Neurology Problem-Based Studies Part III Flashcards

1
Q

what are the top differential diagnoses for general proprioceptive ataxia in camelids?

A

focal spinal ataxia
multifocal disease
brain

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2
Q

what is the most common neurological disease in US camelids?

A

Parelaphostrongylus tenuis
meningeal worm

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3
Q

what is the definitive host of Parelaphostrongylus tenuis?

A

white tail deer
ruminants and camelids are aberrant hosts

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4
Q

how is Parelaphostrongylus tenuis diagnosed?

A

CSF eosinophilia >17% high sensitivity and specificity

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5
Q

what can you use to treat Parelaphostrongylus tenuis?

A

panacur/fenbendazole 40-50 mg/kg 5 days
NSAIDs or corticosteroids
supportive care

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6
Q

what are the viral encephalitis causes in camelids?

A

equine herpesvirus
west nile virus
eastern equine encephalitis
rabies

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7
Q

what is thee CSF like in camelids with west nile virus?

A

increased protein
increased nucleated cell count
predominance of macrophages and small lymphocytes

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8
Q

how can you diagnose eastern equine encephalitis in camelids?

A

PRNT
hemagglutination inhibition
serum neutralization assay
ELISA for IgM

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9
Q

in lower motor neuron weakness, which tail pull is weak?

A

both standing and walking

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10
Q

how does dysfunction and death of motor neurons in equine motor neuron disease occur?

A

oxidative disorder

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11
Q

how can equine motor neuron disease be diagnosed?

A

increased CSF protein in 50%: increased intrathecal production of IgG in many horses
pigment retinopathy: honeycomb mosaic fundic pattern

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12
Q

what is botulism?

A

neuromuscular disorder associated with inhibition of acetylcholine release at neuromuscular junction
generalized symmetric lower motor neuron and parasympathetic dysfunction

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13
Q

how can you test for botulism?

A

grain test
forage/sample analysis: GI content, feces, reflux, forage, wound discharge (no blood)

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14
Q

what are the clinical signs of moldy corn disease (leukoencephalomalacia)?

A

profound dullness- cortical signs
blindness
multiple animals affected
+/- death presenting complaint

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15
Q

what is the pathology of moldy corn disease?

A

severe liquefactive necrosis or malacia of white matter of frontal cortex, perivascular and vascular congestion in white matter of brain

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16
Q

who is impacted by polioencephalomalacia, cerebrocortical necrosis?

A

ruminants
camelids

17
Q

what is CSF like in polyneuritis equi?

A

xanthochromia
mildly increased protein and cell count
nonspecific

18
Q

what does tetanolysin do?

A

damages viable tissue: creates favorable environment for expansion of infection
exotoxin

19
Q

what are the clinical signs of tetanus?

A

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

20
Q

what are the causes of focal spinal ataxia in camelids?

A

trauma
suppurative discospondylitis

21
Q

what are the types of multifocal disease in camelids?

A

P. tenuis
viral encephalitis
listeria

22
Q

what are the causes of brain problems leading to GP ataxia in camelids?

A

PEM
hepatic encephalopathy
both cortical

23
Q

what is the definitive host of P. tenuis?

A

white tail deer

24
Q

how can you prevent P. tenuis?

A

host control
preventative use of avermectins

25
Q

how can you treat P. tenuis?

A

panacur/fenbendazolee
NSAIDs, maybe corticosteroids
supportive care

26
Q

what can EHV-1 cause in camelids?

A

irreversible blindness
some also neurological dysfunction

27
Q

how does WNV affect camelids?

A

higher mortality than in horses
acute onset
CSF changes: macrophages and small lymphocytes

28
Q

is there a familial or heritable predisposition to equine motor neuron disease?

A

not proven

29
Q

what is the chronic form of equine motor neuron disease like?

A

muscle atrophy generally symmetric
tail head held high

30
Q

what does equine motor neuron disease affect?

A

lower motor neurons of spinal cord grey matter

31
Q

how many toxins are identified in botulism?

A

8
horses commonly get type B toxin

32
Q

how can you treat botulism?

A

treat early- poor if recumbent
supportive care
antitoxin early
vaccination

33
Q

how can you treat polioencephalomalacia, cerebrocortical necrosis?

A

eliminate risk factors and underlying disease
thiamine hydrochloride

34
Q

what happens in polyneuritis equi?

A

progressive immun-mediated lymphoplasmacytic infiltration and demyelination of lumbosacral and sacrococcygeal nerve roots

35
Q

how is polyneuritis equi diagnosed?

A

exclusion

36
Q

what does tetanospasmin do?

A

binds irreversibly to presynaptic inhibitory interneurons
spreads hematogenously