FCE, also referred to as ischemic myelopathy, is an occlusion of the spinal vasculature by fibrocartilaginous material likely originating from the nucleus pulposus. There are many hypotheses speculating how the disk material enters the spinal vasculature, although the exact cause is unknown. One hypothesis is that a Valsalva-like maneuver predisposes the patient to this condition, such as straining to defecate, one of the most common associations found with FCE in humans.1
FCE causes a peracute onset of neurologic signs that typically do not progress beyond 24 hours. The clinical signs reflect location of the lesion within the spinal cord and are typically asymmetric. Although reports2,3 have described this disease as nonpainful, patients may yelp in pain prior to onset of neurologic signs; in some cases, the pain can persist for the first 24 hours following injury. FCE is reported more often in large-breed dogs but has also been described in small-breed dogs, with increased risk for miniature schnauzers.4
Definitive diagnosis is achieved with histopathology at necropsy, but antemortem diagnosis is based on a combination of clinical features, diagnostic imaging, and CSF analysis.5 Treatment consists of supportive nursing care and physical therapy. Corticosteroid therapy has not proven beneficial and is not recommended, as associated side effects may increase risk for infection, especially in recumbent patients.
Prognosis ultimately depends on the severity and extent of spinal cord injury. Recovery rates range from 58% to 84%.3 Negative prognostic indicators include severe neurologic deficits (eg, loss of nociception), symmetric neurologic signs, lower motor neuron signs, lack of improvement within the first 14 days after injury, and owner unwillingness to pursue treatment.3