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Neurology > Spinal disease - Problem solving - vidoes > Flashcards

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
Q

Breed predisposition - hemivertebra

A

bulldogs, pugs. Up to 78% clinically normal French Bulldogs have radiographic evidence of hemivertebra

26
Q

Describe hemivertevra

A

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
Q

What can hemivertebra be associated with?

A

other spinal disorders – IVDD, spinal arachnoid diverticula, syringomyelia, myelitis
Hemivertbera often an incidental finding

28
Q

What is the occurence of CS with hemivertebra associated with?

A

degree of kyphosis

29
Q

Tx - hemivertebra

A

Sx – spinal sx to correct kyphosis (plates and screws)

30
Q

Ddx - horse with spinal ataxia

A
  • 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
Q

CVM/S pathogenesis

A
  • 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
Q

When do you use a myelogram for CVM/S?

A

uncommon, usually when sx being considered, dye injected dorsally and ventrally (provided dorsal dicolumn is not narrowed, compression of SC unlikely)

33
Q

What is absolute stenosis (type 2)

A
  • = 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
Q

What spinal congenital malformations can horses get?

A
  • 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
Q

What is torticolis and how do you diagnose it?

A

= twisted neck

Dx - lateral radiograph

36
Q

What is articular process joint osteochondrosis?

A

• 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
Q

What is Wallerian degeneration and what is it associated with?

A

= 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
Q

Dx - CVM/S

A
  • 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
Q

Tx and prognosis of CVM/S

A
  • 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
Q

What does the standing tail pull assess?

A

LMN in lumbosacral plexus

41
Q

What does the walking tail pull assess?

A

UMN

42
Q

What is implied by gluteal mm atrophy being neurogenic?

A

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
Q

Outline occurrence of EPM

A
  • 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
Q

Outline Sarcocystis neurona

A
  • 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
Q

CS - EPM

A 
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
Q

Dx - EPM

A

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
Q

Tx - EPM

A

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
Q

Prognosis - EPM

A

o Guarded to poor (especially severe case)
o Mm atrophy usually permanent
o Ataxia can improve

49
Q

What is the panniculus/ cutaneous trunci reflex used to identify?

A

used to ID segmental SC lesions

50
Q

What horses does EDM affect?

A
  • various breeds
  • clusters in certain farms (familial presentation - likely genetic basis)
  • 6months - 2 years
  • rare
51
Q

CS - EDM

A

o Symmetric ataxia
o Weakness
o HL > TL
o Hyporeflexia over trunk (reduced or absent ++)

52
Q

Pathophysiology - EDM

A
  • 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
Q

What may EDM be associated with?

A

May be associated with vit E deficiency / other antioxidants –> free radical induced neuronal damage

54
Q

Dx - EDM

A

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
Q

Prognosis - EDM

A

o Poor
o Signs may stabilise with high dose vit E tx (alpha tocopherol well absorbed in horses)
o Unlikely to be athletic

Neurology (26 decks)

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