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.
Hemorrhage at the lumbosacral
region.Â No fracture was detected.Â No other significant
findings.Â Sections of the spinal column were
submitted to the Tai Lung Veterinary Laboratory for
histological interpretation.Â 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.
cord: One cross section and one longitudinal section
from the area of lumbar vertebra four (L4) are
examined.Â L4-L6 represents the most devastatingly
affected segment with large areas of gray matter loss
(cavitation).Â 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.Â Blood vessels
radiating from the gray matter into the surrounding
white matter are surrounded by perivascular edema and
hemorrhage.Â 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.Â White matter changes
also include vascular diapedesis and perivascular cuffs
composed of neutrophils, macrophages and
lymphocytes.Â There are multifocal areas of
hemorrhage seen in the white matter and the meninges.
Multifocally, vascular fibrinoid necrosis is also
Spinal cord, lumbar: Myelopathy, necrotizing, ischemic, extensive,
severe, acute, neutrophilic and histiocytic with massive
hemorrhage and Wallerian degeneration, Thoroughbred, equine.
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
- Negri Bodies Negative
- Immunofluorescent Test - Negative
Traumatic spinal cord injury
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.Â 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.Â 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.Â The primary event is the mechanical injury to the tissue, which may include compression.Â 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.Â 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.Â Neurons are dependent on a continuous supply of oxygen to remain viable and if the supply is interrupted, vulnerable neurons will degenerate.Â It is reported that the more rapid the onset of ischemia, the more severe the lesion tends to be.Â 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.Â 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)
Lumbar spinal cord, gray matter:
Hemorrhage and necrosis, diffuse, severe.
Although not reported in the
history, conference participants considered postanesthesia
hemorrhagic myelopathy as a possible
ruleout in this case.Â 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.Â Fuentealba IC, Weeks BR, Martin MT, et al.Â Spinal cord ischemic necrosis due to fibrocartilaginous embolism in a horse.Â Journal of Veterinary Diagnostic Investigation. 1991;3:176-179.
2.Â Maxie MG, Youssef S.Â Nervous system.Â In: Maxie MG, ed.Â Jubb, Kennedy and Palmers Pathology of Domestic Animals. 5th ed.Â Vol 1.Â New York, NY: Elsevier Saunders; 2007: 343-345, 358-9.
3.Â Ragle C, et al.Â Development of equine post anaesthetic myelopathy: Thirty cases (1979-2010).Â Equine Vet Ed.23(12); 2011:630-5.
4.Â Sebastian MM, Giles RC.Â Fibrocartilaginous embolic myelopathy in a horse. Journal of Veterinary Medicine. 2004;51:341-343.
5.Â Summers BA, Cummings JF, de Lahunta A.Â Injuries to the central nervous system.Â In: Veterinary Neuropathology. Mosby, St.Â Louis, MO, Mosby: 195;189-193.
6.Â Zachary JF.Â Nervous system.Â In: McGavin MD, Zachary JF, eds.Â Pathologic Basis of Veterinary Disease. 5th ed.Â St.Â Louis, MO: Mosby; 2011:851-852, 860-861, 892, 899-900.