Spinal Cord Diseases: Congenital, Inflammatory, and Degenerative Disorders Flashcards
(67 cards)
1
Q
What’s cervical spondylomyelopathy?
A
aka wobbler’s.
- seen in large/ giant breeds
- cervical instability
2
Q
What’s the cause of cervical spondylomyelopathy?
A
- unknown, likely a combination of congenital and developmental
3
Q
What are the 2 forms of cervical spondylomyelopathy?
A
- disc-associated compression: more common in mid-aged large breeds (ex. Dobermean), mostly C5-6 or C6-7
- Osseous-associated compression: more common in young adult, giant breeds (ex. Great Dane), combination of vertebral malformation and osteoarthritic-osteoarthrotic changes
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
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
6
Q
How is cervical spondylomyelopathy treated?
A
- 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 - 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
7
Q
What’s degenerative lumbosacral disease?
A
aka “cauda equina syndrome”
- disc protrusion and hypertrophy of soft tissue in L7-S1
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
9
Q
How is degenerative lumbosacral disease diagnosed?
A
MRI (preferred), CT
10
Q
How is degenerative lumbosacral disease treated?
A
- Medical management: initial exercise restriction then leashed walking, weight loss (improvement noted in 55% of patients)
- Epidural steroids (improvement noted in 79% of dogs) - 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
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
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
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)
14
Q
How is extradural synovial cyst diagnosed?
A
MRI, hyperintense on T2
15
Q
How is extradural synovial cyst treated?
A
Mostly surgery, but should start with medical management, as it could be an incidental finding
16
Q
What’s spinal arachnoid diverticula?
A
Cysts
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
18
Q
How is spinal arachnoid diverticula diganosed?
A
MRI
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
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
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
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
23
Q
How is spondylosis deformans diagnosed?
A
- can be noted in routine x-rays
- commonly found in mid-older medium to giant breeds
24
Q
How is spondylosis deformans treated?
A
on its own = no clinical significance, therefore, no tx needed
25
What is disseminated idiopathic skeletal hyperostosis (DISH)?
- 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
26
What the clinical signs of disseminated idiopathic skeletal hyperostosis (DISH)?
- like spondylosis deformans, can cause stiffness/ limited performance in working dogs
- can increase risk of vertebral disease in adjacent vertebrae
27
How is disseminated idiopathic skeletal hyperostosis (DISH) diagnosed?
Radiographs, it can span >4 vertebral bodies (to ddx from spondylosis deformans)
28
How is disseminated idiopathic skeletal hyperostosis (DISH) treated?
no tx necessary
29
What's degenerative myelopathy?
- 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
What are some clinical signs of degenerative myelopathy?
- 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
How is degenerative myelopathy diagnosed?
- commonly seen in Boxers and GSH
- diagnosis of exclusion
- DNA test --> SOD1 (at risk for developing degenerative myelopathy)
32
What's the treatment for degenerative myelopathy?
- 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
What's IVDD?
intervertebral disc disease
- progressive collagenation and calcification in the nucleus pulposus and inner annulus fibrosis occurs at a young age in chondrodystrophic breeds
34
What are the two types of disc herniation in IVDD?
- 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
Which type of IVDD is more common in the neck?
Type I
36
What's the typical age group of cervical IVDD?
4-8y
37
Where is the most common location of cervical IVDD?
for chondrodystrophic breeds:
- C2-C4 (80%)
- C2-C3 (44-59%)
Large breeds:
- C6-C7
- Type II more likely in more caudal location
38
What's the clinical signs of cervical IVDD?
- 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
How is cervical IVDD diagnosed?
- rads can r/o; identification of location only in 35%
- myelogram, CT, or MRI for definitive diagnosis
- CSF to r/o inflammatory diseases
40
How is cervical IVDD treated? When is Sx indicated?
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
What's the success rate for surgery for cervical IVDD?
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
Which type of IVDD is most common in the thoracolumbar region?
Type I, with chondrodystrophic breeds
- French bulldogs
43
At what location is T-L IVDD most common?
T12-T13, L1-L2
L1-L2 = most common for large, non-chondrodystrophic breeds; BUT, German Shepherd Dogs like T1-T5
44
What are the clinical signs of T-L IVDD?
- 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
How is T-L IVDD diagnosed?
- Survey rads have 68-72% accuracy
- CT is mor accurate than myelogram
46
How is T-L IVDD treated?
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
What is atlantoaxial instability?
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
What are the clinical signs of atlantoaxial instability?
- neck pain = most common
- mild postural reaction abnormalities (56%) to tetraplegia (10%)
- abnormal gait in 94%
49
How is atlantoaxial instability diagnosed?
- Can see on survey rads: increased joint space between C1 and C2
- CT/MRI can give more info
50
How is atlantoaxial instability treated?
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
Describe butterfly vertebra.
on VD view, looks like a butterfly
- ventral and lateral portion of the vertebral body didn't form
- often clinically insignificant
52
Describe Hemivertebrae
- 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
Describe Centrum Hypoplaisa.
variable loss of vertebral body, leading to scoliosis
- common in screw-tailed breeds
- mostly congenital, may not see associated signs until 10m old
54
Describe block vertebrae.
Partial or total fusion of 2 vertebrae.
55
Describe articular facet aplasia.
due to dysgenesis of 2 neural arch ossification centres or abnormal development of secondary ossification
- T1-T9
- Asymptomatic
56
Describe transitional vertebrae
- congenital vertebral anomaly
- asymptomatic
- can be associated with disc disease
57
What's meningomyelitis?
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
What's steroid-responsive meningitis-arteritis (SRMA)?
- 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
What are the clinical signs of teroid-responsive meningitis-arteritis (SRMA)?
- hyperesthetic, febrile., cervical rigidity, anorexia
- young adult 8-18m
- medium/large breeds
- can also have immune mediated polyarthritis (esp BMD, Boxers, Akitas)
60
How is teroid-responsive meningitis-arteritis (SRMA) diagnosed?
- 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
How is teroid-responsive meningitis-arteritis (SRMA) treated?
Steroids! need to r/o infectious diseases first
- can have a good outcome, need long term (2y) treatment
- if refractory, try azathioprine
62
What's discospondylitis?
It's infection of the intervertebral disc and adjacent vertebral endplates
- if it's confined to the vertebral body = vertebral osteomyelitis or spondylitis
63
What's the most common etiology for discospondylitis?
- coagulase (+) Staphylococcus spp.
- Aspergillus (young GSH bitch)
- Systemic tuberculosis (young basset hounds)
64
Where is the most common location for discospondylitis?
L7-S1
(L2-4 for plant material migration)
65
What clinical signs are associated with discospondylitis?
spinal pain = most common
- ataxia, paresis, occasional paralysis
- 30% will have signs of systemic illness
66
How is discospondylitis diagnosed?
- 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
What's the treatment for discospondylitis?
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)
