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RUSVM LAM II > Neuro > Flashcards

Neuro Flashcards

1
Q

Where are circling and head tilt lesions usually located?

A

Vestibular

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2
Q

Propulsive movement originates form?

A

Frontal lobe

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3
Q

If you have an animal that is blind or has seizures, where is the lesion localized

A

Brainstem

Blindness — occipital lobe

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4
Q

What is the purpose of the basal ganglia?

A

Processing link, initiates and directs voluntary movement

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5
Q

Spastic ataxia, dysmetria, and tremors are associated with lesions in the _________

A

Cerebellum

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6
Q

If you have normal mentation and facial nerves but bilateral gait abnormalities, where would the lesion be?

A

Spinal cord

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7
Q

UMN/LMN?

Spasticity and hypertonic
Loss of inhibition of myotatic reflexes

Spinal reflexes intact
Paresis

A

UMN

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8
Q

UMN/LMN??

Hypotonia and hyporeflexia
Muscle weakness
Loss of spinal reflexes
Muscle atrophy

A

LMN

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9
Q

What two viruses cause hydrocephalus in ruminants?

A

Bluetongue and akabane

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10
Q

What neurological signs can be caused by a vitamin A deficiency?

A

Interferes with the absorption of CSF at the arachnoid villi

CSF pressure elevates
— results in blindness first followed by seizures
— papillidema at the optic chiasm

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11
Q

What is cerebellar abiotrophy?

A

Autosomal recessive traits of Herefords and short horns

BVD between 100-200 days gestation
— folial degeneration, cavitation of cerebellum

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12
Q

What ocular lesions can be assoicated with BVD?

A

Retinal atrophy and micro-ophthalmia

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13
Q

Hereditary disorder of the vertebral canal in Jerseys?

A

Hypomyelinogenesis

-spastic dysmetric gait if they can walk

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14
Q

Neuraxial edema is an autosomal recessive traits of what breeds?

A

Herefords

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15
Q

Charolais get what disorder of the vertebral canal?

A

Myelin disorders

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16
Q

Pathogenesis of tetanus?

A

Tatanospasim toxin

Necrotizing effect
— decreased tissue oxygenation
— facilitates Bacteria prolifertion

TeNT binds to nerve cell and is taken up by endocytosis
Moves retrograde up the axon

Internalized into interneurosn
Prevent release of glycine and GABA, binding irreversibly

Recovery only with growth of new nerve terminals

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17
Q

Clinical signs of tetanus?

A

Wound

Stiff gait 
Mild bloat, no ruminations  
Difficulty rising 
Pump-handle tail 
Hyperesthesia

Erect ears pulled back to poll, “sardonic grin”

Prolapsed third eyelid- spasm of retractor oculi m.

Spasm of masseter m- lock jaw
Loss of swallowing

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18
Q

Treatment for tetanus?

A

Wound debridement and antibiotics (PPG)

Tetanus antitoxin

Acepromazine and diazepam for relief of muscle spasm

Good nursing care

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19
Q

Prevention of tetanus?

A

Vaccinate with tetanus toxoid
Start at 6 weeks then every 2-4weeks

Clostridium bacterins C and D

Booster pregnant ewes/does in late gestationto protect lambs and kids

Tetanus antitoxin with docking/castratting

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20
Q

Where do cattle usually get botulism?

A

Decaying vegetation, carrion

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21
Q

How do ticks cause paralysis?

A

Tick saliva contains neurotoxin

Rx: remove tick, prog is good if dx quickly

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22
Q

What two types of ticks can cause paralysis?

A

Ixodes holcyclus

Dermacentor spp

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23
Q

How can you prevent rabies?

A

Vaccination of all livestock is NOT recommended

Imrab 3

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24
Q

T/F listeria is zoonotic

A

True

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25
Q

How is listeria spread?

A

In feces of many mammals, birds and fish

Survive in environment for months to years

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26
Q

What are sources of exposure of listeriosis?

A

Silage: pH <5.5 inhibits growth

Fecal contamination
Chronic intramammary infection
Poultry litter used as bedding

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27
Q

When does listeria infection usually occur?

A

Commonly associated with environmental and nutritional stress

Requires wound for entry
Rough browse/hay

Erupting teeth

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28
Q

What are the clinical signs of listeriosis?

