Equine Top 15 Neurologic Diseases - Part 1 Flashcards

1
Q

what horses are most often affected by EPM?

A

more common in horses <4 years

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2
Q

what is the classic clinical presentation of a horse with EPM?

A

usually multifocal lesions of brainstem and/or spinal cord - asymmetric ataxia, asymmetric muscle atrophy, random well-demarcated focal areas of swelling, & teraparesis/paraparesis

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3
Q

what is mayhew’s grading scale for ataxia in regards to EPM?

A

grade 0 - normal strength/coordination, grade 1 - subtle to mild neuro deficits noted only under special circumstances (walking in a circle), grade 2 - mild neuro deficits but apparent at all times/gaits, grade 3 - moderate deficits at all times/gaits that are obvious to all observers regardless of expertise, grade 4 - severe deficits with tendency to buckle, stumble spontaneously, trip, or fall, & grade 5 - recumbency, unable to stand

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4
Q

what is the etiology of EPM?

A

sarcocytis neurona - rare but neospora hughesi

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5
Q

how is EPM diagnosed?

A

based on combo of clinical signs, history, geography/prevalence, labwork, & elimination of other diseases

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6
Q

what is the antemortem gold standard for diagnosing EPM?

A

serum CSF ratio of titers

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7
Q

how are serum titers used for diagnosing a horse with EPM?

A

positive titers mean nothing because many horses are exposed, but negative titers imply absces of disease except in acute cases (< 2 weeks)

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8
Q

what is seen on CSF fluid from a horse with EPM?

A

mononuclear pleocytosis & increased protein

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9
Q

what prevention is used for EPM?

A

keep possums off property, minimize stress

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10
Q

what treatment is used for EPM?

A

long term antiprotozoal therapy of ponazuril or diclazuril (very safe), short term anti-inflammatory drugs, & supportive care

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11
Q

what animal is the definitive host for EPM?

A

possum

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12
Q

what is the prognosis of EPM?

A

guarded to fair - horses with less severe signs tend to do better

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13
Q

what does SAG stand for?

A

surface antigens - SAG2, 4/3 titers

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14
Q

what is the life cycle of sarcocystis neurona?

A

opposum is definitive host, horse is the aberrant dead end host which ingests sporocysts, & merozoites are found in CNS lesions

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15
Q

what is another name for cervical vertebral malformation & malarticulation in horses?

A

equine wobbler’s

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16
Q

what signalment of horses are often affected by CVM type I?

A

developmental - thoroughbreds, warmbloods, & light breeds usually a few months to 4 years old, more often males

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17
Q

what signalment of horses are often affected by CVM type II?

A

acquired - usually seen in middle-aged horses

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18
Q

what is the classic case presentation of CVM?

A

history of over-conditioning or rapid growth, progressive ataxia in pelvic limbs or all four limbs with toe dragging, thoracic limb hypometria, & absent slap test

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19
Q

what is the etiology of type I CVM?

A

developmental dynamic - mid-cervical region

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20
Q

what is the etiology of type II CVM?

A

acquired due to OA or trauma - caudal cervical region

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21
Q

what is seen on radiographs that supports a diagnosis of CVM?

A

vertebral canal stenosis, abnormal articular processes, & angular deformities

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22
Q

what horses with CVM have a good prognosis? what horses with CVM have a guarded prognosis?

A

good - young horses with mild clinical signs & a single site, guarded - young horses requiring surgery may not be able to return to athletic function, older horses, & chronic signs, & poor - multiple site involvement

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23
Q

T/F: horses with multiple sites of CVM have a very poor prognosis

A

TRUE

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24
Q

what treatment is used for equine wobb;er’s?

A

basket surgery (decompression & fusion), young horses can do significant caloric/exercise restriction, older horses can use NSAIDS +/- vertebral facet injections

25
Q

what are signs of spinal trauma in a horse?

A

ataxia, paraparesis/tetraparesis, paraplegia (dog sitting), & urinary/fecal incontinence

26
Q

what are signs of forebrain trauma in a horse?

A

coma, dementia, wandering in circles, seizures, & cortical blindness

27
Q

what are signs of brainstem trauma in a horse?

A

strabismus, nystagmus, ataxia, & facial nerve deficits

28
Q

what is the common signalment & history of a horse with a CNS injury?

A

young/fractious/athletic horse with a cute onset of signs with a history of a fall, thunderstorm, flipping over backwards (basilar bone fracture due to the pull from rectus capitus ventralis muscle)

29
Q

what are signs of fractures involving the middle/inner ear in a horse with a CNS injury?

A

cranial nerve VII deficits (ipsilateral face drooping), cranial nerve VIII deficits (ipsilateral vestibular deficits), dog sitting, & urinary/fecal incontinence

30
Q

how are CNS injuries in horses diagnosed?

A

skull/spinal rads, MRI/CT, +/- CSF tap if unsure that an injury occurred

31
Q

what treatments are used in horses with CNS injuries?

