Chapter 233 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. 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). 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. 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. 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). 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. 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, 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.
Canine Intervertebral Disk Herniation
Pathophysiology of Intervertebral Disk Disease
Intervertebral Disk Degeneration
Intervertebral Disk Herniation
Spinal Cord Injury and Pathologic Features
Epidemiology and Clinical Signs
Spinal Cord Injury Scores
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.
Stay updated, free articles. Join our Telegram channel
Canine Intervertebral Disk Herniation
Only gold members can continue reading. Log In or Register a > to continue