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Compendium March 2009 (Vol 31, No 3)

Canine Thoracolumbar Intervertebral Disk Disease: Pathophysiology, Neurologic Examination, and Emergency Medical Therapy

by John F. Griffin IV, DVM, Jonathan M. Levine, DVM, DACVIM (Neurology), Sharon C. Kerwin, DVM, MS, DACVS, Timea Brady, DVM

    CETEST This course is approved for 3.0 CE credits

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    Thoracolumbar intervertebral disk disease (IVDD) is a common, important cause of paraspinal hyperesthesia, pelvic limb ataxia, paraparesis, paraplegia, and urinary and fecal incontinence in dogs. Research offers insights into the pathophysiology, diagnosis, prognosis, and treatment of this disorder. The comparative efficacy of many familiar therapies remains unknown and controversial. This article reviews the pathophysiology and epidemiology of this condition and the examination and emergency medical therapy of dogs with suspected thoracolumbar IVDD. A companion article addresses diagnosis, prognosis, and treatment.

    Thoracolumbar intervertebral disk disease (IVDD) is a broad term, encompassing disk degeneration and clinical neurologic disease due to disk herniation. Canine IVDD has been reported to be the reason for presentation in 23 of every 1000 cases seen in 13 veterinary colleges in the United States and Canada, and it is the most common cause of thoracolumbar myelopathy with paraspinal hyperesthesia.1,2 A thorough, integrated understanding of spinal anatomy, pathophysiology, and neurologic function forms the foundation for medical decision-making and care for dogs with clinical signs of intervertebral disk herniation.

    Structure and Function

    The average canine vertebral column has 13 thoracic and seven lumbar vertebrae, each consisting of a body, a vertebral arch, and various processes.3 Each vertebral arch consists of right and left pedicles and a lamina. Together, the bodies and vertebral arches form the vertebral canal, which houses the spinal cord.3 The intervertebral disks lie between the vertebral bodies, providing stability and flexibility to the vertebral column.4,5 Each disk is composed of three anatomic regions: the annulus fibrosus, nucleus pulposus, and cartilaginous end plate.4,6 Intervertebral disks account for about 16% of the vertebral column length in the thoracic and lumbar regions.7 The cervical and lumbar intervertebral disk spaces are wider than the caudal thoracic spaces (T9-T10 through T12-T13).8

    The annulus fibrosus arises from mesenchymal cells to form a fibrous ring around the central nucleus pulposus3,9 (FIGURE 1A). The annulus is composed of distinct microscopic lamellae, each arising from the cartilaginous end plate and adjacent vertebrae.10 These lamellae run parallel to one another, are mostly composed of type I collagen, and have the ability to glide over one another during biomechanical loading4,11,12 (FIGURE 1B and FIGURE 1 C). The canine annulus is thickest ventrally and is sparsely innervated peripherally.5,13-15 This nerve supply includes nociceptive and other fibers that may be involved in sympathetic function or proprioception from the intervertebral disk.16 The nociceptive fibers probably play a role in diskogenic pain and could be a source of paraspinal hyperesthesia in some dogs with annular tears or disk degeneration.15

    An embryologic remnant of the notochord, the nucleus pulposus forms the center of the intervertebral disk and comprises an extracellular matrix of water and proteoglycans5,13,17 (FIGURE 1D and FIGURE 2). Associated with this matrix is a sparse network of fibrous material (mostly type II collagen) and various cells (e.g., chondrocytes, fibrocytes, notochordal).4,5 In the healthy nucleus, notochordal cells are found in large clusters connected by functional gap junctions, providing an important means of intercellular communication.18 The notochordal cells produce and assemble proteoglycans and may regulate intervertebral disk chondrocyte proteoglycan production and cell proliferation.19,20 Important proteoglycans include chondroitin sulfate, keratan sulfate, and hyaluronic acid.4,11,21 Proteoglycan content changes with aging in healthy dogs (increased keratan sulfate relative to chondroitin sulfate), and water-binding capacity decreases.11,21,22 It has been noted that nonchondrodystrophoid dogs maintain their intervertebral disk notochordal cells into adulthood, whereas chondrodystrophoid breeds do not, so the preserved notochordal cells may help prevent development of degenerative disk disease.19

    The cartilaginous end plate is the site of attachment between the intervertebral disk and the vertebral body.6,12,13 Histologically, the end plate consists of hyaline cartilage with openings for vascular elements.5 Small particles diffuse across the end plate to supply the intervertebral disk with nutrients.23,24 It is believed that occlusion of end plate openings may lead to insufficient disk nutrition and to disk degeneration, a process that may occur with aging.25-27

    Throughout the thoracolumbar vertebral column, the intervertebral disks are attached ventrally and dorsally to the longitudinal ligaments.13 The dorsal longitudinal ligament lies just dorsal to the vertebral bodies, is narrowest in the middle of the vertebra, and fans out near its attachment to each intervertebral disk.13 The bilateral cranial and caudal vertebral notches in the vertebral arches form the intervertebral foramina, through which spinal nerves and blood vessels pass.13 The lamina are bound to each other by the interarcuate ligaments.13 Each thoracolumbar vertebra has bilateral cranial and caudal articular processes that form synovial articulations with adjacent vertebrae.28-30 The interspinous ligaments run between adjacent spinous processes.13 The supraspinous ligament is a thick band of connective tissue that binds the dorsal-most aspects of the spinous processes.13

    The vertebral column and associated structures must be able to provide flexibility and stability in response to compression, bending, shear, torsion, and tension.4,31 In physiologic movement, several of these forces occur simultaneously.4 Compression occurs during loading of the disk on its neutral axis when adjacent vertebral bodies press together.4,32 Compression increases pressure within the nucleus pulposus that is circumferentially absorbed by the annulus fibrosus.4,31 Bending occurs with flexion or extension of the vertebral column, and torsion occurs with rotation about the long axis of the vertebral column.4,32 Shear refers to forces oriented in a plane perpendicular to the long axis of the vertebral column.31 Tension occurs when adjacent vertebral bodies are pulled apart along the long axis of the vertebral column.31

    Resistance to bending, shear, and torsion is provided by the articular facets and supporting ligaments of the vertebral column in addition to the annulus fibrosus.4,28 The relative importance of these structures may vary with the type and direction of specific forces involved. For example, the annulus seems to be more important than the articular facets in opposing lateral bending forces in the lumbar vertebrae; however, the articular facets probably play a larger role in opposing lateral than dorsoventral bending forces.28,29 The supraspinous and interspinous ligaments impart stiffness to the vertebral column in response to ventral flexion.33

    Each thoracic vertebra articulates bilaterally with the capitulum (head) of the associated rib, and intercapital ligaments bind each rib to its contralateral mate.13 Throughout most of the thoracic vertebral column, the costovertebral joints lie in the same craniocaudal plane as the intervertebral disk.5,13,34,35 Hence, most of the intercapital ligaments lie immediately dorsal to the annulus.5,13,34,35 It has been speculated that the intercapital ligaments aid in strengthening the vertebral column, reducing the risk of disk herniation cranial to the 10th thoracic vertebra.5,13,34,35 Caudal to the 10th thoracic vertebra, the intercapital ligaments may lie caudal to the intervertebral disks and may be smaller or missing.5,13


    Thoracolumbar IVDD encompasses disk degeneration and clinical neurologic disease due to disk herniation (disk prolapse). Two patterns of disk degeneration are commonly recognized in dogs: chondroid and fibroid. Disk herniation manifests as three syndromes: disk extrusion, disk protrusion, and disk bulge. Disk herniation can result in acute or chronic spinal cord injury, with a broad spectrum of associated clinical signs.