A

check airway, stop bleeding, treat shock, sedation if needed for thrashing, no steroids for head trauma, NSAIDS, serial neuro exams, but time is often the best treatment

32
Q

what is the prognosis for a horse with a brain injury? spinal injury?

A

brain - guarded, 40-60% survival depending on type/location, spinal - guarded, depends on location & severity for return to function

33
Q

most spinal injuries in horses occur at what site?

A

between C1 & T2

34
Q

what is the prognosis for a horse with a CNS injury that has bilateral pupil dilation & a coma?

A

very poor

35
Q

what is the classic case presentation of botulism in a horse?

A

any age affected, history of a food change especially in round hay bales - flaccid teraparesis to tetraplegia, dysphagia, hypersalivation, muscle tremors, tongue/tail/eyelids poor tone!!!! wet slippery flaccid tongue, flaccid tail, & lack of audible click of palpebral

36
Q

what is the classic case presentation of tetanus in a horse?

A

history of omphalitis/recent injury/recent surgery - stiff hypometric gait, elevated tailhead, bloat, dysphagia, erect/pulled back ears, prominent nictitatting membranes, flared nostrils, & hypersensitivity to touch/sound

37
Q

what is the etiology of botulism? what is the mechanism of its disease?

A

clostridium botulinum toxin - blocks exocytosis of Ach at presynaptic membrane, toxin is ingested in feed or in toxicoinfectious, organism can grow in a wound or abscess where the toxin is produced - most common neurotoxins in horses are types B, C, & D

38
Q

what is the etiology of tetanus? what is the mechanism of its disease?

A

clostridium tetani toxin - blocks neurotransmitter release from inhibitory interneurons in the spinal cord & brainstem

39
Q

what testing is done for a horse with suspected botulism?

A

PCR (best) or mouse bioassay, grain test is suspected botulism if the horse can’t eat 1 cup of grain within 2 minutes, EMG, & isolation of c. botulinum from feed, feces, or wounds

40
Q

what testing is done for a horse with suspected tetanus?

A

history & classical clinical findings - +/- CSF tap to rule out meningitis

41
Q

what treatment is done for a horse with botulism?

A

antibiotics (not in toxicoinfectious botulism as it may cause release of more toxins), nursing/supportive care, & antiserum if a known/suspected type (expensive)

42
Q

what treatment is done for a horse with tetanus?

A

dark/quiet environment, sedation (phenothiazine, a2 agonist, benzo, or barbiturate), clean/debridement of wounds, penicillin or metronidazole

43
Q

what is it called when a foal has botulism?

A

shaker foal syndrome - usually botulism type b toxin

44
Q

what is the prognosis for a horse with botulism?

A

can range from poor to excellent but adults that are recumbent for more than 24 hours usually have a poor prognosis

45
Q

giving the tetanus antitoxin to a horse vaccinated against tetanus puts it at risk for what?

A

theiler’s disease

46
Q

what is the prognosis for a horse with tetanus?

A

good if the animal can drink, fair to good if not recumbent, & poor if recumbent

47
Q

how is botulism prevented? how is tetanus prevented?

A

botulism - c. botulinum type b toxoid vaccine of mares twice in the last trimester in areas where common & keeping water/food sources clean from dead animals, tetanus - core annual vaccine guidelines followed from AAEP

48
Q

what does EDM/EMND stand for?

A

EMD - equine degenerative myelopathy & EMND - equine motor neuron disease

49
Q

what is the classic case presentation of a horse with EDM?

A

insidious onset of signs - slowly progressive ataxia, hypometria, weakness, poor thoracolaryngeal (slap) test, & poor cutaneous trunci reflex

50
Q

what is the common signalment of a horse with EDM?

A

northeast USA, horses with a lack of access to fresh green forage, 6-12 month old foals, familial in appaloosa, standardbred, & paso fino - possible familial in norwegian fjord, arabian, QH, welsh pony, & haflinger

51
Q

what is the common signalment of a horse with EMND?

A

adult onset with a peak of 16 years - quarter horses, thoroughbreds, & similar breeds

52
Q

what is the classic case presentation of a horse with EMND?

A

elephant ball stance, progressive weakness, increased recumbency, NO ataxia, muscle/weight loss, trembling, low head carriage, unable to lock stifles, weight shifting, & hypometria

53
Q

how is EDM diagnosed?

A

based on clinical signs, history, serum vitamin e, & response to therapy

54
Q

how is EMND diagnosed?

A

sacrocaudalis dorsalis medialis & spinal accessory nerve biopsies, EMG, & necropsy

55
Q

how are EDM/EMND treated?

A

vitamin E supplementation

56
Q

T/F: EMND horses move better than they stand

A

TRUE

57
Q

T/F: for EDM, there is strong evidence that suggests a familial predisposing component

A

TRUE

58
Q

what is the suspected etiology of EDM/EMND?

A

ikely a result of vitamin E deficiency - low serum vitamin E concentration is suggestive but not specific

59
Q

how is EDM/EMND prevented?

A

adequate access to vitamin e-rich forage