Intervertebral Disc Disease - Medical or Surgical?
World Small Animal Veterinary Association World Congress Proceedings, 2014
Wayne Berry, BVSc, MMedVet, MRCVS, DACVIM (Neurology)
Southern California Veterinary Specialty Hospital, Irvine, CA, USA

Degeneration of the intervertebral discs (IVD) is common in dogs and may lead to extrusion (Hansen Type I) or protrusion (Hansen Type II) of disc material into the vertebral canal, resulting in variable spinal cord compression. One of the difficulties that we as veterinarians have is convincing owners that their dog with spinal pain or paresis may require neurosurgery. Many clients will share their personal experience with lumbar disc disease or "sciatica" and fail to understand that disc disease in dogs, particularly chondrodystrophic breeds, is markedly different from that in people.

Anatomy and Degeneration

The intervertebral disc (IVD) is composed of an outer annulus fibrosus (AF) surrounding the gelatinous nucleus pulposus (NP), separated by a transitional zone (TZ). Cranial and caudal boundaries of the disc are hyaline cartilage end plates (EP), with the dorsal and ventral longitudinal ligaments serving as the dorsal and ventral boundaries, respectively. The NP is composed of a network of proteoglycan molecules and hyaluronic acid creating an osmotic gradient, pulling water into the complex such that as much as 80% of the normal NP is water. The surrounding AF is a dense ring meshwork of concentric fibrous lamellae consisting of collagen fibrils and elastin fibres and arranged as concentric and oblique lamellae. The inner fibres of the AF are firmly connected to the EP, whereas the outer AF fibres are more firmly connected via Sharpey's fibres to the vertebral epiphyses. The ventral portion of the AF is thicker than the dorsal AF such that the NP is eccentric (more dorsal) within the AF. The EP is also a highly hydrated structure and is similar in structure to articular cartilage consisting of proteoglycans linked with hyaluronidase and collagen.

Besides providing mobility and stability to the spinal column, the IVD functions in transmitting compressive forces between the vertebral bodies to withstand loading conditions including axial compression, shear, tension, bending, and torsion forces. The highly hydrated NP plays a vital role in absorbing axial compressive forces. The AF and EP keep the NP in place and protect the NP from shearing forces and its own swelling pressure. This maintains disc circumference despite a decrease in disc height when shearing forces are applied. The concentric and oblique arrangement of the lamellae of the AF protect against torsion and bending forces. Nutrition of the NP and inner AF is by diffusion since only the outer layers of the AF have a vascular supply.

The dorsal longitudinal ligament (DLL) is very well innervated with sensory nerve endings, compared to the sparse innervation of the outer third of the AF (inner AF and NP are not innervated), such that the pain of IVD disease results from stretching and tearing of the dorsal longitudinal ligament rather than the disc itself. This is in contrast to the discogenic pain described in man, where the AF is extensively innervated and when distorted will result in considerable pain.

Degenerative changes to the disc are generally different for chondrodystrophic compared to non-chondrodystrophic breeds. In chondrodystrophics, loss of glycosaminoglycans, increased collagen and decreased water content characterizes chondroid metaplasia, and the gelatinous NP becomes progressively fibrocartilaginous. Mineralization occurs and may be identified on radiographs. As the NP matrix deteriorates, losing its hydrostatic properties and becoming more rigid, it no longer functions as an effective hydroelastic cushion. Repair is hampered by the inherently avascular nature of the disc and a cycle of continued deterioration and inadequate repair occurs. As the degenerate NP cannot withstand normal forces, tears develop in the AF, and NP material extrudes/ruptures (Hanson Type I) through the coalesced tears into the vertebral canal. This material may extrude either through, or lateral to, the dorsal longitudinal ligament into the vertebral canal, and on occasions result in laceration of the internal vertebral venous plexus (venous sinus). In non-chondrodystrophic dogs, the AF degenerates and fibrous collagen replacement of the NP occurs as a result of fibrous metaplasia. These discs more commonly protrude into the vertebral canal as a result of partial AF rupture and bulging of the NP material (Hansen's Type II). These protrusions rarely become adherent to the dura, whereas chronic disc extrusions are often found to have fibrous attachments to the dura.

