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Neurology Flashcards

1
Q

Control of PLRs

A

Oculomotor (III)

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2
Q

Localization of brain lesion, and midbrain

A

?

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3
Q

Most sensitive test for rabies

A

Immunofluorescent antibody test in brain Gold standard by public health department

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4
Q

Horse with 3 week history of hind limb ataxia, fecal retention, decreased tail tone, facial nerve paralysis, masseter muscle wasting

A

Polyneuritis equi

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5
Q

Cause of stringhalt

A

False dandelion (Hypochoeris radicata)

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6
Q

Clinical sign in horse with Horner’s syndrome

A

Unilateral sweating

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7
Q

Histology lesion in listeriosis

A

Micro-abscesses in brainstem

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8
Q

Polioencephalomalacia: treatment and prevention

A

• Thiamine: 10 mg/kg IV q6h for 3 days Chelation therapy for lead: CaEDTA, Zn supplement because it chelates too • Dietary management • Water source evaluation • Avoid high sulfur feedstuffs (Gyspum, molasses) • Remove or fence of junk piles • Early identification of cases

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9
Q

Types of botulism in adult horses

A

Mostly type B (A in western USA, B in eastern)

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10
Q

Sheep with alopecia on trunk and axilla, nibble when itched

A

Scrapie

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11
Q

Guttural pouch nerves

A

Accessory (XI) Hypoglossal (XII)

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12
Q

Most indicative lesion on radiographs for Wobbler’s

A

?

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13
Q

Most important cell to fight EHV-1

A

Cytotoxic T lymphocytes –> lyse virus-infected cells

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14
Q

Causative agent of dummy lambs

A

Blue tongue virus, related to MLV to pregnant ewes

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15
Q

Temporohyoid osteoarthropathy

A

?

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16
Q

Clinical signs of equine motor neuron disease

A

○ Trembling ○ Muscle fasciculations ○ Base-narrow stance (“horse-on-a-ball”) ○ Shifting weight rear limbs, better when walking, hypometric steps but no ataxia ○ Abnormal sweating ○ Excessive recumbency, low carriage head ○ Muscle atrophy (esp triceps, quadriceps, gluteal, neck → low head carriage) § Onset 1 month before acute signs ○ Tail elevated (Denervation atrophy and fibrotic contracture of the sacrococcygeous dorsalis) ○ Weight loss despite normal or ravenous appetite ○ No ataxia, move better than stand

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17
Q

Life cycle of Parelaphostrongylus tenuis in white tail deer

A

adult worms in subarachnoid space and venous sinuses–> eggs in venous blood–> lung–> embrionate –>larvae penetrate airways–> cough to pharynx –> swallow–> feces L1 –>penetrate snails and slugs(L1–>L3) –> ingestion snail –> GI wall –> abominal migration 90d–>migration nerve rootlets–>CNS

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18
Q

Cerebral Perfusion Pressure

A

MAP – ICP

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19
Q

Best Diagnostic test for CSF from a horse with suspected Neospora hughesi:

A

IFAT?

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20
Q

What is the Single Nucleotide Polymorphism that differentiates more neuropahtogenic EHV-1 strains?

A

SNP DNA polymerase D752 (neuropathogenic)

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21
Q

In a horse that falls on its back and is bleeding from its nose what is the best choice to perform IV fluid therapy:

A

Hypertonic saline.?

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22
Q

Horse with symmetric muscle atrophy and weakness, sweating one side a spot only, muscle atrophy in the epaxial muscles: what is the best to diagnostic test?

A

Biopsy muscle: sacrocaudalis dorsalis (Se 90%)

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23
Q

Guttural pouch lesion on left side, leading to Horner’s syndrome. Clinical signs?

A

?

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24
Q

Filly with scoliosis neck towards right side, weakness, ataxia in all limbs, analgesia of the right side of the neck. Where is the lesion?

A

Grey mater horns right side?

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25
Q

Neurological sx in steers at feedlot

A

H. somni

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26
Q

Calves in a dairy with signs of otitis media, central vestibular disease, what to prevent it?

