Large Animal Vestibular/Cerebellar/Prosencephalic Diseases

Question 1

how is vestibular disease different in large animals?

Answer 1

1. can be hard to tell central from peripheral!
   -if falling to one side is very dangerous so have to support which makes the rest of neuro exam hard, can’t circle or back up or anything else

Question 2

what are causes of peripheral vestibular disease in horses?

Answer 2

1. DEGENERATIVE: temporohyoid osteoarthropathy
2. trauma (horses are stupid)

Question 3

what are causes of peripheral vestibular disease in ruminants?

Answer 3

1. INFECTIOUS: otitis (mycoplasma and others)
2. trauma: less common than horses, more like being attacked

Question 4

describe temporohyoid osteoarthopathy

Answer 4

1. progressive degenerative changes in the stylohyoid bone, tympanic bulla, and petrous temporal bone in horses ONLY (guttural pouch disease)
2. pathogenesis not entirely known; suspect repetitive movement from constant eating can alter anatomy/trauma and as age can develop arthritis
   -consider infection as a potential cause for NAVLE bc bulla is right there, but otitis is rare in horses

Question 5

describe clinical presentation of THO in horses

Answer 5

1. adult usually, acute onset usually (more like owner noticed acutely)
   -not usually a neonatal disease!
2. vestibular ataxia, head tilt
   -peripheral, but is hard to tell bc OFTEN with cranial nerve deficits (7, 9, 10, 11, and 12) due to guttural pouch anatomy
   -medial compartment: 9, 10, 11, 12 and internal carotid artery
   -lateral compartment: 7 and 8 (tympanic bulla right next door!), and external carotid artery

Question 6

describe diagnosis, treatment, and prognosis of THO

Answer 6

diagnosis
1. guttural pouch endoscopy
2. radiographs
3. can fit them in an MRI but try to avoid because already vestibular and ataxia would just increase badly from anesthesia

treatment:
1. medical:
-antibiotics or steroids NO WORK

2. surgical:
   -ceratohyoidectomy (remove a piece of stylohyoid on affected side= no more movement at temporo-hyoid articulation to reduce inflammation

prognosis:
variable! depends on severity, duration, luck, and money!
-recovery can be prolonged and deficits can persist
-surgical anesthesia also risky bc of ataxia

Question 7

can other guttural pouch diseases cause neurologic signs? (not tested on)

Answer 7

yes but rarely!

1. guttural pouch mycosis: aspergillus
   -can cause epistaxis that can be fatal
2. guttural pouch empyema: pus from strep equi (strangles) commonly
   -discharge, dyspnea, +/- dysphagia
3. guttural pouch tympany: fill with air (foals)
   -swelling, dyspnea

see how they really don’t commonly have neuro signs; so if see a horse with guttural pouch disease and neuro signs, think THO first

Question 8

describe otitis media/interna

Answer 8

1. NOT IN HORSES
   -more in ruminants
2. usually secondary to respiratory infection
   -mycoplasma
   -mannheimia hemolytica
   -pasteurella multicoda
   -histophilus somni
3. usually unilateral
4. may have other sites of infection:
   -pneumonia, septic arthritis, ear mites

Question 9

describe diagnosis and treatment of otitis media/interna

Answer 9

1. not much different from SA but otoscopic exam is harder
   -tiny otoscope can’t look at tympanum in any large animal; need endoscope to see! not practical
   -not all LA patients fit in the CT or have the budget! so sampling for culture is harder
2. systemic antibiotics are usually administered long term based on presumptive diagnosis (see common bacteria in previous card)
3. +/- surgery
   -bulla osteotomy, blind myringotomy
   -total ear canal ablation

Question 10

what are causes of central vestibular disease in horses? what about in cows? key differences from SA?

Answer 10

horses:
1. INFECTIOUS: EPM +/- viral myeloencephalitis viruses
-do guttural pouch endoscopy or skull rads to r/o THO first!
-then work up for EPM
-if very quickly progresses, suspect the viruses more (wear gloves)
2. vascular: air embolus
3. trauma: horses are stupid

cows:
1. INFECTIOUS: P. tenuis, listeria monocytogenes
-P. tenuis classically asymmetric ataxia, multifocal is common localization
–vestibular signs can occur, often with other signs too
2. trauma: sometimes

differences from SA:
1. NOT stroke, neoplasia, or autoimmune like SA
2. metronidazole toxicity uncommon unlikely SA
3. thiamine deficiency presents differently

Question 11

describe listeria monocytogenes

Answer 11

1. acute meningoencephalitis in ruminants and people!
2. gram + rod
   -intracellular pathogen of MONOCYTES and other cells
   -ubiquitous in soils, farms, and SOILED silage (pH >5.5)
   -history of silage feeding but NOT always (also table scraps in pets)
3. shed in feces and milk
   -can have asymptomatic shedders!
   -survives in refrigerator!

