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NAVLE > Equine Neurology > Flashcards

Equine Neurology Flashcards

1
Q

CN I name and function

A

Olfactory nerve: mediates sense of smell

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2
Q

3 ways of testing CN II

A

Optic Nerve

i) drop a cotton ball and watch patient follow it to the ground (II only)
ii) Menace response (II for visual cues + VII for blink)
iii) PLR (II for visual + III for pupil constriction)

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3
Q

function of CN II

A

Optic nerve: carries visual signals from retina to occipital lobe of brain

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4
Q

2 ways of examining CN III function

A

Oculomotor nerve

i) observing for physiologic nystagmus when turning head
ii) observing pupillary constriction (PLR)

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5
Q

function of CN III

A

Oculomotor nerve; provides motor to most of the extraocular muscles (dorsal, ventral + medial rectus) + for pupil constriction

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6
Q

CN IV function

A

Trochlear nerve: provides motor function to the dorsal oblique extraocular muscle and rolls globe medially

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7
Q

Trochlear nerve CN number

A

CN IV

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8
Q

how to examine CN IV function

A

examine by observing for dorsolat. rotation of the pupil

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9
Q

3 branches of the CN V

A

trigeminal nerve: mandibular, maxillary, ophthalmic branches

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10
Q

function of CN V

A

Trigeminal nerve:

  • motor to muscles of mastication (masseter, temporal)
  • sensory: eyelids, cornea, tongue, nasal mucosa + mouth
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11
Q

What nerve are you assessing when checking jaw tone?

A

CN V: trigeminal nerve

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12
Q

What nerve are you assessing by touching the globe and assessing for retraction?

A

CN V: Trigeminal for sensory

CN VI: Abducens nerve for motor

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13
Q

What nerves are you assessing through the menace response?

A

CN II (optic) + CN VII (facial)

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14
Q

What nerves are you assessing when pinching the lips and observing for snarl response?

A

CN V (trigeminal) + CN VII (facial)

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15
Q

function of CN VI

A

Abducens nerve: provides motor function to the lateral rectus extra-ocular muscle and retractor bulbi

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16
Q

CN VII name and function

A

Facial Nerve: provides motor to muscles of facial expression (eyelids, ears, lips) + sensory to medial pinna. Also taste to rostral tongue + parasympathetic innervation to lacrimal glands and some salivary glands.

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17
Q

What nerve are you assessing when you observe for any facial paralysis, deviation of the nose to one side or droopy lips?

A

CN VII: facial

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18
Q

CN VIII name and function

A

Vestibulocochlear: sensory input for hearing and head position

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19
Q

CN IX name and function

A

Glossopharyngeal: provides motor and sensory innervation to pharynx for swallowing (w/ CN X).
Also innervates some salivary glands and provides taste innervation from caudal tongue.

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20
Q

What nerves are you assessing when you elicit a gag reflex?

A

CN IX: Glossopharyngeal

CN X: Vagus

21
Q

CN X name and function

A

Vagus: innervates the larynx, oesophagus and pharynx. Also provides parasympathetic innervation to the heart and viscera.

22
Q

how can you examine vagus nerve function?

A

CN X: Vagus nerve

i) elicit a gag reflex
ii) observe for laryngeal paralysis
iii) assess for megaoesophagus and regurgitation

23
Q

name and function of CN XI

A

Spinal accessory: innervates cranial cervical muscles

24
Q

name and function of CN XII

A

Hypoglossal: provides motor to the tongue

25
Q

how do you examine CN XII

A

examine by observing tongue movements and symmetry or for problems drinking/prehending food

26
Q

what is the tx and px for idiopathic trigeminal neuritis?