A

Pasteurize milk for the calves (Mycoplasma)

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27
Q

What mycoplasma is associated with otitis media in dairies?

A

M. Alkalscesns,?

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28
Q

Ayrshire cow with head pressing and hx blindness. Treatment?

A

Edta treatment plan (lead toxicity)

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29
Q

Listeria relation with

A

winter months in cattle

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30
Q

Meningeal worm related with

A

majority of cases in fall (not all cases have Eosinophilia)

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31
Q

Listeria adhesion and supervivence in macrophages

A

Listeriolysin-O permits escape form phagosomes

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32
Q

Listeria ocular lesions, associated with

A

silage

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33
Q

PEM associated with

A

High levels of Sulfur in water

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34
Q

Tx for viral encephalitis with EHV-1

A

valacyclovir > oral availability

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35
Q

Lamb with posterior ataxia

A

Enzootic ataxia, Cu deficiency

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36
Q

Heifer with dorsomedial strabismus

A

PEM sulfur feed - water

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37
Q

EHV-1 CSF findings

A

Increased RBC, increased protein, increased leukocytes

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38
Q

Tetanus toxin

A

spinal nerves, spinal cord, interneurons, inhibition motor ventral neurons

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39
Q

Botulism toxin

A

Inhibit release of Ach at the neuromuscular junction

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40
Q

What most adequate concent for tx of hypernatremia 178 mmol/L

A

175 mmol/L

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41
Q

In botulism, which chain cleaves?

A

Light chain

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42
Q

7 week old Arabian foal, no menace, hypermetria, head tremors

A

Cerebellar abiotrophy

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43
Q

Lesion of NAD QH/EDM:

A

Axon necrosis and demyelination

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44
Q

PEM in feedlot cattle drinking well water

A

Sulfur toxicity

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45
Q

Tetanospasmin

A

Synaptobrevin

46
Q

How is scrapie transmitted?

47
Q

Horse on sorghum, clinical signs?

A

Flaccid bladder, tail paralysis

48
Q

Virulence factor of listeria

A

Listerolysin O

49
Q

Clinical signs of Horner’s syndrome in horses

A
  • Ptosis upper eyelid
  • Miosis
  • Enophtalmos –> Protrusion nictitating Mb
  • Unilateral facial-C2 sweating
50
Q

What is the origin of the clinical signs in Horner’s syndrome?

A

Dysfunct of sympat nerve supply to the neck and head

51
Q

How can you determine if the lesion for Horner’s syndrome is pre- or postganglionar?

A

Epinephrine application to the eye:

  • Post-ganglionar lesion –> midriasis in 20min
  • Pre-ganglionar lesion –> midriasis retarded (30-50min)
52
Q

What type of propioception is altered in lesions to the cerebrum and midbrain?

A

Concious propiocention –> abnormal potural reactions

  • If lesion rostral to medulla oblongata –> signs are contralateral
53
Q

Signs of cerebellar disease

A
  • Failure to blink to bright light
  • Lack menace response
  • Head tremor
  • Intentional tremors
  • Hypermetry
54
Q

Which of the equine encephalitis has a high viremia, thus it is able to be transmitted from the horse

A

Venezuelan Equine Encephalitis (VEE)

55
Q

Which proteins are important in the virulence of WNV?

A

M (Mb) and E (Envelope)

56
Q

Which receptor is used by WNV to enter the cells?

A

Chemokine CCR5 receptor

57
Q

Diagnosis of equine encephalitis

A

IgM capture ELISA

  • Can distinguish between disease (IgM) and vaccination (IgG)
58
Q

Cranial nerves affected in WNV

A

VII, IX, XII

Head tilt, flaccid muzzle and lips, inability to swallow

59
Q

Pathogenesis of Borna disease

A

Nasal –> transaxonal transport to CNS –> replication neurons and glial cells –> migration to perif nerves and retina –> blindness

*Persistent infection

60
Q

This plant corresponds to Yellow Star Thistle, Knapweed. To which condition in horses it is related?

