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3. Equine 3 > neurology 2 > Flashcards

neurology 2 Flashcards

1
Q

Equine Herpes Virus
- which ones are important to us?

A

EHV 1&4 (2-3) (5-9)

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2
Q
  • EHV - 1 signs? why do we see these signs?
A
  • Respiratory
  • Abortions
  • Neurologic signs
    > Ischemia of neurons due to vasculitis, not neuronal infection (type III allergic hypersensitivity, immune-mediated???)
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3
Q

Equine Herpes Virus
- prevalence?
- what age group is susceptible?
- transmission and nature of infection

A
  • Endemic in horse population
  • Most infected within first year of life
  • Spread by droplets – nasal, ocular, respiratory,
    reproductive
  • Latency – trigeminal nerve, lymphoid tissue
  • Role of virus strains, latency, disease?
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4
Q

EHV, neurologic signs:
- outbreaks
- morbidity and mortality
- who get this disease?
- risk factors?
- season?

A
  • Virus spreads rapidly in outbreaks
  • Morbidity up to 90%
  • Mortality up to 40%
  • Can occur at any age, rarely in foals
  • Lactating & pregnant mares more susceptible
  • Risk factors – age, females, fever
  • More common in winter & spring
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5
Q

EHV – Clinical Signs

A
  • Acute onset ataxia & tetraparesis
  • May be 6 – 10 days post infection
  • Range: subtle signs to recumbency
  • Non-specific – fever, cough, nasal discharge may occur early
  • Also – anorexia, limb edema, ocular lesions
    (conjunctivitis), colic
    <><><><>
    Spinal white matter:
  • Ataxia, paresis, CP deficits
  • Hind limbs > forelimbs, symmetric
  • Urinary incontinence, bladder atonia, dysuria, scalding of legs
  • Tail paralysis, decreased anal tone, decreased perineal sensation, fecal retention
    <><><><>
    May cause more central signs:
  • Cranial nerve signs
  • Blindness
  • Vestibular signs
  • Seizures
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6
Q

EHV disease progression, recovery period

A
  • Progression: usually 24-48 hours, then stabilize. May die or be euthanized especially if recumbent
  • Need to allow months for recovery
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7
Q

EHV
- Diagnosis

A
  • Clinical signs
    <><>
  • PCR
  • Neuropathogenic & non-neuropathogenic strains
  • Fast
  • Nasal swab & blood sample (EDTA)
    <><>
  • Serology – acute & convalescent
  • > 1:256 suggests recent infection
    <><>
  • Virus isolation
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8
Q

EHV
- CSF analysis

A
  • May be normal
  • Xanthochromia
  • Increased protein level
  • May have slight increase in nucleated cell counts
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9
Q

EHV
- Treatment

A
  • Anti-inflammatory medication
  • Fluids, nutrition
  • Decompress bladder, evacuate rectum
  • Sling
  • Anti-viral medication – people have tried acyclovir (useless) and valacyclovir (potentially useful)
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10
Q

EHV Prevention

A
  • Vaccines – none are labelled for protection against neurologic disease
  • Single study – suggests vaccination within 1 year increases likelihood of neuro disease 9-14x
  • Herd management:
    > Isolate new arrivals – 3 weeks
    > Maintain distinct herd groups according to age, sex, occupation; broodmares away from others
    > Minimize stress
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11
Q

Ataxia Scale (Mayhew)

A

0 – Normal
1 – Subtle deficits, noted when special maneuvers performed
2 – Mild deficits, apparent all times & gaits
3 - Moderate deficits, easy to identify, all times & gaits
4 – Severe deficits, may buckle, stumble, fall
5 – Recumbent & cannot stand

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12
Q

Wobbler Syndrome - possible causes in the horse?

A
  • Cervical stenotic myelopathy
  • Cervical static stenosis
  • Cervical vertebral malformation/malarticulation
  • Cervical vertebral dynamic instability
  • Aberration in cartilage & bone metabolism
  • Trauma
  • Degenerative joint disease
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13
Q

Wobbler Syndrome signalment
- age, breeds, sex, etc…
- who gets this? factors?

