EqMed F, Neuro I

  1. Where do seizures localize the lesion to?
  2. What is the main nerve evaluated when assessing tail and anal tone?
    internal pudendal nerve
  3. Horner's syndrome is damage to sympathetic nerve fibers. What are some ways these fibers are damaged?
    • brachial plexus avulsion
    • injury to cranial thoracic spinal cord (sympathetic fibers ascend from here)
    • guttural pouch disease
    • cervical sympathetic trunk injury
  4. what are clinical signs of horner's?
    • enophthalmos
    • ptosis
    • prolapsed 3rd eyelid
    • miosis
    • sweating on affected side
  5. Grade 0 means no deficits. What is the difference between 2 and 3?
    • deficits readily seen but
    • 2: confused with lameness easily
    • 3: not confused with lameness easily
  6. what is the difference between 4 and 5?
    • 4: horse nearly falls, not safe
    • 5: horse recumbent
  7. If horse stands in place ok but then seems very unstable when blindfolded, what neuro disease does this lead you to?
    vestibular disease
  8. What part of the brain does the horse NOT need to be able to walk properly?
    does not need intact cerebrum (but will falter for complicated tasks)
  9. what are some signs of paresis?
    • muscle fasciculations
    • difficulty backing
    • toe drag/wearing toe
    • "bounce" to stride
  10. what are some ways to test paresis?
    • incline
    • tail pull
    • sway test
    • hopping in small foals
  11. what are tests for ataxia?
    • circling
    • incline
    • obstacles
    • move w/head elevated
    • blindfold
  12. what gait is upper motor neuron sign characterized by over-reaching and high stepping?
  13. what are some signs of proprioceptive deficits when standing? when walking?
    • standing w limb crossed over the other w/o correcting
    • walking: circumducting
  14. If signs of paresis, could cerebellum, brainstem or vestibular system be involved?
    paresis - brainstem
  15. If signs of paresis, is this UMN or LMN? could it also be a musculoskeletal issue?
    • UMN or LMN but more likely LMN
    • also possibly MS
  16. If signs of ataxia, could cerebellum, brainstem, or vestibular system be involved?
    all 3 possible, esp. cerebellum
  17. If signs of ataxia, is this UMN or LMN?
    either but more likely UMN
  18. Is hypometria or hypermetria associated with possible musculoskeletal problem?
  19. Is hypometria or hypermetria associated w/ LMN?
    • hypometria - LMN
    • hypo/hyper - both UMN associated
  20. What is normal CSF total protein, cell count, and color?
    • clear
    • TP: <100mg/dl
    • < 6WBC
    • no RBCs unless contamination
  21. what is xanthocromia? what does it indicate?
    previous endothelial inflammation/bleed into CSF
  22. What should be aware of during recovery after taking myelograms?
    transiently worse after taking the films (can pre-tx w NSAIDs)
  23. list 6 cortical brain diseases?
    • rabies
    • EPM
    • alpha virus encephalitis (EEE,WEE,VEE)
    • west nile virus
    • herpes myeloencephalitis
    • leukoencephalomalacia
  24. How long after administration is rabies vaccine effective?
    30 days
  25. what is causative agent of equine protozoal myeloencephalitis? Definitive host?
    • sarcocystis neurona
    • opossum
  26. How do horses get PEM?
    possom eats sarcocyst in muscle tissue - poop sporocyst - horse eats sporocyst
  27. what is the most defining clinical sign for EPM?
    asymmetrical (otherwise can mimic any neuro disease)
  28. how is EPM diagnosed?
    • hx + CS
    • western blot *only if horse neurological*
    • CSF protein/cytology normal
  29. what is western blot testing for? what does it mean that this test has only 89% sensitivity and 39% specificity?
    • S. neurona antibodies (qualitative)
    • many false positives
    • *if CSF positive AND clinical signs = EPM*
  30. what is a quantitative test for EPM w/97% specificity?
    indirect immunoflorescence antibody test (IFAT)
  31. What pathologic findings are suggestive of EPM?
    perivascular cuffing w/mononuclear cells
  32. how is EPM treated? what is efficacy of this tx?
    folic acid inhibitors w/combo of antibiotics (sulfa + pyrimethamine) for 90-120 days
  33. Coccidiostat (ponazuril) for 28days
  34. only about 62% efficacy in both (meas. by improvement/return to function)
  35. Should horses be vaccinated against EPM?
    no, vx no longer available bc not efficacious
  36. Are EEE/WEE/VEE reportable and/or zoonotic?
    yes and yes
  37. What is the vector and amplifying host for these alphaviruses?
    • vector - mosquito (culiseta melanura)
    • amplifier - birds (horse amplifies VEE only)
  38. why is EEE/WEE/VEE known as sleeping sickness?
    somnolence, recumbency, death
  39. what are other signs seen with EEE/WEE/VEE?
    • head pressing, dementia
    • seizures, blindness
    • Cr N deficits
    • hypermetria, ataxia
  40. what is prognosis for EEE? for WEE?
    • EEE: 90% mortality (poor)
    • WEE: <50% mortality (fair to poor)
  41. what is best ante mortem test for the alphaviruses? What are problems with this test?
    • serology
    • horse often dies before collect convalescent titers
    • vaccine antibodies interfere
  42. what are expected CSF findings with alphaviruses?
    • xanthochromia
    • elevated protein
    • neutrophilia
  43. how is alphavirus diagnosed post mortem?
    virus isolation from the brain
  44. Most cases of alphavirus are in UNvaccinated horses. How long is the vaccine good for? when should it be given?
    • lasts about 6 months
    • give before mosquito season
  45. Is west nile virus zoonotic? reportable?
    • yes zoonotic
    • not reportable
  46. how is west nile virus transmitted? reservoir?
    • mosquito
    • birds as reservoir (crows)
  47. what kind of virus is west nile?
    flavivirdae, RNA virus
  48. Do birds show signs of west nile virus? what is mortality in horses and humans?
    • some birds die
    • horse mortality 30% (much lower than alphaviruses)
    • humans 10% (" ")
  49. what are clinical signs of west nile virus?
    • fever
    • acute onset ataxia, *preferentially in rear limbs*
    • face muscle fasciculations, tongue weakness
    • (somnolence, but more w/EEE)
  50. how is WNV diagnosed?

    • IgM capture ELISA (81%sens/100%spec)
    • virus isolation, PCR

    supportive tx
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EqMed F, Neuro I
EqMed F, Neuro I