LAM- Equine Neurology

Is cortical blindness a clinical sign of fore brain disease?

Yes

Classic signs of brainstem disease

Alterations in consciousness/arousal

Cranial nerve deficits

Vestibular signs

Gait&Posture deficits

What coordinates motor activity

Cerebellum

What is the real teller of cerebellar disease?

Intention head tremor

If body movements are on the left side during a seizure, what side is the lesion?

Right side of cerebral cortex

If cortical blindness in right eye, what side is lesion ?

Left side

Place catheter in horse after seizure when recumbant, why?

Because likely to seize again

Drugs for seizure management?

Benzos

Barbs (phenobarb)

What drug is for short term control to avert or mitigate a seizure?

Benzo

Bolus injection

What would you use to suppress seizures in encephalopathic neonatal foals

midazolam CRI

What is used for longer term control?

Phenobarb

Oral daily dose for recurring seizures

Levetiracetum for long term control?

What are some conditions in neonatal foals causing seizures?

Neonatal encephalopathy

due to perinatal oxygen deprivation

Metabolite/electrolyte disturbances

Bacterial meningitis (rare)

Congenital development defects

Seizures can be heritable in foals in what breed?

Arabian

Arabian foals with seizures typical have them at what age?

before 6 months

avg 2 months

What is treatment for lavender foal syndrome?

Nothing- euthanize

What is a developmental disease of egyptian arabian foals?

Cerebellar abiotrophy

Will not grow out of

Cerebellar abiotrophy foals will develop what and by what age?

generalized cerebellar disease

6 months

What is treatment for cerebellar abiotrophy?

No treatment

With cranial trauma, what is the essential lesion?

Brain edema

Common injuries from horses flipping over backwards?

Petrous temporal and occipital injuries

What are some controversial managments of counteracting brain edema?

Dexmethasone/corticosteroids

IV Dimethyl sulfoxide

Can you use mannitol with intracranial hemorr?

No - but it can be used otherwise to counteract brain edema

What two plants may cause nigropallidal encephalomalacia?

Yellow star thistle

Russian knapweed

Clinical signs of nigropallidal encephalomalacia?

Causes dystonia, can't swallow and no prehension, sardonic grin

Is there treatment for nigropallidal encephalomalacia?

No

Ddx clinically but could be MRI

Locoism is an acquired ___________________________ storage disease caused by consuming _____________ of the genera ________________&________________

polysaccharide

plants

Oxytropis

Astragalus

Signs of locoism?

Generalized ataxia, behavioural changes, intention tremor- similar signs to cerebellar disease

With locoism what may you see in the blood lymphocytes?

Intraplasmic vacuoles

Do horses with locoism recover?

No- permanent neurological deficits

What is the fungal species associated with moldy corn poisoning?

Fusarium verticilloides

What is scientific name of moldy corn disease

Leukoencephalomalacia

Whats the principle toxic agent for mcp?

fumonisin B

What does moldy corn disease cause?

Asymetric liquefactive necrosis of the cerebral hemispheres, cerebellum, brainstem and spinal cord

Clinical signs of Moldy corn poisoning?

Rapidly progressive encephalopathy

incoordination, aimless walk, blindness, head pressing

How do you diagnose moldy corn poisoning?

Clinical signs and the feed

No cure- very fatal

Who are brain abcesses most common in and why?

Young horses from whacking their heads

What is a RARE complication of neonatal sepsis?

meningitis

How do diagnose brain infection?

CSF with increasaes neutrophils and protein

MRI can localize abscess

Diagnosis of brain infection?

Inflammatory leukogram with increased fibrinogen

Management for infection in brain?

Abx- penicillin or sulfas

Anti-inflammatories, NSAIDs, DMSO maybe steroids

Phenobarb for sedations or potential seizures

Whats prognosis for brain infection?

GUARDED to poort

What is most common in north america? EEE or WEE?

EEE

Vector for EEE?

Mosquito- so seasonal, year round in warm parts of america

How do you prevent EEE and WEE

Vaccine

Clinical signs of EEE

1-3 weeks incubation

High fever with rapid progressive encephalopathy

How diagnosis confirmed?

IgM capture on Elisa

Prognosis of EEE and WEE?

guarded to poor

Vaccine schedule for EEE and WEE

2 doses 4-6 weeks apart then revaccinate annually

In endemic areas in SE , foal may be started on _____ dose seroes at 3-4 months of age

4

Adults may be immunized semi annually as well

West nile is also a mosquito borne encephalomyelitis virus that affects what part of the brain?

