The neurological horse with normal mentation - ataxias

Question 1

Types of ataxia

Answer 1

• spinal ataxia
• vestibular ataxia
• cerebellar ataxia

Question 2

CS of spinal ataxia

Answer 2

Proprioceptive deficits
- crossing, abduction, circumduction, knuckling (ascending pathways)
- foot dragging, stumbling (descending pathways)

Question 3

CS of vestibular ataxia

Answer 3

• head tilt
• leaning
• falling to 1 side
• wide base stance

Question 4

CS of cerebellar ataxia

Answer 4

Loss of modulatory effect of cerebellum
- wide base stance
- dysmetria: hyper/hypo
- no proprioceptive deficits
- no weakness

Question 5

Causes of spinal ataxias

Answer 5

• cervical vertebral compressive myelopathy (CVCM)
• equine herpesvirus (EHV-1)
• vitamin E related ataxias
• equine protozoal myeloencephalopathy (EPM)
• cervical trauma: kicks, falls

Question 6

Ataxia grading system: Mayhew scale

Answer 6

Grade 0
- no neurologic deficits

Grade 1
- neurological deficits just detected at normal gait, but worsened by backing, turning, loin pressure, or neck extension

Grade 2
- neurologic deficits easily detected at the walk and exaggerated by backing, turning, loin pressure or neck extension

Grade 3
- neurologic deficits prominent at the walk with a tendency to buckle or fall with backing, turning, loin pressure, or neck extension
- postural deficits noted at rest

Grade 4
- stumbling, tripping, and falling spontaneously at normal gait

Grade 5
- horse recumbent

Question 7

CVCM - what is it also known as?

Answer 7

• Wobbler’s syndrome

Question 8

CVCM - prevalence

Answer 8

• most common non-infectious neurologic disease in horses
• prevalence 1.3% TBs

Question 9

CVCM - CS

Answer 9

• moderate to severe ataxia
• inability to perform
• unsafe to ride
• ataxia, weakness and spasiticty
• generally symmetrical deficits, sometimes asymmetric (OA)
• truncal sway, crossing and interferences when turning, hindlimb pivoting

Question 10

CVCM - causes

Answer 10

Multifactorial dz
- genetic predisposition + dietary imbalances _ rapid growth rates

Question 11

CVCM - signalment

Answer 11

• typically diagnosed early in life (<4y/o), but can manifest later in life

Question 12

CVCM - diagnosis

Answer 12

Radiographic sagittal ratios: intervertebral
- normal: C2-C6 >52%, C6-C7 >56%

Radiographic myelography
- dorsal contrast column (C2-C7 = 50%, C7-T1 = 60%)
- total dural diameter (20%)

CT-myelography & MRI
- transverse plane images
- better definition of tissues
- length of scan: anaesthesia risk

Question 13

CVCM - tx

Answer 13

Medical - young horses (<12m)
- NSAIDs ± steroids (acute phase)
- diet restrictions
— limit over nutrition (protein ± starch)
— maintain correct Ca:P in feeds
— avoid excess copper in diet

Medical - adult horses
- NSAIDs ± steroids
- mesotherapy and exercised
- intra-articular facet joint injection (OA)

Surgical
- 1-2 ataxia grade improvement
- ventral interbody vertebral fusion

Question 14

Equine herpes virus 1 - aetiology

Answer 14

1. primary replication in the URT
2. replication in draining LN and cell-associated viraemia
3. establishment of latency int bigeminal ganglia and respiratory lymphoid tissues
4. secondary replication in target organs

10-12d after initial respiratory signs/fever
Might have a 2nd febrile episode

Question 15

EHV-1 - CS

Answer 15

Previous resp dz
- 6-10d prior to presentation
- intermittent cough, serous nasal discharge, conjunctivitis

Consider re-activation of carrier status

Symmetric ataxia ± weakness
- bladder distension/urinary incontinence
- poor anal tone
- recumbency

Inconsistent fever

Chorioretinitis (obvious 2-3w after)

Stabilisation over 48h, improvement starts at 5d

Majority of horses fully recover

Question 16

EHV-1 - diagnosis

Answer 16

Signalment -> high risk
- previous resp dz on yard?
- high number horse movement premises
- recent competition (within last week)

Nasopharyngeal swab PCR

Whole blood PCR

Serology
- complement fixation test if unvaccinated

CSF tap
- often unrewarding
- xanthochromia and increased protein

Question 17

EHV-1 - tx

Answer 17

Prevent spread among other horses at premises
- quarantine
- isolate affected horses to different barn, segregate according to risk, monitor temperatures
- 21d movement restriction
- biosecurity: foot baths, overalls, gloves, booths

Valacyclovir
- 30mg/kg q8h for 48h then 20mg/kg q12h

Low-molecular heparin SC

NSAIDs/steroids?
- treat respiratory dz early enough -> less fever -> less viraemia -> lower likelihood of neurological dz

Time to recover

Question 18

Equine degenerative myeloencephalopathy/axonal dystrophy - what is it?

