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Smith. Neurolgic DZ > Equine Neuro > Flashcards

Equine Neuro Flashcards

1
Q

Evidence of cerebral disease

A

abnormal mentation
seizures
head pressing
compulsive walking
ataxia
blindness (lack of menace, pos PLR)

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2
Q

Evidence of brainstem disease

A

CN deficits
altered consciousness
Gait deficits

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3
Q

Evidence of cerebellar disease

A

ataxia with wide-based stance
intention tremor
maybe absent menace
strength is preserved

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4
Q

Spinal cord segment involved: C1-C5 Clinical signs

A

all 4 limbs (pelvic > thoracic)
-UMN deficits to thoracic and pelvic limbs

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5
Q

Spinal cord segment involved: C6 to T2 Clinical signs

A

all 4 limbs affected (thoracic >pelvic)
-LMN to thoracic limbs
-UMN to pelvic limbs

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6
Q

Spinal cord segment involved: T3-L3 Clinical signs

A

pelvic limbs only affected
-UMN to pelvic limbs

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7
Q

Spinal cord segment involved: L4-S1 Clinical signs

A

pelvic limbs only affected
-LMN to pelvic llimbs

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8
Q

Spinal cord segment involved: S3-S5 Clinical signs

A

urinary incontinance, fecal retention, hypalgesia to tail and perineal areas

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9
Q

Spinal cord segment involved: Coccygeal Clinical signs

A

decreased tail tone, hypoaglesia caudal to lesion

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10
Q

UMN signs

A

exaggerated (hypermetric gait, exaggerated reflex, increased muscle tone

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11
Q

LMN signs

A

weakness, dragging feet, reduced to absent reflexes, decreased muscle tones

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12
Q

Cranial nerves:

A

1: olfactory
2: optic
3: oculomotor
4: trochlear
5: trigeminal
6: abducens
7: facial
8: vestibulocochlear
9: glossopharyngeal
10: vagus
11: accessory
12: hypoglossal

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13
Q

Nerves involved in menace response

A

afferent: optic nerve
through occipital cortex
efferent: facial nerve

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14
Q

nerves involved in pupillary light reflex

A

afferent: optic nerve
efferent: oculomotor nerve

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15
Q

Where is the lesion located if pLRS are intact but menace is absent?

A

through occipital cortex
–cortical–cortical blindness

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16
Q

What nerves are involved in eye position?

A

trochlear: innervates superior/dorsal oblique
abducens: innervates retractor bulbi and lateral rectus
oculomotor: innervates all rest

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17
Q

Ventrolateral strabismus– what cranial nerve is damaged?

A

CN3

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18
Q

dorsal deviation of medial angle (strabismus)– what cranial nerve is damaged?

A

CN 4

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19
Q

Medial strabismus– what cranial nerve is damaged?

A

CN 6

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20
Q

What nerves are involved in palpebral refelx?

A

afferent trigeminal nerve
efferent: facial nerve

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21
Q

What supplies motor innervation ot the tongue?

A

hypoglossal nerve

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22
Q

Signs of cranial VIII: vestibulocochlear nerve involvement

A

nystagmus (fast phase away)
head tilt (poll towards)
widebased stance
ataxia
circling (toward)
hearing

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23
Q

What cranial nerves are invovled in dysphagia

A

IX: glossopharyngeal
X: Vagus
XII: hypoglossal (tongue tone)

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24
Q

Which cranial nerve innervates the trapezius muscle?

A

XI: accessory nerve

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25
Q

What is the grading scale for ataxia?

A

0: no neuro deficits
1: subtle nero deficits
2: mild neuro deficits (apparent at all times)
3: moderate deficits at all times (obvious to all observors at all times)
4: severe neuro deficits & danger of folling
5: recumbent, unable to stand

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26
Q

Describe C/S of horners syndrome

A

vagosympathetic trunk; miosis, ptosis, prolapse of nictitating membrane, enotphthalmus
horse: ipsilateral sweating, poor airflow through affected nostril

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27
Q

What are differentials for horses with cerebral C/S?

A

alpha viruses: WEE, EEE/VEE
WNV
Rabies
Trauma
Leukoencephalomalacia
Mass: PPID, abscess, cholesterole granuloma, neoplasia
meningitis
juvenile epilepsy of arabians

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28
Q

What are differentials for horses with cerebellar C/S?

A

cerebellar abiotrophy
trauma

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29
Q

what are differentials for horses with brain stem C/S?

A

vestibular disease
THO
Trauma
Horners syndrome
Nigropallidal encephalomalacia

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30
Q

What are differentials for horses with spinal cord C/S?

A

EHM
EPM
NAD/EDM
Trauma
cervical vertebral compressive myelopathy
Mass: abscess, neoplasia, hematoma
occipitoatlantoaxial malformation
verminous meningecephalopmyelitis

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31
Q

What are differentials for horses with neuromusclar C/S?

A

EMND
botulism
tetanus
polyneuritis equi
lead poisoning in horses (chronic polyneuritis)

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32
Q

What are reservoir for EEE/WEE

A

birds
EEE: snakes potentially
VEE: small rodents

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33
Q

What is the vector for EEE/WEE/VEE?

A

mosquito

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34
Q

What is the amplifying host for VEE?

A

horses

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35
Q

What are clinical signs seen with EEE/WEE/VEE?

A

fever
cerebral signs (head pressing, compulsive walking, abnormal mentation)

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36
Q

What is the reservoir for WNV?

A

birds

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37
Q

What is the vector for WNV?

A

mosquito

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38
Q

What clinical signs are seen with WNC?

A

mentation change, muscle fasciculations
weakness/ataxia assymetric
CN abnormalities
fever
depression

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39
Q

WNV diagnosis

A

serum IgM capture ELISA (elevated with disease, not vaccination)

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40
Q

What are wildlife reservoirs of rabies?

A

skunks
bats
raccoons

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41
Q

Rabies diagnosis

A

hippocampus and brainstem
–negri bodies (aggregates of viral proteins and nucleic acids
-direct flourescent antibody
-intercerebral inoculation of mice with CNS tissue

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42
Q

Cerebellar abiotrophy is heritable in what breed?