    Predisposition to disk herniation likely reflects both biomechanical forces associated with body type and genetic factors associated with disk degeneration.5,36,37 Dachshunds, poodles, Pekingese, cocker spaniels, shih tzus, Lhasa apsos, and beagles are the most commonly affected small-breed dogs.1,38-40 Basset hounds, German shepherds, Labrador retrievers, and Doberman pinschers are the most commonly affected large-breed dogs.39,41 A study of 8117 cases of disk disease found that dachshunds were 9.9 times more likely to be affected than all breeds combined, while shih tzus, Pekingese, and Lhasa apsos were 3.9, 3.5, and 3 times more likely to be affected, respectively.1 Dachshunds made up 48% of this study population and 72% of another large study population (654 dogs with thoracolumbar IVDD).1,42 The second study found that poodles and Pekingese accounted for 10.6% and 5.4% of affected dogs, respectively.42 Another report found that dachshunds, cocker spaniels, Pekingese, and beagles accounted for 60.3%, 7.3%, 4.7%, and 3.1% of all cases of IVDD, respectively.43 Chondrodystrophoid dogs are most commonly affected between the ages of 4 and 6 years, whereas nonchondrodystrophoid dogs are generally affected between 6 and 8 years of age.1,5,42 Some studies suggest a slight male predisposition.1,44

    As the most susceptible breed, dachshunds have been studied to identify predisposing factors.36,42,45-47 Pedigree analysis suggests that IVDD in dachshunds is inherited in an autosomal polygenic manner that may be related to haircoat type.45 Body weight, body condition score, and various body dimensions do not seem to affect intervertebral disk calcification.48 Shorter vertebral column length (as measured from T1 to S1) and a shorter distance from the tuber calcaneus to the midpatellar tendon do appear to predispose to acute intervertebral disk herniation.36 In addition, longer vertebral column lengths, taller height at the withers, and decreased pelvic circumference were associated with more severe myelopathy.36 When dachshunds were compared with German shepherds, dachshunds were found to have an increased ratio of spinal cord height to vertebral canal height in the lumbar region and a spinal cord that terminates further caudally—differences that could leave less room within the vertebral canal to accommodate disk herniation.36,47

    Disk Degeneration

    Chondroid metaplasia is a predictable, degenerative change in the disks of chondrodystrophoid dogs younger than 2 years5,22,46 (FIGURE 3). This process begins shortly after birth and may be caused by early chondrocyte senescence within the nucleus pulposus, leading to nuclear calcification, disk dehydration, and increased keratan sulfate content relative to chondroitin sulfate content.21,22,48,49 The affected nucleus in turn has abnormal biomechanical properties that may allow annular tearing when torsion and compression are applied to the disk.5,50 In some dogs, the annulus is weakened sufficiently to permit disk herniation. Although chondroid metaplasia is most often associated with disk extrusion, protrusion and bulge are also possible.5

    Fibroid metaplasia is a degenerative change in the disks of older dogs that may be a pathologic response to chronic torsion.5,51 Repetitive microtrauma likely leads to fissures in the annulus fibrosus, altered disk biomechanics, and secondary fibroid metaplasia of the nucleus pulposus.5,51,52 Fibroid metaplasia of the nucleus is histologically characterized by fibrous tissue deposition, disk dehydration, and increased keratan sulfate content relative to chondroitin sulfate content.5,22,52,53 As with disk degeneration in chondrodystrophoid dogs, fibroid degenerated disks may become calcified.5,52

    Disk Herniation

    Disk herniation typically occurs within two disk spaces of the thoracolumbar junction (T13-L1).5,6,40,42,54-61 The spaces between T1-T2 and T9-T10 are seldom affected, probably due to the relative lack of mobility cranial to T10 and the presence of the intercapital ligament.5,34,35,52,62 Herniation usually occurs in a dorsolateral orientation, likely influenced by the presence of the dorsal longitudinal ligament on midline and the decreased width of the annulus dorsally; the ventral aspect of the annulus fibrosus is approximately twice as thick as the dorsal aspect.5,63,64 Young adult chondrodystrophoid dogs are most likely to be affected by disk extrusion (FIGURE 4), whereas older, large-breed dogs are more susceptible to disk protrusion and bulge.5,6,40,42,54-61 Disk herniation in large dogs is most common at the L1-L2 disk space, whereas small dogs tend to have involvement at the T12-T13 or T13-L1 disk spaces.6,40-42,54-61,63 Disk extrusion is usually acute in onset, whereas disk protrusion and bulge are usually chronic.2,5

    Disk extrusion (Hansen's type I IVDD) is defined as complete rupture of the annulus fibrosus with translocation of the nucleus pulposus into the vertebral canal.2,5,6 Complete rupture of the annulus fibrosus is probably caused by abnormal stresses associated with altered biomechanical properties of the nucleus pulposus.5,50,65 Disk extrusion is often associated with chondroid metaplasia.5 The extruded nucleus usually lies in the adjacent epidural space but may also migrate cranially, caudally, or dorsally.5,6 Disk extrusions can lead directly to spinal cord compression and may cause laceration of the ventral vertebral venous sinuses with epidural hemorrhage, compression of the ventral spinal artery with spinal cord ischemia, and fibrocartilaginous embolic myelopathy.66-68 Rarely, the nucleus extrudes into the spinal cord or causes high-velocity concussion.69

    Disk protrusion (Hansen's type II IVDD) is caused by rupture of the inner layers of the annulus fibrosus, partial displacement of the nucleus into the disrupted annulus, and annular hypertrophy.5 Clinical disk protrusion usually leads to chronic spinal cord compression. Spondylosis deformans, a noninflammatory osteophytic reaction associated with the cartilaginous joints of the vertebral column, may be spatially related to sites of disk protrusion, but no link has been demonstrated between spondylosis and disk extrusion.70,71 The putative association between spondylosis deformans and disk protrusion may reflect similar predisposing factors, such as vertebral column biomechanical abnormalities and resulting annular tears.70

    Disk bulge is poorly defined in veterinary medicine and is often equated with disk protrusion. However, although these forms of disk herniation may have a shared pathogenesis, they are distinct entities.6 Disk bulge is defined as symmetric hypertrophy of the annulus fibrosus, probably in response to injury of the annulus and microscopic instability.6,51 Such injury may be associated with nuclear degeneration leading to altered vertebral column biomechanics.5,65

    Intravertebral disk herniation (Schmorl's nodes) is a rare manifestation of disk herniation that may be attributable to weakening of the cartilaginous end plate or of the subchondral trabeculae of the vertebral body.72 Abnormal axial loading causes nuclear material to herniate through the cartilaginous end plate without annular degeneration.11,73 Back pain is the most consistent clinical finding in dogs, with radiography and magnetic resonance imaging demonstrating defects just beneath the cartilaginous end plate.72,74 In one report, three of five affected dogs were German shepherds younger than 4 years.72