A

Equine Nigropallidal Encephalomalacia

  • Toxic principle → repin → inhibits dopamine release
61
Q

Cranial nerves affected in listeriosis

62
Q

Is listerioris a concern for human health?

A

Can infect mammary gland –> excreted in milk –> zoonosis

63
Q

Bacteria implicated in otitis media-interna in calves

A

Mycoplasma bovis (Dairy)

Pasteurella multocida (feedlot)

64
Q

Which is the single nucleotide polymorphism (SNP) related to EHM and why?

A

D752 leads to higher magnitude and duration of viremia (theory)

65
Q

Why are older horses more susceptible to EHM?

A

Greater IFN-γ response to EHV-1

66
Q

Gold standard for diagnosis of EHV-1

A

Virus isolation

  • Nasal/nasopharyngeal swab or buffy coat
67
Q

Test of choice for EHV-1

A

PCR (Glycoprot B)

  • High sensitivity and specificity (Exceeds virus isolation)
  • Nasal samples > nasopharyngeal samples –> Results indicate risk of shedding
  • Uncoagulated blood –> Results indicate active viremia (Not latent infection)
68
Q

Usefulness of serology for diagnosis of EHV-1

A

Screening in-contact horses exposed to virus in outbreak (Indirect evidence EHV-1)

69
Q

For EPM horses ingest _______ from infected feces of opossum

70
Q

How do sporocyts from S. neurona reach the CNS?

A

Leukocyte associated parasitemia

Isn’t this so cool! This parasite is a badass!

71
Q

What is the form of S. neurona that gt stablished in the CNS?

A

Schizonts

Merozoites

72
Q

What does IFAT detect for diagnosis of S. neurona?

A

IgG against whole merozoite

73
Q

What is one of the main downsides of IFAT for the diagnosis of EPM?

A

Unable to differentiate btw S. neurona and S. fayeri

74
Q

Is the use of snSAG1 acceptable for the diagnois of EPM?

A

NO NO NO! The Se is unacceptable

75
Q

What does a C-value > 1 means when using snSAG2

A

CNS production of antibodies

76
Q

Test with best Se and Sp for EPM

A

snSAG 4/3 serum-to-CSF ratio

77
Q

Which test for EPM is ore accurate for CSF samples?

78
Q

Mechanism of action of ponazuril

A

Works at plastid body in merozoite → mitochondria and energy metabolism affected

79
Q

Where do you have to pay more attention when interpreting a myelogram?

A

Compression of the DORSAL column

Compression of ventral column is normal

80
Q

Lesion on EDM/NAD

A

Demyelinization of dorsal funiculi of spinal cord and brainstem (young horses)

  • Caudal brainstem nuclei (medulla oblongata) and spinal cord (dorsal spinocerebellar tracts esp)
  • Diffuse neuronal fiber degeneration (dystrophy) of white matter
  • Astrocytosis, astrogliosis vacuolization, myelin loss, spheroid formation (axonal swelling) and lipofuscin-like pigment accumulation
81
Q

Cause of EDM

A

Unknown, believed combination of dietary vitamin E deficiency and genetic predisposition

82
Q

Breeds where NAD is more described

A

Morgans and Haflingers (familial tendencies) and QH

83
Q

Mode of inheritance of EDM/NAD

A

Autosomal dominant

84
Q

Parasite that causes cervical scoliosis in horses

A

Parelaphostrongylus tenuis

85
Q

Effect of organophosphates in horses

A

Bilateral laryngeal paralysis

86
Q

Enzootic ataxia in sheep (aka awayback) is caused by…

A

Deficient maternal diet in Cu

87
Q

Inheritance of cerebellar abiotrophy

A

Autosomal recessive in Arabians

gene MUTYH

88
Q

In tetanus, which toxin is internalized in axons, transpoted retrograde and after 1-14 days enters CNS, reaches neuronal cell body and binds irreversible to presynaptic inhibitory interneurons?