A

ariabians
– 2 to 6 months of age

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43
Q

Cerebellar abiotrphy clinical signs

A

ataxia
wide-based stance
intention tremor, absent menace
normal strength

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44
Q

Vestibular disease clinical signs

A

head tilt
circling
pathologic nystagmus
assymetric ataxia: ipsilateral extensor hypotonus & contralateral extensor hypertonus

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45
Q

What is the most common C/S of temperohyoid osteoarthropathy (THO)?

A

CN VII and CN VIII signs

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46
Q

Cervical vertebral malformation spinal cord compression has C/S of

A

ataxia worse in hind limbs than forelimbs

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47
Q

Signalment of horses with cervical vertebral malformation?

A

young, fast-growing horses

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48
Q

Cervical vertebral malformation diagnosis

A

cervical vertibral radiographs: minimum ratios: <52% are abnormal for C2-C6 ,<56% abnormal for C6-C7

Myelogram: neutral, felxed, extended

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49
Q

What are radiographic abnormalities of cervical vertebrae?

A

flare of caudal epiphysis (ski slope)
subluxation/malalignment
abnormal ossification
dorsal laminar extensions

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50
Q

Diagnosis of cervical spine compression on myelogram

A

20% or greater reduction in dural diametercompared to adjacent mid-body diameter
–50% or greater reduction on dorsal dye column

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51
Q

Equine degenerative (EDM) is seen in what horses?

A

genetically susceptible individuals deficient in vitamin E in first year of life (young horses)

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52
Q

Equine degenerative (EDM) breeds predisposed

A

mrogan
appaloosa
lusitano

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53
Q

Equine degenerative (EDM) C/S

A

symmetric ataxia & paresis (hind limbs >forelimbs)
spasticity

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54
Q

Equine degenerative (EDM) neuronal degenreation seen on histo

A

EDM: spinocerebellar tracts of cervicothoracic spinal cord
–axonal necrosis, spheroids (Swollen axons)

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55
Q

Prognosis Equine degenerative (EDM)

A

Poor- even with tx of vit E

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56
Q

What is the definitive host of sarcocystis neurona?

A

opposum

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57
Q

EPM C/S

A

assymmetric ataxia
weakness
muscle atrophy
+/- CN abnorma
+/- cerebral signs (mentation change, seizures)

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58
Q

What are the 3 FDA approved tratments for EPM?

A

ponazuril (marquis)
diclazuril (protazil)
sulfadizine/pyrimethamine (Rebalance)

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59
Q

EHV-1 clinical signs

A

symmetric posterior weakness and ataxia
ascending
urine dribbling
poor tail and anal tone
+/- fever

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60
Q

EHM CSF

A

xanthochromic

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61
Q

EHM diagnosis

A

nasal swab PCR: shedding
whole blood PCR: lymphocyte assoc viremia

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62
Q

What is the analagous disease in humans to equine motor neuron disease?

A

Lou Gerigs Disase (ALS)– assoc with Vit E def

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63
Q

Equine motor neuron disease C/S

A

muscle wasting and weakness
fasciculations

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64
Q

Equine motor neuron disease Diagnosis

A

serum vit E levels
tail head mm biopsy (sarcocaudalis dorsalis m)

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65
Q

Equine motor neuron disease treatmnet

A

+/- response to natural Vit E supplementation

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66
Q

Clostridium tetani toxin?

A

tetanospasmic (classic toxin) and tetanolysin
–> irreversibly binds presynaptic inhibitory interneurons (Renshaw cell)– blocks inhibitory synapses by inhibtiing NT release (glycine and GABA)–> disinhibition of motor neurons

**SPASTIC PARALYSIS

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67
Q

Tetanus disease is caused by

A

inoculation of organism in anaerobic wound (ie subsolar abscess)

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68
Q

tetanus c/S

A

spastic paralysis
- “Sawhorse” stance, rigit tail, stiff gait
-hyperesthesia
-prolapse of nictating membrane

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69
Q

Tetanus treatment

A

-antibiotics: stop toxin production from vegetative form
-tetanus antitoxin: neutralize unbound toxin
-diazepam, sedatives: control muscular spasm
-supportive care
-tetanus toxoid: generate active immunity

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70
Q

What are the 3 routes of transmission of clostridium botulinum?

A
  1. forage poisoning: ingestion of preformed toxin
  2. wound botulism: anaerobic
  3. toxicoifnectious botulism (ingestion of spores)
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71
Q

What is the cause of shaker foal syndrome?

A

clostridium botulinum– toxicoinfectious botulism ingestion of spores

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72
Q

What are clinical signs of shaker foal syndrome

A

muscle fasciculations
bunny hopping
dysphagia

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73
Q

describe the pathogenesis of botulism

A

botulinum neurotxin at presynpatic cholinergic NM junction
–> binds to SNARE proteins in nerve terminal
–> prevents fusion of prsynaptic vesicle at NM junction
–> prevents release of acetylcholine

**FLACCID PARALYSIS

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74
Q

What are clinical signs of BOtulism?

A

Flaccid paralysis
-weakness, poor muscle tone
-dysphagia
-hypoventilation

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75
Q

Botulism treatment

A

-eliminate source of toxin: antibiotics
-bind circulating toxin: antitoxin
-supportive

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76
Q

What anitbiotics are contraindicated in the treatment of botulism?

A

gentamicin
procaine (PPG)
**because potentiate NM blockade

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77
Q

What are C/S of cauda equina/polyneuritis equi

A

tail and anal spincter paralysis, peirneal anesthesia, CN deficits

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78
Q

What are palliative treatments for cauda equina?

A

corticosteroids
rectal and bladder evacuation

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79
Q

What are the most competent reservoir for WNV in US?

A
  1. passerine (true perching birds)
  2. Charadrii form (shore bird) spp
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80
Q

Who are the dead end hosts of WNV?

A

horses
humans

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81
Q

How is WNV transmitted to horses?

A

unknown mosquito species

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82
Q

WNV clinical signs are predominantly due to?

A

lesions in gray matter– hindbrain, spinal cord **majority of lesions

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83
Q

Describe the progression of C/S seen with WNV?

A

initial presentation– mild obtundation
–> progress to stupor
–> narcoleptic episodes– midbrain/hindbrain, facial tongue involvement, vestibular signs, ataxia, limb weakness

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84
Q

What are differentials for WNV?

A

alphaviral encephalomyelitis (EEE, WEE)
rabies
verminous or bact encephalitis
EPM
brain or SC trauma
cervical stenotic vertebral myelopathy
hepatic encephalopathy
compressive mass in calvaria/vertebral canal

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85
Q

What are common reported residual effects with horses that recover from WNV?

