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749 - Ex 3 > Equine Neuro > Flashcards

Equine Neuro Flashcards

1
Q

Lack of coordination of muscle movement

A

Ataxia

  • vestibular
  • cerebellar
  • sensory
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2
Q

Paresis

A

UMN, LMN, Muscle

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3
Q

Dysmetria

A

Hypermetria - spinocerebellar disease

Hypometria - stiffness

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4
Q

Reduced inhibition of extensor motor neurons

A

Spasticity

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5
Q

In the horse, _____ ataxia seems to predominate assoc’d with ___ ___ disease in which proprioceptive input to the cerebellum is compromised

A

sensory

spinal cord

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6
Q

Afferent CN deficits (sensation)

A

smell, taste, vision, hearing, balance, and specific proprioception

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7
Q

Efferent CN deficits (motor)

A

pupil diameter, eye ball movement, mastication, facial expression, ear play, swallowing, vocalization, tongue movement

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8
Q

What are the four most commonly seen deficits in the horse (CN)

A
  1. facial nerve paralysis
  2. head tilt
  3. laryngeal dysfunction
  4. dysphagia
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9
Q

Postural deficits, seizures, altered mentation, blindness

A

Cerebral cortex lesion

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10
Q

Ataxia, paresis, dysmetria, dysphagia, anisocoria, or dilated pupils

A

Brain stem lesion

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11
Q

Ataxia, head tilt, pronounced postural deficits

A

Vestibular system lesion

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12
Q

Ataxia, intention tremors

A

Cerebellum

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13
Q

Ataxia, paresis, dysmetria, spasticity…

All 4 limbs, worse in pelvic limbs, +/- Horner’s

A

C1-C5 lesion

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14
Q

Ataxia, paresis, dysmetria, spasticity…

All 4 limbs, worse in thoracic limbs, +/- Horner’s

A

C6-T2 lesion

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15
Q

Ataxia, paresis, dysmetria, spasticity…

Pelvic limbs

A

T3-L3 lesion

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16
Q

Ataxia, paresis, dysmetria, spasticity…

Urinary incontinence, fecal retention, hypalgesia tail and perianal areas

A

S3-S5 lesion

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17
Q

Ataxia, paresis, dysmetria, spasticity…

Decreased tail tone, hypalgesia caudal to lesion

A

Coccygeal

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18
Q

Weakness predominates; within 10-20 days muscle atrophy…

Inability to flex shoulder, extend the lim and fix elbow

A

Radial n

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19
Q

Weakness predominates; within 10-20 days muscle atrophy…

“Sweeney” - shoulder slip: supraspinatus and infraspinatus mm atrophy, abduction of limb, inability to advance shoulder

A

Suprascapular n

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20
Q

Weakness predominates; within 10-20 days muscle atrophy…

Inability to extend stifle

A

Femoral n

21
Q

Weakness predominates; within 10-20 days muscle atrophy…

Inability to adduct pelvic limbs –> “splay legged”

A

Obturator n

22
Q

Weakness predominates; within 10-20 days muscle atrophy…

Limb hangs behind the horse with stifle and hock extended, foot cannot be advanced

A

Sciatic n

23
Q

Grade 0-5 deficit scale (pg 3 notes)

A

Grade 0 = normal

Grade 5 = recumbent horse

24
Q

DAMNIT V!

A 
D - degenerative, developmental 
A - allergic, autoimmune, anomaly 
M - metabolic, mechanical 
N - nutritional, neoplastic 
I - inflammatory, immune-mediated, IA, ischemic, idiopathic 
T - toxic, traumatic 
V - vascular
25
Q

Symmetrical Neuro Signs

A
  1. Infectious - EHV1, EEE/WEE, WNV, rabies, bacterial meningitis
  2. Immune mediated - accompanying inflammation can involve several layers or structures
  3. Trauma - later… when edema, swelling, and pressure alterations develop
  4. Developmental/Congenital
  5. Toxic - can target a specific site within the nervous system
26
Q

Asymmetrical Neuro Signs

A
  1. Infectious - EPM, EHV1, EEE/WEE, WNV, rabies
  2. Neoplasia
  3. Trauma
27
Q

What infectious agents should you consider…

in late spring/summer and early fall?

in winter and spring?

A

EEE/WEE, WNV, rabies

EHV1

28
Q

What is the most common cause of central and peripheral nervous system dysfunction in the horse?

A

Trauma

29
Q

Encephalitis causing viruses!

