Nine-year-old gelding Thoroughbred, Equus caballus, equine.The owner complained that the horse seemed to be lame when riding in sand. Over the next 24 hours there was rapidly ascending paralysis. The horse was dog sitting and then became recumbent with complete loss of deep sensation to the rear limbs. Cerebral spinal fluid (CSF) was collected from the lumbar region and appeared to be blood. CSF collected from the thoracic region was cloudy. The owner opted for humane euthanasia and a post mortem examination was performed.

Gross Description:  

Hemorrhage at the lumbosacral region. No fracture was detected. No other significant findings. Sections of the spinal column were submitted to the Tai Lung Veterinary Laboratory for histological interpretation. These sections of the spinal cord were fixed in 10% neutral buffered formalin, processed, sectioned and stained with haematoxylin and eosin (H&E).

Pathologists findings: On trimming of the spinal cord sections submitted for histological examination, the segment from lumbar vertebra 1 to lumbar vertebra 4 was visibly compressed with a 15 mm x 4 mm dorsal protrusion.

Histopathologic Description:

Spinal cord: One cross section and one longitudinal section from the area of lumbar vertebra four (L4) are examined. L4-L6 represents the most devastatingly affected segment with large areas of gray matter loss (cavitation). In both the dorsal and the ventral gray column there is severe hemorrhage, neuronal necrosis, spheroids, high protein perivascular edema and an inflammatory cell infiltrate consisting of neutrophils, macrophages and fewer lymphocytes. Blood vessels radiating from the gray matter into the surrounding white matter are surrounded by perivascular edema and hemorrhage. Multifocally, in the white matter there are swollen, eosinophilic axons (spheroids) and Wallerian degeneration characterized by the presence of gitter cells in dilated myelin sheaths. White matter changes also include vascular diapedesis and perivascular cuffs composed of neutrophils, macrophages and lymphocytes. There are multifocal areas of hemorrhage seen in the white matter and the meninges. Multifocally, vascular fibrinoid necrosis is also evident.

Morphologic Diagnosis:  

Spinal cord, lumbar: Myelopathy, necrotizing, ischemic, extensive, severe, acute, neutrophilic and histiocytic with massive hemorrhage and Wallerian degeneration, Thoroughbred, equine.

Lab Results:  

Cytology Examination results: Virology Rabies:


Traumatic spinal cord injury

Contributor Comment:  

The most likely cause of the devastating changes seen in the spinal column and considering the rapid onset of clinical signs, aggressive progression of paralysis and the protrusion of the spinal column seen grossly is trauma. There was neither history of degenerative disk disease nor evidence of fibrocartilaginous emboli but these scenarios were considered due to the sudden onset of clinical signs and the ischemia evident histologically.1 However, in the literature it is thought that the cervical spinal cord is the area primarily affected by fibrocartilaginous emboli in the horse.(4)

Despite there being no evidence of vertebral fracture during post mortem examination, acute compression of the spinal column and resultant ischemia would account for the changes seen histologically. It has been reported that direct injuries to the spinal cord can occur without obvious injury to the vertebrae with devastating effects.(2)

Grey matter with its high metabolic rate and dependence on oxygen is much more sensitive than white matter to ischemic changes.(5) This would explain why the gray matter in this case is so much more severely affected than the white matter.

Acute, traumatic spinal cord injury generally occurs by primary and secondary mechanisms. The primary event is the mechanical injury to the tissue, which may include compression. The secondary mechanism consists of the interruption in vascular supply and perfusion.(5)

The gray matter is composed primarily of cell bodies and dendrites of nerve cells. Neurons are the most sensitive to injury out of all the cells in the central nervous system as they have limited energy stores. They are dependent on an intact blood flow to supply oxygen and nutrients, particularly glucose. Neurons are dependent on a continuous supply of oxygen to remain viable and if the supply is interrupted, vulnerable neurons will degenerate. It is reported that the more rapid the onset of ischemia, the more severe the lesion tends to be. The severe hemorrhage seen primarily in the gray matter is consistent with damage to the capillary framework which tends to be more concentrated in the gray matter than in the white matter. There are also fewer anastomoses in the vessels that supply the white matter.(6)

It is thought that the tendency for spinal cord tissue to become soft and suffer liquefactive necrosis is due to the abundance of lipids and enzymes and a lack of fibrous connective tissue in the CNS.(6)

JPC Diagnosis:  

Lumbar spinal cord, gray matter: Hemorrhage and necrosis, diffuse, severe.

Conference Comment:  

Although not reported in the history, conference participants considered postanesthesia hemorrhagic myelopathy as a possible ruleout in this case. When horses are anesthetized and laid in dorsal recumbency, compression of the azygous vein can result in venous infarction and ischemic necrosis, and poliomyelomalacia of the caudal spinal cord is the most common histopathological finding.(3) Another possible cause is fumonisin B1 toxicity from the consumption of corn contaminated with the saprophytic fungus Fusarium verticillioides, which typically causes edema and necrosis of the cerebral white matter, but chiefly cause gray matter necrosis in the brain stem and spinal cord.(2) Also considered was purpura hemorrhagica, which causes vasculitis, vascular necrosis and hemorrhage secondary to antigen-antibody complexes; or endotoxemia, although accompanying inflammation would be expected.(6)


1. Fuentealba IC, Weeks BR, Martin MT, et al. Spinal cord ischemic necrosis due to fibrocartilaginous embolism in a horse. Journal of Veterinary Diagnostic Investigation. 1991;3:176-179.
2. Maxie MG, Youssef S. Nervous system. In: Maxie MG, ed. Jubb, Kennedy and Palmers Pathology of Domestic Animals. 5th ed. Vol 1. New York, NY: Elsevier Saunders; 2007: 343-345, 358-9.
3. Ragle C, et al. Development of equine post anaesthetic myelopathy: Thirty cases (1979-2010). Equine Vet Ed.23(12); 2011:630-5.
4. Sebastian MM, Giles RC. Fibrocartilaginous embolic myelopathy in a horse. Journal of Veterinary Medicine. 2004;51:341-343.
5. Summers BA, Cummings JF, de Lahunta A. Injuries to the central nervous system. In: Veterinary Neuropathology. Mosby, St. Louis, MO, Mosby: 195;189-193.
6. Zachary JF. Nervous system. In: McGavin MD, Zachary JF, eds. Pathologic Basis of Veterinary Disease. 5th ed. St. Louis, MO: Mosby; 2011:851-852, 860-861, 892, 899-900.

Click the slide to view.

Back | VP Home | Contact Us |