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5-year-old FI Beagle History of an acute onset, non-progressive paraplegia three weeks prior to presentation.
There was no improvement during that time. No history of trauma. No medications. The owner reports that the patient defecates and urinates normally. At presentation, the patient was bright, alert and responsive with normal vital parameters. Cardiopulmonary auscultation was unremarkable. Neurologically, the lesion was localized to L4-S3 (paraplegia with intact pain sensation, normal thoracic limb reflexes, and normal mentation/cranial nerves).
Fairly well margined, irregularly shaped and undulating T2 hyperintensity within the spinal cord extending from L2-3 caudally to the conus medullaris. With few exceptions, the hyperintensity is restricted to the gray matter tract, centrally in the cord. The hyperintensity tapers cranially in the dorsal funiculus. This area is hypointense on T1-weighted images, does not contrast enhance, and remains heterogeneously hyperintense on FLAIR images. There are no signal voids on FFE (T2* or GRE) sequences. The spinal cord is increased in diameter over the region of T2 hyperintenstiy. There is minimal disc protrusion into the vertebral canal at L4-5. This disc space is questionably narrowed with minimal decrease in hydration of the nucleus pulposus.
Locally extensive intramedullary myelopathy with spinal cord swelling, lumbar spinal cord.
The differential diagnosis includes intramedullary neoplasia (primary neoplasia of the spinal cord or perhaps other neoplastic processes like lymphoma). Vascular compromise was also considered because of the gray matter distribution. A high-velocity, low volume disc protrusion was another possibility. The degree of T2-hyperintensity without progressive deterioration of the clinical signs made a secondary myelomalacia unlikely. Infectious and primary inflammatory myelitis was considered unlikely because of the acute onset, lack of contrast enhancement, and lack of progression.
The patient was humanely euthanized due to poor quality of life and lack of clinical improvement. Histopathology revealed fibrocartilaginous emboli within meningeal small vessels, gray matter necrosis with numerous Gitter cells and Wallerian degeneration. This correlates with an ischemic event caused by fibrocartilaginous emboli.
Fibrocartilaginous emobolic myelopathy (FCEM) occurs when fibrocartilaginous material identical to nucleus pulposus (a remnant of the notochord) occludes spinal vasculature causing infarction. These patients often present with an acute onset, non-progressive and non-painful (after the first 24 hours) myelopathy with asymmetric neurologic deficits. The asymmetric neurologic deficits are related the asymmetric distribution of the central spinal arteries. The ventral spinal artery gives off central artery branches that penetrate the spinal cord asymmetrically. The central arteries supply most of the gray matter and lateral and ventral white matter. The predominant gray matter localization of this case supports a vascular event. Perhaps the minimal changes to the disc space at L4-5 represent the source of the nucleus pulposus material.
FCEM is a diagnosis of exclusion. Histopathology is the only method to obtain a definitive diagnosis, however, MRI greatly enhances the ability to achieve an antemortem diagnosis.
The prognosis for recovery, in general, is good. However, several negative clinical prognostic factors have been identified. This patient exhibited several of these factors such as lower motor neuron signs, symmetrical neurologic deficits and lack of improvement within the first 14 days.
- Abramson CJ, Garosi L, Platt SR, et al. Magnetic resonance imaging appearance of suspected ischemic myelopathy in dogs. Veterinary Radiology & Ultrasound. 17 Jun 2005. Volume 46 Issue 3: 225-229.
- De Risio L, Platt SR. Fibrocartilaginous embolic myelopathy in small animals. Veterinary Clinics of North America: Small Animal Practice. 2010. Volume 40: 859-869.
- De Risio L, Adams V, Dennis R, et al. Magnetic resonance imaging findings and clinical associations in 52 dogs with suspected ischemic myelopathy. J Vet Intern Med Nov 2007. Volume 21 Issue 6: 1290-1298.