Equine Wobbler Syndrome (Piercey) Flashcards
What is equine wobbler syndrome?
Mixed clinical signs d/t Spinal ataxia and paresis
- most common neuro disease of horses
Ddx for spinal ataxia
- 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
Pathogenesis of CVM/s
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
What does CVM/S cause?
Combined ataxia (sensory) and paresis (motor) d/t compression dorsally and ventrally - progressive signs
What is Wallerian degeneration?
- 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
What diagnostic techniques may potentially be useful in identifying SC compresssion with CVM/S?
> 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
Tx and prognosis of ECVM/S?
- 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)
Case: ataxia in all 4 limbs
- paresis in both pelvic limbs
- muscle atrophy gluteals esp. L
> can this be defined by a single lesion?
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
Where is EPM seen? What is the pathological agent?
- 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)
Pathogenesis of EPM?
- 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
Clinical signs of EPM?
- 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
Dx EPM?
> ocasionaly mild mononuclear monocytosis but often normal
western immunoblot for s. neurona Ab
- iatrogenic haemorrhage contaminated tap -> false +
- Uni Kentucky
- CSFmore specific than serum
Tx EPM
> folate synthesis inhibitors - sulphadiazine - pyrimethamine > coccidiostats - ponazuril(marquis) >NSAIDs >steroids? if acute onset
Prognosis EPM?
- guarded to poor esp if severely affected
- muscle atrophy usually permenant
- ataxia can improve
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?
> EDM (equine degenerative myelopathy)
- variety of breeds, ID as a neuroaxonal dystophy in Morgans
- clusters on some farms
- 6mo-2years
- rare
Clinical signs of EDM?
- 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)
Pathogenesis of EDM?
- 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
Dx EDM?
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
Prognosis EDM?
- poor
- signs may stabilise with high dose Vit E Tx (6000IU/day alpha tocopherol: buy from human health store)
- unlikely to be athletic
Where do sensory and LMN axons enter the spinal cord?
- sensory dorsolateral horns
- LMN cell bodies in ventral grey matter (-> peripheral motor n.)
How may torticolis affect diagnostics of spnal dz?
may need oblique angled rads to get clear view of SC
What may be seen with OCD?
Osteochondral fragments
- NB: may be incidental
- seen with type 2 dz
Outline methodology of myelograms in horses
- remove some CSF
- inject iodohexine dye
> NB low sense and low specificity except for C6-7 lesions
Are myelograms necessary for dx?
Not really - majority of dx can be made on clinical signs, neuro exam and standing lateral radiographs
Which direction do head tilts generally go?
Towards lesion (unless paradoxical central vestibular syndrome)
how can spinal dz of horses be remembered?
All the abbreviations!