A

gait abnormalities
behavioral changes
mm atrophy
lethargy

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86
Q

When horses flip over backwards, why is there facial nerve deficits?

A

courses through facial canal within petrosal bone

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87
Q

The basioccipital and basisphenoid bones are susceptible to fracture due to the dsitracting force of what mm?

A

rectus capitus ventralis mm

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88
Q

Optic nerve injuries occur with flipping over backwards ifor what reason?

A

stretched/damaged with violent gyrations d/t head impact fx through optic canals

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89
Q

When a horse pitches its head first into ground when running, it can fracture the atlas cranially causing trauma to what CN?

A

hypoglossal nerve
**trauma as it exits hypoglossal foramen

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90
Q

Cattle injure what cranial nerve when they are clampedi n the head catch?

A

CN VII: Facial N.
**“stanchion head

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91
Q

What kind of breathing pattern is seen with cerebral injury?

A

Cheyne-stokes breathing (hyperventilation)

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92
Q

What is the main differentiating factor between central vs peripheral C/S?

A

peripheral: horizontal/rotary nystagmus– fast phase away from lesion

central: spontaneous vertical nystagmus

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93
Q

What retinal changes are seen with traumatic optic nerve blindness (in 2 to 4 weeks)?

A

pallor of optic disk
Dec number and caliber of retinal vessels
linear peripappillary pigment

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94
Q

Equine thiamine deficiency can be seen with ingestion of what?

A

diets that contain thiaminases:
-bracken fern (pteridium aquilinum)
horse tails (Equistium avense)
-amprolium

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95
Q

What C/S are seen with equine thiamine deficiency?

A

ataxia
CP deficits
heart block bradycardia
blindness
wt loss
dysuria
hypothermia of extremities
periodic muscular fasciculations
convulsions (terminal development)

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96
Q

Why are intracarotid injections uncommon in cattle?

A

d/t omohyoid mm lies between carotid a and jugular

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97
Q

What are drugs that cause cortical necrosis when injected into carotid a:

A

pheonthiazine tranquilizers
chloramphenicol
chloral hydrate
barbiturate anesthetics
phenylbtuazone
calcium gluconate
Naiodide

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98
Q

What is the pathogenesis of an intracarotid injection leading to neuro signs?

A

intense vasospasm
–> ischemia
–> progress to Ca ion influx, anaerobic metabolism, loss of function and accumulation of excitatotoxi aa, free radicals and eicosanoids

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99
Q

Cholinesteric granulomas in horses are seen in what part of the brain?

A

choroid plexus– 4th and lateral ventricles

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100
Q

A cholinesteric granuloma should be suspected in horses with what C/S

A

forebrain dysfunction and brain stem
**suspect in horses with waxing/waning forebrain dysfunction

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101
Q

What is the etiology of cholinesteric granulomas?

A

chronic inflammatory reaction to cholesterol– extravasated from breakdown RBCs w//in choroid plexus

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102
Q

What is the method of choice for Dx of cholinesteric granuloma?

A

CT

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103
Q

What is seen on necropsy with a cholinesteric granuloma?

A

brownish mass ~3cm in diamater and attached to choroid plexus

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104
Q

What is the cause of equine luekoencephalomalacia?

A

ingestion of fumonsin toxins produced by fusarium certicilloids or fusarium proliferatum (fungi) infecting corn/corn by products

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105
Q

What C/S are seen with equine luekoencephalomalacia?

A

Neuro signs (cerebral): obtundation, dementia, head pressing, blindness, lack of menace, limb ataxia/weakness

hepatic: high liver enzymes, icterus, mm petechiation

CV: dec cardiac contractility, inc systemic vascular resistance

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106
Q

Which species is most susceptible to fumonsin toxins?

A

horses

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107
Q

How is an antemortem diagnosis of equine luekoencephalomalacia?

A

> 10 ppm in feed: B1, B2, B3

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108
Q

What are differentials for equine luekoencephalomalacia?

A

traumatic brain injury
arboviral encephalitidies
hepatic encephalopathy
EPM
botulism

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109
Q

What is seen on necropsy of horses with equine luekoencephalomalacia?

A

vascular damage: liquefactive necrosis, degen or malacia of white matter, flattening of cortical gyri, yellowing of white matter, feltainous fludi in CNS lesions, CNS hemorrahge

visceral organs: hepatic conestion, centrilobular necrosis, hemorrahgic enteritis& cystitis

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110
Q

What are idiopathic causes of epilepsy?

A

genetic predisposition (known or suspected): juvenile idiopathic epilepsy of arabian foals of egyptian lineage, arabian lavender foal syn, familial epilepsy of various cattle breeds

unknown cause (no structural cause

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111
Q

What are structural causes of epilepsy?

A

cerebral disorders:
-vascular
-inflamm/infectious
traumatic
anomalous/developmental
-neoplastic
-degenerative dzes

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112
Q

What is the most common cause of epilepsy in ruminants?

A

polioencephalomalacia

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113
Q

What is the most common cause of structural abnormalities leading to epilepsy?

A

skull fractures

–> cerebral hemorrhage, cerebral edema, neoplasia, cholinesteric granuloma, vasculitis, meningoencephalitis, abscess, IC bascular events, leukocencephalomalacia, congenital abnorm, EPM

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114
Q

Define generalized seizures

A

involving neural networks of both cerebral hemispheres
**generalized bilateral motor activity

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115
Q

Define focal seizures

A

involving one side of forebrain
**lateralized motor signs or sensations

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116
Q

What are autonomic signs of generalized the seizures?

A

salivation
urination
defecation

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117
Q

When are clinical signs seen with juvenile idiopathic epilepsy?

A

2 months old (2d-6months)

118
Q

juvenile idiopathic epilepsy: what are post ictal clinical signs?

A

profound & persistent obtundation
-obtundation
-cortical blindness (last sign to resolve, several days, hrs to 2 weeks)
-loss of maternal bond & interest in suckling

119
Q

Define cataplexy

A

path intrusion of REM sleep into wakefullness or at onset of sleep

120
Q

define narcolepsy

A

tendency for abrupt transitions from wakfullness into non-REM sleep

121
Q

What are equine breeds known to have narcolepsy/cataplexy?