A

Multiple unilateral cranial nerve defects

Circling, head tilt, facial paralysis
Fever-early
Silage eye: uveitis, conjunctivitis, keratitis (secondary to not blinking)

Anorexia, dysphagia

Recumbent- opisthotonos, paddling

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29
Q

What is the pathogenesis of listeria?

A

Rootlet trigeminal —> intra-axonal migration —> brainstem

Bacteria bind to cell via surface proteins
Enter cytoplasm via hemolysis
Multiply, press on internal surface cell membrane, form listeriopods that invaginate into adjacent cell

Cell to cell movement evades phagocytosis

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30
Q

PH must be above ____ for proliferation of listeria to occur?

A

5

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31
Q

Treatment for listeria?

A

Penicillin
OTC **

NSIAD, fluids, vitamins

Mortality approaches 100% if recumbent

32
Q

How can you diagnose listeriosis antemortem ?

A

Clinical signs — doesnt usually cause limb paralysis

Chemistry: stress leukogram, evidence of dehydration

CSF: increased protein (>20mg/dl) and high mononuclear cells (>10 cells.ul)

33
Q

What is the definitive diagnosis for listeriosis

A

PM

Mutifocal-to-coalescing areas of necrosis and severe infiltration of macrophages/neutrophils
Axonal swelling and degeneration

Lesions most severe in pons and medulla

34
Q

Conditions causes by histophilus somni?

A 
Thromboembolic meningoenchepalitis 
Pneumonia 
Arthritis 
UTI 
Abortion 
Myocarditis 
Neurological disease
35
Q

Pathogenesis of TME?

A

Obligate of mucosal surface

Compromised host
Migrates through unprotected epithelial cells

Meets brain epithelial cells, causes cytoskeletal rearrangement

Increased paracellular permeability of vascular endothelial cells— neuro signs
Influx

Inreased CSF in Brian

36
Q

Clinical signs of TEME>

A

Somnolence is the first clinical signs

Ataxia and weakness

Lateral recumbency, profound depression, opisthotonos, convulsions

Closes or partially closed eyelids

37
Q

How can you confirm TEME diagnosis?

A

History and PE

CBC- non specific changes

CSF - cellular changes reflective of bacterial infection + evidence of hemorrhage

38
Q

Treatment for TEME>

A

Only attempt early in dz

Ab with gram - spectrum

Down animals euthanize

Can be prevented with vaccination

39
Q

Brain and pituitary abscesses are most often caused by what bacteria?

A

Trueperella pyogenes

40
Q

Signs of brain/pituitary abscess?

A

Vision loss in contralateral eye, depression, mania, head pressing, circling with head tilt toward the side of lesion

41
Q

How do pituitary abscesses arise?

A

Hematogenous origin — rete mirabile —> mesh of capillaries converging pituitary
— cavernous sinus —> valveless venous system bathing pituitary

Dehorning complication
Head butting

42
Q

Clinical signs of pituitary abscess?

A

Blindness, pupillary dysfunction, nystagmus, dysphagia, facial paralysis, circling, head tilt

43
Q

What is polioencephalomalacia?

A

Swelling and softening of gray matter

Dysfunction of Na-K ATP pump
- intracellular Na- promotes water into cell

Thiamine - cofactor in neuronal ATP production
Rumen microbes needed-thiamine production
Non-ruminants rely on diet

44
Q

What type of diets promotes H2S gas formation which interferes with oxidative processes in mitochondria and deplete ATP

A

Grain

45
Q

Where is H2S found?

A 
Drinking water 
Molasses 
Forage 
Urine acidifiers mineral supplements 
Brassica grass
46
Q

Clinical signs of polioencephalomalacia?

A

Central blindness, ataxia, proprioceptive deficits, head pressing, hyperexcitability

Leads to recumbency, opisthotonus, seizure, coma, and death

Also strabismus and convulsions

47
Q

How an you diagnose polio/?

A

Test food/water for H2S
>1000ppm in water
>4000ppm in diet

> 1000ppm in rumen gas indicates toxic levels

48
Q

Treatment of polio?

