• NAVC Brands

Acute Spinal Cord Injuries

Acute Spinal Cord Injuries


Adam Moeser, DVM, and Charles Vite, DVM, PhD, Diplomate ACVIM (Neurology)

Acute spinal cord injury is a major cause of neurologic dysfunction in dogs and somewhat less so in cats.


  1. History: When a dog or cat presents with evidence of acute spinal cord injury, obtain a detailed history and ascertain whether trauma may have occurred.
  2. Stabilization: Whenever spinal cord injuries secondary to trauma are suspected, manipulate the patient as little as possible. Evaluate the patient’s overall stability first; then address neurologic deficits.
  3. Neurologic Examination: The findings from a comprehensive neurologic examination are the most important part of the diagnostic evaluation.
  4. Differentials: If no trauma or obvious instability has occurred, consider differentials, such as intervertebral disk disease and fibrocartilagenous embolism.
  5. Radiographs: Spinal radiographs are essential in order to identify spinal instability prior to extensive manipulation of the patient.
  6. CT & MRI: Advanced imaging is valuable in diagnosis of acute spinal cord injury. If severe neurologic deficits are present, refer the patient to a hospital with appropriate diagnostic capabilities.
  7. Treatment: Depending on diagnosis, pursue medical management (indicated for patients with pain or minor deficits) or surgery (indicated in patients with severe neurologic deficits, vertebral instability, or significant extradural compression).
  8. Secondary Damage: Be prepared for secondary damage and initiate treatment if necessary.

The most commonly encountered causes of acute spinal cord injury in dogs are, in order of incidence:1-4

  • Intervertebral disk disease (IVDD)
  • Trauma (automobile trauma, gun shots)
  • Infarction (fibrocartilagenous embolism).

In cats, the most common causes of acute spinal cord injury recorded from a population of cats that had been necropsied are, in order of incidence:5

  • Trauma (falling from windows, automobile trauma)
  • IVDD
  • Ischemic disease (infarction, fibrocartilagenous embolism [FCE]).



Whenever spinal cord injuries secondary to trauma are suspected, it is important to manipulate the patient as little as possible.

  • Transport: The use of a stretcher or board can be very helpful for transportation. The patient should be restrained and possibly strapped to the board during transport.
  • Overall Stability: When evaluating a patient with neurologic deficits due to suspect trauma, evaluate the patient’s overall stability first (ie, evaluation of pulmonary and cardiovascular systems). Trauma patients may suffer significant damage to body systems that pose more immediate threats to their lives than neurologic deficits.

Neurologic Examination

  • The neurologic examination is the first and most important tool used by the clinician to localize the site of injury. Please refer to Chapter 3 of A Practical Guide to Canine & Feline Neurology (Dewey CW, Wiley-Blackwell, 2003) for more specifics on the neurologic examination. The presence of certain examination findings will help localize the lesion (Table 1) and direct further diagnostics.
  • However, it is not uncommon to find some discrepancy between neurolocalization based on the neurologic examination and the actual injury localization.
  • One study showed an incorrect neuroanatomic localization within the cervical cord in 12/26 dogs with cervical disk disease, mainly due to inconsistent withdrawal reflexes.6 In addition, incorrect neuroanatomic localization from L4 to S3 can occur due to spinal shock in cases of T3 to L3 myelopathy (spinal cord disease).7

050612 spinal table 1

When assessing a patient with evidence of a myelopathy, the presence/absence of plegia and deep pain are very important indicators of prognosis regardless of the etiology. Plegia and loss of deep pain are usually associated with severe lesions that are causing pathology to a significant percentage of the white matter, while patients that are only painful and ataxic likely have less white matter involvement (Table 2). A theoretical progression of clinical signs following progression of pathology would be:

Pain/ataxia/paresis → Plegia → Loss of deep pain sensation

050612 spinal table 2


Intervertebral Disk Disease

IVDD is a major cause of acute spinal cord injury in dogs; less so in cats. The intervertebral disk is composed of an outer annulus fibrosis and an inner nucleus pulposus (Figure 1). The majority of the annulus and the entire nucleus is avascular; only the peripheral parts of the annulus are innervated.

