The Neurological Horse with Normal mentation: Ataxias

Question 1

What are the different types of ataxia?

Answer 1

Spinal ataxia: Proprioceptive deficits
* Crossing, abduction, circumduction, knuckling (ascending pathways)
* Foot dragging, stumbling (descending pathways)

Vestibular ataxia: head tilt, leaning, falling to one side, wide base stance

Cerebellar ataxia: loss of modulatory effect of cerebellum
* Wide base stance
* Dysmetria:hyper/hypo
* No proprioceptive deficits
* No weakness

Question 2

What are causes of spinal ataxia?

Answer 2

• Cervical Vertebral Compressive Myelopathy (CVCM)
• Equine Herpes Virus (EHV-1)
• Vitamin E related ataxias
• Equine protozoal myeloencephalopathy (EPM)
• Cervical trauma: falls, kicks

Question 3

What can cause cervical vertebral compressive myelopathy? What clinical signs are associated? When is it most likely to be diagnosed? How is it diagnosed? How is it treated?

Answer 3

Multifactorial disease: Genetic predisposition + dietary imbalances + rapid growth rates
Incongruence between soft tissue and bones growth around spinal cord.

Clinical signs
Moderate to severe ataxia: inability to perform, unsafe to ride
* Ataxia, weakness and spasticity
* Generally symmetrical deficits, sometimes asymmetric (OA)
* Truncal sway, crossing and interferences when turning, hindlimb pivoting

Diagnosis
Typically diagnosed early in life (<4yo), but can manifest later in life
Radiographic sagittal ratios: intravertebral
- Normal: C2-C6 >52% / C6-C7>56%

Radiographic Myelography
- Dorsal contrast column (C2-C7=50%; C7-T1=60%)
- Total Dural diameter (20%)

CT-Myelography And MRI
- Transverse plane images
- Better definition of tissues
- Length of scan: anesthesia risk

Treatment
Medical
Young horses <12months
* NSAIDs ± Steroids (acute phase)
* Diet restrictions
* Limit overnutrition (protein and/or starch)
* Maintain correct Ca:P in feeds
* Avoid excess copper in diet

Adult horses
* NSAIDs ± Steroids
* Mesotherapy and exercises
* Intra-articular facet joint injection (OA)

Surgical (1-2 grades improvement)
- Ventral interbody vertebral fusion

Question 4

Why can we see neurological signs with equine herpes virus? How can they be prevented?

Answer 4

• Time of viraemia is long
• Allows the virus to get in contact with the endothelium
• Early treatment with NSAIDs will reduce the risk of developing neurological signs

Question 5

What clinical signs are associated with equine herpes virus? How is it diagnosed? How is it treated?

Answer 5

Clinical signs
* Previous respiratory disease: intermittent cough, serous nasal discharge, conjunctivitis
* 6-10 days prior to presentation
* Consider re-activation of carrier status
* Symmetric ataxia ± weakness
* Bladder distension/urinary incontinence
* Poor anal tone
* Recumbency
* Inconsistent fever
* Chorioretinitis (obvious 2-3 weeks after)
* Stabilization over 48h, improvement starts at 5 days
* Majority of horses fully recover

Diagnosis
* Signalment»>high risk
* Previous respiratory disease in the yard?….but re-activation is possible - may not still be present on nasopharyngeal swab if neurological signs appear much later
* 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 increase protein

Treatment
* Prevent spread among other horses at the premises»>Quarantine
* Isolate affected horses different barn, segregate according to risk, monitor temperatures»21 days movement restriction
* Biosecurity: foot baths, overalls, gloves, boots….
* Valacyclovir 30mg/kg q 8h for 48h, then 20mg/kg q12h
* Low-molecular heparin SC
* NSAIDs/Steroids?: treat respiratory disease early enough>less fever»less viraemia»lower likelihood of neurological disease
* Time to recover

Question 6

What are the different vitamin E related ataxias and weaknesses?

Answer 6

• Equine degenerative myeloencephalopathy/axonal dystrophy
• Equine Motoneuron disease

Question 7

What is equine degenerative myeloencephalopathy? What clinical signs are associated? How can it be prevented?

Answer 7

• diffuse degenerative disease of the equine spinal cords and caudal portion of the brainstem
• primarily affects young horses (<1yo), but can take longer to dx (<5yo)

Clinical signs:
* insidious onset of symmetric spasticity, ataxia, and paresis
* pelvic limbs are usually more severely affected than the thoracic limbs
* Some horses will have decease menace response , lethargy or behavioural changes
* Long-term poor performance in adult horses
* Clinical signs may progress slowly: onset around 1 year-old

Low Vit E <2ug/ml but non-responsive to treatment: Antemortem DX

Prevention
* Some breed lines might be predisposed (QH?), areas with Low VitE
* Supplementation last month pregnancy and nursing period

Question 8

What is equine motorneuron disease? What clinical signs are associated? How is it diagnosed? How is it treated?

Answer 8

• Acquired progressive neurodegenerative disease that affects neurons in brain and spinal cord (LMD)
• Triggered by Vit-E deficiency for periods longer than 18 months
• Risk factors: Excess copper and no access to green forage

Clinical signs
* Generalized weakness: slow gait, dragging to, base-narrow stance
* Shifting weight between limbs
* Muscle fasciculations of anti-gravitatory muscles (T>P)
* Generalized sweating
* Neurogenic muscle atrophy: Type I fibres
* Pigmentary retinopathy

Diagnostics
* Low Vit E in serum <2ug/,l
* Confirmatory: sacrocaudalis dorsalis medialis muscle (tail) biopsy
* Myelinated axons degeneration
* Post-mortem: Loss of motor neurons from ventral horn spinal cord

Treatment
Vitamin E (water dispersible better): 5000-7000 IU/day for 3 months
* 40% showed improvement in 6 weeks, normal in 3 months
* 40% stable clinical signs: chronic deficits
* 20% progression despite treatment

Question 9

What is equine protozoal myelocephalopathy? What clinical signs are associated? How is it diagnosed? How is it treated?

Answer 9

• 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
• Ingestion of contaminated feed: concentrate/hay/grass..
• Seropositive ≠ aetiology

Clinical signs
* Any possible neurological sign/insidious or acute
* Asymmetric ataxia with/without cranial nerve deficits (VIII, VII, X)
* Weakness and muscle atrophy (gluteus, biceps femoris, epaxial musculature)
* Poor anal tone, “cauda equina syndrome”

Diagnostics
* Challenging but intrathecal production of Antibody (S.neurona): SAG
* Serum: CSF ratio< 1
* Do not trust serum + results in areas of high prevalence
* Routine CSF analysis often unrewarding: high protein and high WBC rare
* Clinical signs + area with opossums
* Response to treatment?
* Post-mortem: Histopathology confirmation

Treatment
* Pyrimethamine and sulfadiazine (90 days treatment)
* Rapid absorption into CNS
* Diclazuril/ponazuril (60 day treatment)
* Takes 7 days to achieve adequate CNS concentrations
* NSAIDs/Steroids acute severe stages
* Long term Vitamin E supplementation?