Gray matter primariily in brainstem and spinal cord

Clinical signs of WNV

Generalized weakness, gait deficits, stumbling falling

Muscle fasciculations, blinking and twitching of muzzle

With rabies, encephalopathic signs may take sime time to appear, when they do show, they progress ____________

rapidly

Encephalopathy with rabies is often characterized as?

hyperesthesia, self mutilation, recumbence and death

How do horses sometimes feel about water with rabies?

Hydrophobia

Horses exposed to rabies be re-vaccinated and undergo observation for how many days?

60 days

How long is quarantine for non vaccinated horses?

6 months

Immunization is best prevention!

What type of vaccine is rabies vax?

Killed

How many doses do adults need?

1 single dose followed by yearly booster

When do foals get vaxxed for rabies?

Foals of vaccinated mares get two doses at 6&7 months

When do foals of unvaccinated mares get vaxxed?

3-4 months or as per label

What is the definitive host for equine protozoal myeloencephalitis

opossum

skunk, raccoon, cat, and 9 banded armadillo are intermediate hosts

What is the dead end host for equine protozoal myeloencephalitis?

Horses

It is most common infectious equine CNS disease in the united states

What protozoan parasite cause equine protozoal myeloencephalitis?

Sarcocystis neurona

Where will equine protozoal myeloencephalitis localize most commonly?

Brain stem and spinal cord

Can be anywhere tho

With EPM are lesions local or multifocal?

Can be both!

It can also affect gray and white matter

______________________ signs are typcial and LMN signs are common

asymmetrical

What are the characteristic signs for EPM?

Asymmetrical ataxia and muscle atrophy

Three A's

What do lesions of the cervical intumescense cause with EPM?

asymmetrical flaccid paresis and focal atrophy of fore limb muscles and long tract signs in rear limbs

What do lesions of the lumbar intumescence with EPM cause?

asymmetrical flaccid paresis and focal muscle atrophy of gluteal and thigh muscles

Do you see facial paralysis with EPM?

Yes you can

How do you diagnose EPM?

Rule out other options with CT or MRI

Immunodiagnostic testing

EPM diagnosis is made complicated by what?

High seropositivity

Low prevalence

Major differentials are common

Common differentials for EPM?

CSM

EDM

WNV

EHV1

What is immunodiagnostic testing good for?

S neurona antibodies in serum and CSF

What serum to CSF ratio is stronly supportive of EPM?

Serum to CSF ratio < 100

less than 100 tells us theres a high antibody titre in the csf which is strongly supportive of EPM

What are the treatments for EPM?

Ponazuril (marquis)

Diclazuril

Potentiated sulfas - sulfadiazine/pyrimethamine

With mild cases- what percent have full recovery of EPM?

50% have full recovery

With severe cases of EPM, what % have full recovery?

10-20%

What can Parelaphostrongylus cause?

Verminous myeloencephalitis

What is treatment for Verminous myeloencephalitis?

anthelmintics and supportive care, but prognosis is GUARDED

Vestibular disease

• functions to

  • maintain posture, muscle tone and equilibrium

  • orientation of head with respect to eyes, trunk, limbs

    • special proprioception

• clinical signs

  • head tilt

  • drifting or listing to one side

  • resting nystagmus

• can be

  • central, involving the medulla, pons and or cerebellum

  • peripheral involving the vestibular branch of CN8; peripheral vestibular disease is common in horses

Peripheral vestibular disease

• components of the vestibular branch of CN8 are ‘

  • the receptor organ in the middle ear (hair cells in endolymph)

  • the vestibular ganglion

  • the afferent axons projecting into the brainstem

• these structures are located within and near the petrous temporal bone

• the signs of disequilibrium are ipsilateral to the lesion

  • head tilt, leaning, drifting, falling, rolling

• resting horizontal nystagmus, fast phase is away form the side of the lesion; sometimes rotary

Peripheral vestibular disease and facial nerve paralysis

• common disease in horses

• occurs with traumatic, infectious, inflammatory, or degenerative conditions of petrous temporal bone and or nearby structures (tympanic bullae / inner ear)

  • examples are petrosal impact/fractures, temporohyoid osteo-arthorpathy (THO), maybe otitis media-interna

• there is a close anatomic relationship of CNs 7 and 8 such that dz in this area may result in vestibular signs, facial nerve paralysis or both

  • trauma and THO are common cause of each / both

  • polyneuritis equi and LSA are add causes of FNP

Temporohyoid oestoarthropathy

• bony proliferation, enlargement and sclerosis of the temporohyoid articulation and adjacent bone

  • periosteal reaction involving stylohyoid bone, petrous temporal bone and tympanic bulla

  • end result is fusion of the temporohyoid articulation, stenosis of external ear canal, obliteration of tympanic bulla

• cause is incompletely understood; possibilities include:

