Neurology Problem-Based Studies Part III Flashcards
what are the top differential diagnoses for general proprioceptive ataxia in camelids?
focal spinal ataxia
multifocal disease
brain
what is the most common neurological disease in US camelids?
Parelaphostrongylus tenuis
meningeal worm
what is the definitive host of Parelaphostrongylus tenuis?
white tail deer
ruminants and camelids are aberrant hosts
how is Parelaphostrongylus tenuis diagnosed?
CSF eosinophilia >17% high sensitivity and specificity
what can you use to treat Parelaphostrongylus tenuis?
panacur/fenbendazole 40-50 mg/kg 5 days
NSAIDs or corticosteroids
supportive care
what are the viral encephalitis causes in camelids?
equine herpesvirus
west nile virus
eastern equine encephalitis
rabies
what is thee CSF like in camelids with west nile virus?
increased protein
increased nucleated cell count
predominance of macrophages and small lymphocytes
how can you diagnose eastern equine encephalitis in camelids?
PRNT
hemagglutination inhibition
serum neutralization assay
ELISA for IgM
in lower motor neuron weakness, which tail pull is weak?
both standing and walking
how does dysfunction and death of motor neurons in equine motor neuron disease occur?
oxidative disorder
how can equine motor neuron disease be diagnosed?
increased CSF protein in 50%: increased intrathecal production of IgG in many horses
pigment retinopathy: honeycomb mosaic fundic pattern
what is botulism?
neuromuscular disorder associated with inhibition of acetylcholine release at neuromuscular junction
generalized symmetric lower motor neuron and parasympathetic dysfunction
how can you test for botulism?
grain test
forage/sample analysis: GI content, feces, reflux, forage, wound discharge (no blood)
what are the clinical signs of moldy corn disease (leukoencephalomalacia)?
profound dullness- cortical signs
blindness
multiple animals affected
+/- death presenting complaint
what is the pathology of moldy corn disease?
severe liquefactive necrosis or malacia of white matter of frontal cortex, perivascular and vascular congestion in white matter of brain
who is impacted by polioencephalomalacia, cerebrocortical necrosis?
ruminants
camelids
what is CSF like in polyneuritis equi?
xanthochromia
mildly increased protein and cell count
nonspecific
what does tetanolysin do?
damages viable tissue: creates favorable environment for expansion of infection
exotoxin
what are the clinical signs of tetanus?
muscle rigidity
3rd eyelid prolapse with globe retraction of eye
hyperthermia
spasticity, “sawhorse” stance
stiff gait
sensitivity to sound
gas-bloat, colic
potentially autonomic response
what are the causes of focal spinal ataxia in camelids?
trauma
suppurative discospondylitis
what are the types of multifocal disease in camelids?
P. tenuis
viral encephalitis
listeria
what are the causes of brain problems leading to GP ataxia in camelids?
PEM
hepatic encephalopathy
both cortical
what is the definitive host of P. tenuis?
white tail deer
how can you prevent P. tenuis?
host control
preventative use of avermectins
how can you treat P. tenuis?
panacur/fenbendazolee
NSAIDs, maybe corticosteroids
supportive care
what can EHV-1 cause in camelids?
irreversible blindness
some also neurological dysfunction
how does WNV affect camelids?
higher mortality than in horses
acute onset
CSF changes: macrophages and small lymphocytes
is there a familial or heritable predisposition to equine motor neuron disease?
not proven
what is the chronic form of equine motor neuron disease like?
muscle atrophy generally symmetric
tail head held high
what does equine motor neuron disease affect?
lower motor neurons of spinal cord grey matter
how many toxins are identified in botulism?
8
horses commonly get type B toxin
how can you treat botulism?
treat early- poor if recumbent
supportive care
antitoxin early
vaccination
how can you treat polioencephalomalacia, cerebrocortical necrosis?
eliminate risk factors and underlying disease
thiamine hydrochloride
what happens in polyneuritis equi?
progressive immun-mediated lymphoplasmacytic infiltration and demyelination of lumbosacral and sacrococcygeal nerve roots
how is polyneuritis equi diagnosed?
exclusion
what does tetanospasmin do?
binds irreversibly to presynaptic inhibitory interneurons
spreads hematogenously