A

american mini horse
lipizzaner
suffolk
shetland
fell pony

122
Q

What are ruminant breeds known to have narcolepsy/cataplexy?

A

suffolk lamb
spanish fighting bulls
Guernsey bull
brahman bull

123
Q

Rabies is shed in what secretions?

A

saliva

124
Q

Rabies is inactivated by

A

dried/exposed to UV light

125
Q

Describe the pathogenesis of rabies

A

binds to acetylcholine receptors of peripheral n migrates to CNS through peripheral N, spinal rootlets and SC traveling to brain along nerve tracts into CSF
**spreads centrifugally to salivary galnds and nasal epithelium

126
Q

How does Rabies causing neuron destruction lead to death?

A

multifocal loss of lower motor n and autonomic dysfunction
–> leads to cardiorespiratory paralysis as virus infects medullary centers of brainstem

127
Q

What are the forms of rabies disease?

A

dumb: mentally depressed
furious: hyperexcitable, fearful or enraged
paralytic: dumb with flaccid paraperesis, tetraparesis, teraplegia

128
Q

What bacteria are most commonly isolated from foals and calves with meningitis?

A

Gram neg enteric bacteria:

escherichia coli
salmonella spp
klebsiella spp

129
Q

What bacteria are commonly isolated from goat kids?

A

mycoplasma spp

130
Q

What bacteria is commonly isolated from juvenile cattle in feedlots with meningitis?

A

Histophilus somni
listeria monocytogenes

131
Q

CSF analysis indicative of meningitis

A

color: turbit, white amber in color, may foam when shaken, may clot
+/- xanthochromia
WBC: calves >100 neuts/uL, 20 - 270 mg/dL protein
gluc: <50% of corrresponding serum

132
Q

What is the recommended antibiotic treatment with calves with gram negative enteric bacterial meningitis?

A

florfenicol

133
Q

What is the recommended antibiotic treatment for horses with meningitis?

A

3rd generation cephalosporins:
-ceftazidime
-ceftizoxime
-ceftriaxone
-cefoprazone
-ceftazxime

134
Q

If cannot use 3rd generation cephalosprins and suspect enteric organisms, what antibiotic is recommended

A

Na ampicillin (better spectrum than PPG)

135
Q

EHV-1 can manifest in what forms?

A

respiratory disease
reproductive disease
neurologic disease

136
Q

How is EHV-1 transmitted?

A

inhalation or ingestion
respiratory secretions, most commonly:
– direct or indirect contact
–aerosol, short distance, less important

137
Q

What is the incubation period of EHV-1

A

2 to 10 days

138
Q

How long does EHV-1 remain infective in the environment?

A

for 14 days and on horse hair for 35 to 42 days

139
Q

How does EHV-1 evade the immune response?

A

EHV-1 downregulated MHC-1 expression to evade immune response
**trigeminal ganglion and lymphoreticular system

140
Q

Describe the pathogenesis of EHV-1 respiratory disease:

A

after inhalation/ingestion
–virus infects cells of nasopharyngeal epitheliuma nd assoc lymphoid tissue
–> infection & erosion of resp epithelium–> respiratory disease

141
Q

Describe pathogenesis of EHV-1 neurologic disease

A

virus infected phagocytic cells migrate into circulation–> viremia assoc with mononuclear cells, T lymphs
– intracellular location is protection from immune sys & antibodies
–>endotheliotropism– vasculitis, thrombosis of arterioles
–spinal cord, brain –> neuro disease
–placental endothelial cells– reproductive disease

142
Q

EHV-1 non-neuroapthic genotype

A

A2254= N752

143
Q

Neuropathic genotype

A

G2254=D752

144
Q

Can either strain of EHV-1 cause neurologic disease?

A

yes: N752 and D752

145
Q

What are risk factors for the development of EHV-1?

A

-risk based on viral, host and environ factors
-presence of EHV-1 and/or shedding horse with susceptible horses
-season: late autumn, winter, spring
-Age >3 years; mares >20 years of age
-past exposure
-biphasic fever
-stress assoc with weaning, transport, intro of new horses, secondary infection, immune suppression
-mares more commonly affected: ponies and smaller breed less common
-magnitude and duraiton of viremia
-infection with D752 genotype
-geographic region (NZ, AUS less common)
-vaccination within 5 weeks of event

146
Q

What are potential differentials for EHV-1/EHM?

A

EPm
cervical vertebral malformation
vertebral fx/trauma
viral encephalitis (WNV, EEE, WEE)
equine degnerative myelopathy
rabies
botulism
intoxication
anaplasma phagocytophilum
borrelia burgdorferi

147
Q

PCR testing for EHM/EHV-1 recommendation from AAEP guidelines

A

PCR for glycoprotein B (gB) gene, then PCR for N752D mutation

148
Q

In acute suspected cases of EHV-1/EHM that are initially negative, when should you retest?

A

in 24 to 72 hours

149
Q

EHV-1 serology, what is indicative of recent infection?

A

four-fold rise indicates recent infection

150
Q

What is the mechanism of action of acyclovir against EHV-1?

A

synthetic purine nucleoside analog
– inhibits viral DNA polymerase and viral replication
– inhibitory action against several human herpresviruses
–inhibitory effect on EHV-1 in invitro
–> prevents viremia, reduces nasal shedding severity and abortion

151
Q

The prodrug of acyclovir gets higher bioavailability, what drug is this?

A

valacyclovir: 27 mg/kg q8h for 2 days, then 18 mg/kg a12h for 1 to 2 weeks

152
Q

The greatest effect of valacylovir was seen when?

A

greatest effect when administered prophylactically

153
Q

What are differentials to rule out with headshaking in horses?

A

skull lesions
alelrgic rhinitis
vasomotor rhinitis
otitis externa/media/interna
trombicula autumnalis (harvest mite)
sinus sx
cervical arthritis
ocular lesions
alelrgic oconjucntivitis
blocked lacrimal ducts
fungal sinusitis
THO
mites/ticks– external ear canal
guttural pouch mycosis
onchocerca dermatitis
dental problems

154
Q

What diagnostic is used to determine integrity of auditory pathway of inner ear adn medulla oblongata

A

auditory evoked potentials

155
Q

What should you suspect when a horse with vestibular disease, shows clinical signs of systemic sepsis (fever, tachycardia, tachypnea), limb ataxia/weakness, other CN deficits, obtundation?

