Spinal disease - Problem solving - vidoes Flashcards

1
Q

Define FCE

A

Fibrocartilagenous embolism

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2
Q

Define ANNPE

A

Acute non-compressive NP extrusion

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3
Q

What is ANNPE?

A

o = hyperacute extrusion of hydrated and non-degenerated NP through small fissure in annulus fibrosus, spinal cord contusion but no compression. Don’t confuse with IVDD

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4
Q

Other names - ANNPE

A

: high velocity, low-volume disk extrusion, traumatic intervertebral disc extrusion.

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5
Q

What is the typical signalment and history for both FCE and ANNPE?

A

o Adult large breed dogs
o Hyperacute onset of CS (seconds)
o Occurs during strenuous activity or external trauma for ANNPE
o Typically non-painful (FCE

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6
Q

Ddx - 7 yo ME Doberman Pinscher, chronic, painful, progressive, non-lateralising C6-T2 myelopathy

A

o CIVDD (type 1 or 2)
o Cervical spondylomyelopathy
o Neoplasia
o Cervical spondylomyelopathy (many terms in literature, this is correct term)

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7
Q

What is cervical spondylomyelopathy?

A
  • Complex neurological syndrome

* Covering term: describe cervical vertebral canal stenosis d/t soft tissue and bony structure

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8
Q

Animals affected by cervical spondylomyelopathy

A

• Large and giant breeds

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9
Q

CS - cervical spondylomyelopathy

A
  • Variety of CS, lesions, synonyms
  • These are perhaps distinct clinical syndromes (?)
  • Cervical hyperaesthesia, ataxia, paresis
  • Wide-based ataxia and paresis of HL in combination with short-stilted gait of TL  ‘disconnected’ or ‘two-engine gait’
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10
Q

What are the 2 forms of cervical spondylomyelopathy?

A

Disc-associated cervical spondylomyelopathy and osseous-associated cervical spondylomyelopathy

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11
Q

Typical dog affected by Disc-associated cervical spondylomyelopathy

A

o Older large breed dogs (>6yo)

o Doberman Pinscher

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12
Q

What happens in disc-associated cervical spondylomyelopathy?

A

o Intervertebral disc protrusion(s) – one or more caudal cervical, C6-C7 and C5-7 most commonly affected
o Vertebral abnormalities: abnormal shape and position of vertebral bodies
o Ligamentum flavum hypertrophy ( mid-dorsal extradural compression)
o C5-C6 and C6-C7
o Multiple compression sites in 25-50% cases
o Multifactorial syndrome

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13
Q

What are the side effects of myelography? Incidence?

A

 Post-myelographic seizures (27%)

 Neurological deterioration (14%)

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14
Q

Tx - disc-associated cervical spondylomyelopathy

A

 Controversial, surgical and medical options
 Surgical
• > 20 techniques reported
• Most authors claim 75% success rate
• Up to 25% will demonstrate a recurrence of CS after initial improvement (adjacent segment disease or ‘domino lesion’)
 Medical
• 40% asuccess
• Failure characterised by rapid deterioration

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15
Q

What dogs does osseous-associated cervical sponylomyelopathy affect?

A

o Young-adult giant breeds (18-24 months)

o Great Dane, Dogues de Bordeaux

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16
Q

What happens in osseous-associated cervical spondylomyelopathy?

A

o Articular process abnormalities (hypertrophy/ degeneration. Causes dorsolateral or lateral SC compression)
o Ligamentum flaum and dorsal lamina hypertrophy ( dorsal compression)
o Ventral abnormalities too
o Also more cranial sites
o Multiple sites in 85%

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17
Q

What is the imaging modality of choice for cervical spondylomyelopathy?

A

• MRI is the imaging modality of choice, preferred over myelogram (25% (Dobermans?) have seizure when recover from anaesthesia)

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18
Q

If only HL is affected, where is the spinal lesions?