    Acute Spinal Cord Injury

     Acute spinal cord injury is usually divided into primary and secondary events. Primary injury refers to the initial mechanical insult to the spinal cord and associated vascular structures. Primary injury can involve compression, concussion, contusion, or laceration.75,76 Compression occurs when adjacent structures exert pressure on the spinal cord.32 Concussion results from abrupt acceleration and deceleration of the spinal cord in response to trauma and may involve temporary axonal impairment.77 More severe trauma may result in contusion, which is defined as a loss of vascular integrity resulting in hemorrhage into the spinal cord parenchyma and meninges.77 Laceration occurs when the spinal cord is physically torn or disrupted.77 Disk extrusion can cause primary injury by each of these mechanisms, although laceration is rare.6,58,69,77–79 The severity of the injury is thought to correspond to the rate of extrusion, amount of disk material extruded, and duration of compression; the amount of material extruded is not necessarily proportional to the severity of the injury.6,60,80–82

    Primary injury results in a cascade of events that initially affect the spinal cord gray matter.76,83,84 Secondary injury results in neuronal cell death by necrosis and apoptosis. Necrosis typically occurs shortly after the primary injury, whereas apoptosis can occur for weeks following the injury.85 Secondary injury can involve many interconnected systemic, local, and cellular mechanisms.75,83,86 Systemic mechanisms include arterial hypotension and hypoxemia.83,87 Local mechanisms include loss of autoregulation of spinal cord circulation, ischemia, vasogenic edema, neurotransmitter release, oxidative injury, release of matrix-degrading enzymes, loss of neurotrophic factor support, and inflammation.76,83,86,88–93 Cellular mechanisms include ionic derangements, altered membrane permeability, and loss of energy metabolism.


    About 5% to 10% of dogs with severe spinal cord injury (absent nociception) may develop myelomalacia—gross softening of the spinal cord resulting from hemorrhagic necrosis.5,58,60,77 Myelomalacia may ascend and descend through the spinal cord parenchyma and is believed to result from secondary spinal cord injury.5,58,77,94 Dogs with a lesion initially involving the T3–L3 spinal cord segments that develop myelomalacia may have decreased pelvic limb reflexes, anal and urethral sphincter hypotonia, cranial migration of panniculus reflex, flaccid abdominal muscles, and ultimately flaccid forelimb paralysis and respiratory arrest.2,58 The prognosis is grave, and there is no known treatment. It is not known how many dogs with focal myelomalacia develop ascending and descending myelomalacia.2,5,95,96

    Spinal Shock

    Spinal shock consists of temporary hypotonia and hyporeflexia caudal to a severe spinal cord injury; such decreases in reflexes are not caused by lower motor neuron injury.97 Spinal shock may be caused by an acute disruption of upper motor neuron facilitatory input to lower motor neurons.97 In dogs with experimentally induced spinal cord injury, some reflexes may return in minutes (patellar), whereas others may take hours (flexor withdrawal).97,98 With time, adaptations such as altered excitatory neurotransmitter levels and receptor modifications often restore function in lower motor neurons caudal to the injury.97,98 The exact time course of spinal shock and the return of reflexes in clinical cases of disk herniation remain unknown.

    Chronic Spinal Chord Injury

    Disk herniation may result in chronic spinal cord compression.5,86,99–101 Although the increased pressure is thought to be distributed throughout the cross-sectional area of the cord, dogs with compressive lesions can have asymmetric clinical signs.86,102 Interestingly, the lateralization of the clinical signs does not necessarily coincide with the source or side of compression.102 Chronic spinal cord compression results in gliosis, demyelination, perivenous fibrosis, loss of cells in the gray matter, vasogenic edema, and permanent axonal loss.77,86,103,104 Decreased expression of neurotrophic factors in chronic spinal cord compression is probably an important cause of neuronal loss by apoptosis.105 Histopathologic analysis reveals degeneration of descending upper motor neuron fibers caudal to the lesion and ascending proprioceptive fibers cranial to the compressive lesion (Wallerian degeneration).106,107 The oxytocin content of cerebrospinal fluid is increased in dogs with chronic spinal cord compression and may be involved in pain modulation.108

    In both the acute and chronic settings, the fiber diameter of the white matter dictates the progression of spinal cord injury.2,86,99 The variable susceptibility to injury in the white matter may be explained by the law of Laplace, which states that wall tension is directly related to pressure and radius.99,109 Thus, larger myelinated fibers under pressure would be expected to sustain more severe injury due to increased cell membrane tension. Conversely, small, unmyelinated fibers that carry nociceptive information to the brain are relatively resistant to injury.84,99,109,110 Loss of deep nociceptive fibers indicates severe spinal cord injury.2,58,60,63,110,111

    Clinical Signs

    Paraspinal hyperesthesia is the earliest and most consistent clinical sign of thoracolumbar disk herniation.38,82 Progressive spinal cord dysfunction may occur and usually results in overlapping development of clinical signs. Pelvic limb proprioceptive ataxia is also seen early, followed by ambulatory paraparesis (pelvic limb weakness). Later clinical signs include nonambulatory paraparesis, urinary retention, fecal incontinence, paraplegia, and loss of nociception progressing from superficial to deep structures.38,40,41,58,60,61,63,82,100,110,112–114 This process can take minutes to months.2

    Neurologic Findings

    With few exceptions (e.g., myelomalacia, Schiff-Sherrington posture), neurologic examination reveals abnormalities limited to the pelvic limbs.2 Gait analysis may show general proprioceptive ataxia, alterations in stride length (elongated with upper motor neuron involvement, shortened with lower motor neuron involvement), paraparesis, and paraplegia.115 The presence of motor function in a nonambulatory dog should be evaluated by supporting the dog’s weight in the tail or inguinal region and walking the dog on a leash while observing for purposeful pelvic limb movement.110 It is important to evaluate the dog on a surface that provides good traction, such as grass or concrete. Postural reactions (knuckling, hopping, hemi-walking) are decreased or absent in dogs with paraparesis and paraplegia.110,115

    Pelvic limb myotatic reflexes may be normal, increased, or decreased.58,94,97,98,110 Lesions causing dysfunction of the T3–L3 segments are usually associated with normal to increased pelvic limb reflexes.110 Lesions causing dysfunction of segments L4 to S2 are usually associated with decreased pelvic limb reflexes.110 Spinal shock may complicate differentiation between T3–L3 and L4–S2 lesions. Depression of the patellar reflex in clinically normal geriatric dogs can also complicate neuroanatomic localization of spinal cord injury.116 Patellar hyporeflexia in older dogs with myelopathy must be interpreted with caution, as a subset of these patients may not have a true lesion in the L4–L6 segments.

    The cutaneous trunci (panniculus) reflex may be weak or absent in some dogs with thoracolumbar disk herniation.110,115 This reflex can be assessed by using hemostats to lightly pinch the skin of the dorsal trunk, cranial to the wings of the ilia, on each side of the midline110,115; in healthy dogs, this produces ipsilateral “twitching” of the skin by the cutaneous trunci muscles.110,115 The afferent limb of the reflex involves the dorsal cutaneous branches of the spinal nerves. Ascending fibers course bilaterally through the fasciculus proprius to the C8–T1 cord segments, where they synapse on lower motor neurons of the lateral thoracic nerve (efferent limb), which innervates the cutaneous trunci muscle. Loss of the cutaneous trunci reflex in an animal with T3–L3 myelopathy usually implies a lesion located one or two vertebrae cranial to the cutoff point.110,115

    The crossed-extensor reflex occurs with upper motor neuron lesions due to decreased descending inhibitory input to lower motor neurons.98,117 The measurable outcome is extension of the limb ipsilateral to the lesion after flexor withdrawal is performed on the contralateral limb.110,115,117 This reflex must be carefully distinguished from the dog’s attempt to escape the noxious stimulus applied to initiate the withdrawal reflex.

