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RUSVM LAM II > Neuro > Flashcards

Neuro Flashcards

(75 cards)

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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
How is listeria spread?
In feces of many mammals, birds and fish | Survive in environment for months to years
26
What are sources of exposure of listeriosis?
Silage: pH <5.5 inhibits growth Fecal contamination Chronic intramammary infection Poultry litter used as bedding
27
When does listeria infection usually occur?
Commonly associated with environmental and nutritional stress Requires wound for entry Rough browse/hay Erupting teeth
28
What are the clinical signs of listeriosis?
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
29
What is the pathogenesis of listeria?
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
30
PH must be above ____ for proliferation of listeria to occur?
5
31
Treatment for listeria?
Penicillin OTC **** NSIAD, fluids, vitamins Mortality approaches 100% if recumbent
32
How can you diagnose listeriosis antemortem ?
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
What is the definitive diagnosis for listeriosis
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
Conditions causes by histophilus somni?
``` Thromboembolic meningoenchepalitis Pneumonia Arthritis UTI Abortion Myocarditis Neurological disease ```
35
Pathogenesis of TME?
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
Clinical signs of TEME>
Somnolence is the first clinical signs Ataxia and weakness Lateral recumbency, profound depression, opisthotonos, convulsions Closes or partially closed eyelids
37
How can you confirm TEME diagnosis?
History and PE CBC- non specific changes CSF - cellular changes reflective of bacterial infection + evidence of hemorrhage
38
Treatment for TEME>
Only attempt early in dz Ab with gram - spectrum Down animals euthanize Can be prevented with vaccination
39
Brain and pituitary abscesses are most often caused by what bacteria?
Trueperella pyogenes
40
Signs of brain/pituitary abscess?
Vision loss in contralateral eye, depression, mania, head pressing, circling with head tilt toward the side of lesion
41
How do pituitary abscesses arise?
Hematogenous origin — rete mirabile —> mesh of capillaries converging pituitary — cavernous sinus —> valveless venous system bathing pituitary Dehorning complication Head butting
42
Clinical signs of pituitary abscess?
Blindness, pupillary dysfunction, nystagmus, dysphagia, facial paralysis, circling, head tilt
43
What is polioencephalomalacia?
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
What type of diets promotes H2S gas formation which interferes with oxidative processes in mitochondria and deplete ATP
Grain
45
Where is H2S found?
``` Drinking water Molasses Forage Urine acidifiers mineral supplements Brassica grass ```
46
Clinical signs of polioencephalomalacia?
Central blindness, ataxia, proprioceptive deficits, head pressing, hyperexcitability Leads to recumbency, opisthotonus, seizure, coma, and death Also strabismus and convulsions
47
How an you diagnose polio/?
Test food/water for H2S >1000ppm in water >4000ppm in diet >1000ppm in rumen gas indicates toxic levels
48
Treatment of polio?
Thiamine Increase forage adding gluogenic precursors Dexamethasone
49
What can cause a nervous ketosis?
Negative energy balance
50
Most common CS of nervous ketosis
Anorexia | Drop in milk production
51
What is the pathology in nervous ketosis?
Diffused cerebrocortical neuronal necrosis — bilateral blindness with intact PLR Cerebellar purkinje cell necrosis
52
Rx for nervous ketosis?
Glucose | Propylene glycol
53
Main isolate from otitis media/interna in ruminants?
Mycoplasma bovis
54
What are sources of lead toxicity?
Grease, oil, old paint, lead-headed nails, batteries, linoleum, smelter discharges
55
What type of lead is readily absorbed?
Lead salts (eg acetate, phosphate, carbonate, hydroxide)
56
Sudden death, central blindness, tremors, chewing fits, seizures, bellowing DDX?
Polio | Lead toxicity
57
How can you confirm diangosis of lead toxicity?
Basophilic stippling and normocytic, normochronic anemia Blood lead measurement
58
Treatment for lead toxicity?
Usually die before/in spite of treatment Remove from source immediately Intermittent CaEDTA to chelate from bone Early in disease — thiamine
59
A copper deficiency during prenatal/perinatal period can lead to what condition?
Sway back AKA enzootic ataxia
60
Copper deficiency prenatally results in bilateral symmetrical ____ in the dorsolateral spinal cord
Myelin degradation
61
Clinical signs of sway back?
Rear limb ataxia Muscle atrophy and paresis Tetraparesis seen at birth Signs are static in neonates but progressive in older animals
62
What is the diagnosis for swayback?
Definitive dx on necropsy Measure body tissue Cu Plasma copper status (blood Cu increase with stress) and assess dietary Cu
63
Treatment of swayback
Hypomyelinogenesis and demyelination is irreversible Supplement Cu to prevent more cases Cu to molybdenum ratio 6:1
64
Progressive ataxia is a recessive defect in purebred/ mixed breed _________ calves at 6-36 months
Charolais
65
What is the major lesion in progressive ataxia?
Eosinophilic plaques on white matter in the brain/spinal cord
66
What are clinical signs of progressive ataxia?
Stiff neck Dragging rear toes Stumbling Proprioceptive deficits worsening with exercise Difficulty in maintain posture during urination and pulsatile micturition
67
What is another name for progressive degenerative myeloencophalopathy?
“Weaver syndrome”
68
Weaver syndrome is an inherited disorder in purebred ___________
Brown Swiss and Angler cattle
69
Clinical signs of progressive degenerative myeloencephalopathy?
``` Paraparesis Ataxia Dysmetria of pelvic limbs Insidious progression Muscle wasting over hindquarters ```
70
What is the MOA of organophosphate toxicity?
Bind with acetylcholinesterase —> increases ACh
71
Clinical signs of organophosphate toxicity?
Muscarinic: Dyspnea, hypersalivation, diarrhea, bradycardia, pupillary contrition Nicotinic: muscle tremors, tetany, recumbency, and opisthotonos
72
What is the treatment for organophosphate toxicity?
Atropine Oral activated charcoal Oximes — break bone of OP and AChase within first 24hours 2-PAM
73
What bacteria are often the cause of veterbral osteomyelitis and spinal abscess?
Trueperella pyogenes | Fusobacterium necrophorum
74
How can you confirm vertebral osteomyelitis/spinal abscess?
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
Treatment for spinal abscess ?
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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