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Fibrocartilaginous Emboli of the Spinal Cord

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Newsletter, 2006 Vol. 12, Issue 1


Probably the second most common cause of acute-onset paresis or paralysis we see in our practice involves embolization of the spinal cord.

Fibrocartilaginous emboli (FCE) of the spinal cord can occur in any breed of dog, but seems to be more common in large breeds. Presentation may mimic acute-onset disc disease, and the differential for these dogs should consider disc rupture.

Pathogenesis of these emboli is not well-defined. The source of the disc material seen in the spinal cord embolus seems to be the nucleus pulposus of the disc. In man, extrusion of fibrocartilaginous material into an adjacent vertebral body (Schmorl's nodules) places this disc material in close proximity to the sinusoidal venous channels in the bone marrow. In the dog, however, Schmorl's nodules have not been identified. The mechanism of transportation of fibrocartilaginous material from the disc, into the spinal cord vasculature, may vary between dog and man.

Regardless of the mechanism of transport, histopathological examination of affected dogs shows the presence of fibrocartilaginous material in the spinal cord vasculature. This embolization of the spinal cord is responsible for the clinical signs noted.

The clinical signs noted can vary from mild ataxia, to severe ataxia, paresis or paralysis. There may be subtle differences in presentation between a dog with an FCE and a dog with a ruptured disc that may help distinguish between the two conditions to some extent. The most common findings which may help distinguish between the two are:

  • Lack of pain. Dogs with FCE very rarely exhibit hyperesthesia.
  • Non-progressive. Symptoms are static and do not worsen over time.
  • Lateralization of signs. Many times a dog with an FCE is markedly more paretic on one side of the body vs. the other.
  • Breed. Preponderance of large breed dogs affected.

Diagnosis is based upon exclusion of other causes for spinal cord dysfunction. Plain film radiographs are initially obtained to exclude fractures, luxations, and overt bone lesions of the vertebrae such as neoplasia or discospondylitis. Anesthesia and a myelogram is done to rule out a compressive lesion (either intramedullary, intra-dural/extra-medullary, or extra-dural). In the absence of another cause (normal myelogram), a diagnosis of FCE is presumptively made. Definitive diagnosis, at this time, can only be made by histopathological examination of the cord.

Treatment is supportive. In our practice, most dogs presenting with a severe spinal cord lesion are treated initially with high-dose corticosteroids (Solu Medrol); however, corticosteroid therapy has not been shown to affect outcome. Since most dogs have treatment initiated prior to myelography and diagnosis, it seems reasonable to initiate therapy as would be done for a general spinal cord insult.

Prognosis is somewhat dependent on the area of the spinal cord affected. Dogs with LMN lesions are much less likely to recover than dogs with UMN lesions. This is most likely because infarction of an area of the cord containing the cell bodies (grey matter) is less likely to recover than an infarction of the white matter, or long tracts, of the cord. As mentioned above, presence or absence of deep pain sensation is important in rendering a prognosis.


We have secured space immediately next door to the Animal Emergency Center and are in the process of "building-out" our new practice facility.

We are excited about this new specialty clinic, and plan our grand-opening announcement in July!