    A common mistake in the assessment of spinal cord injury is to confuse the withdrawal reflex with nociception. The withdrawal reflex can localize a lesion.2,110,115 A decreased withdrawal reflex can localize the lesion to either central (L4–S2) or peripheral lower motor neuron disease but provides no specific prognostic information.2,63,110,115 This reflex may remain intact in dogs with a spinal cord that is completely severed between the T3 and L3 spinal cord segments.98,110

    Nociception can be confirmed only by observing a brain-mediated response to a painful stimulus.2,110,115 This may be behavioral (biting, vocalizing, panting) or physiologic (increased heart rate, mydriasis). In dogs with spinal cord disease, nociception can help to evaluate lesion severity.110 Many clinicians differentiate between deep and superficial nociception.110 Superficial nociception is tested by pinching the skin with fingers or forceps. Deep nociception is tested by applying heavy pressure with forceps to bones of the digits or tail.58,60 Deep nociception depends on a network of small-diameter, bilateral, multisynaptic fibers that are relatively resistant to injury.3,118,119

    Dogs with severe T3–L3 myelopathy may adopt the Schiff-Sherrington posture: increased thoracic limb extensor tone with normal thoracic limb postural reactions. Damage to border cells or their ascending projections within the fasciculus proprius results in disinhibition of thoracic limb extensor motor neurons.110 Pelvic limb reflexes are classically decreased (which may relate to spinal shock) but may be normal or increased.75,110

    Traditionally, modified Frankel spinal cord injury scores (BOX 1) have been used in veterinary medicine to assess the extent of myelopathy.120 A number of different schemes have been employed.36,54,59,61,74,92,110,111,121,122 A more specific functional scoring system was proposed to facilitate clinical outcome trials in ambulatory dogs with pelvic limb dysfunction caused by acute spinal cord injuries.123,124 This 14-point scale compared favorably with a visual analog scale in terms of intraobserver and interobserver variability in gait evaluation. These scores can be used to characterize therapeutic outcomes and compare studies in the future.123

    Emergency Medical Therapy

    The goal of emergency therapy is to improve the likelihood of recovery by subsequent surgical or nonsurgical means. Severely affected (nonambulatory) or rapidly deteriorating dogs should be regarded as surgical emergencies because their prognosis worsens as clinical signs progress.2,41,55,55,58,60,63,74,113,125 Because ischemia and hypoxia are important pathophysiologic mediators of spinal cord injury, intravenous (IV) fluid replacement should be implemented.83,87 Physical examination, packed cell volume, and total protein levels are unreliable indicators of hydration, so it is prudent to apply 1.5 to 2 times maintenance fluid rates.126 Appropriate analgesia should be administered as well.127 Catheterization or expression can be used to relieve urine retention and bladder distention.128,129 Surgical candidates should be closely monitored for progression of clinical signs.

    In practices that do not perform spinal surgery, it is crucial to determine whether the case should be referred to a surgical facility. Surgery is advisable in dogs with progressive, nonresponsive, or severe clinical signs such as nonambulatory paraparesis. Conservative management is usually reserved for cases with recent-onset mild myelopathy or paraspinal hyperesthesia.94,130–134 When the clinician is in doubt, the dog should be reevaluated and monitored at the surgical facility. The sooner a nonambulatory dog is admitted to a surgical facility, the better.2,41,55,56,58,60,63,74,113,125

    High-Dose Methylprednisolone

    Therapy with high-dose methylprednisolone sodium succinate (MPSS) is widely used to treat acute spinal cord injury. MPSS is thought to be integrated into cell membranes, decreasing lipid peroxidation through a nongenomic mechanism of action.135–140 Its use in humans is controversial, appearing to yield little benefit and sometimes producing serious side effects.135,141–150 Evidence supporting its use in dogs with intervertebral disk herniation is likewise lacking. Several retrospective studies found no significant benefit from MPSS in this setting.63,151,152 Spinal cord injury models in dogs, cats, and rats have produced inconsistent and inconclusive histopathologic and functional results.99,153,155


    Dexamethasone is also widely used in the treatment of canine thoracolumbar intervertebral disk herniation despite a similar lack of supporting data.59,61,63,83,113,152,156,157 MPSS was reported to be superior to dexamethasone in promoting functional and histopathologic outcomes in one rat model of spinal cord injury.155 A rodent model of gradual spinal cord compression over 7 days demonstrated improved motor function in rats treated with high- and low-dose dexamethasone compared with nontreated rats; mortality was higher in the high-dose group.157


    The complications of high-dose corticosteroid therapy are well known. Studies have shown that 33% of dogs treated with high-dose prednisolone had gastrointestinal (GI) side effects and that nine of 10 healthy dogs treated with high-dose MPSS had severe gastric hemorrhage.158,159 Dachshunds treated with MPSS were more likely to have GI side effects, required more GI protectant drugs, and had an increased cost of hospitalization.151 Most GI side effects are not life threatening, but increased rates of sepsis and pneumonia have been linked to MPSS.147,151 Colonic perforation is a life-threatening side effect reported in a few dogs treated with dexamethasone.160,161

    Other Therapies

    21-Aminosteroid compounds such as tirilazad inhibit lipid peroxidation and may be beneficial in minimizing secondary spinal cord injury. An advantage of these compounds is that they do not have many of the side effects of high-dose corticosteroids.135 Nonetheless, a clear demonstration of therapeutic benefit is lacking.99,135 Other pharmacologic options include IV surfactants, which may seal cell membrane defects and thereby repair spinal axons.162 Dogs with acute disk herniation treated with two surfactants, polyethylene glycol and poloxamer 188, exhibited no adverse drug effects and recovered spinal cord function faster than historical controls. Other medications have been tried (e.g., dimethyl sulfoxide, solcoseryl, mannitol, naloxone, crocetin, thyrotropin-releasing hormone), but none has shown clinical efficacy in dogs; mannitol has had harmful effects in a feline model of acute spinal cord injury.154,156

    Read the companion article: Canine Thoracolumbar Intervertebral Disk Disease: Diagnosis, Prognosis, and Treatment

    Downloadable PDF

    1. Priester WA. Canine intervertebral disc disease—occurrence by age, breed, and sex among 8117 cases. Theriogenology 1976;6(2-3):293-303.

    2. Dewey CW. A Practical Guide to Canine and Feline Neurology. Ames: Iowa State University Press; 2003.

    3. Evans HE. Miller’s Anatomy of the Dog. 4th ed. Philadelphia: WB Saunders; 1993.

    4. Bray JP, Burbidge HM. The canine intervertebral disk, part 1: structure and function. JAAHA 1998;34:55-63.

    5. Hansen HJ. A pathologic-anatomical study on disk degeneration in the dog, with special reference to the so-called enchondrosis intervertebralis. Acta Orthop Scand Suppl 1952;11:1-117.

    6. Besalti O, Pekcan Z, Sirin YS, et al. Magnetic resonance imaging findings in dogs with thoracolumbar intervertebral disk disease: 69 cases. JAVMA 2006;228(6):902-908.

