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Neuro > Equine Wobbler Syndrome (Piercey) > Flashcards

Equine Wobbler Syndrome (Piercey) Flashcards

1
Q

What is equine wobbler syndrome?

A

Mixed clinical signs d/t Spinal ataxia and paresis

- most common neuro disease of horses

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2
Q

Ddx for spinal ataxia

A
  • CVM/CVS/CVSM: cervical vertebral malformation/stenosis
  • neck trauma
  • EHV1: myeloencephalitis
  • EDM: equine degenerative myeloencephalopathy
    ~ EPM: equine protozoal myeloencehalopathy (seen foreign imports from america)
    ~ migrating parasites
    ~ ryegrass staggers
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3
Q

Pathogenesis of CVM/s

A

neuro signs d/t compression of SC
> dynamic type 1
- neck flexed/hyperextended
- vertebrae move excessively causing cord compression
- commonly C3-C5 flexion, or C5-C7 extension
- most prevalent in young animals
> static/absolute type 2
- mishapen articular process joint surface (osseus changes)
- facets (process joints) v close to SC cf. smallies so especially axial joint affected can -> compression
- compression ventral and dorsal SC
- often older horses @ C5-C7
- congenital malformations eg. occipito atlanto-axial malformation/subluxation of Arabs or OA articular process joint facets

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4
Q

What does CVM/S cause?

A 
Combined ataxia (sensory) and paresis (motor) d/t compression dorsally and ventrally
- progressive signs
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5
Q

What is Wallerian degeneration?

A
  • ascending tracts cranial to the lesion and desceding tracts caudal to the lesion degenerate (???different to what pathologists said - maybe neuron swelling cell body side of lesion and degeneration distal to cell body)
  • both white mattter and grey matter changes at site of lesion
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6
Q

What diagnostic techniques may potentially be useful in identifying SC compresssion with CVM/S?

A 
> Myelography 
- useful for C6-7 lesions 
- NB: ventral dye column often lost (not pathological cf. smallies) 
> CT? 
- doesnt go very far down neck (C4) 
- bigger machines for fat people :D 
> CSF tap lumbosacral standing (or atlantoaxial under GA) 
- r/o other dz
- should be normal with wobblers
> scintigraphy
- not v. useful 
- may show spondylosis of spine
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7
Q

Tx and prognosis of ECVM/S?

A
  • pace diet ^fat/v carbs, limit protein (slow growth) start early
  • articular process joint medication under u/s (crorticosteroids)
  • ventral stabilisation prevent articulation (good for dynamic form, also works for static but takes some time for remodelling)
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8
Q

Case: ataxia in all 4 limbs
- paresis in both pelvic limbs
- muscle atrophy gluteals esp. L
> can this be defined by a single lesion?

A

NO
- gluteal mm atrophy (neurogenic) implies damage to peropheral nerves/cell bodies in ventral horn of SC L3-S3
- ataxia in thoracic limbs suggest SC white matter lesion C1-T2
> dz must be multifocal

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9
Q

Where is EPM seen? What is the pathological agent?

A
  • common USA and south america
  • seen elsewhere in imported horses from endemic areas
  • no seasonal influence
  • 50% normal horses US seropositive to
    > sarcocystis neurona
    (exposied but no dz)
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10
Q

Pathogenesis of EPM?

A
  • s. neurona cycles normally between birds and opossums (and domestic cats)
  • feacal contamination of pasture/feed -> horses
  • not transmitted horse-horse
  • diffuse multifocal, asymmetric, non-supparative inflammaotry lesions in brain and spinal cord
  • Grey and white matter affected
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11
Q

Clinical signs of EPM?

A
  • insiduous OR sudden onset
  • highly variable - can mimic all other neuro diseases
  • asymmetric sensory or motor (UMN/LMN)
    > ataxia
    > paresis
    > musce atrophy
    > CN signs
  • depending on site of lesion
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12
Q

Dx EPM?

A

> ocasionaly mild mononuclear monocytosis but often normal
western immunoblot for s. neurona Ab
- iatrogenic haemorrhage contaminated tap -> false +
- Uni Kentucky
- CSFmore specific than serum

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13
Q

Tx EPM

A 
> folate synthesis inhibitors
- sulphadiazine
- pyrimethamine 
> coccidiostats 
- ponazuril(marquis) 
>NSAIDs
>steroids? if acute onset
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14
Q

Prognosis EPM?

A
  • guarded to poor esp if severely affected
  • muscle atrophy usually permenant
  • ataxia can improve
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15
Q

Case: 2yo colt stabled for early life d/t lack of pastrure, hx of abnormal gait developed over 2-3months, initially progressive, now static. Looks drunk. Neuro: ataxic all 4 limbs, worse hind. Panniculus decreased bilat. Well muscled. Dx?

A

> EDM (equine degenerative myelopathy)

  • variety of breeds, ID as a neuroaxonal dystophy in Morgans
  • clusters on some farms
  • 6mo-2years
  • rare
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16
Q

Clinical signs of EDM?

A
  • symetrical ataxia and paresis (most SC is symmetrical)
  • hind limbs > forelimbs affects (because pelvic limb tracts more superficial in SC so affected first)
  • hyporeflexia over trunk
  • sometimes panniculus reflex reduced or absent (identify segmental SC lesion)
17
Q

Pathogenesis of EDM?

A
  • neuronal fibre degeneration and demyelination in white matter of ascending and descending tracts of SC
  • mid-thoracic region worst affected
  • degenerative lesions spinal and brain stem nuclei
  • Vit E deficieny?? -> free radical induced neuronal damage?
  • familial predisposition: genetic likely
18
Q

Dx EDM?

A

DX OF EXCLUSION
- r/o other dz (esp CVM/S - much more common!!)
- measure vit E plasma conc (not dx though)
- usually made PM
> NO segmental wallerian degneration along spine (unlike classical Wobblers)
- ascending and descending both affected along length of spine

19
Q

Prognosis EDM?

A
  • poor
  • signs may stabilise with high dose Vit E Tx (6000IU/day alpha tocopherol: buy from human health store)
  • unlikely to be athletic
20
Q

Where do sensory and LMN axons enter the spinal cord?

A
  • sensory dorsolateral horns

- LMN cell bodies in ventral grey matter (-> peripheral motor n.)

21
Q

How may torticolis affect diagnostics of spnal dz?

A

may need oblique angled rads to get clear view of SC

22
Q

What may be seen with OCD?

A

Osteochondral fragments

  • NB: may be incidental
  • seen with type 2 dz
23
Q

Outline methodology of myelograms in horses

A
  • remove some CSF
  • inject iodohexine dye
    > NB low sense and low specificity except for C6-7 lesions
24
Q

Are myelograms necessary for dx?

A

Not really - majority of dx can be made on clinical signs, neuro exam and standing lateral radiographs

25
Q

Which direction do head tilts generally go?

A

Towards lesion (unless paradoxical central vestibular syndrome)

26
Q

how can spinal dz of horses be remembered?

A

All the abbreviations!

Neuro (30 decks)

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