Intervertebral Disc Disease
World Small Animal Veterinary Association World Congress Proceedings, 2006
Richard A. LeCouteur, BVSc, PhD, DACVIM (Neurology), DECVN
University of California
Davis, CA, USA

Type I Disk Extrusion

The appropriate treatment for animals with type I disk extrusion depends on an individual animal's neurological status. Medical treatment directed at decreasing spinal cord edema by means of corticosteroids is indicated only in those animals with an acute onset of neurological deficits, that are examined within eight hours of the injury. The recommended agents and dosages are as described for spinal cord trauma. The use of corticosteroids in dogs with type I disk extrusion has been associated with pancreatitis, gastrointestinal bleeding, or colonic perforations.

Nonsurgical (medical or conservative) treatment is recommended for animals with apparent pain only or animals that have mild neurologic deficits but are ambulatory and have not had previous clinical signs associated with disk disease. These animals should be strictly confined to a small area such as a hospital cage or a quiet place away from other pets for at least 2 weeks, and walked (on a leash or harness) only to urinate and defecate. The objective of confinement is to allow fissures in the anulus fibrosus to heal, thus preventing further extrusion of disk material, and allowing resolution of the inflammatory reaction caused by small amounts of extruded disk material.

Use of analgesics, muscle relaxants, or non-steroidal anti-inflammatory agents, is not recommended in most cases as it is believed that their use encourages animals to exercise and risk further disk extrusion. Very cautious use of analgesics or non-steroidal anti-inflammatory agents occasionally may be indicated. However, strict confinement followed by a period of restricted exercise is imperative. Owners should also be warned that an animal's neurological status may deteriorate owing to extrusion of further disk material despite this treatment and to observe the animal very carefully. If the neurological status worsens, an animal's treatment should be reevaluated immediately. Owners should also be warned that a recurrence of clinical signs is common due to further disk extrusion at the same or a different site, and subsequent episodes may be more severe, especially in the thoracolumbar spine.

Animals with severe cervical pain frequently do not respond to cage rest. These dogs often have large amounts of disk material within the spinal canal, and dogs that do not show improvement after 7 to 10 days of confinement should be evaluated further by means of radiographs and myelography, and ventral cervical decompression should be considered.

Surgical disk fenestration has been recommended as a prophylactic measure to prevent further extrusion of disk material into the spinal canal. Fenestration of the disks most likely to herniate (C2-3 through C6-7 in the cervical spine and T11-12 through L3-4 in the thoracolumbar spine) is recommended in animals that have had one or more episodes of apparent neck or back pain and have evidence of intervertebral disk disease on radiographs. Various surgical techniques have been described. Fenestration of disks does not remove disk material from the spinal canal and therefore is not recommended as the sole surgical procedure in dogs that have evidence of disk material within the spinal canal and spinal cord compression on radiographs and myelography.

The role of disk fenestration in the management of intervertebral disk disease is controversial. Disk fenestration in the thoracolumbar region is not easily done, and complications such as scoliosis, pneumothorax, and hemorrhage may occur. Disk fenestration in the cervical region is achieved more easily and rarely is associated with such complications. Fenestration does not prevent recurrence of disk extrusion in all animals. The effectiveness of fenestration depends largely on the amount of nucleus pulposus removed. Completion of disk fenestration is recommended at the time of spinal cord decompression.

Animals with neurological deficits such as paresis or paralysis with deep pain perception intact, animals with recurrent bouts of apparent back or neck pain, or animals with apparent back or neck pain (or mild neurological deficits) that are unresponsive to strict confinement, should be evaluated by means of spinal radiographs, CSF analysis, and myelography. Surgical decompression of the spinal cord and removal of disk material from the spinal canal should be considered. Although many dogs with moderate or severe paresis improve neurologically if treated with cage rest, neurologic recovery is often more rapid and more complete in animals following surgical decompression of the spinal cord. In addition, the neurological status of some dogs with type I disk extrusion, especially in the thoracolumbar spine, suddenly worsens over a period of hours or days despite medical treatment. Such deterioration usually results from further disk extrusion that may result in irreversible spinal cord damage and permanent paralysis. This progression of signs always is a risk with medical treatment of animals with thoracolumbar disk disease. Progression is impossible to predict on the basis of history, clinical signs, or radiography. Owners should be made aware of treatment options and offered the opportunity of referral to an appropriate surgical facility when animals are initially presented. Surgical decompression should be done as soon as possible to prevent further spinal cord damage incurred as a result of sustained compression or further extrusion of disk material. In addition, if surgery is delayed 2 to 3 weeks, disk material hardens and becomes adherent to dura mater, and becomes difficult or impossible to remove from the spinal canal.