050612 spinal fig 1
Types of IVDD

  • Fibrous metaplasia is part of the normal aging process in dogs and cats, which results in weakening of the annulus and fibrous collagenization of the nucleus pulposus. This can lead to bulging of the intervertebral disk and a Hansen Type II intervertebral disk lesion (outermost layers of annulus fibrosus remain intact).
  • Chondroid metaplasia occurs within the nucleus pulposus at an early age in chondrodystrophic breeds, such as the dachshund.8 With chondroid metaplasia, the nucleus pulposus becomes abnormal and is no longer able to disperse forces evenly, leading to herniation. This herniation can occur acutely and cause a Hansen Type I intervertebral disk lesion (complete perforation of annulus fibrosus with extrusion of nucleus pulposus into the spinal canal). Since the nucleus pulposus is eccentrically placed more dorsally within the annulus, the herniated material tends to herniate toward the spinal cord.
  • Traumatic noncompressive intervertebral disk herniation occurs when the nucleus pulposus is extruded and causes a concussive injury to the spinal parenchyma (Figure 2). In some cases this extruded material causes a dural tear, which can be found below the level of the dura mater.9,10

050612 spinal fig 2


  • Plain radiographs can help determine the correct region of interest by identifying abnormalities, such as narrowing of the intervertebral disk space, mineral opacities within the canal/foramen, and the vacuum effect (area of radiolucency at the level of the affected intervertebral disk space caused by loss of disk material).
    • However, plain radiographs (without contrast) cannot accurately diagnose IVDD with spinal cord compression.
    • The accuracy of identifying the correct site based on plain radiographs alone is reported to range from 51% to 61%, and advanced imaging is needed for accurate localization and diagnosis of IVDD.11
  • Computed tomography (CT) and myelography have a sensitivity over 80% for localizing the correct site, but magnetic resonance imaging (MRI) remains the best imaging modality for cases of IVDD (Figure 3).12,13
    • CT and/or myelogram may be appropriate for young and middle-age chondrodystrophic breeds where IVDD is very high on the differential list.
    • In older animals and nonchondrodystrophic breeds, MRI should be recommended to the owner as an option since most areas now have a facility with MRI within a reasonable distance.
    • MRI has been reported to have complete agreement with surgical findings, with respect to the site of disk extrusion.
    • In cases of noncompressive traumatic intervertebral disk herniation, the affected disk space may have decreased signal on MRI T2 weighted images, along with mild extradural compression seen at the level of the affected disk space.14,15

050612 spinal fig 3


Once spinal cord imaging is complete, a decision can be made whether to pursue surgical decompression or medical management.

Medical Management
Conservative management typically consists of:1,2,16

  • Strict cage rest for 2 to 6 weeks
  • Anti-inflammatory drugs
  • Analgesics
  • Physical therapy.

Alternative therapies, such as acupuncture, have been described, but not enough evidence is available to determine their efficacy.

A recent retrospective report describing the use of medical management for suspected thoracolumbar IVDD reported a success rate of about 55% once dogs with episodes of relapse were factored in17; if dogs with only minor deficits (ie, pain) are included in the success group, the success rate increases to 66%. A similar retrospective study showed comparable results when disk herniation was localized to the cervical region.18

Conservative management is not an ideal choice for patients with severe neurologic deficits (severe paresis, plegia, loss of deep pain) or those that have already failed conservative management. However, if the client cannot pursue surgery, conservative management is an option for these patients.

Surgical Management
In patients that have severe neurologic dysfunction at time of presentation, significant compression of the cord may be present, which has the potential to severely impair local blood flow and cause progressive secondary damage to the cord. Candidates for surgery include:

  • Significant vertebral instability (luxation, fracture)
  • Patients with significant neurologic deficits, such as severe paresis or paralysis
  • Deep-pain negative dogs.

The latter condition has a significantly worse prognosis if treated with medical management alone. Seven percent or less of deep-pain negative dogs recover with medical management alone.19

Surgical treatment for acute disk extrusions includes:

  • Cervical IVDD: Ventral slot or hemilaminectomy
  • Thoracic/Lumbar IVDD: Hemilaminectomy or dorsal laminectomy.
  • Modifications of the typical hemilaminectomy, such as a pediculectomy and mini-hemilaminectomy, can also be performed.


Indicators by disease type/presentation include:

  • Acute Hansen Type 1 Disk Herniation/Intact Nociception: Patients have an excellent prognosis with surgery. One retrospective study found that 96% of these patients were ambulatory within 3 months of surgery.19
  • Loss of Deep Pain Sensation/Lack of Nociception: These patients have a more guarded prognosis. Decompressive surgery allows about 62% of deep pain negative dogs with thoracolumbar disk extrusions to regain nociception and ability to ambulate without assistance.20
  • Noncompressive Traumatic Intervertebral Disk Herniation: One retrospective study reported that 46/48 dogs with this condition made significant improvements and all were ambulatory with medical management.21 Prognosis may be worse for patients that have lost deep pain sensation. Surgery is a potential therapy for patients with suspected dural tears, and prognosis appears good based on limited reports.22,23


Common causes of trauma include:

  • Automobile accidents
  • Gun-shot wounds
  • Vertical falls in cats, among others.