Spinal Mobility

In man, the most mobile region of the spinal column distal to the cervical spine is at the lumbosacral junction. In man, about 70% of disc protrusions occur at L4–L5. Considering human anatomy, where the terminal spinal cord is located within the L1–L2 vertebral canal, disc protrusions within the caudal lumbar spine will compress the cauda equina and not the spinal cord.

In the dog, the spinal cord terminates within the L6–L7 vertebral canal, however, the most mobile region of the dog's spinal cord is between T11 and L3, since the dog flexes and extends the thoracolumbar spine when running. This is the region where the greatest wear and tear will occur on the intervertebral disc, and where early degeneration of discs will occur. The spinal cord resides within this region of the vertebral canal, allowing little room for extraneous material, such that should the degenerating disc protrude, or even worse, extrude nuclear material into the vertebral canal, it is the spinal cord that takes the force of the compression and not the cauda equine, as in the case of man or lumbosacral disc disease in the dog. The cauda equina is far more tolerant of compression than the spinal cord. Cauda equina compression will certainly result in pain; however, compression of the cord quickly leads to paresis, which can lead to paralysis and likely incontinence. Since lumbar disc disease in man results in discogenic pain and in severe cases cauda equina compression, surgical decompression is usually delayed until all non-surgical therapeutic modalities have been attempted. Many of us live with the discomfort of lumbar disc disease and do not require surgery - we modify our lifestyles since the process is unlikely to result in paralysis.

Degenerative Process

In man the degenerative process is fibroid degeneration of the nucleus pulposus, resulting in disc protrusion, distortion of the annulus and discogenic pain. Disc extrusion or rupture is less common in man. In dogs, particularly the chondrodystrophic breeds, the nucleus pulposus undergoes chondroid degeneration, resulting in changes that eventually result in mineralization/calcification and predispose the disc to an explosive extrusion. Extruded disc material results in a space occupying mass lesion within the vertebral canal, compressing the structures within the bony vertebral canal.

Medical Versus Surgical Treatment?

Intervertebral disc disease should be considered a surgical disease. However, it would be naïve to consider all cases require surgery. The question is rather that of: If the spinal cord were compressed, would it not be ideal to decompress it before further or permanent damage occurs? Medical therapy is directed at reducing spinal cord oedema, providing pain relief, and attempting to prevent further protrusion or extrusion of disc material by restricting activity. The hope is that confinement allows for tears in the AF to heal, and that the extruded disc material is soft enough to spread around the spinal cord and no longer act as a compressive mass. Many chondrodystrophics with cervical disc extrusions exhibit only pain, despite considerable compression of the cervical spine. In contrast, even small compressions of the T3–L3 cord will result in neurological deficits. Delaying decompression often results in adhesions to the dura, making later removal more challenging and potentially less successful. Successful medical management is often temporary and most reports indicate at least 1/3–½ of patients represent with recurrence of signs and therapeutic failure.

Patient confinement is required for at least three weeks, either limiting the patient to a crate or pen large enough so that they can reposition themselves and be able to escape any excrement. Soft absorbent bedding is necessary, especially if the patient is left unattended for more than 5–6 hours. The only activity should be limited to being taken outside for elimination purposes.

Antiinflammatory and analgesic therapy is usually provided since it is difficult to justify not treating for pain in the fear that the patient becomes more active. Generally, a COX-2 cyclooxygenase inhibitor (NSAID) is preferred, since steroid therapy could confound a diagnosis of steroid responsive meningitis should later investigation occur and cerebrospinal fluid analysis be found normal. Meloxicam at 0.1 mg/kg q 24 h allows small breed dogs (chondrodystrophics) to be more accurately dosed, and deracoxib at 1–2 mg/kg q 24 h for non-chondrodystrophic breeds, are the preferred NSAIDs. Should a steroid be prescribed, prednisone at antiinflammatory doses are used: 0.5 mg/kg q 12–24 h for 5 days, reducing to 0.25 mg q 12–24 h for 10 days, then 0.25 mg q 24–48 h for 10 days. An H2 blocker (famotidine 0.5 mg/kg q 24 h) or proton pump inhibitor (omeprazole 0.25–0.5 mg/kg q 24 h) is often prescribed to reduce the risk of gastric ulceration. Transdermal fentanyl (1–2 mcg/kg/h) or buprenorphine (0.05 mg/kg q 6 h), oral tramadol (2–4 mg/kg q 6–12 h) are narcotic analgesics often prescribed.

