Unit 2 - Neuro 2 Flashcards
What is the pathophysiology of cervical vertebral stenotic myelopathy?
Compression of the spinal cord due to impingement from the vertebrae narrowing the vertebral canal
When can impingement in patients with cervical vertebral stenotic myelopathy occur?
It can be static (at rest) or dynamic (when the neck is flexed/extended)
What horses are typically affected by cervical stenotic myelopathy?
Big and young horses (CVSM type 1) or older and arthritic (CVSM type 2)
What clinical signs are associated with cervical vertebral stenotic myelopathy?
Normal physical exam, normal mentation, normal cranial nerve exam, and ataxia affecting all four limbs (hindlimbs may be 1-2 grades worse than forelimbs)
How is cervical vertebral stenotic myelopathy diagnosed?
radiographs or myelogram
What are the cons to using radiographs to diagnose cervical vertebral stenotic myelopathy?
It is a 2D image of a 3D structure - you need to get really good laterals
What are the pros to using a myelogram to diagnose cervical vertebral stenotic myelopathy?
Current gold standard for static and dynamic compression
What are cons to using a myelogram to diagnose cervical vertebral stenotic myelopathy?
More expensive, requires general anesthesia, and the horse may wake up from general anesteshia 1-2 grades worse than before (temporary)
How is Cervical vertebral stenotic myelopathy treated?
Basket’ surgery, time and decrease caloric intake if the horse is still growing, retirement, or euthanasia
What is the goal with basket surgery for cervical vertebral stenotic myelopathy?
To prevent them from doing worse and get 1-2 grades better within the next year
What etiologic agent causes equine protozoal myeloencephalitis?
Sarcocystis neurona
How do horses get S. neurona?
by eating opossum feces
Where does S. neurona travel?
wherever it wants to go
In practice, what clinical signs can equine protozoal myeloencephalitis have?
anything it wants to be
Accorind to the NAVLE, what clinical signs does equine protozoal myeloencephalitis have?
Asymptomatic, hind limb ataxia and atrophy
How is equine protozoal myeloencephalitis diagnosed?
serology, CSF antibody titres, and necropsy
When is serology for equine protozoal myeloencephalopathy valuable?
When you get a negative test. Serology tests for exposure which 90% of horses have, so if you get a negative test it means they havent been exposed.
What is the gold-standard for diagnosis for EPM?
necropsy to find the parasite
What is the ante-mortem gold standard for diagnosis of EPM?
CSF antibody titers
How is EPM treated?
Sulfadiazine/pyrimethamine (Rebalance), ponazuril (Marquis), or Diclazuril (Protazil) +/- NSAIDs, +/- steroids, vitamin E and corn oil with Marquis
What is the prognosis for EPM?
60% of horses improve by at least 1 grade
What is the pathophysiology of Equine Herpes Myeloencephalomalacia?
EHV-1 can cause microthromboses of the spinal cord in SOME horses
True or False: Only the neuropathic strain of EHM can cause neurologic signs.
False - although there is a neuropathic strain, but all strains have the potential
What is EHM vaccination not protective against?
neurologic disease - it does not protect against viremia
What clinical signs are associated with EHM?
Often have a fever proceeding clinical signs, can have a fever at the time of clinical disease, ataxia, tetraparesis, urine +/- fecal retention, incontinence, occasionally changes in mentation, ocular lesions
What must you do first if you suspect EHM?
contact your state vet - it is reportable
Once you have contacted your state vet, what should be done next if you have a patient you suspect to have EPM?
Nasal sqabs, buff coats from affected horses(s) for PCR
Stop traffic at the barn
BID rectal temperatures from other horses at the farm If possible
Quarantine confirmed or suspected horses
How is EHM treated?
Supportive care - keep them in a safe place and provice them with fluid and nutrition, bladder catheterization and fecal elimination may be necessary
What is the prognosis for EHM?
50% case fatality
What is the pathophysiology of rabies?
Local replication of the rabies virus (bite), travel via Ach receptors to the CNS via peripheral nerves and then replicates in the brain before it reaches the salivary glands
What are the wildlife reservoirs of rabies infection in horses?
foxes, skunks, bats, and racoons
What clinical signs are associated with a rabies infection?
Wide variety of clinical manifestations.
Suspect with any horse that has intracranial dysfunction.
Dysphagia, weakness, paresthesia (intense pruritus), colic-like signs, increased salivation, and stuporness
How is rabies treated?
There is no treatment - submit all suspects for post-mortem and contact the state veterinarian
How is rabies prevented?
rabies vaccination
What causes equine leukoencephalomalacia?
Ingestion of mycotoxin fumosin B1 in growing moldy corn
When is equine leukoencephalomalacia most common?
in late fall and early spring
What are the initial clinical signs associated with equine leukoencephalomalacia?
Incoordination, aimless walking, intermittent anorexia, lethargy, obtundation, head pressing, and blindness
What are the progressive clinical signs associated with equine leukoencephalomalacia?
delirium, hyperexcitability, belligerence, and sweating
What are the end stage clinical signs associated with equine leukoencephalomalacia?
recumbency, seizures, and death
How is equine leukoencephalomalacia treated?
there is no treatment
What will you find on necropsy in patients with equine leukoencephalomalacia?
Liquifactive necrosis and degeneration of the cerebral hemispheres
What causes nigropallidal encephalomalacia?
Yellow-star thistle and russian knapweed ingestion
Where is yellow star thistle and russain knapweed found?
in the western US
What clinical signs are associated with Nigropallidal encephalomalacia?
inability to prehend, masticate and deglutinate, swallowing appears to be intact, hypertonicity of facial muscles, tongue protrusiton, and constant chewing
How is Nigropallidal encephalomalacia treated?
there is notreatment
What will you find on necropsy in horses with Nigropallidal encephalomalacia?
Unilateral to bilateral softening and necrosis of the globus pallidus and substantia nigra