  • chronic changes initiated by otitis media, maybe GP disease

  • cribbing

  • or maybe a primary degenerative process

• progressive bony changes and ultimate fusion of the joint results in

  • signs of discomfort such as difficulty with mastication, rubbing the head on the affected side, head-shaking

  • **spontaenous fracture of the petrous temporal bone

    • due to tension on the fused articulation from muscle contractions of the tongue, pharynx and neck

• fx results in acute vestibular ataxia and or facial paralysis

• signs and lesions are most often unilateral ,although up to 20% have bilateral bony changes

management of THO

• Acute vestibular signs ± facial paralysis is treated with anti-inflammatory drugs and antibiotics

  • antibiotics are indicated due to potential for bacterial translocation into the brain case; also if active otitis or osteomyelitis is suspected

  • with facial paralysis* the eye on the affected side should be protected with topical antibiotic ointments or tarsoraphy

• surgical intervention can prevent the fracture*

  • disarticulation of the hyoid apparatus on the affected side via ceratohyoidectomy

otitis media-interna

• presumably it can cause acute vestibular signs ± facial palsy in horses

• diagnosis can be challenging

  • definitive dx with tympanocentesis, cytology and culture

  • imaging: rads / CT / MRI

• antibiotic treatment should resolve mild/early cases

• extension of infection beyond the inner ear can lead to osteoyelitis of the calivarium

  • extension of infection centrally which leads to subdural abscess and or meningitis and severe CNS signs

  • also secondary pathologic fx can result in hematoma/hemorrhage into the brain case and acute vestibular signs

  • both have guarded prognosis

• for less severe cases, aggressive antibiotic and anti-inflammatory tx are indicated and may resolve the signs

CN IX and X: pharyngeal and laryngeal paresis / paralysis

• signs/complications include dysphagia, choke, upper respiratory obstruciton, aspiration, DDSP; feed in nostrils is a clinical sign of dysphagia

• causes

  • guttural pouch disease mycosis

  • GP and laryngela surgies

  • idiopathic left laryngeal hemiplegia

  • laryngeal hemiplegia also occurs with injuries to recurrnet laryngeal nerve; can occur on either side

  • bilateral laryngela paresisi paralysis occurs with

    • lead poisoning; causes generalized polyneuritis in horses; laryngeal / pharyngeal signs clinically prominent; abnormal phonition often sites as early / characteristic sign

    • botulism: early signs are weak tongue and masticatory efforts difficuly swallowing (dysphagia) may present as choke

    • bilateral laryngela pralysis with pyrodizadine tox/hep encephaloaphty

Horner syndrome in horses

• signs are ptosis, enophthalmus, 3rd eyelid prolapse, miosis

• facial sweating in horses

  • focal sweating occurs with any local sympathic injury in horses

  • the pattern of sweating is helpful in localizations

• some causes of horner syndrome in horses include

  • cranial trauma

  • GP disease

  • cervical injuries ex injection site injury***

  • spinal cord disease or injury at T2

  • brachial plexus / nerve root disease or injury (avulsion)

  • thoracic trauma or mass

Neuropathic head shaking

• hyperesthesia caused by neuropathy of ophthalmic branch of CN V (sensory trigeminal neuropathy)

• head shaking is induced by exposure to light and other environmental stimuli

• may also show sneezing, snorting, nose rubbing

• many have seasonal pattern

• dx supported when headshaking is improved with dark environment, blindfold and or UV mask

• other causes of headshaking are ruled out

• management

  • mechanical distractors example nose nets

  • drug treatments include cyrproheptadine and carbamazepin

• many cases are progressive and debilitating resulting in loss of use and or humane euthanasia

cauda equine neuritis / polyneuritis equi

• chronic, progressive granuloamtous inflammation causing fibrosis and adhesions of peripheral nerve roots

• classically affects the nerves of the cauda equina resulting in cauda equina syndrome

• less commonly, cranial nerves and other spinal nerve are affected

• the cause is unknown believed to be an immune-mediated process

Polyneuritis equi

• initial signs inlcude hyperesthesia around the rump and tail-head manifested as tail rubbing; m/b mild dysuria

• over weeks to months there is progressive development of a cauda equine sydnrome

  • flaccid bladder with overflow incontinence and urine scalding, fecal rentention, atrophy and paralysis of tail head muscles, perineal anesthesia, penile prolpase and anesthesia, hyperesthesia peripheral to perinuem

  • some show atrophy of hind quarters and mild hind limb ataxia

  • cranial n deficits when present are typically unilateral

• there is no specific treatment

  • corticosteroids and other immunosuppressive drugs may have a temporary benefit

  • can be temporarily managed with urinary bladder catherization and manual rectal emptying as needed and nursing care

  • humane euthanasia is the usual course