In cases of acute spinal injury related to trauma, stabilization is the most important aspect of initial care. See Patient Assessment.


  • Lateral and dorsal/ventral radiographs of the entire vertebral column can help identify any fractures (Figure 4) or luxations without manipulating the patient excessively.

050612 spinal fig 4

  • Atlanto-axial luxations must be considered in dogs with a lesion localized from the C1 to C5 spinal cord after suffering suspected trauma; it is important to minimize cervical flexion in these dogs.
  • CT is the gold standard for detecting vertebral fractures and instability, and should be recommended for any patient with suspected vertebral fractures or instability.24
  • While an MRI provides good evaluation of the spinal cord, a CT scan offers much better visualization of the vertebral column’s pathology.
  • In some patients with vertebral fracture(s) and/or luxations, both MRI and CT may be ideal. Figure 5 shows an atlanto-axial luxation for which the CT allowed proper surgical planning.

050612 spinal fig 5


Treatment of trauma patients with significant neurologic deficits ranges from rest to immobilization using external braces to surgical intervention/stabilization.

  • Rest: Rest is appropriate for a patient with pain and/or minor deficits and no evidence of significant instability of the cord.
  • Stabilization: Cervical lesions need more rigorous stabilization due to the inherent mobility of this region. When using braces and/or bandage material to decrease motion, significant cutaneous lesions due to rubbing or moisture can occur, and respiratory status can be compromised by tight neck bandaging. Frequent bandage changes and rechecks may be necessary.
  • Surgery: Surgery may be indicated for patients with significant neurologic deficits and instability. Once stabilized, these patients should be transported to a veterinarian that is comfortable with such procedures for evaluation and treatment.


According to available literature, prognosis for acute spinal cord injuries related to trauma seems to be more guarded than for other types of acute spinal cord injuries.

  • One report evaluating prognosis for dogs with vertebral fractures and/or luxations as well as absent nociception reported that 0/9 had return of nociception.25 Therefore, obvious vertebral instability (ie, fracture, luxation), paralysis, and no evidence of nociception indicates a poor prognosis.
  • A better prognosis is indicated if patients with significant deficits but intact sensation receive surgical stabilization. Unfortunately, these patients are often euthanized.


Surgery should be performed as early as possible in patients with severe deficits in an effort to minimize secondary damage from extradural compression.

Most papers regarding this subject show the following trend: Once the patient loses deep pain sensation, as more time passes, the prognosis worsens. The recommended time frame for pursuing surgery varies but, for patients that have lost deep pain in the past 12 to 24 hours, most publications support emergency surgery. As the time frame extends past 24 hours, the evidence supporting emergency surgery becomes weaker and these patients may be able to wait until the morning for surgery without worsening their prognosis.

Similarly, patients that have become plegic in the previous 24 hours are also considered surgical emergencies in order to preserve an excellent prognosis, by intervening prior to development of extensive secondary damage to the spinal cord and loss of deep pain sensation (more guarded prognosis).

Fibrocartilagenous Embolism

FCE is encountered frequently in dogs; cats are also affected by it, but much less frequently.

  • An FCE occurs when material identical to the nucleus pulposus of the intervertebral disk space forms an embolus that obstructs either arterial, venous, or both types of vasculature within the spinal cord.
  • FCE commonly affects large- and giant-breed dogs, but may also affect small-breed and chondrodystrophic dogs.14,15,26-28 Miniature schnauzers appear to be affected at a higher incidence than other small breeds.29
  • Dogs typically present with a history of peracute neurologic deficits that progress within a 24-hour period.15,26,27 History often involves some form of physical activity at the time clinical signs develop.15
  • Patients are usually not painful at presentation and a substantial percentage will have asymmetrical neurological deficits.15,26


Diagnosis is usually made using advanced imaging. MRI is the best antemortem diagnostic tool, but CT and myelography can also be used to make a presumptive diagnosis.

  • MRI will usually show an intramedullary hyperintensity on T2-weighted images (Figure 6).
  • In some instances, lesions detected by MRI will not be detectable since the changes may require several days to develop.28
  • The main feature that helps differentiate an FCE from other common causes of acute spinal cord injury is the lack of extradural compression. A herniated disk will have extradural compression.

050612 spinal fig 6


Definitive diagnosis of FCE is made using histopathology. Emboli found within the spinal cord vasculature will be histologically identical to the nucleus pulposus.


