THORACOLUMBAR INTERVERTEBRAL DISC DISEASE

INTERVERTEBRAL DISC DEGENERATION

Intervertebral disc disease is the most common neurologic syndrome in the dog. Disc degeneration has been reported in 84 breeds with particular susceptibility in certain small breeds. These breeds (Dachshund, Pekinese, Poodle, Beagle, etc.) have characteristic skeletal changes that predisposes the disc to change at a very early age.

Intervertebral discs act as cushions between the vertebrae and function as the shock absorbers of the spine. A normal disc has 2 regions: a resilient gelatinous nucleus in the center and an outer fibrous ring that encircles the nucleus (Fig.1). A degenerative disc loses its resiliency when its jelly-like center calcifies and takes on a gritty, hardened consistency. No longer able to cushion the vertebrae, the center is predisposed to bulging and to rupture (extrusion), resulting in pressure on the spinal cord, pain and paralysis.

A mild disc rupture may cause back pain while a more moderate rupture causes weakness and a wobbly gait (Fig.2). If a large amount ruptures, or if it ruptures quickly and causes spinal cord swelling, the pressure results in a potentially life-threatening paralysis (Fig.3).

DIAGNOSIS

A tentative diagnosis of thoracolumbar intervertebral disc disease is made on the History and Neurologic Examination. Radiographs (X-rays) can reveal the presence of degenerative, calcified discs and may outline narrowed disc spaces with evidence of extruded (ruptured) calcified disc material in the spinal canal. A definitive diagnosis may require a special x-ray test. The Myelogram (a contrast dye study of the spine) is used to confirm and document not only the location of the ruptured disc but also the amount of spinal cord swelling. With new gas anesthetics, advanced monitoring equipment, and modern "contrast" agents for the dye study, the myelogram is now a common and safe diagnostic procedure when performed with care and under the proper conditions.

The individual’s prognosis depends on many factors:

1) The severity of neurologic dysfunction
2) The number of previous episodes of back pain
3) The amount of disc material that has ruptured
4) The degree of accompanying spinal cord swelling
5) How quickly the disc ruptured (minutes to over several days)
6) The length of time the disc has been ruptured
7) The overall physical condition of the patient

This means that paralysis is not the only factor in the individual patient’s prognosis for recovery.

In general the ability to perceive deep pain in the rearlimbs and tail area remains the key prognostic indicator. If paralysis is present, how quickly they "went down" and how quickly they may have lost deep pain perception are the keys to determining if permanent damage has occurred. Therefore, the neurologic status and radiographs (x-rays) are used to determine the severity of each individual’s condition and, subsequently, the best treatment.

TREATMENT

Individuals experiencing their first episode of back pain with minimal neurologic dysfunction may be treated medically. The medications include corticosteroids (cortisones) to relieve the cord swelling and pain caused by intense inflammation. Patients with recurring painful episodes or significant neurologic deficits are candidates for a Hemilaminectomy. This procedure removes one wall of the vertebrae allowing the surgeon to delicately extract the disc material from the spinal canal without injuring the spinal cord (Fig.4). With pressure removed from around the cord, neurologic function may then begin to return.

A second procedure is then performed to remove the center of the adjacent degenerative discs. This procedure can include up to 6 intervertebral discs and involve cutting a window in the outer fibrous ring of the disc followed by extraction of the calcified, degenerative center. This Fenestration of the disc centers should prevent recurrence of any disc rupture, while allowing normal, pain free motion at each disc site. As the resected center of each disc center scars, there is little to no effect on back mobility (Fig.5).

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