A

T3-L3 or L4-S3 (then look for spinal reflexes and mm tone to differentiate)

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19
Q

Ddx - pug puppy with progressive neurological deficits - 3

A
  1. Arachnoid diverticulum
  2. Vertebral malformation – hemivertebra, kyphosis
  3. Infectious inflammatory – CDV, toxoplasmosis, neosporosis
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20
Q

What is spinal arachnoid diverticulum?

A

= focal fluid filled dilations of the subarachnoid space  progressive SC compression

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21
Q

Aetiology - arachnoid diverticulum

A
  • multifactorial (congenital or acquired)

- pug and french bulldogs

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22
Q

Sx - arachnoid diverticulum

A

Sx- challenging, incise into cyst to collapse it

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23
Q

Dx - arachnoid diverticulum.

A
  • myelography,
  • CT-myelography
  • MRI.
  • Look for typical teardrop-shaped dilatation subarachnoid space
24
Q

What is the commonest vertebral malformation?

A

hemivertebra

25
Breed predisposition - hemivertebra
bulldogs, pugs. Up to 78% clinically normal French Bulldogs have radiographic evidence of hemivertebra
26
Describe hemivertevra
Incomplete formation of vertebral body  wedge shaped vertebral body - Mid thoracic region (T5 and T8) - Vertebral canal stenosis, instability with subluxation and abnormal angulation of the vertebral column - Often mild CS, which can stabilise
27
What can hemivertebra be associated with?
other spinal disorders – IVDD, spinal arachnoid diverticula, syringomyelia, myelitis Hemivertbera often an incidental finding
28
What is the occurence of CS with hemivertebra associated with?
degree of kyphosis
29
Tx - hemivertebra
Sx – spinal sx to correct kyphosis (plates and screws)
30
Ddx - horse with spinal ataxia
* CVM/S = Cervical vertebral malformation/ stenosis = commonest * EHV-1 myeloencephalitis (CS this afternoon) * EDM = equine degenerative myeloencephalitis * Trauma * Migrating parasites (rare UK) * EPM = equine protozoal myeloencephalitis (USA) * (Foreign imports) * Ryegrass staggers (occasionally UK, warmer and damper climates – NZ, fungus which infects ryegrass)
31
CVM/S pathogenesis
* Neuro signs results from progressive SC compression * 2 main types: 1 (dynamic) and 2(absolute – i.e. occurring all time) * Damage ascending proprioceptive and descending motor fibres * When neck flexed or hyperextended, vertebrae move excessively  cord compression. Usually C3-5, usually young animals. Often worse with flexion (C3-C5) and extension (C5-C7)
32
When do you use a myelogram for CVM/S?
uncommon, usually when sx being considered, dye injected dorsally and ventrally (provided dorsal dicolumn is not narrowed, compression of SC unlikely)
33
What is absolute stenosis (type 2)
* = osseous change in vertebrae  SC compression * Usually older horses, C5-7 * Osteoarthritic changes in articular process joints (Facets) as result of congenital OCD - perhaps? * Other malformed vertebrae
34
What spinal congenital malformations can horses get?
* Seen occasionally * Abnormal atlas –fused to back of occiput * Axis – weird shape and fused too * = occipito atlanto-axial malfomation (foals, possibly genetic in Arabians)
35
What is torticolis and how do you diagnose it?
= twisted neck | Dx - lateral radiograph
36
What is articular process joint osteochondrosis?
• Some changes in neck occur due to this • Any articular cartilage joint susceptible • Usually this  OA  type 2 CVM/S OA in neck usually  CS of ataxia Intervertebral foramina = exit for spinal nn
37
What is Wallerian degeneration and what is it associated with?
= distal end of axons, below site of compression, start to die (ventral funiculus lesions predominate). D/t distal ends of axons are separated from cell body. - CVM/S
38
Dx - CVM/S
