 Apr.

Abstract

Traumatic spinal cord injuries represent a significant source of morbidity in humans. Despite decades of research using experimental models of spinal cord injury to identify candidate therapeutics, there has been only limited progress toward translating beneficial findings to human spinal cord injury. Thoracolumbar intervertebral disk herniation is a naturally occurring disease that affects dogs and results in compressive/contusive spinal cord injury. Here we discuss aspects of this disease that are analogous to human spinal cord injury, including injury mechanisms, pathology, and metrics for determining outcomes. We address both the strengths and weaknesses of conducting pre-clinical research in these dogs, and include a review of studies that have utilized these animals to assess efficacy of candidate therapeutics. Finally, we consider a two-species approach to pre-clinical data acquisition, beginning with a reproducible model of spinal cord injury in the rodent as a tool for discovery with validation in pet dogs with intervertebral disk herniation.

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Figures

FIG. 1.
FIG. 1.
Hematoxylin and eosin stained spinal cord sections from dogs with thoracolumbar disk extrusion, showing the range of histopathologic lesions. Dog 1 (A) was paraplegic with preserved nociception for 6 h prior to sample acquisition. The spinal cord displays very mild white matter vacuolation (axonal degeneration and secondary demyelination) within the ventral and lateral funiculi (arrow). Dog 2 (B) was paraplegic without nociception for 2 days and has more extensive injury, including severe white matter vacuolation, intraparenchymal hemorrhage, and a discrete area of necrosis (asterisk). Dog 3 (C) was paraplegic without nociception for 14 days and also has extensive white matter vacuolation and a discrete area of necrosis that has become cavitated (asterisk). Dog 4 (D) was paraplegic without nociception for 3 months and had a discrete area of axonal loss and gliosis in the dorsal funiculi (arrow). Dog 5 (E) had paraplegia and absent nociception for 1 day. There is massive necrosis of both the white and gray matter of the spinal cord with intraparenchymal hemorrhage. Image F is a higher-magnification view of the discrete necrotic area in B. The necrotic, pale-staining area on the left (asterisk) contrasts with the still viable white matter on the right. Swollen axons (black arrow) and reactive blood vessels (white arrow) are evident. Image G is a closer view of the necrotic area in C. The necrotic area (asterisk) has become cavitated and contains numerous gitter cell macrophages (black arrow). Swollen axons (white arrow) are evident in the adjacent white matter. Image H is a higher-magnification view of the dorsal funiculi of image D, showing relatively normal white matter on the right side of the image with axonal loss and gliosis on the left.
FIG. 2.
FIG. 2.
Sagittal (A) and transverse (B and C) T2-weighted magnetic resonance images from a dog with acute-onset non-ambulatory paraparesis. At the T13–L1 vertebral articulation there is severe ventral extradural spinal cord compression (A and C). The compressive material is non-dispersed and hypointense, which is common in some cases of disk extrusion that do not result in epidural hemorrhage. The spinal cord parenchyma cranial to the lesion (B), and at the lesion (A and C), has normal signal characteristics.
FIG. 3.
FIG. 3.
Sagittal (A) and transverse (B and C) T2-weighted magnetic resonance images from a dog with acute-onset paraplegia and no deep nociception. At the L5 vertebra (A and C) there is dispersed, mixed-signal, ventral extradural compression due to disk extrusion and epidural hemorrhage. The spinal cord parenchyma cranial to the lesion (A and B) is hyperintense, suggesting severe spinal cord injury.

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