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Where do seizures localize the lesion to?
cerebrum
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What is the main nerve evaluated when assessing tail and anal tone?
internal pudendal nerve
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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
-
what are clinical signs of horner's?
- enophthalmos
- ptosis
- prolapsed 3rd eyelid
- miosis
- sweating on affected side
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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
-
what is the difference between 4 and 5?
- 4: horse nearly falls, not safe
- 5: horse recumbent
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If horse stands in place ok but then seems very unstable when blindfolded, what neuro disease does this lead you to?
vestibular disease
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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)
-
what are some signs of paresis?
- muscle fasciculations
- difficulty backing
- toe drag/wearing toe
- "bounce" to stride
-
what are some ways to test paresis?
- incline
- tail pull
- sway test
- hopping in small foals
-
what are tests for ataxia?
- circling
- incline
- obstacles
- move w/head elevated
- blindfold
-
what gait is upper motor neuron sign characterized by over-reaching and high stepping?
hypermetria
-
what are some signs of proprioceptive deficits when standing? when walking?
- standing w limb crossed over the other w/o correcting
- walking: circumducting
-
If signs of paresis, could cerebellum, brainstem or vestibular system be involved?
paresis - brainstem
-
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
-
If signs of ataxia, could cerebellum, brainstem, or vestibular system be involved?
all 3 possible, esp. cerebellum
-
If signs of ataxia, is this UMN or LMN?
either but more likely UMN
-
Is hypometria or hypermetria associated with possible musculoskeletal problem?
hypOmetria
-
Is hypometria or hypermetria associated w/ LMN?
- hypometria - LMN
- hypo/hyper - both UMN associated
-
What is normal CSF total protein, cell count, and color?
- clear
- TP: <100mg/dl
- < 6WBC
- no RBCs unless contamination
-
what is xanthocromia? what does it indicate?
previous endothelial inflammation/bleed into CSF
-
What should be aware of during recovery after taking myelograms?
transiently worse after taking the films (can pre-tx w NSAIDs)
-
list 6 cortical brain diseases?
- rabies
- EPM
- alpha virus encephalitis (EEE,WEE,VEE)
- west nile virus
- herpes myeloencephalitis
- leukoencephalomalacia
-
How long after administration is rabies vaccine effective?
30 days
-
what is causative agent of equine protozoal myeloencephalitis? Definitive host?
- sarcocystis neurona
- opossum
-
How do horses get PEM?
possom eats sarcocyst in muscle tissue - poop sporocyst - horse eats sporocyst
-
what is the most defining clinical sign for EPM?
asymmetrical (otherwise can mimic any neuro disease)
-
how is EPM diagnosed?
- hx + CS
- western blot *only if horse neurological*
- CSF protein/cytology normal
-
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*
-
what is a quantitative test for EPM w/97% specificity?
indirect immunoflorescence antibody test (IFAT)
-
What pathologic findings are suggestive of EPM?
perivascular cuffing w/mononuclear cells
-
how is EPM treated? what is efficacy of this tx?
folic acid inhibitors w/combo of antibiotics (sulfa + pyrimethamine) for 90-120 days
-
Coccidiostat (ponazuril) for 28days
-
only about 62% efficacy in both (meas. by improvement/return to function)
-
Should horses be vaccinated against EPM?
no, vx no longer available bc not efficacious
-
Are EEE/WEE/VEE reportable and/or zoonotic?
yes and yes
-
What is the vector and amplifying host for these alphaviruses?
- vector - mosquito (culiseta melanura)
- amplifier - birds (horse amplifies VEE only)
-
why is EEE/WEE/VEE known as sleeping sickness?
somnolence, recumbency, death
-
what are other signs seen with EEE/WEE/VEE?
- head pressing, dementia
- seizures, blindness
- Cr N deficits
- hypermetria, ataxia
-
what is prognosis for EEE? for WEE?
- EEE: 90% mortality (poor)
- WEE: <50% mortality (fair to poor)
-
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
-
what are expected CSF findings with alphaviruses?
- xanthochromia
- elevated protein
- neutrophilia
-
how is alphavirus diagnosed post mortem?
virus isolation from the brain
-
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
-
Is west nile virus zoonotic? reportable?
- yes zoonotic
- not reportable
-
how is west nile virus transmitted? reservoir?
- mosquito
- birds as reservoir (crows)
-
what kind of virus is west nile?
flavivirdae, RNA virus
-
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% (" ")
-
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)
-
how is WNV diagnosed?
Treatment?
- IgM capture ELISA (81%sens/100%spec)
- virus isolation, PCR
supportive tx
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