- Myelography – look for changes in dicolumns in ventral and dorsal part of spinal column, referral only, low sensitivity and low specific --> suspect wobbler syndrome, most cases don’t need this (dx – based on PE, neuro exam and lateral neck radiographs). High specificity with lesions at C6-7. - CT – only reaches to C4 (often compression in cd neck, so not worth risk of GA) - CSF analysis – lumbosacral area, to r/o other dz, usually a referral, iatrogenic haemorrhage a common complication--> confuses interpretation. Normal in CVM/S. - Scintigraphy – not useful for most CVM/S cases but for evaluating spine curvature.
39
Tx and prognosis of CVM/S
* PACE DIET – young, fast growing horses (TBs), protein intake limited (75-80% normal to slow growth), balance properly (minerals etc.) * ARTICULAR PROCESS JOINT MEDICATION – usually corticosteroids into joint, not helpful if bony changes * VENTRAL STABILISATION –limited to certain referrals, GA, dorsal recumbency, incision along middle neck. Drill out compression b/w adjacent vertebrae and screw in titanium implant to stop vertebrae rubbing. Good for dynamic CVM/S also good for static type (but longer). Also many post-op complications. £10,000-12,000.
40
What does the standing tail pull assess?
LMN in lumbosacral plexus
41
What does the walking tail pull assess?
UMN
42
What is implied by gluteal mm atrophy being neurogenic?
implies damage to peripheral nn or cell bodies in ventral horn of SC L3-S3 (i.e. LMN problem in gluteal region of SC
43
Outline occurrence of EPM
- common in USA and S. America • Elsewhere if imported (endemic) • No seasonal influence • About 50% USA horses are sero+ (hard to diagnose those with dz)
44
Outline Sarcocystis neurona
- can cause EPM, animals seroconvert so not all have EPM o Cycles between birds and opossums (= DH, cats =IH) o Faecal contamination of pasture/feed horse (aberrant host) o Not horse-horse spread o Diffuse, multifocal, asymmetric, non-suppurative inflammatory lesion, brain + SC o White + grey matter o Localisation  many different CS
45
CS - EPM
``` o Insidious or sudden o Highly variable – can mimic most other neuro dz o Asymmetric, sensory, motor (UMN or LMN) signs possible o Ataxia o Paresis o Mm atrophy o CN signs (sometimes) o Above CS on own or in combination ```
46
Dx - EPM
o CSF analysis (usually) – occasionally mild mononuclear pleocytosis, often normal o Western immunoblot for S.neurona Abs (CSF and serum levels compared). If leakage of blood into CSF  false positive (as 50% horses seropositive in USA).
47
Tx - EPM
o INHIBITORS OF FOLATE METABOLSIM: sulfadiazine + pyrimethamine (for 3 months) o COCCIDIOSTATS: Ponazuril (Marquis, orally, 3-4 weeks) o NSAIDs (d/t inflammatory component) o STEROIDS (if v acute onset)
48
Prognosis - EPM
o Guarded to poor (especially severe case) o Mm atrophy usually permanent o Ataxia can improve
49
What is the panniculus/ cutaneous trunci reflex used to identify?
used to ID segmental SC lesions
50
What horses does EDM affect?
- various breeds - clusters in certain farms (familial presentation - likely genetic basis) - 6months - 2 years - rare
51
CS - EDM
o Symmetric ataxia o Weakness o HL > TL o Hyporeflexia over trunk (reduced or absent ++)
52
Pathophysiology - EDM
* Neuronal fibre degeneration and demyelination in white matter in ascending and descending tracts * Mid-thoracic region often worst affected * Degenerative lesions in spinal and brainstem nuclei (but classically spinal ataxia)
53
What may EDM be associated with?
May be associated with vit E deficiency / other antioxidants --> free radical induced neuronal damage
54
Dx - EDM
o r/o other dz (CVM/S) o Measure [vitamin E ] in plasma (often normal but damaged occurred early in life) o Usually PME dx
55
Prognosis - EDM
o Poor o Signs may stabilise with high dose vit E tx (alpha tocopherol well absorbed in horses) o Unlikely to be athletic