A

extension of infection along fracture line to meninges

156
Q

Antibiotic Treatment of otitis media/interna

A

**should directed with culture
– gramp ps: PPG, Kpenn, ceftiofur sodium
Staph: enrofloxacin
oral tx: TMS, chloramphenicol

157
Q

Temperohyoid osteoarthropathy is a progressive disease, with enlargement and sclerosis of:

A

stylehyoid bone
tympanic bulla
petrous portion of the temporal bone

158
Q

Fusion of the Temporohyoid joint causes interference in the coordinated movement of what structures?

A

tongue
hyoid apparatus
larynx

159
Q

WIth THO, what causes stress on fused joints?

A

chewing
swallowing
vocalizing
veterinarian– passing NG tube, dental work

160
Q

What is a normal schirmer tear test?

A

normal >20 mm

**injury to parasymp. lacrimal brach of facial nerve causes decreased tear production

161
Q

Fusion of THJ causes a sudden onset of C/S

A

CN VII and VIII deficits
**toward the affected side: head tilt, neck turn, body lean, tight circling

162
Q

What are the percentages of hroses that died as a consequence of THO with what treatment options?

A

medical therapy: 13/20- 65%
certahyoid ostectomy 1/25 4%
partial stylohyoid ostectomy 1/8 12.5%

163
Q

What are management changes to help prevent the progression of THO?

A

cribbing collars– prevent cribbing
bitless bridle
minimize dental/other prof procedures

164
Q

What is the cause of equine nigropallidal encephalomalacia?

A

yellow star thistle: centaura solstitalis
Russian knapweed: rhapoticem repens

165
Q

What are characteristic C/S of equine nigropallidal encephalomalacia?

A

faciala nd lingual dystonia
variable: obtundation (mild-mod)
behavioral signs
ataxia

166
Q

What do horses that have nigropallidal encephalomalacia do when drinking?

A

immerse the muzzle deep into bucket to force water to back of pharnyx

167
Q

What are the toxic principles of yellow star thistle/russian knapweed?

A

repin- sequeseterpen lactone
– high affinity for neural tissue- inhibit dopamine release

168
Q

Nigropallidal encephalomalacia lesions are similar to human toxic envorment parkinsomism, seen where?

A

lesions globus pallidus and susbtantia nigra pars reticulata

169
Q

What are the most common fungal organisms cultured in guttural pouch mycosis?

A

Aspergillus fumigatus
Emericella nidulans

170
Q

In guttural pouch mycosis, what causes the epistaxis, local pain and. neurologic signs

A

erosion of major vessels and major nerves involved
medial pouch: CN 9-12, cranial cervical ganlgion, postganglionic sympathetic n, internal carotid a
lateral pouch: external carotid a, facial n VII paralysis

171
Q

Definitive diagnosis of guttural pouch mycosis is performed with what diagnostic?

A

endoscopy

– can see other C/S: dorsal displacement of soft palate, inability to swallow, larygneal hemiplegia

172
Q

What treatment has the best prognosis for cure in guttural pouch mycosis?

A

15 days to 5 weeks after arterial catheterization for fungal plaques

173
Q

What are differentials for epistaxis (guttural pouch mycosis)

A

EIPH
ehtmoid hematoma
guttural pouch or pharyngeal neoplasia
tracheobronchial foreign bodies

174
Q

What are differentials for dysphagia (guttural pouch mycosis)?

A

hyoid apparatus fracture
pharyngeal & guttural pouch fistula
cleft pallate
esophagitis
pharyngeal paralysis
bacteria, viral & mycotic CNS infections
FB entrapment in mouth/esophagus
pharyngeal neoplasia
PB poisoning

175
Q

Horners syndrome: damage to sympathetic nerve supply along pre/post ganglionic nerves orders?

A

First order: brain stem– ipsilat brain stem (rare), spinal cord (T1-T3)– horses met neoplasia & EPM

Second order: cranial thoraic nerve roots, spinal nerves, cervical sympthatic trunk

Third order: CCG (cranial cervical ganglion) in the skull and behind the eye

176
Q

Preganglionic sympathetic motor fibers that innervate structures of the head originate from where?

A

the first 3 thoracic segments

177
Q

Cattle with horners syndrome have what C/S?

A

dryness of ipsilateral planum nasale
– mediation of norm sweat gland secretion by postganglionic symp. fibers & alpha adrenergic receptors in cattle

178
Q

Using hydroxyamphetamine (1% solution) as a diagnostic causes release of norepinephrine form postganglionic sympathetic neurons, no response (no pupillary dilation) indicates:

A

postganglionic nerve damaged

179
Q

Horners syndrome:
Using hydroxyamphetamine (1% solution) as a diagnostic causes release of norepinephrine form postganglionic sympathetic neurons, response (pupillary dilation) indicates:

A

preganglionic n damage

180
Q

Horners syndrome:
After administration of hydroxyamphetamine and no response is elicited, then what can be administered?

A

topical adinistration of epinephrine

–> activates iris musculature produces mydraisis within 20 m, within 40 m if preganglionic disorder

181
Q

Horners syndrome:
Topical administration of phenylephrine solution (2.5 to 10 %) causes pupillary dilation is indicative of what lesion location?

A

postganglionic lesion

– INC d/t denervation hypersensitivity

182
Q

Horners syndrome: if administer epinephrine parenterally, what C/S are seen in effected horses?

A

affected horses sweat profusely over affected side of face
**does not differentiate post to pre-ganglionic lesions

183
Q

What is the treatment in xylazine associated horners syndrome?

A

condition disappears spontaneously

184
Q

With horners syndrome caused by necrotizing perivascular drug injection, what treatment can be performed?

A

immediate dilution or irrigation or both (lg vol of saline infiltrated into perivascular tissues)

185
Q

With abnormalities seen in CN IX, X and XI, what C/S are seen

A

dysphagia
dysphonia (stridor, roaring)
inspiratory dyspnea

186
Q

CN X deficits (visceral efferent component) can be caused by what other diseases in ruminants?

A

vagal indigestion
ruminal distension with fluid
ruminal tympany
abomasal stasis
+/- hypochloremic, hypokalemic met alkalosis

187
Q

define abiotrophy

A

spontaneous premature degeneration resulting from an inborn error of development

188
Q

cerebellar abiotrophy is described in what breeds?

A

arabian
gotland pony
eriskay pony

189
Q

What is the genetic basis for cerebellar abiotrophy in arabians?

