Spinal Cord Diseases: Congenital, Inflammatory, and Degenerative Disorders Flashcards
What’s cervical spondylomyelopathy?
aka wobbler’s.
- seen in large/ giant breeds
- cervical instability
What’s the cause of cervical spondylomyelopathy?
- unknown, likely a combination of congenital and developmental
What are the 2 forms of cervical spondylomyelopathy?
- 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
What are the clinical signs cervical spondylomyelopathy?
- “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
How is cervical spondylomyelopathy diagnosed?
- MRI = gold standard
- rads good for rule outs
- CT is a good start, but cannot precisely localize
How is cervical spondylomyelopathy treated?
- 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
What’s degenerative lumbosacral disease?
aka “cauda equina syndrome”
- disc protrusion and hypertrophy of soft tissue in L7-S1
What are the clinical signs of degenerative lumbosacral disease?
- 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
How is degenerative lumbosacral disease diagnosed?
MRI (preferred), CT
How is degenerative lumbosacral disease treated?
- 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
What’s extradural synovial cyst?
- cysts arising from the prearticular joint tissue
- 2 types:
1. synovial cysts = have synovial lining
2. Ganglionic cysts = no specific lining
What’s the cause of extradural synovial cyst?
Could be degeneration of the zygopophyseal joint –> protrusion of the synovial membrane –> formation of cyst
What are the clinical signs ofextradural synovial cyst?
- ## 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)
How is extradural synovial cyst diagnosed?
MRI, hyperintense on T2
How is extradural synovial cyst treated?
Mostly surgery, but should start with medical management, as it could be an incidental finding
What’s spinal arachnoid diverticula?
Cysts
What’s the cause of spinal arachnoid diverticula?
- 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
How is spinal arachnoid diverticula diganosed?
MRI
What are the clinical signs associated with spinal arachnoid diverticula?
- proprioceptive ataxia
- various degree of para to tetraparesis
- no apparent pain
- may have pseudo hypermetria in thoracic limbs
What’s the treatment for spinal arachnoid diverticula?
Surgery = treatment of choice (65-80% success) but medical management may be attempted initially
What’s spondylosis deformans?
- 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
What clinical signs are associated with spondylosis deformans?
- usually no c/s
- in working dogs, can see reduction in activity level
- can lead to other issues in adjacent vertebrae
How is spondylosis deformans diagnosed?
- can be noted in routine x-rays
- commonly found in mid-older medium to giant breeds
How is spondylosis deformans treated?
on its own = no clinical significance, therefore, no tx needed
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
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
How is disseminated idiopathic skeletal hyperostosis (DISH) diagnosed?
Radiographs, it can span >4 vertebral bodies (to ddx from spondylosis deformans)
How is disseminated idiopathic skeletal hyperostosis (DISH) treated?
no tx necessary
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
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
How is degenerative myelopathy diagnosed?
- commonly seen in Boxers and GSH
- diagnosis of exclusion
- DNA test –> SOD1 (at risk for developing degenerative myelopathy)
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
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
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
Which type of IVDD is more common in the neck?
Type I
What’s the typical age group of cervical IVDD?
4-8y
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
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
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
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
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%
Which type of IVDD is most common in the thoracolumbar region?
Type I, with chondrodystrophic breeds
- French bulldogs
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
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%
How is T-L IVDD diagnosed?
- Survey rads have 68-72% accuracy
- CT is mor accurate than myelogram
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%
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
What are the clinical signs of atlantoaxial instability?
- neck pain = most common
- mild postural reaction abnormalities (56%) to tetraplegia (10%)
- abnormal gait in 94%
How is atlantoaxial instability diagnosed?
- Can see on survey rads: increased joint space between C1 and C2
- CT/MRI can give more info
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
Describe butterfly vertebra.
on VD view, looks like a butterfly
- ventral and lateral portion of the vertebral body didn’t form
- often clinically insignificant
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
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
Describe block vertebrae.
Partial or total fusion of 2 vertebrae.
Describe articular facet aplasia.
due to dysgenesis of 2 neural arch ossification centres or abnormal development of secondary ossification
- T1-T9
- Asymptomatic
Describe transitional vertebrae
- congenital vertebral anomaly
- asymptomatic
- can be associated with disc disease
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
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
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)
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
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
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
What’s the most common etiology for discospondylitis?
- coagulase (+) Staphylococcus spp.
- Aspergillus (young GSH bitch)
- Systemic tuberculosis (young basset hounds)
Where is the most common location for discospondylitis?
L7-S1
(L2-4 for plant material migration)
What clinical signs are associated with discospondylitis?
spinal pain = most common
- ataxia, paresis, occasional paralysis
- 30% will have signs of systemic illness
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
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)