  1. What are the main 3? and the 4th?
  2. What kind of virus are these?
  3. Whats the reservoir?
  4. Which are considered core vaccines?
  5. Can this be transmitted from horse to horse, or horse to humans?
  6. Which is the most fatal?
  7. Most often, horses that are infected develop an inapparent infection with a mild and short-lived fever…. For many cases of WEE and VEE that is where it ends… However, in some cases (and most cases of EEE), the disease progresses into a general febrile illness. What clinical signs then follow?
  8. When the disease progresses further, what is seen?
  9. What is the hallmark of treatment of these viral diseases?
  10. When do we vaccinate these guys?
A
  1. EEE, WEE, VEE, and WNV
  2. Arboviruses! Arthropod-borne
  3. Songbirds, small rodents (VEE)
  4. Core = EEE, WEE, WNV
  5. Viremia in the host is not high enough - can’t be transmitted from horse to horse or horse to human
  6. EEE&raquo_space;> VEE > WEE
  7. anorexia, depression, tachycardia, and diarrhea.
  8. Obtundation and dementia (head-pressing, irritability, teeth-grinding, leaning against walls or fences, compulsive walking, and circling. Others… blindness and mm twitching, development of a head tilt, dysphagia, recumbency and finally death.
  9. Supportive care
  10. Before mosquito season! Depending on location this is either annually or biannually
30
Q

Encephalomyelitis!

  1. What is the the leading cause of infectious neuro dz in the US?
  2. What kind of virus is this?
  3. Where is it seen?
  4. Whats the reservoir? and how it is transmitted? is the viremia high in horses?
  5. Most cases in the horse are subclinical… but about 10% have clinical disease that develops. Explain the signs
  6. Whats the case fatality rate?
  7. How do we dx?
  8. How do we treat?
A
  1. WNV
  2. Flavivirus
  3. Everywhere! except Antarctica
  4. Birds! transmitted by mosquitoes. Low viremia in horses (incidental or dead end host)
  5. Incubation period is about 9-11 days. CS consist of fever, anorexia, and depression…. later followed by brain involvement - depression, obtundation, and coma. Muscle fasciculations are a very prominent feature as well as gait abnormalities and CN deficits.
  6. about 30% (100% for recumbent horses); in those that survive… they often have clinical signs again later on as well as other difficulties
  7. Dx: serum or CSF tested on IgM ELISA (VI or PCR also used)
  8. Similar to other encephalitides (supportive)
31
Q

Rabies!

  1. Is this a core vaccine for horses?
  2. How does the virus spread?
  3. What are the three stages?
  4. Whats the incubation time? How long after CS appear a fatal encephalopathy?
  5. Whats the major reservoir spp in CO?
  6. What are the most common CS?
  7. How do we test?
A
  1. Yep!
  2. Virus replication at site of entry –> retrograde axonal transport into SC –> centripetal spread into the brain
  3. Prodromal, Acute excitative/Furious stage, and the Paralytic/dumb or end-stage (weakness and ataxia)
  4. 12 days; 5-7 days
  5. Skunks/bats
  6. gait deficits and neuro signs (ataxia, weakness); also recumbency, weakness of pharynx, and abdominal pain
  7. Only post-mortem (IFT on brain) - REPORTABLE!
32
Q

This usually occurs in conjunction or following severe liver disease; PE may show icterus and abnormal behavior and ancillary diagnostics may show elevated serum liver enzymes/products

A

Hepatoencephalopathy

33
Q

Fumonisins are mycotoxins produced by fungi that grow on corn (products) and cause rapid break down of white matter in the brain. This disease is also called “hole in the head syndrome”

A

Leukoencephalomalacia

34
Q

________ block ACh-esterase resulting in excess ACh in the body. CS include seizures and SLUD

A

Organophosphate

35
Q

Common etiologies of facial nerve paralysis

A

trauma, EPM, THO, guttural pouch disease

36
Q

Common etiologies of Vestibulo-cochlear dz

A

trauma, EPM, THO, guttural pouch disease

37
Q

What is Temporohyoid osteoarthropathy?

A

THO is a degenerative jt dz of the joint between the stylohyoid bone, which is part of the tongue skeleton, and the temporal bone, which is part of the skull

38
Q

CVCM!

  1. What is the full name?
  2. Cause?
  3. Typical signalment
  4. Etiology and pathogenesis
  5. What are the CS?
  6. Dx ante-mortem?
  7. Tx?
A
  1. Cervical Vertebral Compression Myelopathy
  2. Caused by malformation of cervical vertebrae leading to narrowing/stenosis of the vertebral canal, malalignment of vertebral bodies due to changes at the jts between vertebral bodies, osteochondrotic lesions at the facets and attempts of the body to stabilize through production of CT
  3. Young horses - some breeds are predisposed (THB, TWH, QH and WB). Males > females
  4. Multifactorial! Nutrition, genetics, Cu and Zn ratios, rapid growth rates and trauma
  5. Symmetrical ataxia and dysmetria in thoracic and pelvic limbs. Often seen as acute (trauma) or more gradual onset
  6. Rads or other imaging
  7. Conservative management primarily; cervical interbody fusion. Search continues for better sx management
39
Q

EPM! Multifocal dz!

