Canine Intervertebral Disk Herniation

Chapter 233


Canine Intervertebral Disk Herniation



Intervertebral disk herniation (IVDH) is the most common cause of spinal cord injury (SCI) in the dog, accounting for 2.3% of admissions to academic veterinary centers (Priester, 1976). The clinical signs associated with IVDH are numerous and reflect a combination of primary (biomechanical) injury to surrounding neuroparenchyma and secondary (biochemical) mechanisms. A basic understanding of the epidemiology and pathophysiology of this disease process is essential in making diagnostic and treatment recommendations.



Pathophysiology of Intervertebral Disk Disease


The intervertebral disk has three anatomic zones: the anulus fibrosus, nucleus pulposus, and cartilaginous end plate. The anulus fibrosus arises from mesenchymal cells and consists of overlapping lamellae, which are predominantly composed of type I collagen. These lamellae attach to the cartilaginous end plate and are capable of parallel motion during biomechanical loading. In some species, the outermost portions of the anulus are supplied by minute blood vessels and innervated by small, penetrating nerve fibers. The nucleus pulposus is centrally located, bounded by the anulus fibrosus, and contains an abundance of extracellular matrix. It arises from remnant notochordal and chondrocyte-like cells. These cell populations are responsible for the synthesis and maintenance of proteoglycans that bind extracellular water. The cartilaginous end plate serves as a connection between the bony end plate and anulus fibrosus. The hyaline cartilage that composes this structure has pores, which are essential in providing nutrition and removing waste materials from the largely avascular nucleus and anulus.



Intervertebral Disk Degeneration


Disk degeneration has been defined as structural failure of the intervertebral disk associated with abnormal or accelerated changes seen in aging (Adams and Roughley, 2006). Both mechanical and biochemical factors are responsible for disk degeneration. Mechanical degeneration results from chronic vertebral column loading, which leads to anular tearing with subsequent histologic changes in the nucleus and cartilaginous end plate. Biochemical degeneration results from either failure of nutrient delivery or premature senescence of remnant notochordal cells.


In veterinary medicine, disk degeneration traditionally is classified as chondroid or fibroid. This scheme probably is a vast oversimplification of complex, inherently interwoven processes. Chondroid metaplasia is primarily biochemical and is identified most commonly in young chondrodystrophoid dogs. Specifically, early notochordal cell senescence within the nucleus pulposus results in loss of proteoglycans, shifts in proteoglycan ratios, disk dehydration, and nuclear mineralization (Cappello et al, 2006). Fibroid metaplasia is identified frequently in older large-breed dogs and is believed to be principally the result of mechanical influences. The affected nucleus contains abundant fibrous tissue, has shifts in proteoglycan ratios, and is dehydrated; nuclear mineralization also has been recognized. A recent large-scale study suggested that disk degeneration in dogs and disk degeneration in humans bear critical similarities with reference to gross morphological changes, reductions in nuclear glycosaminoglycans, and increases in matrix metalloproteinases; histologic differences in degenerative patterns were not detected between chondrodystrophoid and nonchondrodystrophoid dogs (Bergknut et al, 2012).


It is important to note that disk degeneration may not result in clinically detectable signs. Clinical neurologic disease is believed to occur only when IVDH is present. Some individuals use the expression intervertebral disk disease as an umbrella term to refer to disk degeneration, subclinical IVDH, and clinical IVDH.



Intervertebral Disk Herniation


Intervertebral disk herniation is synonymous with the term intervertebral disk prolapse and refers to abnormal focal displacement of the intervertebral disk. Most frequently, displacement is dorsal or dorsolateral and impacts structures within the vertebral canal or intervertebral foramen. In dogs IVDH most often occurs in the setting of a previously degenerated disk. Traumatic IVDH has been reported and occurs when a supraphysiologic load is applied to the vertebral column. In such a case, it is possible for nondegenerate intervertebral disks to herniate. Disk herniation is classified as disk extrusion (Hansen’s type I disk herniation) or disk protrusion (Hansen’s type II disk herniation). Many investigators have ceased using Hansen’s terminology because these eponyms are specific to veterinary medicine and do not reflect pathologic mechanisms.


Disk extrusion is defined as rupture of the anulus fibrosus with displacement of the nucleus pulposus into the vertebral canal or intervertebral foramen. In dogs disk extrusion typically is an acute event and is associated with chondroid metaplasia. Disk extrusion can be subclassified as nondispersed, dispersed, sequestered, and noncompressive. Nondispersed disk extrusion is contiguous with the intervertebral disk space and extruded material does not extend significantly over vertebral bodies. Dispersed disk extrusion is more extensive and implies that herniated material extends beyond the limits of the vertebral articulation. Disk sequestration occurs when extruded material is no longer contiguous with the anulus fibrosus. Noncompressive disk extrusion results in minimal displacement of nervous system tissues, even in the setting of significant clinical signs.


Disk protrusion is defined as rupture of the inner layers of the anulus fibrosus, partial displacement of the nucleus into the disrupted anulus, and annular hypertrophy. It is associated most frequently with fibroid metaplasia and may result in slowly progressive clinical signs. Spatial relationships with spondylosis deformans may exist. Disk bulge is reported uncommonly in veterinary medicine and is technically not a form of IVDH (Fardon and Milette, 2001). It is defined as symmetric hypertrophy of the anulus fibrosus over greater than 50% of the disk circumference without nuclear displacement.



Spinal Cord Injury and Pathologic Features


Mechanisms of nervous system injury typically are described as primary and secondary. Primary injury refers to the initial mechanical insult delivered to tissues. Subcategories of primary injury may include compression, contusion, concussion, laceration, and traction. Secondary injuries occur following primary events and are biochemical in nature. Inflammation (innate and adaptive), oxidative stress, excitotoxicity, and vascular injury are just a few of the often overlapping processes involved in secondary injury.