A
  • Age – months to years
  • Breed – any
    > Many TB, STB, QH
    > Older horses – Warmbloods, any breed
  • Sex – male > female
  • Fast growing young horses – part of developmental orthopedic diseases.
  • Multifactorial
    > Genetic
    > Nutrition – high protein & calories, micromineral imbalance (Cu, Zn)
    > (Trauma)
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14
Q

Onset & Progression of wobblers

A
  • Often insidious
  • May be acute
  • Vague lameness
  • Progression over months, wax & wane
  • Spontaneous recovery uncommon
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15
Q

wobblers presenting complaints and clinical signs

A
  • Clumsiness or stumbling when move out of stall
  • Rider – looseness or “losing the back end” on turns
  • Reluctance to change leads
  • Stumble & fall
    <><><><><>
  • Spinal ataxia
  • Spastic gait
  • Conscious proprioceptive deficits
  • Weakness
  • Hind limbs > forelimb signs (C1-C5)
    > Why? pelvic tracts of spinal cord more superficial
  • Forelimb signs more pronounced (C6-T2)
    > Why? brachial plexus and thoracic tracts more superficial here
    <><><><>
    Degree of difference
  • if there is a difference between fore and hind limbs with Wobblers, it will only be ~1 degree, important because if we have a horse will multifocal disease we will see a difference of more than 2 grades
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16
Q

Wobbler - Radiographs

A
  • Vertebral canal stenosis
    > Intraventricular sagittal ratios
    => Min. canal diameter and max. vertebral body diameter
    => C3-C6 <50%
    => C7 <52%
  • Degenerative joint disease, OCD, malformation
  • Physeal flaring (caudal, ventral canal)
    > “ski jumps”
  • Caudal extension of the caudal laminae
  • Angulation between vertebral bodies
17
Q

Wobblers Dx

A
  • Neurologic evaluation
  • Spinal radiographs, myelogram
  • Rule out other diseases
    > EPM, EHV-1, EDM
    > Space-occupying lesion (cyst, abscess, tumor)
    > Aberrant parasite migration
18
Q

wobblers Tx

A
  • Rest, stall restriction
  • Anti-inflammatory medication
  • Ultrasound-guided joint injections (may help with pain associated with arthritis)
  • (Feed restriction) > if you detect this early in life
  • Surgery (?) > invasive, difficult, many complications…
19
Q

Equine Protozoal Myeloencephalitis
- pathogen? hosts?

A
  • Sarcocystis neurona, (Neospora hughesi)
    <><>
  • Definitive host – opossum
    > Didelphis virginiana
    > Sexual reproduction in intestine, shed oocysts
    <><>
  • Intermediate host
    > Unknown – asexual reproduction → sarcocysts
    > Skunk, raccoon, domestic cat, armadillo
    > Horse – aberrant intermediate host (CNS)
20
Q

EPM - Pathogenesis

A
  • Fecal – oral contamination (water, feed)
  • Ingestion
  • Parasite locates to CNS
    > brain, spinal cord
    > Not peripheral nerves or nerve roots
  • Found in neuronal cells, mononuclear cells, endothelial cells
21
Q

EPM clinical signs? differential and how to tell them apart?

A
  • Depends on extent & distribution
  • Can present with any CNS signs
  • Usually spinal ataxia (often resembles Wobbler syndrome)
    > EPM more likely if there is notable asymmetry
    > Also if large disparity between forelimb and hind limb signs
    > Also if there is muscle loss
22
Q

EPM diagnosis

A
  • Rule out other diseases
  • Detect S. neurona specific antibodies – serum, CSF
  • Serology – depends on geographic area. Up to 90% positive in some areas. Only means exposure.
    <><>
    Tests:
  • Western blot
  • IFA - indirect fluorescent antibody (react w S. fayeri)
  • SAG testing
23
Q

EPM Treatment? considerations?

A

Sulfadiazine-pyrimethamine
- V rarely - blood dyscrasia, neonatal or reproductive problems
- Pyrimethamine interferes with dihydrofolate reductase
> Do NOT supplement w folic acid during treatment
> Stop pyrimethamine therapy
> Can supplement with folinic acid
<><>
Ponazuril (give loading dose) – was currently on back order
<><>
Diclazuril – Protazil (Merck Animal Health, USA)
<><>
Toltrazuril
<><><><>
<><><><>
- Anti-inflammatory medication > Parasite die-off
- Vitamin E – antioxidant

24
Q

EPM prognosis, prevention?

A

Prognosis:
– guarded, do not know extent of neural damage; need to see response to treatment
> Moderate to severe signs – 60% improved at least 1 grade
> 10-20% may recover completely
<><><><>
Prevention: try to inhibit the opossums from getting into feed
> Avoid possum feces in feed.

25
Q

Equine Degenerative Myeloencephalopathy (EDM)
- who is affected? age, breed, sex?

A
  • Age: Young horses <1 year up to 3 years of age
  • Breeds: Many
    > Horses, ponies, donkey, Przewalski, zebra
    > Heritability strongly suggested in Morgan, Appaloosa, Lusitano
    > More common in some familial lines
  • Sex: no predilection
  • How common is it? > a big question still.
26
Q

EDM
- etiology??

