2.9 Principles of Myelopathies in Large Animals

Question 1

How does LA spinal disease relate to SA spinal disease?

Answer 1

both display paresis and ataxia in the face of a myelopathy; the principles of recognizing disease remain the same

BUT, we cannot easily assess the spinal reflexes of large animals
- we assume the spinal reflexes are intact if the animal is standing

Question 2

What are the most common myelopathies of the horse?

Answer 2

1. cervical vertebral malformations / stenosis (CVM/S)
2. equine herpes virus 1 (EHV-1)
3. equine degerative myelopathy (EDM)
4. trauma
5. migrating parasites (strongylus spp.)
6. ryegrass staggers

top three all have POOR prognosis

Question 3

What is CVM/S?

Answer 3

cervical vertebral malformations / stenosis: POOR prognosis

(1) pathogenesis:
- paresis and ataxia
- neurologic signs result from progressive spinal cord compression

two main types of osseous malformation/stenosis:

CVM TYPE I: dynamic stenosis
- when neck is flexed for hyperextended, the vertebrae move excessively causing compression
- commonly C3-C5 (can be C5-C7)
- most often young animals
- worse when neck is flexed (C3-C5) ot hyperextended (C5-C7)
- subluxations: acute or chronic

CVM TYPE II: absolute stenosis (static)
- osteoarthritic changes in the vertebrae (due to congenital OCD) that cause spinal cord compression independent of neck position
- commonly C5-C7
- other malformed vertebrae may exist

both forms of CVM can cause wallerian degeneration

Question 4

What is Wallerian Degeneration?

Answer 4

a pattern of degeneration related to spinal cord compression from CVM/S

1. rostral to lesion: ascending proprioceptive tract lesions
2. at the site of lesion: white and grey matter changes
3. caudal to lesion: descending (motor) tract lesions

this pattern exists because neuronal degeneration occurs where the axon is no longer attached to the nucleus (in this case due to compression).

• proprioceptive nuclei exist caudal in the spinal cord
• motor tract nuclei exist cranial: up by the brain

a defect causing functional “detachment” of nerves from their nuclei will create degenerative changes on the side of the nerve that is “cut off” from its nuclei, while the portion of the tract between the lesion and the nucleus will remain functional

Question 5

How do you diagnose CVM/S?

Answer 5

1. clinical and neurological examination
2. standing cervical radiographs (subjective and objective interpretation)
3. myelography: invasive (dye injected into spinal canal), many false positives, but good in rare instances (e.g., neoplasia)
4. CSF analysis: US-guided atlantoaxial (C1-C2) or lumbosacral, rules out other diseases (normal CSF with CVM)
5. scintigraphy

MOST IMPORTANT objective assessment of standing cervical radiographs: “inter and intra-vertebral ratios”
- the ratio of canal diameter to vertebral thickness:
- smallest diameter of the spinal canal : maximum diameter of vertebral thickness
- if the ratio is 0.52 or less (the spinal canal is less than 52% the size of the vertebra), there is a high likelihood of spinal compression due to narrowing of the spinal canal
- great in young horses (90% accuracy) not as good for older horses with type II CVM

other measurements exist (e.g., “caudal epiphyseal flare”, “caudal extension of the dorsal vertebral lamina”, and the vertebral “step”), but they are less reliable

Question 6

How is CVM/S treated?

Answer 6

oftentimes horses with this condition are not treated, and are instead euthanized or retired (QOL dependent)
- can be “wobbly” and physically unstable
- danger to themselves and others

if treating:
1. PACE diet: reduces protein in the diet to slow growth (allows the spinal canal to “catch up” to the growth of the spinal cord) -> not many studies to support this, but use has little consequence
2. articular process joint medication: local injection of a long-acting corticosteroid; good for use in patients with severe osteoarthritic changes of the vertebral articular processes
3. vertebral stabilization: major surgery, massive neck incision, drill toward spinal cord, insert titanium basket to stabilize the vertebrae; requires specialist surgeon and ~20-30,000 GBP

Question 7

How can EHV-1 lead to spinal cord disease?

Answer 7

EHV-1 may cause little to no symptoms, or respiratory symptoms alone; in some horses, however it can enter the blood

• transmission via inhalation, fomites (feed, water, hands)
• viral replication in the nasal epithelium
• life-long infection (trigeminal ganglion latency)
• one major predilection site is the blood vessels of the spinal cord, where the virus causes a blockage to the blood supply (vasculitis via immune-complex formation)
• sharply demarcated hemorrhages throughout the spinal cord

clinical signs:
- ascending paresis/ataxia
- pyrexia/depression
- urinary incontinence (urine scalding), tail paresis
- occasionally cranial nerve signs

Question 8

What is equine degerative myeloencephalopathy?

Answer 8

neuronal fiber degeneration and demyelination in white matter of ascending and decending SC tracts
- mid-thoracic region most affected
- unknown cause, though genetics and vitamin E deficiency (lack of access to good pastures in early life -> free radical damage) is suspected
- POOR prognosis: may stabilize with high vit E therapy

clinical signs:
- symetric ataxia
- hindlimbs more effected than forelimbs
- hyporefflexia over trunk (cutaneous trunci reflex may be reduced or absent)

while clinical signs are similar to CVM, hyporeflexia and/or hindlimb severity may help distinguish the two

diagnosis:
- usually PM exam
- measure Vit E serum concentrations (though may be normal by the time of clinical signs)
- rule out other diseases (CVM/S which is more common)