Dogs with acute SCI resulting from IVDH typically have significant spinal cord compression and contusion. The pathologic lesions seen with IVDH involve white and gray matter (Smith and Jeffery, 2006). White matter involvement may predominate and usually is most obvious in the dorsolateral, lateral, and ventral portions of the spinal cord. Intraparenchymal hemorrhage, axonal fragmentation, and demyelination typically occur in combination. In some cases wedge-shaped, infarctlike lesions are located within the white matter. Within the gray matter, ischemic neuronal necrosis, hemorrhage, and neuronal chromatolysis have been recognized.


Limited data are available concerning the pathologic alterations seen with chronic SCI resulting from IVDH, especially in the setting of disk protrusion. At the site of compression there is typically axonal loss and demyelination in all white matter funiculi. Cranial and caudal to the compression, stereotypical loss of white matter tracts reflecting wallerian-like degeneration has been described.



Epidemiology and Clinical Signs


Dogs with IVDH typically are young to middle-aged males of chondrodystrophoid breeds. Dachshunds have been reported to represent 48% to 72% of affected animals and may have a lifetime incidence of IVDH that approaches 20% (Levine et al, 2011). In one study, 83.6% of dogs with IVDH had compression located in the thoracolumbar vertebral column, whereas 16.4% had lesions in the cervical vertebral column (Gage, 1975).


The clinical signs associated with IVDH are variable. In the cervical vertebral column, IVDH may result in hyperesthesia, root signature, tetraparesis, and general proprioceptive ataxia in all limbs. Severely affected dogs may be tetraplegic and require mechanical ventilation. Many dogs with cervical IVDH have hyperesthesia as their only clinical sign, perhaps because the ratio of vertebral canal diameter to spinal cord diameter is larger in the cervical region than in other vertebral column locations.


In dogs with thoracolumbar IVDH either the T3 to L3 or L4 to S3 spinal cord can be involved. Animals may have hyperesthesia, paraparesis or paraplegia, pelvic limb general proprioceptive ataxia, urinary voiding disability, fecal incontinence, and loss of pelvic limb nociception. Animals with acute IVDH localized to T3 to L3 may have Schiff-Sherrington syndrome. In some instances of acute IVDH, spinal shock can occur. Spinal shock results from interruption of corticospinal tracts and is manifest as a transient loss of pelvic limb spinal reflexes in the setting of an upper motor neuron lesion (Smith and Jeffery, 2005). About 5% to 10% of dogs with IVDH that lack pelvic limb deep nociception develop ascending-descending myelomalacia. The clinical signs of myelomalacia may include severe hyperesthesia, loss of pelvic limb reflexes in the setting of a compression located in the T3 to L3 vertebral column, anal dilation, flaccid bladder paralysis, and cranial migration of the cutaneous trunci reflex. In some instances myelomalacia may result in thoracic limb paresis and ventilatory compromise due to involvement of the cervical spinal cord.



Spinal Cord Injury Scores


Recently several groups have advocated the routine use of physical examination–based SCI scores in dogs with IVDH and other myelopathies. Examples of currently validated systems are the modified Frankel score, Texas Spinal Cord Injury Score, and 14-point gait score (Table 233-1) (Levine et al, 2011). These systems allow for objective, reliable measurement of clinical facets of SCI, such as nociception and gait. Scoring systems enhance medical record keeping, facilitate clinician communication, and provide objective functional milestones during recovery.



TABLE 233-1


Comparison of Validated Ordinal Physical Assessment–Based Spinal Cord Injury Scales Commonly Used in Dogs











































MFS* TSCIS–Gait* (Individual Limb) 14-Point Motor Score
0 = No motor function or deep nociception caudal to lesion site. 0 = No limb movement. 0 = No motor function or deep nociception caudal to lesion site.
1 = No motor function and no superficial nociception caudal to lesion site; deep nociception preserved. 0 = No limb movement. 1 = No motor function caudal to lesion site, but deep nociception preserved.
2 = No motor function caudal to lesion site, but deep and superficial nociception preserved. 0 = No limb movement. 1 = No motor function caudal to lesion site, but deep nociception preserved.
3 = Nonambulatory status with paresis and general proprioceptive ataxia. 1 = Limb protraction with no ground clearance. 3 = Non–weight-bearing protraction in at least one joint.
  2 = Limb protraction with inconsistent ground clearance. 5 = Non–weight-bearing protraction with more than one joint involved >50% of the time.
  3 = Limb protraction with consistent ground clearance.  
4 = Ambulatory with paresis and ataxia. 4 = Ambulatory, consistent ground clearance, moderate paresis-ataxia (falls occasionally). 7 = Weight-bearing protraction 10%-50% of the time.
  5 = Ambulatory, consistent ground clearance, mild paresis-ataxia (does not fall). 10 = Weight-bearing protraction 100% of the time with reduced strength. Mistakes 50%-90% of the time.
5 = Normal gait. Spinal hyperesthesia and hyperreflexia may be present. 6 = Normal gait. 14 = Normal gait.

MFS, Modified Frankel scale; TSCIS, Texas Spinal Cord Injury Scale (gait component).


*From Levine GJ et al: Description and repeatability of a newly developed spinal cord injury scale for dogs, Prev Vet Med 89:121, 2009.


Only the gait component of the TSCIS is displayed. The TSCIS gait component scores each limb individually on a scale of 0 to 6.


From Olby NJ et al: Development of a functional scoring system in dogs with acute spinal cord injuries, Am J Vet Res 62:1624, 2001.

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Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Canine Intervertebral Disk Herniation
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