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Internal Medicine/ Ettinger > Spinal Cord Diseases: Congenital, Inflammatory, and Degenerative Disorders > Flashcards

Spinal Cord Diseases: Congenital, Inflammatory, and Degenerative Disorders Flashcards

1
Q

What’s cervical spondylomyelopathy?

A

aka wobbler’s.
- seen in large/ giant breeds
- cervical instability

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2
Q

What’s the cause of cervical spondylomyelopathy?

A
  • unknown, likely a combination of congenital and developmental
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3
Q

What are the 2 forms of cervical spondylomyelopathy?

A
  1. disc-associated compression: more common in mid-aged large breeds (ex. Dobermean), mostly C5-6 or C6-7
  2. Osseous-associated compression: more common in young adult, giant breeds (ex. Great Dane), combination of vertebral malformation and osteoarthritic-osteoarthrotic changes
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4
Q

What are the clinical signs cervical spondylomyelopathy?

A
  • “two engine” gait: LMN thoracic limbs & UMN pelvic limbs.
  • thoracic gait = short, choppy
  • pelvic gait = wide based, long
  • GP deficit may not be obvious in chronic cases
  • cervical hyperesthesia is not prominent
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5
Q

How is cervical spondylomyelopathy diagnosed?

A
  • MRI = gold standard
  • rads good for rule outs
  • CT is a good start, but cannot precisely localize
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6
Q

How is cervical spondylomyelopathy treated?

A
  1. medical management: exercise restriction & anti-inflammatory dose of steroids –> reduces vasogenic edema, protect from glutamate toxicity, reduce neuronal and oliogodendroglial apoptosis
    - 50% will improve with medical management alone
  2. Surgery: direct decompression (ex. ventral slot, dorsal laminectomy) and indirect decompression (ex. distraction techniques). No proven superior one
    - 70-80% will improve with surgical management. May deteriorate after 2-3y
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7
Q

What’s degenerative lumbosacral disease?

A

aka “cauda equina syndrome”
- disc protrusion and hypertrophy of soft tissue in L7-S1

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8
Q

What are the clinical signs of degenerative lumbosacral disease?

A
  • reluctant to sit, jump
  • lameness, “stiff
    weakness in hindlimbs
  • lumbosacral pain
  • deficits in proprioceptive positioning tests
  • reduced flexion (esp hock), normal patella
  • severe cases may have urinary/ fecal incontinence
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9
Q

How is degenerative lumbosacral disease diagnosed?

A

MRI (preferred), CT

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10
Q

How is degenerative lumbosacral disease treated?

A
  1. Medical management: initial exercise restriction then leashed walking, weight loss (improvement noted in 55% of patients)
    - Epidural steroids (improvement noted in 79% of dogs)
  2. Surgical management: usually dorsal laminectomy of L7-S1 with removal of hypertrophied soft tissue (improvement noted in 66.7-95% of patients). If fecal/urinary incontinent, 55-87% will persist
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11
Q

What’s extradural synovial cyst?

A
  • cysts arising from the prearticular joint tissue
  • 2 types:
    1. synovial cysts = have synovial lining
    2. Ganglionic cysts = no specific lining
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12
Q

What’s the cause of extradural synovial cyst?

A

Could be degeneration of the zygopophyseal joint –> protrusion of the synovial membrane –> formation of cyst

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13
Q

What are the clinical signs ofextradural synovial cyst?

A
  • ## depend on the location, most commonly in the lumbosacral (lameness or weakness, +/- pain), or in association with the osseous from of Wobbler’s (proprioceptive ataxia, tetraparesis)
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14
Q

How is extradural synovial cyst diagnosed?

A

MRI, hyperintense on T2

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15
Q

How is extradural synovial cyst treated?

A

Mostly surgery, but should start with medical management, as it could be an incidental finding

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16
Q

What’s spinal arachnoid diverticula?

A

Cysts

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17
Q

What’s the cause of spinal arachnoid diverticula?

A
  • genetic predisposition in Pugs
  • 55% in the cervical region, 45% in the thoracolumbar region
  • Large breed: cervical, C2, C3, T9-T13
  • small breed: thoracolumbar
  • 88% located in the dorsal aspect of the spinal cord
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18
Q

How is spinal arachnoid diverticula diganosed?

A

MRI

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19
Q

What are the clinical signs associated with spinal arachnoid diverticula?

A
  • proprioceptive ataxia
  • various degree of para to tetraparesis
  • no apparent pain
  • may have pseudo hypermetria in thoracic limbs
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20
Q

What’s the treatment for spinal arachnoid diverticula?

A

Surgery = treatment of choice (65-80% success) but medical management may be attempted initially

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21
Q

What’s spondylosis deformans?

A
  • very common degenerative process: changes in the annulus fibrosus of the intervertebral discs in an effort to stabilize the disc region
  • no clinical significance on its own
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22
Q

What clinical signs are associated with spondylosis deformans?

A
  • usually no c/s
  • in working dogs, can see reduction in activity level
  • can lead to other issues in adjacent vertebrae
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23
Q

How is spondylosis deformans diagnosed?

