Signalment:  
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:
- Cerebrospinal fluid (lumbosacral per submitting
veterinarian): Field was entirely composed of red
blood cells and marked numbers of neutrophils and
macrophages.
- CSF for culture No significant findings
- PCR for Japanese Encephalitis Negative
- PCR for West Nile Virus Negative
Virology Rabies:
- Negri Bodies Negative
- Immunofluorescent Test - Negative
Condition:  
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)
References:
1. Fuentealba IC, Weeks BR, Martin MT, et al. Spinal cord ischemic necrosis due to fibrocartilaginous embolism in a horse.Â
Journal of Veterinary Diagnostic Investigation. 1991;3:176-179.
2. Maxie MG, Youssef S. Nervous system. In: Maxie MG, ed.Â
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).Â
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.Â
Pathologic Basis of Veterinary Disease. 5th ed. St. Louis, MO: Mosby; 2011:851-852, 860-861, 892, 899-900.