Surgical treatment for IVD disease is the treatment of choice, particularly in patients with cervical pain or paraparesis/paraplegia where spinal or nerve root compression has been confirmed with MRI/CT/myelography. Ventral slot decompression is the most commonly performed technique for decompressing cervical IVD extrusions and protrusions. Dorsal laminectomy and hemi-dorsal laminectomy are usually performed in the cervical region for decompressing dorsal or lateral compressions, or intra-foraminal disc extrusions. A lateral approach to the cervical spine is not commonly performed because of limited exposure and the risk of inadvertent vertebral artery laceration. Reports vary in the prognostic figures for recovery but dogs that are ambulatory at the time of cervical surgical decompression, are typically ambulatory postoperatively (99% resolution of signs). Recurrence rate for cervical IVD treated surgically is reported as 5.6%. Recovery rates for non-ambulatory tetraparetic patients vary: some reporting rates of 58–62% for full recovery; small breeds regaining ambulatory status sooner than large breeds; ambulatory status within 96 h of surgery being associated with a greater chance of a full recovery; peracute patients having more severe neurological deficits taking longer to recover; recovery rates of 83% in tetraplegic patients; recurrence of signs after surgery are reported between 0 and 17%.

Hemilaminectomy (commonly) or dorsal laminectomy (rarely), are the techniques most commonly performed to decompress T3 to caudal compressive disc disease. Functional recovery rates for dogs with intact deep pain perception (DPP) range between 86% and 96%, with time to ambulation between 10 and 12 days. No difference in recovery is reported between LMN and UMN location of spinal cord injury. Recovery in DPP absent dogs ranges from 25–78% (average 50%) with improved chances if decompressed within 12 h of losing DPP. Prophylactic fenestration remains controversial: 60% recurrence rate at the decompression site without fenestration; recurrence rate without adjacent fenestration 3–41%, and with adjacent disc fenestration 0–24% range has been reported. More recently, a prospective study revealed a recurrence rate of disc extrusion as 17.89% for single-site fenestration (at site of decompression) and 7.45% for multiple (T11–L4) fenestrations.

Postoperative pain management consists of oxymorphone or hydromorphone (0.05–0.1 mg/kg q 4 h) until transdermal fentanyl (1–2 mcg/kg/h) becomes effective. Tramadol (2–4 mg/kg q 6–8 h) may be combined with a NSAID (meloxicam 0.1 mg/kg q 24 h). Methocarbamol (20–45 mg/kg q 8 h) or other muscle relaxants (cyclobenzaprine 0.25 mg/kg q 8 h) are only indicated in cases of cervical muscle spasm. Gabapentin is prescribed for radicular pain at 5–10 mg/kg q 8–12 h.


Patients with spinal pain, without neurological deficits, may respond to non-surgical management. However, many patients with considerable cervical compression may exhibit pain as the only sign, and investigation to confirm a diagnosis is ideal. Should signs return, or neurological deficits are present at the time of initial evaluation, investigation as to the cause is warranted. The nature of disc degeneration in chondrodystrophic dogs allows for extrusion (rupture) of a mass of tissue into the spinal canal with compression of the spinal cord, which is poorly tolerated. Not only is the degenerative process different from that in man, anatomical differences in pain fibre distribution, length of spinal cord, and fulcrum points exist. The human annulus fibrosus is innervated with a much greater number of nociceptors than that of the dog. Distortion of the annulus fibrosus in man results in stimulation of these pain fibres and is the origin of discogenic pain. In the dog, discogenic pain is not a major contributor to pain from annular distortion, but the dorsal longitudinal ligament is well innervated with pain fibres, such that when a dog is clinical for spinal pain, it reflects deviation of the dorsal longitudinal ligament, a structure within the vertebral canal. Considering the length of the canine spine and the natural thoracolumbar fulcrum compared to man where the spinal cord ends at L1–L2, paralysis from disc extrusion is more likely in the dog, and warrants early surgical intervention.


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Speaker Information
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Wayne Berry, BVSc, MMedVet, MRCVS, DACVIM (Neurology)
Southern California Veterinary Specialty Hospital
Irvine, CA, USA

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