A
  • can be noted in routine x-rays
  • commonly found in mid-older medium to giant breeds
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24
Q

How is spondylosis deformans treated?

A

on its own = no clinical significance, therefore, no tx needed

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25
Q

What is disseminated idiopathic skeletal hyperostosis (DISH)?

A
  • systemic disorder
  • fibrocartilaginous proliferation followed by endochondral ossification within soft tissues of the axia land appendicular skeleton
  • effects one region rather than specific anatomical site
  • likes T6-T10, L2-L6
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26
Q

What the clinical signs of disseminated idiopathic skeletal hyperostosis (DISH)?

A
  • like spondylosis deformans, can cause stiffness/ limited performance in working dogs
  • can increase risk of vertebral disease in adjacent vertebrae
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27
Q

How is disseminated idiopathic skeletal hyperostosis (DISH) diagnosed?

A

Radiographs, it can span >4 vertebral bodies (to ddx from spondylosis deformans)

28
Q

How is disseminated idiopathic skeletal hyperostosis (DISH) treated?

A

no tx necessary

29
Q

What’s degenerative myelopathy?

A
  • commonly noted in thoracolumbar in medium-large breeds
  • Familial degenerative myelopathy noted in Boxers and Rhodesian Ridgebacks
  • segmental degeneration of the axon and associated myelin
30
Q

What are some clinical signs of degenerative myelopathy?

A
  • progressive paraparesis to tetra paresis with mild proprioceptive ataxia initially
  • takes 6-12m to become severe paretic and non-ambulatory
  • T3-L3
  • extensor tone always increased in the early phase of the disease
31
Q

How is degenerative myelopathy diagnosed?

A
  • commonly seen in Boxers and GSH
  • diagnosis of exclusion
  • DNA test –> SOD1 (at risk for developing degenerative myelopathy)
32
Q

What’s the treatment for degenerative myelopathy?

A
  • steroids don’t help
  • no drugs can alter the disease progression
  • try physiotherapy
  • long-term prognosis = poor
  • 6-12m for development of severe pelvic limb dysfunction
33
Q

What’s IVDD?

A

intervertebral disc disease
- progressive collagenation and calcification in the nucleus pulposus and inner annulus fibrosis occurs at a young age in chondrodystrophic breeds

34
Q

What are the two types of disc herniation in IVDD?

A
  • Hansen Type I: herniation of the nucleus pulposus through the annulus fiber, with extrusion of nuclear material into the spinal canal; chondroid disc degeneration
  • Hansen Type II: protrusion of the annulus fiber due to central shifting of the nuclear material; fibroid disc degeneration
  • chondrodystrophic breeds –> Type I, acute
  • older, non-chondrodystrophic breeds –> type II
35
Q

Which type of IVDD is more common in the neck?

A

Type I

36
Q

What’s the typical age group of cervical IVDD?

A

4-8y

37
Q

Where is the most common location of cervical IVDD?

A

for chondrodystrophic breeds:
- C2-C4 (80%)
- C2-C3 (44-59%)
Large breeds:
- C6-C7
- Type II more likely in more caudal location

38
Q

What’s the clinical signs of cervical IVDD?

A
  • neck pain (up to 60%), no neuro deficits (90%)
  • slower on set of clinical signs
  • nerve root signature (discomfort/ lameness associated with a single limb) - 22-50%
  • Neurological deficits are more common in C4-5 and C6-7
39
Q

How is cervical IVDD diagnosed?

A
  • rads can r/o; identification of location only in 35%
  • myelogram, CT, or MRI for definitive diagnosis
  • CSF to r/o inflammatory diseases
40
Q

How is cervical IVDD treated? When is Sx indicated?

A

Conservative therapy:
- strict cage rest for 4-6 weeks
- anti-inflammatory, acupuncture, muscle relaxant, analgesics

3 groups of symptomatic patients:
1. first time, neck pain only
2. neck pain only, recurrent
3. neck pain + neurological deficits

Conservative therapy ok for Group 1
Sx most appropriate for Group 2
Sx required for Group 3

41
Q

What’s the success rate for surgery for cervical IVDD?

A

ventral slot…
For smaller breeds:
- up 90% complete recovery in 1 month, 98% in 12m
For large breeds:
- only 66% success rate

  • recurrence rate for all = 5-10%
42
Q

Which type of IVDD is most common in the thoracolumbar region?

A

Type I, with chondrodystrophic breeds
- French bulldogs

43
Q

At what location is T-L IVDD most common?

A

T12-T13, L1-L2
L1-L2 = most common for large, non-chondrodystrophic breeds; BUT, German Shepherd Dogs like T1-T5

44
Q

What are the clinical signs of T-L IVDD?

A
  • if peracute, can have spinal shock or Schiff-Sherrington
    (this does not determine prognosis)
  • can have hyperesthesia only to paraplegia +/- deep pain perception
  • ascending/ descending myomalacia in 10%
45
Q

How is T-L IVDD diagnosed?

A
  • Survey rads have 68-72% accuracy
  • CT is mor accurate than myelogram
46
Q

How is T-L IVDD treated?

