LA eye and CN diseases

Question 1

describe differentials for eye/cranial nerve diseases in horses, ruminants, and give key differences from SA

Answer 1

horses:
infectious: EPM, polyneuritis equie
TRAUMA
vascular: intracarotid injections, air embolus
metabolic: hepatic encephalopathy, hyperammonemia, electrolyte issues
toxic: fumonisin, yellow star thistle/knapweed +/- lead
degenerative: THO

ruminants:
infectious: P. tenuis, viruses, literiosis, OMI
metabolic: polioencephalomalacia, vitamin A deficiency
toxic: lead

differences from SA:
TRAUMA is a more important cause in LA
-NOT immune mediated
-not hypothryoidism, neoplasia super rare
-not as evenly divided into uni versus bilateral

Question 2

describe polyneuritis equi

Answer 2

1. immune mediated destruction of LMN
2. USUALLY CAUDA EQUINA
   -but can involve CN 5, 7, 9, 10, 11, 12
3. uni or bilateral
4. uncommon

Question 3

describe metabolic causes of eye and CN disease

Answer 3

1. bilateral symmetric!!!
2. cortical blindness common

Question 4

describe vascular causes of eye and CN disease

Answer 4

1. usually see seizure/collapse, +/- blindness, and/or vestibular signs (once they get up from the seizures)
2. sometimes followed by variable CN deficits
3. uni or bilateral

Question 5

describe how THO relates to eye and CN disease

Answer 5

usually mostly vestibular signs BUT since guttural pouch also see 7, 9, 10, 11, and 12 deficits too!!

Question 6

describe facial nerve compression, a traumatic cause of CN disease

Answer 6

1. from halter during recumbency (anesthesia or disease)
2. buccal branches of CN 7, so ears and eyes usually okay but can see CN 7 deficits (droopy face)
3. usually recover with time! (local inflam squished nerve)

Question 7

describe traumatic optic nerve blindness

Answer 7

1. trauma causes stretching of optic nerves
   -or impact fracture causes local inflammation
2. clinical presentation: uni or bilateral
   -ACUTE blindness
   -loss of PLRs
   -mydriasis
   -in 2-4 weeks, will see fundic changes on ophthalmoscopic exam
3. diagnosis: history and clinical presentation in a horse
   -+/- CT or MRI
4. treatment: aggressive and early anti-inflammatory treatment
   -poor/no response to treatment :(

Question 8

generally describe head trauma in horses

Answer 8

1. other clinical presentation than optic nerve blindness
2. poll impact often causes guttural pouch hemorrhage/trauma
   -7, 8, 9, 10, 11, 12 deficits
3. basihyoid fractures:
   -3, 4, 6 signs: PLR issues, strabismus
   -may also see 5 and 7 deficits

Question 9

describe toxins that affect eyes/CN in horses (NOT COMMON but IMPORTANT)

Answer 9

1. fumonisin:
   -fungal toxins on moldy corn
   -pathology: leukoencephalomalacia
   -signs: sudden onset prosencephalic signs AND blindness, loss of facial sensation, facial nerve paralysis
   -FATAL
2. yellow star thistle/knapweed
   -requires long term ingestion to have issues
   -pathology: nigropallidal encephalomalacia
   -signs: weight loss, altered mentation, ataxia, yawning
   -also: protruding tongue, tongue/lip tremors, facial muscle hypertonicity/grimace and INABILITY TO EAT
   -permanent deficits so usually euthanasia

Question 10

describe vitamin A deficiency

Answer 10

1. retinol and precursors found in green plants; important for eye, CNS< bone development
2. deficiency causes blindness via 3 mechanisms
   -night blindness: not enough retinal rhodopsin: most mild and reversible!
   -degeneration of retinal layers: reversible if treat early!!
   -stenosis of optic foramen and thickening of dura mater; causes increased CSF pressure, compression of optic nerve; IRREVERSIBLE

Question 11

who is most susceptible to vitamin A defiency?

Answer 11

ruminants in feedlots: minimal green plants in diet + increased needs with growth and immune activation

Question 12

how do you distinguish vitamin A deficiency from polioencephalomalacia?

Answer 12

clinical presentation!

calves: ill thrift, diarrhea, blindness (NO PLRs) (polio still has PLRs)

adults: stargazing, nystagmus, strabismus, exophthalmus, seizures, diarrhea, BLINDNESS NO PLRs

BILATERALLY SYMMETRIC

Question 13

describe lead toxicity

Answer 13

1. any LA but cattle most often
2. inhibits many important enzymes and causes capillary dysfunction
3. pathology: polioencephalomalacia
4. clinical presentation:
   -horses: weight loss, ataxia, laryngeal paralysis, dysphagia, facal paralysis, difficulty chewing, secondary aspiration pneumonia, emaciation

-cattle: depression, hyperesthesia, facial and generalized muscle twitching, then ataxia, encephalopathy, cortical blindness, seizures, and GI signs (bloat, diarrhea)

5. treatment: chelation (expensive!!)