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.

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]).

PATIENT ASSESSMENT

Stabilization

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

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

DIFFERENTIAL DIAGNOSIS

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.

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

Imaging

• 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

Treatment

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.

Prognosis

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

Trauma

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.

Imaging

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

• 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.

Treatment

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.

Prognosis

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.

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

Imaging

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.

Histopathology

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

Treatment

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

• 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

SECONDARY DAMAGE

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

References

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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 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 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.