    7. Dyce KM, Sack WO, Wensing CJG. Textbook of Veterinary Anatomy. 2nd ed. Philadelphia: WB Saunders; 1996:40.

    8. Dallman MJ, Moon ML, Giovannitti-Jensen A. Comparison of the width of the intervertebral disc space and radiographic changes before and after intervertebral disc fenestration in dogs. Am J Vet Res 1991;52(1):140-145.

    9. Sadler TW. Langman’s Medical Embryology. 9th ed. Philadelphia: Lippincott Williams & Wilkins; 2004:193-194.

    10. Inoue H. Three-dimensional architecture of lumbar intervertebral discs. Spine 1981;6(2):139-146.

    11. Ghosh P, Bushell GR, Taylor TKF, et al. Collagens, elastin and noncollagenous protein of the intervertebral disk. Clin Orthop Relat Res 1977;129:124-132.

    12. Marchand F, Ahmed AM. Investigation of the laminate structure of lumbar disc annulus fibrosus. Spine 1990;15(5):402-410.

    13. Evans HE. Miller’s Anatomy of the Dog. 4th ed. Philadelphia: WB Saunders; 1993.

    14. Willenegger S, Friess AE, Lang J, et al. Immunohistochemical demonstration of lumbar intervertebral disc innervation in the dog. Anat Histol Embryol 2005;34(2):123-128.

    15. Adams MA, Roughley PJ. What is intervertebral disc degeneration, and what causes it? Spine 2006;31(18):2151-2161.

    16. Ozawa T, Ohtori S, Inoue G, et al. The degenerated lumbar intervertebral disc is innervated primarily by peptide-containing sensory nerve fibers in humans. Spine 2006;31(21):2418-2422.

    17. Hendry NG. The hydration of the nucleus pulposus and its relation to intervertebral disk derangement. J Bone Joint Surg 1958;40-B(1):132-144.

    18. Hunter CJ, Matyas JR, Duncan NA. The functional significance of cell clusters in the notochordal nucleus pulposus: survival and signaling in the canine intervertebral disc. Spine 2004;29(10):1099-1104.

    19. Erwin WM, Inman RD. Notochord cells regulate intervertebral disc chondrocyte proteoglycan production and cell proliferation. Spine 2006;31(10):1094-1099.

    20. Cappello R, Bird JLE, Pfeiffer D, et al. Notochordal cells produce and assemble extracellular matrix in a distinct manner, which may be responsible for the maintenance of healthy nucleus pulposus. Spine 2006;31(8):873-882.

    21. Ghosh P, Taylor TKF, Braund KG, et al. The collagenous and non-collagenous protein of the canine intervertebral disc and their variation with age, spinal level and breed. Gerontology 1976;22(3):124-134.

    22. Ghosh P, Taylor TKF, Braund KG, et al. A comparative chemical and histochemical study of the chondrodystrophoid and nonchondrodystrophoid canine intervertebral disc. Vet Pathol 1976;13(6):414-427.

    23. Urban JPG, Holm S, Maroudas A, et al. Nutrition of the intervertebral disk. An in vivo study of solute transport. Clin Orthop 1977;129:101-114.

    24. Crock HV, Goldwasser M. Anatomic studies of the circulation in the region of the vertebral end-plate of adult greyhounds. Spine 1984;9(7):702-706.

    25. Benneker LM, Heini PF, Alini M, et al. Vertebral endplate marrow contact channel occlusions and intervertebral disc degeneration. Spine 2004;30(2):167-173.

    26. Urban JP, Smith S, Fairbank JCT. Nutrition of the intervertebral disc. Spine 2004;29(23):2700-2709.

    27. Rajasekaran S, Babu JN, Arun R, et al. A study of diffusion in human lumbar discs: a serial magnetic resonance imaging study documenting the influence of the endplate on diffusion in normal and degenerate discs. Spine 2004;29(23):2654-2667.

    28. Corse MR, Renberg WC, Friis EA. In vitro evaluation of biomechanical effects of multiple hemilaminectomies on the canine lumbar vertebral column. Am J Vet Res 2003;64(9):1139-1145.

    29. Hill TP, Lubbe AM, Guthrie AJ. Lumbar spine stability following hemilaminectomy, pediculectomy, and fenestration. Vet Comp Orthop Traumatol 2000;13(4):165-171.

    30. Werner T, McNicholas WT, Kim J, et al. Aplastic articular facets in a dog with intervertebral disk rupture of the 12th to 13th thoracic vertebral space. JAAHA 2004;40(6):490-494.

    31. White AA, Panjabi MM. Clinical Biomechanics of the Spine. Philadelphia: JB Lippincott; 1978.

    32. Dorland’s Medical Dictionary. 25th ed. Philadelphia: WB Saunders; 1995.

    33. Smith GK, Walter MC.: Spinal decompressive procedures and dorsal compartment injuries: comparative biomechanical study in canine cadavers. Am J Vet Res 1988;49(2):266-273.

    34. Liptak JM, Watt PR, Thomson MJ, et al. Hansen type I disk disease at T1-2 in a dachshund. Aust Vet J1999;77(3):156-159.

    35. Wilkens BE, Selcer R, Adams WH, et al. T9-T10 intervertebral disc herniation in three dogs. Vet Comp Orthop Traumatol1996;9(4):177-178.

    36. Levine JM, Levine GJ, Kerwin SC, et al. Association between various physical factors and acute thoracolumbar intervertebral disk extrusion or protrusion in dachshunds. JAVMA 2006;229(3):370-375.

    37. Braund KG, Taylor TKF, Ghosh P, et al. Spinal mobility in the dog. A study in chondrodystrophoid and non-chondrodystrophoid animals. Res Vet Sci 1977;22(1):78-82.

    38. Ferreira AJA, Correia JHD, Jaggy A. Thoracolumbar disc disease in 71 paraplegic dogs: influence of rate of onset and duration of clinical signs on treatment results. J Small Anim Pract 2002;43(4):158-163.

    39. Gage ED. Modifications in dorsolateral hemilaminectomy and disc fenestration in the dog. JAAHA 1975;11:407-411.

    40. Mayhew PD, McLear RC, Ziemer LS, et al. Risk factors for recurrence of clinical signs associated with thoracolumbar intervertebral disk herniation in dogs: 229 cases (1994-2000). JAVMA 2004;225(8):1231-1236.

    41. Cudia SP, Duval JM. Thoracolumbar intervertebral disk disease in large, nonchondrodystrophic dogs: a retrospective study. JAAHA 1997;33(5):456-460.

    42. Gage ED. Incidence of clinical disc disease in the dog. JAAHA1975;11:135-138.

    43. Goggin JE, Franti CE. Canine intervertebral disk disease: characterization by age, sex, breed and anatomic site of involvement. Am J Vet Res 1970;31(9):1687-1692.

    44. Brown NO, Helphrey ML, Prata RG. Thoracolumbar disc disease in the dog: a retrospective analysis of 187 cases. JAAHA 1977;13:665-672.

    45. Ball MU, McGuire JA, Swaim SF, et al. Patterns of occurrence of disk disease among registered dachshunds. JAVMA 1982;180(5):519-522.

    46. Jensen VF, Arnbjerg J. Development of intervertebral disk calcification in the dachshund: a prospective longitudinal radiographic study. JAAHA 2001;37(3):274-282.