Prognosis for neurological recovery in animals that retain deep pain perception postsurgically is fair to very good. The major factors that correlate with the degree of neurological improvement seen postsurgically are the animal's neurological status prior to surgery, the rapidity of onset of clinical signs, and the time interval between onset of clinical signs and surgical decompression. Animals that have severe neurological signs, a rapid onset of clinical signs (hours), and a long period of time before surgery generally have a prolonged recovery period and may have varying degrees of permanent neurological deficit.

The incidence of recurrence of clinical signs due to disk extrusion is greater in nonsurgically than surgically treated dogs. One author found that one-third of dogs with type I disk herniation that were treated nonsurgically had a recurrence of clinical signs, and generally showed greater severity of neurological deficits at the time of recurrence. Another author reported a recurrence rate of 40 per cent in nonsurgically treated dogs.

The advantages and disadvantages of various techniques for spinal cord decompression have been discussed. Surgical treatment is not without risks. Anesthesia is necessary, and surgery occasionally results in further spinal cord damage due to surgical manipulation. Nonsurgical treatment should be attempted in animals that are poor anesthesia or surgical candidates or if surgical treatment is not possible financially.

In animals with clinical signs of a complete transverse myelopathy, without deep pain perception for a period of more than 24 hours, the prognosis for return of spinal cord function is poor despite medical or surgical treatment. Some of these animals may improve neurologically if given sufficient time. However, it is a matter of controversy whether surgical treatment increases the probability of improvement or not. In cases in which deep pain perception has been absent for less than 24 hours, the prognosis for return of spinal cord function is poor. However, surgical treatment may increase the likelihood of neurological improvement in this group.

Regardless of whether medical or surgical treatment is instituted, animals that are paretic or paralyzed require intensive nursing care. Neurological improvement may take weeks or months and this requires owner cooperation and enthusiasm regarding care and physical therapy. Manual expression, intermittent catheterization, and /or indwelling catheterization of the bladder are often required to ensure emptying of the bladder. Weekly urinalysis, especially in animals that do not have voluntary control of micturition, is important in monitoring for urinary tract infection. It is also important to keep animals well padded, clean, and dry to prevent formation of pressure sores, and to ensure that caloric and water intake is adequate. Physical therapy does not result in neurologic improvement but helps to prevent disuse muscle atrophy associated with paraplegia or tetraplegia. Physical therapy should not be attempted in animals treated medically for at least the first 2 weeks following onset of signs, as further extrusion of disk material may occur.

Type II Disk Protrusion

Treatment with corticosteroids may result in neurological improvement for variable periods of time in animals with type II disk protrusion. However, corticosteroid therapy is not curative. The reason for this improvement is not clear, as intramedullary hemorrhage and edema seen in cases of acute spinal cord injury are not a feature of chronic spinal cord compression. In the thoracolumbar spine, surgical removal of protruded disk material may result in clinical improvement. However, the neurological status of some dogs is worsened permanently despite careful surgical technique. The reasons for this are not known, but increased vascular permeability has been described in the spinal cord associated with release of chronic spinal cord compression and this probably plays a role in this phenomenon. Ventral decompression in the cervical spine allows removal of protruded type II disk material and neurologic improvement may occur over several months; however, some dogs, especially those with moderate to severe neurologic deficits prior to surgery, may manifest temporary or permanent worsening of clinical signs postoperatively.

Speaker Information
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Richard A. LeCouteur, BVSc, PhD, DACVIM (Neurology), DECVN
University of California
Davis, California, USA

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