Treatment of FCE usually includes physical therapy and rest. Different treatments, such as steroids, have been attempted, but no significant positive association has been found.28


  • Prognosis is generally good, and most patients will show signs of significant improvement within 2 weeks,27,28 but maximal improvement may take months.15 When patients are given time to recover, success rates as high as 84% have been cited.14
  • Negative prognostic factors may include lack of nociception, involvement of an intumescence (disputed in the literature), and intramedullary hyperintensity on (1) T2-weighted images of the spinal cord that are longer than the length of two L2 or two C6 vertebral bodies or (2) an intramedullary hyperintensity on transverse section that is greater than 66% the height of the spinal cord.15,26-28


The pathology that results secondary to a primary spinal cord injury (IVDD, trauma, infarct) is often more serious than the primary injury.1-4,30 Secondary pathology can result from changes in the local ion concentrations, disturbances to blood flow and ischemia, production of free radicals, and inflammation.1-4,30 The chemical environment of an injured spinal cord may also delay the regeneration of injured axons.31

Therapeutic Recommendations

Currently, treatment is aimed at relieving the insult caused by the primary injury with:

  • Surgery (if indicated)
  • Medical management (anti-inflammatory drugs and analgesics).

Potential therapies for secondary injuries include:

  • Calcium channel antagonists
  • Free-radical scavengers (ie, vitamin E, selenium, methylprednisolone)
  • N-methyl-D-aspartate (NMDA) antagonists
  • Opioid agonists and antagonists
  • Thyroid releasing hormone.2,3

Free-Radical Scavengers

Most of these therapies are still being tested for efficacy, but the free-radical scavenger methylprednisolone has been used with modest success to treat human patients. It is believed to exert a protective effect through its free radical scavenging properties, which may prevent further lipid peroxidation. In humans, methylprednisolone may offer some benefit against secondary damage to the cord if used within 8 hours of the primary injury.32 Limited studies have been performed in veterinary medicine, and mixed results have been seen in small numbers of dogs.22,23

As we understand more about the secondary damage that occurs within the spinal cord following a primary insult, hopefully new and more effective treatments will become available.

CT = computed tomography; FCE = fibrocartilagenous embolism; IVDD = intervertebral disk disease; MRI = magnetic resonance imaging; NMDA = N-methyl-D-aspartate