A
  • genetic basis, but also:
  • Problem with Vitamin E
    > Deficiency (feed, dry lots)
    > May be inability to handle Vit E once absorbed
    > Analyze feed levels of Vit E (α-tocopherol)
    > Analyze blood levels of Vit E(α-tocopherol)
    => (point in time measurement; may not reflect past levels)
27
Q

EDM - clinical signs, differentials

A
  • Clinical signs – symmetric spinal ataxia
  • Diagnostic Rule outs: Wobbler Syndrome, EPM
28
Q

EDM - treatment, prevention

A
  • Treatment – not likely to be effective
  • Prevention !!!
  • Supplement Vit E (natural > synthetic)
    > Especially if familial problem, stored feed, lack of pasture, (exposure to insecticides, wood preservatives)
29
Q

Equine Motor Neuron Disease
- what is this?
- anatomy affected?
- signalment?
- risk factor?

A
  • Acquired neurodegenerative disease, sporadic (ALS-like); systemic oxidative stress
  • Ventral horns, gray matter of the spinal cord & select brainstem nuclei
  • Age: adult horse (2-27 years of age)
  • Vitamin E deficiency – lack of pasture, dry lots, dried feed, pelleted feed
30
Q

EMND - clinical signs

A
  • Weakness – profound
    > Stand camped under
    > May rest against solid objects
    > Head & neck may droop
    > NO ataxia or neurologic deficits
  • Muscle atrophy
  • Trembling in anti-gravity muscles
  • Sweating
  • Frequently shift weight
    > Inability to use the stay apparatus
  • Recumbency
  • Raised tail head (muscle atrophy, fibrosis of the dorsal coccygeal muscles)
  • Note: Eyes – retinal pigmentopathy (40%)
    > Ceroid lipofuscinosis
    > Black/brown/yellow deposits tapetal/non-tapetal junction, reticulated/mosaic
31
Q

EMND - diagnostics

A
  • CK & AST – may be mildly to moderately elevated if rapid progression
  • CSF – protein may be elevated; ncells– normal
  • Electromyography
  • Muscle biopsy – sacrocaudalis sacralis m. (tail head) – atrophy of type 1 myocytes in response to denervation (high sensitivity, low specificity)
  • Nerve biopsy – spinal accessory nerve, medial belly of the sternocephalicus m.
32
Q

Polyneuritis equi
- what is this?
- what is affected?
- cause?
- cells?

A
  • Cauda Equina Syndrome
  • Progressive granulomatous polyradiculoneuritis
  • Cranial nerves & other spinal nerves – less
    common
  • Cause?? (unknown) – allergic, autoimmune, viral associated, other
  • Infiltration of macrophages & Tc cells
33
Q

Polyneuritis equi
- signs, outcomes

A
  • Progressive paralysis of tail, bladder, rectum, anus, penis
  • May have initial hypersensitvity & hyperesthesia esp. tail head; leads to desensitization of tail head, perineum,
    caudal thighs, caudal rump
  • May lead to hind limb ataxia, muscle atrophy
34
Q

Polyneuritis equi
- Cranial nerves affected (often asymmetric):

A
  • Cr. V – motor branch
  • Cr. VII
  • Cr. VIII
  • Others > III, IX, X, XII
35
Q

Polyneuritis equi - Differential dx

A

– fracture, subluxation, EHM, rabies, sorghum toxicity, other infectious diseases

36
Q

Polyneuritis equi diagnostic tests, treatment, prognosis

A
  • CSF
    > Mononuclear pleocytosis
    > Lesser increase in neutrophils
  • Abnormal EMG
  • (Increased P2 myelin basic protein)
  • Treatment – anti-inflammatory dose corticosteroids, symptomatic treatment
  • Prognosis – hopeless (may sustain for months)
37
Q

Epilepsy - types, who gets them, what we see?

A

Primary – idiopathic
- Heritable conditions:
- Juvenile idiopathic - line of Egyptian Arabians (respond well to treatment, may outgrow)
- Arabian Lavender foal syndrome
<><>
- Secondary – other disease processes
<><><><>
- Abnormal, synchronous electrical discharges
- Spontaneous, paroxysmal, involuntary movements
- Generalized or partial

38
Q

Epilepsy - dx, tx

A
  • Diagnostics – many to determine, rule out primary disease
    <><>
    Treatment
  • Diazepam
  • Phenobarbital
  • Potassium bromide – this is in addition to phenobarbital
39
Q

Narcolepsy/Cataplexy
- what is this?
- signs?
- Dx, ddx
- tx

A
  • Excessive sleepiness
  • Paradoxic form of sleep
  • Rapid eye movement (REM) sleep
  • May involve muscle weakness, recumbency
  • Diagnostic rule outs: chronic sleep deprivation, seizures
  • Diagnosis – signs, EEG, physostigmine provocation (central acting cholinesterase inhibitor)
  • Treatment – transient improvement with atropine; other: imipramine (cataplexy)??

3. Equine 3 (9 decks)

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