A

mutY homolog gene (MUTYH)
**single nucleotide polymorphism upstream of MUTYH gene

190
Q

cerebellar abiotrophy inheritance in arabians is

A

autosomal recessive

191
Q

C/S of cerebellar abiotrophy in arabians is seen at what age?

A

6 weeks to 4 months

192
Q

What are C/S of cerebellar abiotrophy?

A

basewide posturing in thoracic limbs
head tremors
+/- menace response
gait: wobble side to site, swaying, learching, stiff thoracic limbs/paddling

193
Q

Does blindfolding exacerbate signs of cerebellar abiotrphy?

A

No

194
Q

What is the diagnostic for cerebellar abiotrophy?

A

homozygosity for cerebellar abiotrophy allele–> 20 to 30 hair roots of vet genetics

195
Q

Cerebellar hypoplasia is seen with what infection?

A

BVDV at 90 to 170 days pregnancy

196
Q

conditions promoting poisoning with locoism (swainsonine tox)

A

hot dry weather
scarcity of alternative forage
horses prone to grazing v cattle
cattle– chornicly exposed addicted to locoweed

197
Q

swainsonine toxic principle

A

indolizidine alkaloid

198
Q

what is the pathogenesis of locoism (swainsonine tox)?

A

potent inhibition of mammalian alpha-D-mannosidase and golgi-mannosidase II

199
Q

What are clinical signs of locoism (swainsonine tox)?

A

cerebellar signs: high stepping gait, intention tremor of head,
ataxia
obtundation
dysphagia

200
Q

Why are weak calves seen from cattle diagnosed with locoism (swainsonine tox)?

A

abnormal suckling behavior
– indolizidine alkaloids secreted in milk

201
Q

in utero calves exposed to locoism (swainsonine tox) have what C/S

A

weak/fail to thrive
flexural limb contractions
lateral carpus rotation

202
Q

locoism (swainsonine tox) can potentiate the C/S of what disease?

A

core pulmonale

203
Q

In sheep, the immunosuppressive effects of locoism (swainsonine tox) can predispose to:

A

-pyogenic infections
– pneumonia
–keratoconjunctivitis
– foot rot

204
Q

locoism (swainsonine tox) defintive diagnosis

A

alpha- D-mannosidase, swainsonine– blood concentrates measured with assays

***swainsonine measurements on blood samples collected within 2 days of eating locoweed

205
Q

what liver abnormalities are seen with locoism (swainsonine tox)?

A

INC liver enzymes (INC AST, ALP)
– liver prominent vacuolation of hepatocytes

206
Q

What the is the pathogenesis behind the secondary fungal metablolites indole diterpenoid tremorgens?

A

act by blocking K outflow from cells via inhibition of cell membrane large conductance Ca-activated K channels

207
Q

What is the associated fungus with Perennial Rygrass staggers?

A

Neotyphodium lolii

208
Q

What are conditions that increase the toxicity of perennial ryegrass pastures?

A

-high proportions of endophyte infected plants
-late seasons growth
-hot,dry, summer and fall after wet spring
-ryegrass domination of pastures
ambient temperature higher than 23C
-ryegrass that is allowed to flower before consumption and close grazing

209
Q

what is the toxic principle of rye grass staggers produced by the fungus neotyphodium lolii?

A

lolitrem B

210
Q

When are clinical signs of rye grass staggers seen after introduction to pasture?

A

5 to 10 days onto endophyte rich pastures (as early as 48h, as late as 2 weeks)

211
Q

Horses show what C/S with grass staggers?

A

-fine muscle fasciulcations & tremors– esp shoulders, chest & thoracic limbs
-apparent after exercise
-fine tremors of eyes during ophtho exam
-wide based gait
-trunkal sway
-rapid stumbling
**blindfolding makes these signs worse (consistent with bilateral vestibular disease)
-hyperresponsiveness– C/S worsen with handling

212
Q

Ruminants show what C/S with grass staggers

A

-limb stiffness
-unpredictable inconsistent leg movement
-hypermetria
-head tremor
-falling
-generalized tetanic convulsions
-variable progression of ataxia
-vestibular, veneral proprioceptive then cerebller

213
Q

Treatment of rye grass staggers?

A

recover days to weeks, handle infrequently.

214
Q

What is the toxic principle of PasPalum staggers?

A

indole diterpene metabolite: paspalitrem B (mostly), also A & C

215
Q

What are preventative measures for Paspalum staggers?

A

mowing toxic pastures and removing
burning infected seed heads

216
Q

What is the definitive host of Sarcosystis neurona?

A

opposum: didelphis virgiania- N. America

217
Q

What are intermediate hosts of sarcocystis neurona?

A

nine-banded armadillo
striped skunk
raccoon
domestic cat

218
Q

What is the aberrant host of sarcocystis neurona?

A

Horses

219
Q

What stage of Sarcocystis neurona is ingested by the hrose?

A

sporocyst

220
Q

What is the mechanism of entry into the CNS of sacocystis neurona and Neospora hughesi ?

A

leukocyte associated parasitemia

221
Q

On histology which life stage is observed of sarcocystis neurona/Neospora hughesi in cytoplasma of nerons, mononuclear phagocytes, or capillary enodthelial cells?

A

free merezoites

222
Q

what are risk factors for infection of sarcocystis neurona and neospora hughesi?

A

-prevoius dx EPM
-INC exposure to opposums in environment, feces consistently identified
– physiologic stress important role in onset of disease:
-primary use of the horse– show and race horses
-recent transport
-recent adverse health problems, parturition, management changes

223
Q

What is serum S. neurona antibody PPV?

A

A negative test strong evidence that the horse doesn’t have EPM

224
Q

What ist he only way tot distinguish horses with EPM from exposed horses?

A

detect specific ab made within the CNS
– western blot
-serum to CSF ab ratios
–C values

225
Q

IS PCR of CSF for S. neurona DNA useful?

A

**useful for PM diagnosis
false negatives are common– enzymes destroy DNA in CSF, merezoites rarely enter CSF

226
Q

What percentage of horses with moderate to severe neurologic signs due to EPM improve?

A

60% improve 1 grade

227
Q

What percentage of horses have a complete recovery from neurologic signs due to EPM?

A

10-20% have a complete recovery

228
Q

What percentage of horses with neurologic signs due to EPM suffer at least one relapse?