A

Thiamine

Increase forage adding gluogenic precursors

Dexamethasone

49
Q

What can cause a nervous ketosis?

A

Negative energy balance

50
Q

Most common CS of nervous ketosis

A

Anorexia

Drop in milk production

51
Q

What is the pathology in nervous ketosis?

A

Diffused cerebrocortical neuronal necrosis
— bilateral blindness with intact PLR

Cerebellar purkinje cell necrosis

52
Q

Rx for nervous ketosis?

A

Glucose

Propylene glycol

53
Q

Main isolate from otitis media/interna in ruminants?

A

Mycoplasma bovis

54
Q

What are sources of lead toxicity?

A

Grease, oil, old paint, lead-headed nails, batteries, linoleum, smelter discharges

55
Q

What type of lead is readily absorbed?

A

Lead salts (eg acetate, phosphate, carbonate, hydroxide)

56
Q

Sudden death, central blindness, tremors, chewing fits, seizures, bellowing

DDX?

A

Polio

Lead toxicity

57
Q

How can you confirm diangosis of lead toxicity?

A

Basophilic stippling and normocytic, normochronic anemia

Blood lead measurement

58
Q

Treatment for lead toxicity?

A

Usually die before/in spite of treatment

Remove from source immediately
Intermittent CaEDTA to chelate from bone

Early in disease — thiamine

59
Q

A copper deficiency during prenatal/perinatal period can lead to what condition?

A

Sway back AKA enzootic ataxia

60
Q

Copper deficiency prenatally results in bilateral symmetrical ____ in the dorsolateral spinal cord

A

Myelin degradation

61
Q

Clinical signs of sway back?

A

Rear limb ataxia
Muscle atrophy and paresis
Tetraparesis seen at birth

Signs are static in neonates but progressive in older animals

62
Q

What is the diagnosis for swayback?

A

Definitive dx on necropsy

Measure body tissue Cu
Plasma copper status (blood Cu increase with stress) and assess dietary Cu

63
Q

Treatment of swayback

A

Hypomyelinogenesis and demyelination is irreversible

Supplement Cu to prevent more cases
Cu to molybdenum ratio 6:1

64
Q

Progressive ataxia is a recessive defect in purebred/ mixed breed _________ calves at 6-36 months

A

Charolais

65
Q

What is the major lesion in progressive ataxia?

A

Eosinophilic plaques on white matter in the brain/spinal cord

66
Q

What are clinical signs of progressive ataxia?

A

Stiff neck
Dragging rear toes
Stumbling
Proprioceptive deficits worsening with exercise

Difficulty in maintain posture during urination and pulsatile micturition

67
Q

What is another name for progressive degenerative myeloencophalopathy?

A

“Weaver syndrome”

68
Q

Weaver syndrome is an inherited disorder in purebred ___________

A

Brown Swiss and Angler cattle

69
Q

Clinical signs of progressive degenerative myeloencephalopathy?

A 
Paraparesis 
Ataxia 
Dysmetria of pelvic limbs 
Insidious progression 
Muscle wasting over hindquarters
70
Q

What is the MOA of organophosphate toxicity?

A

Bind with acetylcholinesterase —> increases ACh

71
Q

Clinical signs of organophosphate toxicity?

A

Muscarinic: Dyspnea, hypersalivation, diarrhea, bradycardia, pupillary contrition

Nicotinic: muscle tremors, tetany, recumbency, and opisthotonos

72
Q

What is the treatment for organophosphate toxicity?

A

Atropine

Oral activated charcoal

Oximes — break bone of OP and AChase within first 24hours
2-PAM

73
Q

What bacteria are often the cause of veterbral osteomyelitis and spinal abscess?

A

Trueperella pyogenes

Fusobacterium necrophorum

74
Q

How can you confirm vertebral osteomyelitis/spinal abscess?

A

Acute signs after fracture, veterbral collapse, or spinal cord compression

Malaise, fever, stiffness, lack of proprioceptive, paresis, and/or recumbency

Rads — proliferation, lysis, sclerosis and soft tissue swelling

75
Q

Treatment for spinal abscess ?

A

Surgical curettage, lavage,and drainage

Long term antibiotics

Subsequent meningitis is often associated with poor prognosis

RUSVM LAM II (22 decks)

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