A

Conservative therapy:
- 1st timer
- spinal pain only
- mild/ moderate paraparesis
- tx similar to cervical IVDD, 82-100% success; 30-50% recurrence

Surgery:
- recumbent
- recurrent or progressive
- paraplegia +/- pain perception
- prolonged loss of pain perception = poor prognosis
- high dose of steroids does NOT improve outcome
- recurrence 2-42%

47
Q

What is atlantoaxial instability?

A

AA join instability leads to compression and concussion of the cervical spinal cord
- most common in small/miniature breeds
- malformation of the dens (congenital/ developmental), due to aberrations of physeal growth plate closure
- can happen in large breeds too
- very rare in cats

48
Q

What are the clinical signs of atlantoaxial instability?

A
  • neck pain = most common
  • mild postural reaction abnormalities (56%) to tetraplegia (10%)
  • abnormal gait in 94%
49
Q

How is atlantoaxial instability diagnosed?

A
  • Can see on survey rads: increased joint space between C1 and C2
  • CT/MRI can give more info
50
Q

How is atlantoaxial instability treated?

A

Conservative therapy: strict cage rest and giant splint (head to chest) –> 38% success rate
Surgery: can fuse the AA joint, prevent recurrence, but will not address and underlying parenchymal diseases
- periop mortality = 10-30%
- even dogs that can’t walk can have a good outcome

51
Q

Describe butterfly vertebra.

A

on VD view, looks like a butterfly
- ventral and lateral portion of the vertebral body didn’t form
- often clinically insignificant

52
Q

Describe Hemivertebrae

A
  • failure of 1 sagittal half of the vertebra to develop
  • bulldog and Boston Terriers
  • most common in T5-T9
  • not associated with severe spinal stenosis (more so from the kyphosis and subluxation)
  • but other spinal issues can occur at that location
  • may required surgical realignment and stabilization
53
Q

Describe Centrum Hypoplaisa.

A

variable loss of vertebral body, leading to scoliosis
- common in screw-tailed breeds
- mostly congenital, may not see associated signs until 10m old

54
Q

Describe block vertebrae.

A

Partial or total fusion of 2 vertebrae.

55
Q

Describe articular facet aplasia.

A

due to dysgenesis of 2 neural arch ossification centres or abnormal development of secondary ossification
- T1-T9
- Asymptomatic

56
Q

Describe transitional vertebrae

A
  • congenital vertebral anomaly
  • asymptomatic
  • can be associated with disc disease
57
Q

What’s meningomyelitis?

A

Inflammation of the spinal cord and its parenchyma.
Unlikely to occur without encephalitis.
Infectious: canine distemper, protozoa.
Non-infectious MUE
- c/s depends on location
- need MRI/ CSF

58
Q

What’s steroid-responsive meningitis-arteritis (SRMA)?

A
  • immune-mediated
  • results in vasculitis, without a specific trigger
  • can see increase in serum/CSF IgA, CSF and blood B-cell/T-cell ratios, and CSF IL-6 and IL-8 levels
  • high expression of CD11a = important pathogenesis for SRMA
59
Q

What are the clinical signs of teroid-responsive meningitis-arteritis (SRMA)?

A
  • hyperesthetic, febrile., cervical rigidity, anorexia
  • young adult 8-18m
  • medium/large breeds
  • can also have immune mediated polyarthritis (esp BMD, Boxers, Akitas)
60
Q

How is teroid-responsive meningitis-arteritis (SRMA) diagnosed?

A
  • marked peripheral neutrophilia with L shift , non degenerative
  • CSF = marked neutrophilic pleocytosis and protein elevation
  • elevation in serum C-reactive protein and amyloid-A
61
Q

How is teroid-responsive meningitis-arteritis (SRMA) treated?

A

Steroids! need to r/o infectious diseases first
- can have a good outcome, need long term (2y) treatment
- if refractory, try azathioprine

62
Q

What’s discospondylitis?

A

It’s infection of the intervertebral disc and adjacent vertebral endplates
- if it’s confined to the vertebral body = vertebral osteomyelitis or spondylitis

63
Q

What’s the most common etiology for discospondylitis?

A
  • coagulase (+) Staphylococcus spp.
  • Aspergillus (young GSH bitch)
  • Systemic tuberculosis (young basset hounds)
64
Q

Where is the most common location for discospondylitis?

A

L7-S1
(L2-4 for plant material migration)

65
Q

What clinical signs are associated with discospondylitis?

A

spinal pain = most common
- ataxia, paresis, occasional paralysis
- 30% will have signs of systemic illness

66
Q

How is discospondylitis diagnosed?

A
  • urine cytology
  • blood / urine culture should be performed in all suspected cases
  • positive up to 75% and 50%, respectively
  • spinal rads for definitive diagnosis (may take 2-4 weeks after infection to show signs)
  • CT/MRI can give more detail
67
Q

What’s the treatment for discospondylitis?

A

appropriate antibiotics, cage rest, analgesia
- may required long term antibiotics
- fungal infection prognosis not as good (or have multiple lesions, vertebral fractures/ subluxation, or endocarditis)

Internal Medicine/ Ettinger (93 decks)

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