A

10-20%

229
Q

Equine degenerative myeloencephalopathy/neuroaxonal dystrophy clinical signs?

A

acute insidious onset
-symmetric ataxia
-trunk/limb paresis
-age 1-12 m
-posture/gait wide based (hypometric (aspsicity)
-usu mroe severe in hind limbs

**neurogenic mm atrophy note seen in EDM/NAD

230
Q

Equine degenerative myeloencephalopathy/neuroaxonal dystrophy diagnostic?

A

consistently associated with low serum/plasma vitamin E
normal >2 microg/ml
marginal 1.5-2 microg/ml
deficient <1.5 microg/ml

231
Q

What role does vitamin E have in the body?

A

-neuroprotective effects
-inhibition of oxidation of CNS membrane lipids
-falcification axonal transport macromolecules
-preventing accumulation of oxidized cholesterol (oxysterol) in lipid peroxidation and demyelination

232
Q

How to diagnose Equine degenerative myeloencephalopathy/neuroaxonal dystrophy?

A

low serum/plasma vit E:
marginal-low (<2 microg/ml)
collect 3 blood samples over 24 hours
*store blood without contact to rubber stopper

**diagnosis of exclusion

233
Q

absorption of vitamin E requires what?

A

fat– give with feed or oil

234
Q

DDX for Equine degenerative myeloencephalopathy/neuroaxonal dystrophy

A

EPM
trauma
wobblers (CVCM)
EHV-1 (EHM)

235
Q

Which horse breeds have a familial predisposition for the development of Equine degenerative myeloencephalopathy/neuroaxonal dystrophy?

A

-standardbreds
-paso finos
-Norwegian fjords
-arabians
-welsh ponies
-haflingers

236
Q

What are the histological hallmarks of Equine degenerative myeloencephalopathy/neuroaxonal dystrophy?

A

spheroids, axonal loss and secondary demyelination w/in caudal brain stem adn spinal cord

237
Q

eNAD and EDM are clinically indistinguishable, with EDM being a more advanced form of the disease. What are the differences between these diseases?

A

eNAD: histological lesions are confined to the cuneate and gracile nuclei of the caudal medulla oblongata

EDM: lesions are more widespread and include demyelination within the ascending tracts of the spinal cord

238
Q

what are risk factors for the development of Equine degenerative myeloencephalopathy/neuroaxonal dystrophy?

A

-application of insecticde
-exposure to wood preservatives
-frequent time spent on dirt lots

239
Q

Once clinical signs of ataxia are present in horses with Equine degenerative myeloencephalopathy/neuroaxonal dystrophy, is supplementatin with alpha tocopherol beneficial?

A

– supplementation will not improve neurologic deficits
-progression of disease can be halted through supplementation
–C/S typically stabilize at 2 years of age

240
Q

What is the best management practice in the prevention of Equine degenerative myeloencephalopathy/neuroaxonal dystrophy?

A

maintain pregnant mares, foals, weanlings, yearlings and 2 year old horses on lush green pastures

241
Q

Is treatment of postanesthetic myelopathy and encephalopathy rewarding?

A

no– majority of cases euthanized d/t progressing C/S

242
Q

What are clinical signs observe diwth postanesthetic myelopathy & encephalopathy?

A

apparent in recovery
-paraperesis
-ataxia
-recumbency
-paraplegia
-cutaneous hypoagesia
-areflexia of hind quarteres
-dementia
-pacing
-cortical “central” blindness

243
Q

What are the 5 groups of occipitalatlantoaxial malformation?

A
  1. Heritable conditin Arabian horses
  2. Congenital assymetric OAAMs
  3. Assym atlantoccipital fusion
  4. duplication of axis or atlas
  5. symmetric OAAms iin nonArabian horses
244
Q

What are clinical signs of occipitalatlantoaxial malformation?

A

-+/- abnormal head position
-sudden unexpected death
-stillbirth
-sudden death
-reluctance to move head/neck
-symmetric C/S: hyperreflexia, hypertonia, weakness, ataxia in all 4 limbs, hold head in extension “weathervane posture”

245
Q

What are reasons for congenital vertebral malformations?

A
  • disruption in early gestation spinal cord development
    –> genetic defects, mechanical injury, teratogens, nutrient deficiency microbial infections, maternal abnormalities
246
Q

What are viruses that cause congenital vertebral malformations?

A

schmalenberg virus
akabane virus
aino virus
cache valley virus

247
Q

What are teratogenic viruses that do not cause congental vertebral maloformations?

A

blue tongue
BVD
border disease

248
Q

Spina bifida is seen in what livestock breeds?

A

charolais calves
hereford calves

249
Q

define acquired torticollis

A

neck mm contract, cause head to twist to one side

250
Q

What horse breed is predisposed to torticollis?

A

draft horses

251
Q

What species are most susceptible to tetanus?

A

horses
small ruminants
cattle

252
Q

Which neurotoxin is produced by Clostridium tetani?

A

tetanospasmin

253
Q

Tetanospasmin bind irreversibly where in the nervous system?

A

to presynpatic inhibitory interneurons, preventing hte release of GABA/glycine inhibitory NTs

**growth of new nerve terminals required

254
Q

What is seen on gram stain of wound exudate with horses with tetanus?

A

drumstick shaped, gram pos bacilli

255
Q

What are classic C/S of tetanus?

A

-trismus: INC masticatory mm tone
-risus sardonicus– rigidity of facial expression
-prolapse of membrane nictitans (horses prominant, cattle incosistent, sheep no observed)
-“sawhorse stance”- limbs and neck head in extended posture
-“pump handle” tail- tail evelated

256
Q

What is an effective fluid additive in patients with tetanus?

A

magnesium– b/c blocks neruomuscular transmission, interferes wtih vatecholamine release from nerves and adrenal medulla, antagonizes action so ca, (spares resp mm)

257
Q

What are the goals in treatment of tetanus?

A
  1. provide mm relaxation
  2. enxure good footing
  3. eliminate infection
  4. neutralize unbound toxin
  5. maintain hydration & nutrition
  6. establish active anti-toxic immunity
258
Q

the virulence factor tetanolysin does what in tetanus?

A

damages healthy tissue – anaerobic conditions

259
Q

What is polyneuritis equi?