A

Tetanospasmin, LIGHT chain

89
Q

Effects of light chain of tetanospasmin

A

Inhibits release of inhibitory neurotransmitters GLYCINE and GABA ==> muscle rigidity and spasms

90
Q

Effects of Mg infusion in cases of tetanus

A

Blocks neuromuscular transmission, interfere with catecholamine release, reduces receptor responsivenes to catecholamines, antagonizes action of Ca, anticonvulsivant and vasodilator

91
Q

Which antimicrobial is preferred to manage tetanus in horses and cattle

A

Horse: metronidazole

Cattle: penicillin

*penicillin has anti-GABA and proconvulsant properties*

92
Q

tetanus immunization for foals from nonvaccinated mares

A

3 doses at 4 week intervals, beginning at 1-4 months old

93
Q

most common route of infection of botulism in horses and cattle

A

Ingestion preformed toxin

94
Q

Diagnosis for C. botulinum

A
  1. Demonstrate preformed toxin in serum, GI contents or wound
  2. Demonstrate C. botulinum spores in GI contents or feed, with compatible clinical signs
  3. Detec Ab response in recovering animals
95
Q

Best test for C. botulinum

A

Mouse bioassay –> the most Se (before PCR available)

PCR

96
Q

What is the effect of the botulinum toxin?

A

light chain is released into cytosol → inactivates the SNARE complex

→ Prevents fusion of synaptic vesicles → prevents exoxitosis and release of the Acetilcholine at NEUROMUSCULAR JUNCTION

97
Q

In cases of botulism, why is it important to treat promptly with the antitoxin?

A

It binds only toxin that is not bound to neuromusc junction

98
Q

Characteristics of EMND

A

Generalized neuromuscular weakness

Neurogenic muscle atrophy

99
Q

In chronic form of EMND, what ocular abnormality can be found?

A

retinopathy (mosaic pattern→lipofuscin-like pigm deposition in fundus, no visual impair)

100
Q

Where to do muscle or nerve biopsy for diagnosis of EMND?

A
  • Sacrocaudalis dorsalis (Se 90%)
  • Ventral branch of spinal accessory nerve (more sensitive in chronic cases): Bungner’s bands
101
Q

Characteristics of polyneuritis equi (neuritis of cauda equina)

A

tail and anal sphincter paralysis, often accompanied by cranial and peripheral nerve damage

102
Q

Cause of polyneuritis equi

A

unknown. Suggested primary immune reaction and viral inflammatory disease

103
Q

Diagnosis of polyneuritis equi

A
  • Definitive: post-mortem
  • Inflammatory leukogram
  • CSF: elevated prot + elevated WBC (mononuclear) / or normal
  • P2 myelin Ab *in CSF (weak evidence because can be observed in adenovirus and EHV-1)
104
Q

Diagnosis for equine grass sickness

A

Topical phenylaphine (0.5%) –> reversion ptosis within 30 mins is supportive for diagnosis

Hystopathology enteric ganglia and autonomic ganglia (gutt pouch: cranial cervical ganglia) –> Gold standard

105
Q

What type of nerve damage correlates to the picture

(Stifle and hock extended, fetlock flexed)

A

Sciatic nerve paralysis

  • Can support weight if limb is placed under body
  • Limb is held to the rear
106
Q

Official test for rabies according to the CDC guidelines?

A

Fresh samples of the brain for detection of viral antigen by fluorescent antibody test (FAT)

Transverse section of the cerebellum and the underlying brainstem

107
Q

Which muscle is used for biopsy when a case is suspected of EMND?

A

Sacrocaudalis dorsalis medialis

108
Q

Which alphaviruses are more neuroinvasive?

A

EEE and epizootic VEE

109
Q

For which equine encephalitis the horse is an important vector? Yes… it is actually a risk for human outbreaks!

A

Epizootic Venezuelan Equine Encephalitis

  • Subtypes IAB, IC
  • High viremia
110
Q

Which receptor does WNV uses to enter cells

A

Chemokine CCR5

111
Q

Which proteins and cells are involved in neuronal apoptosis of WNV?

A
  • Caspase 9
  • CD8+ T cells
112
Q

What is the fundamental lesion in PEM

A

Neuronal edema with necrosis

  • ATP depletion –> decrease function of Na/K pump –> edema
  • Edema leads to pressure necrosis

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