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Spinal Cord Injury

Intervertebral disc herniation (IVDH)- associated SCI is the most common cause of SCI in pet dogs, with upwards of 20,000 cases managed by veterinary spinal surgeons in the United States every year.

Human Equivalent

Acute spinal cord injury (SCI); Intervertebral disc herniation-associated SCI


Injury is most commonly observed in the thoracolumbar region, although lower lumbar and cervical injuries are observed at a lower frequency. Intervertebral disc herniation (IVDH)- associated SCI is the most common cause of SCI in pet dogs, with upwards of 20,000 cases managed by veterinary spinal surgeons in the United States every year. Severity of neurologic injury caused by IVDH-associated SCI spans a spectrum up to and including sensorimotor complete injury,  with predictable patterns of recovery across different severities

Similarities in humans

Intervertebral disc herniation-associated SCI produces an acute injury with a mix of concussive and compressive forces. Dogs with this disease are managed by neurologic and surgical specialists in a veterinary clinical setting with advanced imaging, surgical decompression and rehabilitation therapy. Histologic abnormalities consist of varying degrees of gray matter hemorrhage and necrosis, inflammation and gliosis, axonal swelling, sparing of peripheral and small diameter axons, and variable but mild degrees of demyelination. As in people, individual changes within the injured canine spinal cord span a relatively broad spectrum related to type and severity of injury, thus reflecting the general heterogeneity of the disease itself.

Differences in humans

The anatomy of the canine spinal cord differs from humans in that the spinal cord of dogs terminates at approximately the sixth lumbar vertebra in most animals (there are 13 thoracic vertebrae and 7 lumbar vertebrae in dogs). As such, herniation of intervertebral disc material in the thoracolumbar spine causes injury to the spinal cord, the clinical ramifications of which are akin to a mid-thoracic injury in a person. Additionally, the rate of spontaneous recovery of dogs with severe injuries (AIS-A equivalent) is higher than that noted in humans, where dogs with sensorimotor complete injuries have a 40-50% recover rate for return of ability to walk. Those dogs with clinically ‘complete’ injuries which do make some recovery often have major long-term neurologic deficits including fecal and urinary incontinence and gait abnormalities

Disease etiology

There is a high prevalence of spontaneous intervertebral disc degeneration, predominantly affecting chondrodystrophic small breed dogs such as miniature Dachshunds, Beagles, Shih Tzu, Pekingese, and others. Dogs with intervertebral disc degeneration have an increased risk of acute herniation of degenerate calcified nucleus pulposus, which results in a mixed compressive and contusive injury to the spinal cord. In some cases, this herniation of nucleus pulposus may be explosive and occurs over seconds to minutes. In other cases it develops more gradually over hours. The degree of both compression and contusion varies from animal to animal relating to the speed and volume of herniated disc material, and therefore the force of the impact.

Clinical presentation

Affected dogs typically present to the emergency department with a complaint of difficulty walking (paresis or paralysis) and in severe cases may also experience loss of sensation below the level of injury, and incontinence.


Dogs with severe neurologic deficits associated with IVDH-associated SCI are typically managed with decompressive surgery (laminectomy) followed by rehabilitation therapy. Additionally, several recent trials have evaluated neuroprotective strategies in acute injury, or regenerative strategies in subacute and chronic injury both as a means to improve recovery for dogs and as a translational model of human SCI.

Recent Publications

  1. Wang-Leandro A, Hobert MK, Kramer S, Rohn K, Stein VM, Tipold A. The role of diffusion tensor imaging as an objective tool for the assessment of motor function recovery after paraplegia in a naturally-occurring large animal model of spinal cord injury. J Transl Med 2018; 16: 258.
  2. Moore SA, Zidan N, Spitzbarth I, Nout-Lomas YS, Granger N, da Costa RC, Levine JM, Jeffery ND, Stein VM, Tipold A, Olby NJ. Development of an international canine spinal cord injury observational registy: a collaborative data-sharing network to optimize tranlsational studies of SCI. Spinal cord 2018; 56:656-665.
  3. Moore SA, Granger N, Olby NJ, Spitzbarth I, Jeffery ND, Tipold A, et al. Targeting translational successes through CANSORT-SCI: using pet dogs to identify effective treatments for spinal cord injury. J Neurotrauma 2017; 34: 2007-2018.
  4. Gorney AM, Blau SR, Dohse CS, Griffith EH, Williams KD, Lim JH, et al. Mechanical and Thermal Sensory Testing in Normal Chondrodystrophoid Dogs and Dogs with Spinal Cord Injury caused by Thoracolumbar Intervertebral Disc Herniations. J Vet Intern Med. 2016 Mar;30(2):627-35.
  5. Anderson KM, Welsh CJ, Young C, Levine GJ, Kerwin SC, Boudreau CE, et al. Acute Phase Proteins in Cerebrospinal Fluid from Dogs with Naturally-Occurring Spinal Cord Injury. J Neurotrauma. 2015 Nov 1;32(21):1658-65.
  6. McMahill BG, Spriet M, Siso S, Manzer MD, Mitchell G, McGee J, et al. Feasibility Study of Canine Epidermal Neural Crest Stem Cell Transplantation in the Spinal Cords of Dogs. Stem Cells Transl Med. 2015 Oct;4(10):1173-86.
  7. Levine JM, Cohen ND, Heller M, Fajt VR, Levine GJ, Kerwin SC, et al. Efficacy of a metalloproteinase inhibitor in spinal cord injured dogs. PLoS One. 2014 May 1;9(5):e96408.
  8. Lim JH, Muguet-Chanoit AC, Smith DT, Laber E, Olby NJ. Potassium channel antagonists 4-aminopyridine and the T-butyl carbamate derivative of 4-aminopyridine improve hind limb function in chronically non-ambulatory dogs; a blinded, placebo-controlled trial. PLoS One. 2014 Dec 31;9(12):e116139.
  9. Bock P, Spitzbarth I, Haist V, Stein VM, Tipold A, Puff C, et al. Spatio-temporal development of axonopathy in canine intervertebral disc disease as a translational large animal model for nonexperimental spinal cord injury. Brain Pathol. 2013 Jan;23(1):82-99.
  10. Boekhoff TM, Ensinger EM, Carlson R, Bock P, Baumgartner W, Rohn K, et al. Microglial contribution to secondary injury evaluated in a large animal model of human spinal cord trauma. J Neurotrauma. 2012 Mar 20;29(5):1000-11.
  11. Granger N, Blamires H, Franklin RJ, Jeffery ND. Autologous olfactory mucosal cell transplants in clinical spinal cord injury: a randomized double-blinded trial in a canine translational model. Brain. 2012 Nov;135(Pt 11):3227-37.
  12. Jeffery ND, Hamilton L, Granger N. Designing clinical trials in canine spinal cord injury as a model to translate successful laboratory interventions into clinical practice. Vet Rec. 2011 Jan 29;168(4):102-7.
  13. Jeffery ND, Lakatos A, Franklin RJ. Autologous olfactory glial cell transplantation is reliable and safe in naturally occurring canine spinal cord injury. J Neurotrauma. 2005 Nov;22(11):1282-93.
  14. Blight AR, Toombs JP, Bauer MS, Widmer WR. The effects of 4-aminopyridine on neurological deficits in chronic cases of traumatic spinal cord injury in dogs: a phase I clinical trial. J Neurotrauma. 1991 Summer;8(2):103-19.