    47. Morgan JP, Atilola M, Bailey CS. Vertebral canal and spinal cord mensuration: a comparative study of its effect on lumbosacral myelography in the dachshund and German shepherd dog. JAVMA 1987;191(8):951-957.

    48. Jensen VF, Ersboll AK. Mechanical factors affecting the occurrence of intervertebral disc calcification in the dachshund—a population study. J Vet Med A Physiol Path Clin Med 2000;47(5):283-296.

    49. Ghosh P, Taylor TK, Braund KG. The variation of the glycosaminoglycans of the canine intervertebral disc with ageing. I. Chondrodystrophoid breed. Gerontology 1977;23(2):87-98.

    50. Keller TS, Holm SH, Hansson TH, et al. The dependence of intervertebral disc mechanical properties on physiologic conditions. Spine 1990;15(8):751-761.

    51. Farfan HF, Cossette JW, Robertson GH, et al. The effects of torsion on the lumbar intervertebral joints: the role of torsion in the production of disc degeneration. J Bone Joint Surg 1970;52-A(3):468-497.

    52. Bray JP, Burbidge HM. The canine intervertebral disk, part 2: degenerative changes—nonchondrodystrophoid versus chondrodystrophoid disks. JAAHA 1998;34:135-144.

    53. Ghosh P, Taylor TK, Braund KG. Variation of the glycosaminoglycans of the intervertebral disc with ageing. II. Non-chondrodystrophoid breed. Gerontology 1977;23(2):99-109.

    54. Besalti O, Ozak A, Pekcan Z, et al. The role of extruded disk material in thoracolumbar intervertebral disk disease: a retrospective study in 40 dogs. Can Vet J 2005;46(9):814-820.

    55. Ito D, Matsunaga S, Jeffery ND, et al. Prognostic value of magnetic resonance imaging in dogs with paraplegia caused by thoracolumbar intervertebral disk extrusion: 77 cases. JAVMA 2005;227(9):1454-1460.

    56. Lubbe AM, Kirberger RM, Verstraete FJM. Pediculectomy for thoracolumbar spinal decompression in the Dachshund. JAAHA 1994;30(3):233-238.

    57. McCartney W. Partial pediculectomy for the treatment of thoracolumbar disc disease. Vet Comp Orthop Traumatol 1997;10(2):117-121.

    58. Olby N, Levine J, Harris T, et al. Long-term functional outcome of dogs with severe injuries of the thoracolumbar spinal cord: 87 cases. JAVMA 2003;222(6):762-769.

    59. Schulman A, Lippincott CL. Dorsolateral hemilaminectomy in the treatment of thoracolumbar intervertebral disk disease in dogs. Compend Contin Educ Pract Vet 1987;9(3):305-310.

    60. 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(9):417-422.

    61. Yovich JC, Read R, Eger C. Modified lateral spinal decompression in 61 dogs with thoracolumbar disc protrusion. J Small Anim Pract 1994;35(7):351-356.

    62. Breit S. Osteological and morphometric observations on intervertebral joints in the canine pre-diaphragmatic thoracic spine (Th1-Th9). Vet J 2002;164:216-223.

    63. Ruddle TL, Allen DA, Schertel ER, et al. Outcome and prognostic factors in non-ambulatory Hansen Type I intervertebral disc extrusions: 308 cases. Vet Comp Orthop Traumatol 2006;19(1):29-34.

    64. Gordon SJ, Yang KH, Mayer PJ, et al. Mechanism of disc rupture: a preliminary report. Spine 1991;16(4):450-456.

    65. Adams MA, McNally DS, Dolan P. “Stress” distributions inside the intervertebral discs. J Bone Joint Surg 1996;78-B(6):965-972.

    66. Cauzinille L. Fibrocartilaginous embolism in dogs. Vet Clin North Am Small Anim Pract 2000;30(1):155-167.

    67. Griffiths IR. Spinal cord infarction due to emboli arising from the intervertebral disc in the dog. J Comp Pathol 1973;83:225-232.

    68. Hayes MA, Creighton SR, Boysen BG, et al. Acute necrotizing myelopathy from nucleus pulposus embolism in dogs with intervertebral disc degeneration. JAVMA 1978;173(3):289-295.

    69. Sanders SG, Bagley RS, Gavin PR. Intramedullary spinal cord damage associated with intervertebral disk material in a dog. JAVMA 2002;221(11):1594-1596.

    70. Levine GJ, Levine JM, Walker MA, et al. Evaluation of the association between spondylosis deformans and clinical signs of intervertebral disk disease in dogs: 172 cases (1999-2000). JAVMA 2006;228(1):96-100.

    71. Morgan JP, Ljunggren G, Read R. Spondylosis deformans (vertebral osteophytosis) in the dog. A radiographic study from England, Sweden and U.S.A. J Small Anim Pract 1967;8(2):57-66.

    72. Gaschen L, Lang J, Haeni H. Intravertebral disc herniation (Schmorl’s node) in five dogs. Vet Radiol Ultrasound 1995;36(6):509-516.

    73. Jayson MIV, Herbert CM, Barks JS. Intervertebral discs: nuclear morphology and bursting pressures. Ann Rheum Dis 1973;32(4): 308-315.

    74. Kazakos G, Polizopoulou ZS, Patsikas MN, et al. Duration and severity of clinical signs as prognostic indicators in 30 dogs with thoracolumbar disk disease after surgical decompression. J Vet Med A Physiol Pathol Clin Med 2005;52(3):147-152.

    75. Bergman R, Lanz O, Shell L. Acute spinal cord trauma: mechanisms and clinical syndromes. Vet Med 2000;95(11):846-850.

    76. McDonald JW, Sadowsky C. Spinal-cord injury. Lancet 2002;359: 417-425.

    77. Summers BA, Cummings JF, DeLahunta A. Veterinary Neuropathology. St. Louis: Mosby-Year Book; 1995.

    78. Liptak JM, Allan GS, Krockenberger MB, et al. Radiographic diagnosis: intramedullary extrusion of an intervertebral disc. Vet Radiol Ultrasound 2002;43(3):272-274.

    79. Martin RA, Shell L, Dodds WJ. Focal intramedullary spinal cord hematoma in a dog. JAAHA 1986;22:545-550.

    80. Carlson GD, Gorden CD, Oliff HS, et al. Sustained spinal cord compression: part I: time-dependent effect on long-term pathophysiology. J Bone Joint Surg 2003;85A:86-94.

    81. Anderson TE. Spinal cord contusion injury: experimental dissociation of hemorrhagic necrosis and subacute loss of axonal conduction. J Neurosurg1985;62(1):115-119.

    82. Sukhiani HR, Parent JM, Atilola MA, et al. Intervertebral disk disease in dogs with signs of back pain alone: 25 cases (1986-1993). JAVMA 1996;209(7):1275-1279.

    83. Olby NJ. Current concepts in the management of acute spinal cord injury. J Vet Intern Med 1999;13(5):399-407.

    84. Smith PM, Jeffery ND. Histological and ultrastructural analysis of white matter damage after naturally-occurring spinal cord injury. Brain Pathol 2006;16(2):99-109.

    85. Crowe MJ, Bresnahan JC, Shuman SL, et al. Apoptosis and delayed degeneration after spinal cord injury in rats and monkeys. Nat Med 1997;3(1):73-76.