Question 12

describe the pathogenesis of listeria monocytogenes

Answer 12

1. exposure is common but disease is rare!
   -immunocompromised more likely
2. route of infection:
   -ingestion, breaches oral mucous membranes
   -migrates along nerves to brainstem
   -phagocytosed by monocyte/macrophage cells
   –low pH of phagolysosome activates listeriolysin O, allowing escape of organism into cytoplasm, organism can travel from cell to cell
   -microabscesses form in affected areas (brainstem usually)!!!!
   -+/- meningitis, myelitis

Question 13

describe clinical presentation of listeriosis

Answer 13

1. fever and depression common!!
2. classic signs: central vestibular
   -unilateral head tilt, circling, nystagmus
   -often with other cranial nerve deficits (facial nerve paralysis, dysphagia, etc.); helps you know is central when can’t hop a cow!
3. BUT can look like anything
   -depends on what CNs involved
   -if diffuse meningitis, may have multifocal or diffuse signs
   -myelitis, flaccid paralysis, recumbency

Question 14

describe diagnosis and treatment of listeria monocytogenes

Answer 14

diagnosis:
1. CSF: mononuclear pleiocytosis (too many cells)
-testing for the organism in CSF can be false negative (organism is deep in brainstem, not in CSF)

2. necropsy:
   -multifocal micro-abscesses +/- meningitis
   -PCR or immunohistochemistry for the organisms

treatment: weeks or longer!
1. penicillin, ampicillin
2. oxytetracycline
3. florfenicol
4. supportive care also key!

Question 15

describe air embolus

Answer 15

1. can happen in any species but horses are dumb and often have a central line in
   -usually just in a hospital setting
2. if air bubbles reach the CNS vasculature, neuro signs!:
   -seizure, collapse
   -vestibular signs can occur
3. either self limiting or permanent damage
4. diagnosis based on clinical presentation, very acute obvi
5. treatment: stay safe, supportive care post seizure

Question 16

describe causes of cerebellar disease in young large animals? adult large animals? all are pretty rare!!

Answer 16

young:
1. ANOMALOUS: hypoplasia (calves + BVD), malformation
2. DEGENERATIVE: abiotrophy (arabian horses), storage diseases (super rare)

adult:
1. INFECTIOUS: EPM, P. tenuis, abscess (super rare to localize cerebellar)
2. TOXIN: locoweed, grass staggers, metronidazole

Question 17

describe cerebellar hypoplasia in calves

Answer 17

1. exposed to bovine virus diarrhea (BVD) in utero
2. cow infected between 90-170 days of pregnancy
   -damages developing germinal cells and purkinjie cells
3. abortion/stillbirth, hydranencephaly, or cerebellar hypoplasia
4. signs present from birth

Question 18

describe cerebellar abiotrophy

Answer 18

1. arabian horses!
   -single gene mutation in almost 20% of arabians but autosomal recessive so onyl homozyogotes have clinical presentation
   -gene mutation causes decreased ability to repair oxidative damage to cerebellum
2. signs may be present at birth or develop later (weeks to months)
3. no treatment, but can survive if handled safely

Question 19

describe tremoregenic toxins in LA

Answer 19

1. locoweed
   -toxin is swainsonine: inhibits alpha-mannosidase and messes with neuronal metabolism (like an acquired storage disease)
   -HORSES, ruminants too
   -cerebellar signs + altered mentation (manic), dysphagia
   -no treatment, permanent deficits if they survive
2. grass staggers:
   -toxin: mycotoxin from fungal ergots growing on grass
   -all livestock affected
   -cerebellar signs + generalized muscle tremors
   -treatment: remove from grass, can recover

Question 20

describe prosencephalic diseases in LA

Answer 20

signs are same in all species!!

mentation changes:
-depression, agitation, odd behavior, encephalopathy
-consider temperament and socialization
-can be quite dramatic in LA

also seizures! focal or generalized; also pretty dramatic and dangerous
-nystagmus can be sign of a seizure!!

