spinal cord disorders Flashcards
most common spinal cord pathology:
trauma and cervical vertebral compressive myelopathy
etiology of traumaa
neck or back injury
etology of cervial vertebral compressive myelopathy
spinal cord compression due to developmental malformation or instability
etiology of equine protozoal meningitis
Sarcocytis neurona (90%)
Neospora hughesi
etiology of neuroaxonal dystrophy/Equine degenerative myelopathy
progressive axonal loss
geneti and nutritional factors (vitamin E)
etiology of herpesvirus myeloencephalitis
equine herpes virus 1
breed and age predilection of trauma
any age
breed and age predilection of CVCM
wealings to 2 years
thoroughbreds and warmbloods
breed and age predilection of EPM
65% < 4years
breed and age predilection of NAD/EDM
weanlings to 2 years old
breed and age predilection of Herpesvirus myeloencephalitis
adults
pregnant mares
prognosis for trauma
variable, may be good if not recumbent
prognosis for CVCM
guarded
surgery may improve 50% 2 grades, a few 3 grades, but only by 1 grade of signs
prognosis of EPM
fair
prognosis of NAD/EDM
poor
prognosis of herpesvirus myeloencephalopathy
good in non-mutated forms
guarded in mutant Herpes form
recumbency is a poor sx
what are the two types of myelopathy seen in CVCM?
types 1: dynamic-intermittent compression, instability, younger horses, typically C3-C4 or C4 to C5
type 2: static or stenotic-constant compression, osteoarthritis, trauma, adults, typically C5 to C6 or C6 to C7
CVCM clinical signs
may be slowly progressive or acute associated with trauma
symmetrical UMN signs to all four: ataxia, weakness, difficulty backing
pelvic limbs often 1 grade worse
may have stiffness with neck flexion to one or both sides
wide base stance
during circling: circumduction, interference, pivoting, knuckiling, neck flexion
weakness: tail pull, dragging toes
CVCM diagnosis
radiographs-standing cervical radiographs
stenosis, subluxation, malformation, osteoarthritis
sagittal ratio: minimal sagittal diameter divided by width of the vertebral body should be >50% cranially and >52% in caudal cervical canal
myelogram: base on dorsal column
CVCM medical therapy
diet
rest-paced growth diet for foals less than 6 months
Antiinflammatories-NSAIDs and intra-articular steroid injections
articular supplements-Glycosamine, Chondroitin
antioxidants-Vitamin E/selenium
CVCM surgical treatment
basket surgery-fuses joint
spinal cord trauma dx
clinical signs and history
PE to localize lesion
radiography (adults cervical spine, foal entire spine)
may require myelogram
spinal cord trauma clinical signs
peracute
C1-T2: tetraparesis to recumbency
T3 to L6: horse may dog sit
sacral fx
urinary and fecal incontinence
trauma treatment
phenylbutazone
DMSO
glucocorticoids
Mannitol (cerebral edema)
NAD/EDM pathogenesis
progressive neuraxonal dystrophy
epidemiology: young, growing horses, many different breeds, cluster of cases can occur on single farm, usually beging before 6 months of age
vitamin E deficiency and underlying familial predisposition
lesions most prominent mid-thoracic region
NAD/EDM clinical signs
symmetric ataxia, paresis and hypometria
+/- poor panniculus
NAD/EDM dx
rule out other diseases
vitamin E deficiency support but normal doesn’t not r/o
typically disease of younger horses
NAD/EDM Prognosis
poor
NAD/EDM treatment
no specific tx
vitamin E supplementation does not improve affected cases-give to pregnant mares and foals during the 1st year of life
dietary modification of unaffected animals-fresh grass or other roughage