    86. Kraus KH. The pathophysiology of spinal cord injury and its clinical implications. Semin Vet Med Surg (Small Anim) 1996;11(4):201-207.

    87. Vale FL, Burnes J, Jackson AB, et al. Combined medical and surgical treatment after acute spinal cord injury: results of a prospective pilot study to assess the merits of aggressive medical resuscitation and blood pressure management. Neurosurg Focus1999;6(1):Article 4.

    88. Nishisho T, Tonai T, Tamura Y, et al. Experimental and clinical studies of eicosanoids in cerebrospinal fluid after spinal cord injury. Neurosurgery 1996;39(5):950-957.

    89. Olby NJ, Sharp NJ, Munana KR, et al. Chronic and acute compressive spinal cord lesions in dogs due to intervertebral disc herniation are associated with elevation in lumbar cerebrospinal fluid glutamate concentration. J Neurotrauma 1999;16(12):1215-1224.

    90. Azbill RD, Mu X, Bruce-Keller AJ, et al. Impaired mitochondrial function, oxidative stress and altered antioxidant enzyme activities following traumatic spinal cord injury. Brain Res 1997;765(2):283-290.

    91. Brown SA, Hall ED. Role of oxygen-derived free radicals in the pathogenesis of shock and trauma, with focus on central nervous system injuries. JAVMA 1992;200(12):1849-1859.

    92. Levine JM, Ruaux CG, Bergman RL, et al. Matrix metalloproteinase-9 activity in the cerebrospinal fluid and serum of dogs with acute spinal cord trauma from intervertebral disk disease. Am J Vet Res 2006;67(2):283-287.

    93. Griffiths IR. Vasogenic edema following acute and chronic spinal cord compression in the dog. J Neurosurg 1975;42(2):155-165.

    94. Funkquist B. Thoraco-lumbar disk protrusion with severe cord compression in the dog. II. Clinical observations with special reference to the prognosis in conservative treatment. Acta Vet Scand 1962;3:317-343.

    95. Lu D, Lamb CR, Targett MP. Results of myelography in seven dogs with myelomalacia. Vet Radiol Ultrasound 2002;43(4):326-330.

    96. Platt SR, McConnell JF, Bestbier M. Magnetic resonance imaging characteristics of ascending hemorrhagic myelomalacia in a dog. Vet Radiol Ultrasound 2006;47(1):78-82.

    97. Smith PM, Jeffery ND. Spinal shock—comparative aspects and clinical relevance. J Vet Intern Med 2005;19(6):788-793.

    98. Blauch B. Spinal reflex walking in the dog. Vet Med Small Anim Clin 1977;72(2):169-173.

    99. 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(2):128-139.

    100. Hoerlein BF. Intervertebral disc protrusions in the dog. II. Symptomatology and clinical diagnosis. Am J Vet Res 1953;14(51):270-274.

    101. Moissonnier P, Meheust P, Carozzo C. Thoracolumbar lateral corpectomy for treatment of chronic disk herniation: technique description and use in 15 dogs. Vet Surg2004;33(6):620-628.

    102. Smith JD, Newell SM, Budsberg SC, et al. Incidence of contralateral versus ipsilateral neurological signs associated with lateralised Hansen type I disc extrusion. J Small Anim Pract 1997;38(11):495-497.

    103. Yamaura I, Yone K, Nakahara S, et al. Mechanism of destructive pathologic changes in the spinal cord under chronic mechanical compression. Spine 2002;27(1):21-26.

    104. Ikeda H, Ushio Y, Hayakawa T, et al. Edema and circulatory disturbance in the spinal cord compressed by epidural neoplasms in rabbits. J Neurosurg 1980;52(2):203-209.

    105. Kasahara K, Nakagawa T, Kubota T. Neuronal loss and expression of neurotrophic factors in a model of rat chronic compressive spinal cord injury. Spine 2006;31(18):2059-2066.

    106. Yovich JV, LeCouteur RA, Gould DH. Chronic cervical compressive myelopathy in horses: clinical correlations with spinal cord alterations. Aust Vet J 1991;68(10):326-334.

    107. Tator CH, Schmoll B, Rivlin AS, et al. Effect of acute spinal cord injury on axonal counts in the pyramidal tract of rats. J Neurosurg 1984;61(1):118-123.

    108. Brown DC, Perkowski S. Oxytocin content of the cerebrospinal fluid of dogs and its relationship to pain induced by spinal cord compression. Vet Surg 1998;27(6):607-611.

    109. Stillwell GK. The Law of Laplace. Mayo Clin Proc 1973;48(12): 863-869.

    110. De Lahunta A. Veterinary Neuroanatomy and Clinical Neurology. 2nd ed. Philadelphia: WB Saunders; 1983.

    111. Scott HW. Hemilaminectomy for the treatment of thoracolumbar disc disease in the dog: a follow-up study of 40 cases. J Small Anim Pract 1997;38(11):488-494.

    112. Cerda-Gonzalez S, Olby NJ. Fecal incontinence associated with epidural spinal hematoma and intervertebral disk extrusion in a dog. JAVMA 2006;228(2):230-235.

    113. Anderson SM, Lippincott CL, Gill PJ. Hemilaminectomy in dogs without deep pain perception. Calif Vet 1991;45:24-28.

    114. Chen AV, Bagley RS, West CL, et al. Fecal incontinence and spinal cord abnormalities in seven dogs. JAVMA 2005;227(12):1945-1951.

    115. Bagley RS. Fundamentals of Veterinary Clinical Neurology. 1st ed. Ames, Iowa: Blackwell; 2005.

    116. Levine JM, Hillman RB, Erb HN, et al. The influence of age on patellar reflex response in the dog. J Vet Intern Med 2002;16(3):244-246.

    117. Aggelopoulos NC, Burton MJ, Clarke RW, et al. Characterization of a descending system that enables crossed group II inhibitory reflex pathways in the cat spinal cord. J Neuroscience 1996;16(2):723-729.

    118. Casey KL, Morrow TJ. Supraspinal nocifensive responses of cats: spinal cord pathways, monoamines, and modulation. J Comp Neurol 1988;270(4):591-605.

    119. Lorenz MD, Kornegay JN. Handbook of Veterinary Neurology. 4th ed. St Louis: WB Saunders; 2004.

    120. Frankel HL, Hancock DO, Hyslop G, et al. The value of postural reduction in the initial management of closed injuries of the spine with paraplegia and tetraplegia. Paraplegia 1969;7(3):179-192.

    121. Muir P, Johnson KA, Manley PA, et al. Comparison of hemilaminectomy and dorsal laminectomy for thoracolumbar intervertebral disc extrusion in dachshunds. J Small Anim Pract 1995;36(8):360-367.

    122. Tartarelli CL, Baroni M, Borghi M. Thoracolumbar disc extrusion associated with extensive epidural haemorrhage: a retrospective study of 23 dogs. J Small Anim Pract2005;46(10):485-490.

    123. Olby NJ, De Risio L, Munana KR, et al. Development of a functional scoring system in dogs with acute spinal cord injuries. Am J Vet Res2001;62(10):1624-1628.

    124. Olby N, Harris T, Burr J, et al. Recovery of pelvic limb function in dogs following acute intervertebral disc herniations. J Neurotrauma 2004;21(1):49-59.