Question 21

describe infectious causes of prosencephalic diseases in LA

Answer 21

1. viral: EEE/WEE/VEE, rabies, others
2. parasitic: EPM, P. tenuis
3. fungal: rare
4. bacterial: listeriosis, brain abscess
   -abscesses: secondary to sepsis, trauma (bites), or DEHORNING

diagnosis: clinical signs, MRI

treatment: antimicrobial, +/- surgery

Question 22

describe intracarotid injections as a vascular cause of prosencephalic diseases in LA

Answer 22

intracarotid injections:

-common complication in equine, injecting a drug into the wrong blood vessel (shooting for jug and hit internal carotid instead, send drug to brain)

-any drug can cause, some can be fatal

-try to avoid by:
-injecting in the proximal 1/3 of the neck
-use a larger gauge needle and detach through the syringe (if hit carotid
-will see pulsating blood), and use catheters for large volume

Question 23

describe neonatal encephalopathy, a vascular cause of prosencephalic disease in LA

Answer 23

1. any species, but common in foals!
   -also called dummy foal, hypoxemic ischemic encephalopathy, neonatal maladjustment syndrome
2. unknown pathogenesis but we know/think that impaired cerebral oxygenation/energy delivery during gestation ad parturition causes neuronal damage
3. clinical presentation: variable
   -slow to stand/nurse
   -loss of suckle/interest in mare
   -altered mentation (depressed or crazy)
   -also recumbency or seizures
   -opisthotonous, altered respiration, coma

diagnosis:
-clinical signs and signalment
-neonatal herbivore + prosencephalic signs
-ensure glucose, lytes, and liver are all normal to r/o other causes

treatment:
-time, supportive care, anticonvulsants if needed
-sepsis is an important comorbidity! give antibiotics!
-pursue CSF tap and imaging if no response to treatment

prognosis: fair with enough time and money if seizures can be controlled

Question 24

generally describe metabolis causes of prosencephalic disease

Answer 24

not really species specific mostly! a COMMON problem in lawrge animals!

hepatic encephalopathy, hypoglycemia, hyper/hyponatremia

correct slowly!!

Question 25

what are 4 common causes of hyponatremia/hypernatremia in LA?

Answer 25

1. loss of pasture water source, followed by free choice H2O
   -salt intoxication
2. misfeeding salt/electrolyte
3. improperly mixed milk replacer
4. diarrhea

Question 26

describe polioencephalomalacia, a metabolic cause of prosencephalic disease in LA

Answer 26

1. softening of grey matter in brain
2. causes:
   -salt toxicity
   -lead poisoning: exposure to car batteries
   -sulfur toxicosis
   -thiamine (B1) deficiency in ruminants: vital for neuronal ATP production

Question 27

describe how thiamine deficiency can occur in ruminants and result in polioencephalomalacia

Answer 27

1. disruption of rumen flora
   -by inappetance, illness, diet change causes loss of rumen thiamine production
   -AND/OR overgrowth of thiaminase-producing bacteria
2. ingestion of thiaminase I:
   -bracken fern
   -nardoo fern (australia)
3. treatment with inactive thiamine analogs: amprolium (CORID)

Question 28

describe polioencaphalomalacia clinical signs

Answer 28

mild:
1. blindness (PLRs) present
2. dorsomedial strabismus (only vestibular sign)
3. altered mentation

moderate:
1. head press/circle
2. opisthotonos
3. seizures

severe (poor prognosis)
1. recumbency
2. coma
3. sudden death

rapid progression or slower onset; rapid onset has poorer prognosis

Question 29

describe diagnosis, management, and prevention of polioencephalomalacia

Answer 29

diagnosis:
1. history and clinical signs: ruminant with acute prosencephalic signs
2. necropsy :(

management:
1. thiamine 20mg/kg IV q 6hr
2. rumen support

prevention is key!! any inappetent ruminant should get thiamine!!!

Question 30

describe intestinal hyperammonemia, a metabolic cause of prosencephalic disease in LA

Answer 30

1. in HORSES
2. like hepatic encephalopathy, except
   -overproduction of NH3 from the GUT due to disruption of GI flora
3. may have sign of colitis but not always!
   -ACUTE presentation or prosencephalic signs
4. treat like hepatic encephalopthy
   -fluids, lactulose, antibiotics, prayers
   -better prognosis than hepatic encephalopathy!

Question 31

describe idiopathic epilepsy in LA

Answer 31

1. uncommon (horses) to rare (ruminants) in LA
   -EXCEPT juvenile idiopathic epilepsy in arabian foals (EGYPTIAN arabian foals only during the 1st year of life)
2. onset over days to 6 months, most by 2 months of age
   -just like SA: normal during interictal periods
   -still a diagnosis of exclusion!
3. seizures resolve by 1 year of age
   -but can have permanent injury from head trauma if fall and bump head
4. treat: anticonvulsants and safe environment

Question 32

describe cholesterinic granulomas, a neoplastic cause of prosencephalic lesions in horses

Answer 32

1. cholesterol-containing granulomatous masses derived from choroid plexus located in the lateral ventricles
2. unsure of cause but causes
   -chronic bleeding, cholesterol crystal formation, and inflammation
3. usually asymptomatic, incidental finding in 20% of older horses at necropsy!
   -just MAY cause seizures