A
  • supportive care w/ fluids and hand feeding of soft food

- prognosis is excellent w/ most dogs regaining function w/in 1-2wks and return to normal in 3-4wks

27
Q

compare mortality rates of the togavirus encephalitides

A

Eastern equine encephalitis: 75-100% mortality
Venezuelan equine encephalitis: 40-80%
Western equine encephalitis: 20-50%

28
Q

Dx of togavirus encephalitides

A

CS + CSF (inc. protein and cell count) + serology/necropsy evaluation

29
Q

CS of togavirus encephalitides

A
  • most profound in non-vax horses; fever, anorexia, depression, somnolence (sleeping sickness) to hyperasethesia, proprioceptive deficits, recumbency + cerebral/cranial nerve signs (head pressing, propulsive walking, circling, head tilt)
30
Q

Dx of West Nile Virus

A

CS + CSF (inc. protein + mononuclear pleocytosis) –> antigen (IgM) capture ELISA, virus isolation + plaque reduction neutralisation

31
Q

CS of WNV

A
  • not all horses infected w/ WNV develop CS of disease. Horses that are vax. against WNV demonstrate decreased, if any, clinical manifestations. Those that do develop CS;
  • depressed, ataxia, weakness, muscle fasciculations, fever, recumbency
32
Q

CS of equine herpes myeloencephalitis

A
  • fever, lethargy, depression
  • ataxia, paresis, esp. Hind end
  • urinary incontinence, loss of tail tone
  • rarely concurrent resp. signs, can cause abortion in pregnant mares
33
Q

Dx
Tx
Px
of equine herpes myeloencephalitis

A

Dx: nasal swab PCR
Tx: supportive care + antivirals
Px: fair depending on severity, but recovery is prolonged

34
Q

CS of EPM

A
  • chronic w/ mild/vague signs, unilat. hind-end m. atrophy, shifting leg/vague asymm. lameness, weakness, mild ataxia
  • animals are almost always BAR
35
Q

tx of EPM

A

Ponazuril (Marquis) tx up to 6months

36
Q

what disease is prevented with opossum control?

A

EPM: Sarcocystis neurona

37
Q

Pathogenesis of tetanus

A

Clostridium tetani enters through a wound (esp. anaerobic wounds) + proliferates to release a neurotoxin that travels to the CNS.
- Incubation period 1-3wks

38
Q

prevention of tetanus

A
  • annual tetanus toxoid vax., prophylactic tetanus antitoxin in unvax. horses w/ a wound
39
Q

3 forms of rabies CS

A

i) Furious/cerebral form: odd/aggressive behaviour, self-mutilation, ataxia, vocalisation
ii) Dumb/brainstem form: somnolence, dementia, dysphagia, ataxia
iii) Paralytic/Spinal cord: progressive ascending paralysis

40
Q

prevention of rabies

A

AAEP core annual/biannual vax

41
Q

risk factors assoc. w/ botulism

A

silage, poorly stored forage, round hay bales

42
Q

tx and px of botulism

A

Tx: botulinum antitoxin + supportive
Px: poor

43
Q

pathogenesis of cauda equina

A

granulomatous perineuritis of peripheral nerves and cranial nerves, thought to be an immune-mediated event that may be triggered by other bacterial or viral infections

44
Q

pathogenesis of equine degenerative myeloencephalopathy

A

EDM: Vit.E deficiency + a genetic component cause severe neuroaxonal dystrophy

45
Q

pathogenesis of equine motor neuron disease

A

EMND: chronic Vit.E deficiency in adult horse causes peripheral motor neuron cell death

46
Q

CS of EMND

A

weakness, low head carriage + high tail carriage muscle atrophy, muscle fasciculations, weight and muscle loss w/ good appetite
- NO ataxia

47
Q

CS of wobblers

A

Cervical vertebral malformation

  • usu. gradual but can be acute in onset
  • ataxia, usu. worse in HLs than FLs dt HL innervation being SF in the spinal cord
  • freq. perceived as poor performance/vague lameness
  • no CN/brainstem signs
48
Q

Dx of equine cervical vertebral malformation

A

Dx: Suspected based on signalment (young, rapidly growing horse) + CS (symmetric HL weakness and ataxia) + survey rads w/ or w//out myelopgraphy

i) Sagittal ratio is determined by measuring the smallest sagittal diameter of the vertebral canal of each cervical vertebra + dividing this number by the width of the cranial aspect of the vertebral body at its widest pt
ii) The sagittal ratio should be greater than 52% (C4-6) to 56% (C7)
iii) Myelographic studies are necessary for definitive ante-mortem diagnosis of CVM

NAVLE (1 decks)

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