A

a progressive granulomatous polyganglioradiculneuritis of cauda equina

260
Q

Cauda equine C/S:

A

dysuria
tail rubbing
cutaneous & muscular hyperestehsia around hind quarters
paresis: tail, bladder, rectum (fecal retention), anal sphincter, penis, neurogenic tail atrophy

lumbosacral nerve roots involved: pelvic limb weakness, mm atrophy

spinal n roots: discrete areas of mm atrophy

+/- CN involvement– variable

261
Q

What are differentials for polyneuritis equi?

A

ca spine fx/luxations
EHM
sorghum-sudan gass tox
rabies
other infectious dzes involving ca spine and/or lower urinary tract

262
Q

What is seen on muscle biopsy with polyneuritis equi?

A

mononuclear neuritis: sacrocaudalis dorsalis mm

263
Q

Treatment of polyneuritis equi?

A

corticosteroids– early on in dz course
general supportive care: fluid therapy, manual rectal & bladder evaucation
**with careful management can live for months

264
Q

What gait is seen with sorghum toxicity?

A

hopping gait in hind limb
** pelvic limb ataxia, worsens with backing

265
Q

What are C/S seen with sorghum toxicity?

A

flaccid distended bladder– cystitis secondary to urinary retention
–> progress to pyelonephritis- fatal

pelvic limb ataxia

266
Q

What is the toxic principle of sorghum toxicity?

A

unknown

267
Q

What are the two stringhalt syndrome?

A
  1. classical stringhalt: persistent condition of individual horses involving one limb
  2. pasture assoc/Australian stringhalt: inovles both pelvic limbs; outbreaks in horses in pasture
268
Q

Describe the stringhalt gait?

A

abrupt hyperflexion of hock and stifle

269
Q

The stringhalt gait is exacerbated by?

A

excitement, cold weather, hard exercise

backing, sharp turning, when horse goes down slope, sudden stops, transition from standing to walking

270
Q

What is the cause of classical stringhalt?

A

unknown cause

271
Q

Pasture associated stringhalt primarily effects what nerves?

A

primarily large myelinated axons of peripheral nervous system
–> long nerves: recurrent laryngeal nerve, peroneal and tibial branch of sciatic nerve

272
Q

What histologic changes show evidence of nerve regeneration?

A

regenerative nerve clusters
“onion bulb” formations
Schwann cell proliferation

273
Q

Differ between the two types of cervical stenotic myelopathy

A

type 1: focal or multifocal stenosis of vertebral canal, C1-C6

Type 2: boney and ST imingement-remodeling of articular process joints of ca cervical vertebrae, C5-T1

274
Q

What are risk factors for the development of cervical stenotic myelopathy in foals?

A

genetic
physical
dietary factors
COD articular process & metaphyseal growth plates

275
Q

What are normal intervertebral sagittal ratios to be known for diagnosis for cervical stenotic myelopathy?

A

ratio <0.52 C4: C6
ratio <0.54 C7
**89% sensitivity and specificity for spinal cord compression

276
Q

What is Equine motor neuron disease?

A

acquired neurodegenerative disorder in ventral horns, gray matter, spinal cord and brainstem nuclei

277
Q

What are clinical signs of equine motor neuron disease?

A

**do not. have ataxia
-skeletal mm denervation– mm weakness, carry head below shoulders
-“horse on a ball” stance
-fundic exam: horizontal band of pigment above optic disk at tapetal-non-tapetal junction

278
Q

What abnormalities are seen on bloodwork with equine motor neuron disease?

A

vit E levels: low-normal
CK/AST: mild-mod INC
CSF: no cytology abnormalities, +/- INC TP, INC CK

279
Q

What is diagnostic on muscle biopsy for equine motor neuron disease?

A

sacrocaudalis dorsalis mm (biopsy of tailhead mm)
– rich in T 1 myofibriers- sensitive to denervation

**neurogenic atrophy– variable numbers of angular atrophied fibers

280
Q

What are the three forms of botulism?

A
  1. forage poisoning- ingestion of preformed toxin (most common form)
  2. toxicoinfectious- germination of ingested spores in GIT– shaker foal syndrome (T. B)
  3. wound- cotaminated of wounds with spores and vegetative growth
281
Q

Botulism toxin (BoNT) inactivates what protein?

A

inactivates SNARE (soluble N-ethylmalide sensitive factor attachment protein receptor

282
Q

What is the significance of botulism toxin inactivating SNARE?

A

prevents docking and fusion of synaptic vesicles containing acetylcholine
–> prevents exocytosis and relase of neurotransmitter at neuromuscular junction
–>flaccid paralysis of striated mm

283
Q

Shaker foal syndrome is caused by

A

C. botulinum T B

284
Q

When is shaker foal syndrome caused by C. botulinum T B age typically seen?

A

peak age 4 weeks (70% 2-6 weeks)

285
Q

How is botulism diagnosed?

A
  1. botulinum toxin in serum, GI contents, tissues or wounds
  2. antibody against botulinum toxin in serum
  3. C. botulinum spores in GIT contents or suspect feed materials
286
Q

Clinical signs of botulism are dose dependent, and what are they

A

low dose: dysphagia, progression 5 to 7 days, recover with minimal tx

high dose: recumbency 8-12 h, death within 48h

dysphagia- green nasal discharge
generalized mm weakness
increased effort to swallow

287
Q

What are differentials for muscular weakness and dysphagia in horses?

A

-infectious encephalomyelitis: EPM, EEE, WEE, VEE, EHM, WNV
-generalized myopathy: nutritional, seasonal, PSSM
-equine motor neuron dz
-grass sickness
-HYPP
-heavy metal toxicosis

288
Q

What are differentials in cattle for muscular weakness and dysphagia?

A

hypocalcemia
hypokalemia
sulfur toxicity
listeriosis
epidural lymphosacroma
organophosphate tox

289
Q

BoNT T B toxoid vaccine is effective at preventing disease, however what are reasons for failure of vaccine protection in foals?

A

-insufficient ab production in dam
-failure of passive transfer
-overwhelming toxin production
-loss of passive immunity

290
Q

Tick paralysis is caused by what tick spp in the US?

A

Dermacenter andersoni

291
Q

Equine grass sickness is what kind of dz

A

debilitating, often fatal dysautonomia (polyneuropathy)

292
Q

What is the cause of equine grass sickness?

A

unknown
(toxic principle- hypoglycin A in ACer spp seeds)

Smith. Neurolgic DZ (2 decks)

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