    125. Coates JR. Intervertebral disk disease. Vet Clin North Am Small Anim Pract 2000;30(1):77-110.

    126. Hansen B, DeFrancesco T. Relationship between hydration estimate and body weight change after fluid therapy in critically ill dogs and cats. J Vet Emerg Crit Care 2002;12(4):235-243.

    127. Hansen BD. Analgesia and sedation in the critically ill. J Vet Emerg Crit Care 2005;15(4):285-294.

    128. Atalan G, Parkinson TJ, Barr FJ, et al. Urine volume estimations in dogs recovering from intervertebral disc prolapse surgery. Berl Munch Tierarztl Wochenschr 2002;115(7-8):303-305.

    129. Stiffler KS, Stevenson MA, Sanchez S, et al. Prevalence and characterization of urinary tract infections in dogs with surgically treated type 1 thoracolumbar intervertebral disc extrusion. Vet Surg 2006;35(4):330-336.

    130. Funkquist B. Decompressive laminectomy in thoraco-lumbar disc protrusion with paraplegia in the dog. J Small Anim Pract 1970;11(7):445-451.

    131. Hoerlein BF. Further evaluation of the treatment of disc protrusion paraplegia in the dog. JAVMA 1956;129(11):495-502.

    132. Janssens LA, De Prins EM. Treatment of thoracolumbar disk disease in dogs by means of acupuncture: a comparison of two techniques. JAAHA 1989;25(2):169-174.

    133. Scavelli TD, Schoen A. Problems and complications associated with the nonsurgical management of intervertebral disc disease. Probl Vet Med 1989;1(3):402-414.

    134. Wilcox KR. Conservative treatment of thoracolumbar intervertebral disc disease in the dog. JAVMA 1965;147(12):1458-1460.

    135. Bracken MB, Shepard MJ, Holford TR, et al. Administration of methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treatment of acute spinal cord injury. Results of the Third National Acute Spinal Cord Injury Randomized Controlled Trial. National Acute Spinal Cord Injury Study. JAMA 1997;277(20):1597-1604.

    136. Hall ED. The neuroprotective pharmacology of methylprednisolone. J Neurosurg 1992;76(1):13-22.

    137. Hall ED. Importance of pharmacologic considerations in the evaluation of new treatments for acute spinal cord injury. J Neurotrauma 1992;9(2):173-176.

    138. Hall ED. Lipid antioxidants in acute central nervous system injury. Ann Emerg Med 1993;22(6):1022-1027.

    139. Hall ED, Braughler JM, McCall JM. Antioxidant effects in brain and spinal cord injury. J Neurotrauma 1992;2(suppl 1):S165-S172.

    140. Hall ED, Cox JW, Anderson DK, et al. Biochemistry and pharmacology of lipid antioxidants in acute brain and spinal cord injury. J Neurotrauma 1992;9(suppl 2):S425-S442.

    141. Bracken MB. Treatment of acute spinal cord injury with methylprednisolone: results of a multicenter, randomized clinical trial. J Neurotrauma 1991;8(suppl1):S47-S52.

    142. Bracken MB, Shepard MJ, Holford TR, et al. Methylprednisolone or tirilazad mesylate administration after acute spinal cord injury: 1-year follow up. Results of the third National Acute Spinal Cord Injury randomized controlled trial. J Neurosurg 1998;89(5):699-706.

    143. Bracken MB, Holford TR. Effects of timing of methylprednisolone or naloxone administration on recovery of segmental and long-tract neurological function in NASCIS 2. J Neurosurg 1993;79(4):500-507.

    144. Bracken MB, Holford TR. Neurological and functional status 1 year after acute spinal cord injury: estimates of functional recovery in National Acute Spinal Cord Injury Study II from results modeled in National Acute Spinal Cord Injury Study III. J Neurosurg 2002;96(3 suppl):259-266.

    145. Bracken MB, Shepard MJ, Collins WF, et al. Methylprednisolone or naloxone treatment after acute spinal cord injury: 1-year follow-up data. Results of the second National Acute Spinal Cord Injury Study. J Neurosurg 1992;76(1):23-31.

    146. Bracken MB, Shepard MJ, Collins WF, et al. A randomized controlled trial of methylprednisolone or naloxone in the treatment of acute spinal cord injury: Results of the Second National Acute Spinal Cord Injury Study. N Engl J Med 1990;322(20):1405-1411.

    147. Hurlbert RJ. Methylprednisolone for acute spinal cord injury: an inappropriate standard of care. J Neurosurg 2000;93(1 suppl):1-7.

    148. Short DJ, El Masry WS, Jones PW. High-dose methylprednisolone in the management of acute spinal cord injury: a systematic review from a clinical perspective. Spinal Cord 2000;38(5):273-286.

    149. Hurlbert RJ, Moulton R. Why do you prescribe methylprednisolone for acute spinal cord injury? A Canadian perspective and a position statement. Can J Neurol Sci 2002;29(3):236-239.

    150. Pollard ME, Apple DF. Factors associated with improved neurologic outcomes in patients with incomplete tetraplegia. Spine 2003;28(1):33-38.

    151. Boag AK, Otto CM, Drobatz KJ. Complications of methylprednisolone sodium succinate therapy in dachshunds with surgically treated intervertebral disc disease. J Vet Emerg Critical Care 2001;11(2):105-110.

    152. Davis GJ, 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(6):513-518.

    153. Faden AI, Jacobs TP, Patrick DH, et al. Megadose corticosteroid therapy following experimental traumatic spinal injury. J Neurosurg 1984;60(4):712-717.

    154. Hoerlein BF, Redding RW, Hoff EJ, et al. Evaluation of naloxone, crocetin, thyrotropin releasing hormone, methylprednisolone, partial myelotomy, and hemilaminectomy in the treatment of acute spinal cord trauma. JAAHA 1985;21(1):67-77.

    155. Sharma A, Tiwari R, Badhe P, et al. Comparison of methylprednisolone with dexamethasone in treatment of acute spinal injury in rats. Indian J Exp Biol 2004;42(5):476-480.

    156. Hoerlein BF, Redding RW, Hoff EJ, et al. Evaluation of dexamethasone, DMSO, mannitol, and solcoseryl in acute spinal cord trauma. JAAHA 1983;19:216-226.

    157. Delattre JY, Arbit E, Rosenblum MK, et al. High dose versus low dose dexamethasone in experimental epidural spinal cord compression. Neurosurgery1988;22(6 Pt 1):1005-1007.

    158. Culbert LA, Marino DJ, Baule RM, et al. Complications associated with high-dose prednisolone sodium succinate therapy in dogs with neurological injury. JAAHA 1998;34(2):129-134.

    159. Rohrer CR, Hill RC, Fischer A, et al. Gastric hemorrhage in dogs given high doses of methylprednisolone sodium succinate. Am J Vet Res 1999;60(8):977-981.

    160. Toombs JP, Caywood DD, Lipowitz AJ, et al. Colonic perforation following neurosurgical procedures and corticosteroid therapy in four dogs. JAVMA 1980;177(1):68-72.

    161. Toombs JP, Collins LG, Graves GM, et al. Colonic perforation in corticosteroid-treated dogs. JAVMA 1986;188(2):145-150.

    162. Laverty PH, Leskovar A, Breur GJ, et al. A preliminary study of intravenous surfactants in paraplegic dogs: polymer therapy in canine clinical SCI. J Neurotrauma 2004;21(12):1767-1777.

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