Answer 18

• diffuse degenerative disease of the equine spinal cords and caudal portion of the brainstem

Question 19

Equine degenerative myeloencephalopathy/axonal dystrophy - cause

Answer 19

• vitamin e deficiency
• some breed lines may be predisposed (QH?)
• areas with low VitE

Question 20

Equine degenerative myeloencephalopathy/axonal dystrophy - signalment

Answer 20

• primarily affects young horses (<1y/o) but can take longer to dx (<5y/o)

Question 21

Equine degenerative myeloencephalopathy/axonal dystrophy - CS

Answer 21

• insidious onset of symmetric spasticity, ataxia and paresis
• pelvic limbs are usually more severely affected than the thoracic limbs
• some horses will have decreased menace response, lethargy or behavioural changes
• long-term poor performance in adult horses
• CS may progress slowly: onset ~1y/o

Question 22

Equine degenerative myeloencephalopathy/axonal dystrophy - diagnosis

Answer 22

• low vitamin E (<2ug/ml) but non-responsive to treatment

Question 23

Equine degenerative myeloencephalopathy/axonal dystrophy - prevention

Answer 23

Supplementation last month of pregnancy and during nursing period

Question 24

Equine motoneuron disease - what is it?

Answer 24

• acquired progressive neurodegenerative disease that affects neurone in brain and spinal cord (LMB)

Question 25

Equine motoneuron disease - trigger?

Answer 25

- VitE deficiency for periods longer than 18months

Question 26

Equine motoneuron disease - risk factors

Answer 26

- excess Cooper and no access to green forage

Question 27

Equine motoneuron disease - CS

Answer 27

- generalised weakness: slow gait, dragging to, base-narrow stance - shifting weight between limbs - muscles fasciculations of anti-gravitatory muscles (T>P) - generalised sweating - neurogenic muscle atrophy: type I fibres - pigmentary retinopathy - weakness NOT ataxia

Question 28

Equine motoneuron disease - diagnostics

Answer 28

Low VitE in serum (<2ug/l) Confirmatory - sacrocaudalis dorsalis medialis muscle (tail) biopsy --- myelinated axons degeneration PM - loss of motor neurone from ventral horn spinal cord

Question 29

Equine motoneuron disease - tx

Answer 29

VitE (water dispersible better) (Nano E): 5000-7000 IU/day for 3 months - 40% show improvement in 6w, normal in 3m - 40% stable CS: chronic deficits - 20% progression despite tx

Question 30

Equine protozoal myeloencephalitis (EPM) - cause

Answer 30

Sarcocystis neurona and Neospora hughesi - horse only aberrant host - migration of schizonts and merozoites to CNS --- N. hughensi transplacental too? - USA and South America most common --- S. neurona prevalence 10-90% --- N. hughensi prevalence 10% - ingestion of contained feed: concentrate/hay/grass - seropositive ≠ aetiology

Question 31

Equine protozoal myeloencephalitis (EPM) - CS

Answer 31

- any possible neurological sign/insidious or acute - asymmetric ataxia ± CN deficits (VIII, VII, X) - weakness and muscle atrophy (gluteus, biceps femoris, epaxial musculature) - poor anal tone, 'cauda equina syndrome'

Question 32

Equine protozoal myeloencephalitis (EPM) - diagnosis

Answer 32

Challenging but intrathecal production of antibody (S.neurona): SAG - serum:CSF ratio <1 - don't trust serum + results in areas of high prealence - routine CSF analysis often unrewarding: high protein and high WBC rare CS + areas with opossums Response to tx? PM - histopath confirmation

Question 33

Equine protozoal myeloencephalitis (EPM) - tx

Answer 33

Pyrimethamine and sulfadiazine (90d tx) - rapid absorption into CNS Diclazuril/ponazuril (60d tx) - takes 7d to achieve adequate CNS concentrations NSAIDs/steroids - acute severe stages Long term VitE supplementation? Relapses in 10% cases