  1. Olby N. Current concepts in the management of acute spinal cord injury. J Vet Intern Med 1999; 13:399-407.
  2. Olby N. The pathogenesis and treatment of acute spinal cord injuries in dogs. Vet Clin North Am Small Anim Pract 2010; 40:791-807.
  3. Webb AA, Ngan S, Fowler JD. Spinal cord injury I: A synopsis of the basic science. Can Vet J 2010; 51:485-492.
  4. Webb AA, Ngan S, Fowler D. Spinal cord injury II: Prognostic indicators, standards of care, and clinical trials. Can Vet J 2010; 51:598-604.
  5. Marioni HK. Feline spinal cord diseases. Vet Clin North Am Small Anim Pract 2010; 40:1011-1028.
  6. Forterre F, Konar M, Tomek A, et al. Accuracy of the withdrawal reflex for localization of the site of cervical disk herniation in dogs: 35 cases (2004-2007). JAVMA 2008; 232:559-563.
  7. Smith PM, Jeffery ND. Spinal shock-comparative aspects and clinical relevance. J Vet Intern Med 2005; 19:788-793.
  8. Ghosh P, Taylor TK, Braund KG. The variation of the glycosaminoglycans of the canine intervertebral disc with aging; I. Chondrodystrophoid breed. Gerontol 1977; 23(2):87-98.
  9. Kent M, Holmes S, Cohen E, et al. Imaging diagnosis—CT myelography in dog with intramedullary intervertebral disc herniation. Vet Radiol Ultrasound 2011; 52(2):185-187.
  10. Poncelet L, Heimann M. Intradural vertebral disc herniation in a dog. Vet Rec 2011; 168:486A.
  11. Lamb CR, Nichols A, Targett M, Mannion P. Accuracy of survey radiographic diagnosis of intervertebral disc protrusion in dogs. Vet Radiol Ultra 2002; 43:222-228.
  12. Israel SK, Levine JM, Kerwin SC, et al. The relative sensitivity of computed tomography and myelography for identification of thoracolumbar intervertebral disk herniations in dogs. Vet Radiol Ultra 2009; 50:247-252.
  13. Robertson I, Thrall DE. Imaging dogs with suspected disc herniation: Pros and cons of myelography, computed tomography, and magnetic resonance. Vet Radiol Ultra 2011; 42:S81-S84.
  14. Risio LD, Adams V, Dennis R, et al. Association of clinical and magnetic resonance imaging findings with outcome in dogs suspected to have ischemic myelopathy: 50 cases (2000–2006). JAVMA 2008; 233:129-135.
  15. Risio LD, Platt, SR. Fibrocartilaginous embolic myelopathy in small animals. Vet Clin North Am Small Anim Pract 2010; 40:859-869.
  16. Brisson BA. Intervertebral disc disease in dogs. Vet Clin North Am Small Anim Pract 2010; 40:829-858.
  17. Levine JM, Levine GJ, Johnson SI, et al. Evaluation of the success of medical management for presumptive thoracolumbar intervertebral disk herniation in dogs. Vet Surg 2007; 36:482-491.
  18. Levine JM, Levine GJ, Johnson SI, et al. Evaluation of the success of medical management for presumptive cervical intervertebral disk herniation in dogs. Vet Surg 2007; 36:492-499.
  19. Davis GL, Brown DC. Prognostic indicators for time to ambulation after surgical decompression in nonambulatory dogs with acute thoracolumbar disk extrusions: 112 cases. Vet Surg 2002; 31:513-518.
  20. Scott HW, McKee WM. Laminectomy for 34 dogs with thoracolumbar intervertebral disc disease and loss of deep pain perception. J Small Anim Pract 1999; 40:417-422.
  21. McKee WM, Downes CJ, Pink JJ, Gemmill TJ. Presumptive exercise-associated peracute thoracolumbar disc extrusion in 48 dogs. Vet Rec 2010; 166:523-528.
  22. Coates JR, Sorjonen DC, Simpson ST, et al. Clinicopathologic effects of a 21-aminosteroid compound (U74389G) and high-dose methylprednisolone on spinal cord function after simulated spinal cord trauma. Vet Surg 1995; 24:128-139.
  23. Siemering GB, Vomering ML. High dose methylprednisolone sodium succinate: An adjunct to surgery for canine intervertebral disc herniation. Vet Surg 1992; 21:406 (abstract).
  24. Jeffery ND. Vertebral fracture and luxation in small animals. Vet Clin North Am Small Anim Pract 2010; 40:809-828.
  25. Olby N, Levine J, Harris T, et al. Long-term functional outcome of dogs with severe injuries of the thoracolumbar spinal cord: 87 cases (1996–2001). JAVMA 2003; 222:762–769.
  26. Cauzinille L, Kornegay JN. Fibrocartilaginous embolism of the spinal cord in dogs: Review of 36 histologically confirmed cases and retrospective study of 26 suspected cases. J Vet Intern Med 1996; 10(4):241-245.
  27. Gandini G, Cizinauskas S, Lang J, et al. Fibrocartilaginous embolism in 75 dogs: Clinical findings and factors influencing the recovery rate. J Small Anim Pract 2003; 44:76-80.
  28. Nakamoto Y, Ozawa T, Katakabe K, et al. Fibrocartilaginous embolism of the spinal cord diagnosed by characteristic clinical findings and magnetic resonance imaging in 26 dogs. J Vet Med Sci 2009; 71(2):171-176.
  29. Hawthorne JC, Wallace LJ, Fenner WR, Waters DJ. Fibrocartilaginous embolic myelopathy in miniature schnauzers. JAAHA 2001; 37:374-383.
  30. Jeffry ND, Blakemore WF. Spinal cord injury in small animals; 2. Current and future options for therapy. Vet Rec 1999; 145:183-190.
  31. Brosamle C, Huber AB, Fiedler M, et al. Regeneration of lesioned corticospinal tract fibers in the adult rat induced by a recombinant, humanized IN-1 antibody fragment. J Neurosci 2000; 20:8061-8068.

Bracken MB, Shepard MJ, Holford TR, et al. Methylprednisolone or tirilazad mesylate administration after acute spinal cord injury: 1-year follow up. J Neurosurg 1998; 89:699-706.

Adam MoeserAdam Moeser, DVM, is a second-year neurology resident at University of Pennsylvania School of Veterinary Medicine. He received his DVM from University of Wisconsin – Madison and completed a rotating internship at the VCA Aurora/Berwyn veterinary hospitals in the Chicago, Illinois, area.



Charles ViteCharles Vite, DVM, PhD, Diplomate ACVIM (Neurology), is an assistant professor in the section of neurology and neurosurgery in the Department of Clinical Sciences at University of Pennsylvania School of Veterinary Medicine. His clinical interests include epilepsy as well as neurodegenerative and neurodevelopmental processes. He also has specific interests in vestibular dysfunction and myotonia congenita. Dr. Vite received his DVM from Purdue University and completed a residency in neurology at UPenn, followed by a fellowship in neuromagnetic resonance. He received his PhD from the same university.