NAVLE Nervous

Feline Fibrocartilaginous Embolism Study Guide

Fibrocartilaginous embolism (FCE), also known as fibrocartilaginous embolic myelopathy (FCEM), is an acute, non-compressive vascular disorder of the spinal cord caused by embolization of spinal vasculature with fibrocartilaginous material...

Overview and Clinical Importance

Fibrocartilaginous embolism (FCE), also known as fibrocartilaginous embolic myelopathy (FCEM), is an acute, non-compressive vascular disorder of the spinal cord caused by embolization of spinal vasculature with fibrocartilaginous material histologically identical to the nucleus pulposus of the intervertebral disc. FCE causes ischemic necrosis of dependent spinal cord regions, resulting in sudden-onset neurological deficits. While more commonly documented in dogs, FCE is an important differential diagnosis in cats presenting with peracute myelopathy and represents a high-yield topic for NAVLE examination.

Unlike compressive intervertebral disc disease, FCE is a non-surgical condition requiring conservative management with physical rehabilitation. The pathophysiology involves acute ischemic injury similar to a "spinal stroke," making early recognition and differentiation from other causes of acute myelopathy essential for appropriate patient management.

Vessel Territory Supplied Clinical Significance
Anterior Spinal Artery (ASA) Ventral 2/3 of spinal cord including ventral horns, lateral columns, and corticospinal tracts Most commonly affected in FCE; ASA narrowest at C2 in cats
Posterior Spinal Arteries (paired) Dorsal 1/3 of spinal cord including dorsal columns and dorsal horns Less commonly affected; proprioception preserved if posterior columns spared
Radicular Arteries Segmental supply reinforcing longitudinal vessels Provide collateral circulation; fewer in thoracic region (watershed area)

Etiology and Pathophysiology

Source of Embolic Material

The embolic material in FCE is histochemically identical to nucleus pulposus of the intervertebral disc. The nucleus pulposus is the gel-like center of the intervertebral disc, composed of fibrocartilaginous material rich in proteoglycans. The exact mechanism by which this material enters the spinal vasculature remains incompletely understood, but several theories have been proposed:

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