  1. Full name?
  2. Cause?
  3. Clinical signs
  4. Who is the definite host? What kind of host is the horse?
  5. Are horses often exposed to S. neurona?
  6. How do we test?
  7. Tx?
  8. Px?
A
  1. Equine Protozoal Myeloencephalitis
  2. Sarcocystic neurona (most common), Neospora hughesi
  3. Most consistent with damage to the spinal cord and brain stem. Gradual progression of signs. ASYMMETRIC; ataxia, dysmetria, weakness, and focal mm atrophy.
  4. DH = Opossum; IH = skunks, armadillos, and cats; DEH or aberrant hosts = horses
  5. Commonly exposed –> CS only seen once the sporulated merozoites penetrate the BBB
  6. Can test serum and CSF for Abs - BUT this does not indicate disease
  7. Tx: ponazuril, diclazuril, or pyrimethamine-sulfadiazine
  8. Px: favorable if detected early and affection is mild-moderate; in severely affected cases, prognosis is guarded at best
40
Q

NAD or EDM

  1. Full name
  2. Progression of disease?
  3. Cause?
  4. Dx?
  5. What could be low in these guys?
A
  1. Neuroaxonal Dystrophy, Equine degenerative myelopathy
  2. Slowly progression dz of spinal cord white matter (and brain stem)
  3. Suspect genetic basis
  4. Dx made by exclusion
  5. Plasma Vit E conc may be low
41
Q
  • Young (or aged)
  • Symmetric
  • Focal
  • UMN
  • Acute onset
  • Dx: Myelography
  • Tx: Diet/Sx
A

CVCM

42
Q
  • 1-12 mo
  • Symmetric, multifocal
  • UMN
  • progressive
  • Dx: Vit E low
  • tx with Vit E
A

EDM/NAD

43
Q
  • adult
  • asymmetric
  • multifocal
  • UMN/LMN
  • gradual onset; progressive
  • Dx: serum/CSF analysis
  • Tx: antiprotozoal drugs
A

EPM

44
Q

Herpes! (EHV1)

  1. Equine Herpesvirus Myelopathy is a rare phenomenon… so why do we need to talk about it?
  2. Clinical Signs?
  3. Recovery?
  4. Risk factors
  5. Primary infection site
  6. Can this be passed to fetus?
  7. What part of nervous system is affected
  8. Dx
A
  1. its contagious, presents as an outbreak, and can have a strong impact on horse community (competitions, rares, horse transportations, international transportations, quarantines)
  2. Severity of CS varies widely… high fever for several days, followed by RAPID development of neuro signs (ASYMMETRICAL ataxia, dysmetria, and paresis, UMN bladder)
  3. Recovery depends on severity and extent of damage
  4. Outbreak with fevers and (mild) resp dz, typically follows w/ the return from an event, Fall-Winter-Spring, tall breeds
  5. Primary infection at resp epithelium
  6. Yes! Can be passed to fetus as well as CNS
  7. Mostly spinal cord gray and white matter… infrequently brainstem
  8. PCR (nasal swabs) - rapid
45
Q

Case

Hx:

  • possible fever and travel (other horses)
  • more than one horse affected (contagious!)
  • rapid progression (hours)
  • asymmetrical ataxia and weakness is common, hind limbs&raquo_space;> front limbs, UMN bladder
  • No CN involvement
A

EHM!

46
Q
  • Any age
  • horses more susceptible than pony
  • insidious onset, gradual progression (wks), one horse at a time, hx of earlier EPM cases
  • More commonly asymmetrical ataxia, dysmetria, UPM weakness in 1 to all 4 limbs; LMN weakness can also occur, weak ‘standing tail pull’, bladder dysfunction (uncommon), CN deficits (common)
  • will these guys get better with ‘stall rest’ and wait-and-see approached?
A

EPM!

  • more likely to worsen gradually
47
Q
  • adult horse (8-15 years)
  • tall breeds, excludes most pure-bred pony breeds
  • fever, rapid progression (hours) and usually more than 1 horse affected
  • (fever), asymmetrical ataxia, dysmetria, UMN weakness in 1 to all limbs. Commonly, LMN weakness, weak ‘standing tail-pull’. Often hind limbs more affected than fore. CN deficits very uncommon. UMN-bladder very common
  • gradual improvement is possible with time (stall rest and wait and see)
A

EHV-1, EHM

48
Q

Tetanus!

  1. What causes it?
  2. Two big exotoxins and what they do?
  3. How sensitive are horses to it?
  4. How do they get it?
  5. When do CS appear? What are they?
  6. Tx?
  7. Prevention
A
  1. C. tetani; Gram+, spores, anaerobic, rod shaped
  2. Tetanolysin - tissue destruction; tetanospasmin - neurotoxin (enters NMJ and travels to CNS –> blocks GABA and glycine, 2 inhibitory NT)
  3. Super sensitive!
  4. Deep puncture wound
  5. within 5-10 days; increased sensitivity/nervousness, stiff gait/sawhorse stance, altered facial expression (Risus sardonicus), lockjaw, colic
  6. keep away from loud noises and light, tranquilizers, tetanus toxoid, tetanus antitoxin
  7. Vaccine! tetanus toxoid

749 - Ex 3 (4 decks)

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