Flashcards in Equine Wobbler Syndrome (Piercey) Deck (26):
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?
- useful for C6-7 lesions
- NB: ventral dye column often lost (not pathological cf. smallies)
- 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
- 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?
- 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)
> musce atrophy
> CN signs
- depending on site of lesion
> ocasionaly mild mononuclear monocytosis but often normal
> western immunoblot for s. neurona Ab
- iatrogenic haemorrhage contaminated tap -> false +
- Uni Kentucky
- CSFmore specific than serum
> folate synthesis inhibitors
>steroids? if acute onset
- 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
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 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
- 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?
- 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)