Degenerative spinal cord diseases Flashcards
Where does the vertebral disc sit?
- Between the endplates of the vertebrae
Where does the disc not sit between the endplates of the vertebrae?
- C1 and C2
What are the two structures in the disc?
- Annulus fibrosus (it’s the fibrous outer part)
- Nucleus pulposus (gelatinous structure on the inside)
Compare the blood supply to the AF and NP
- Only blood supply to the outer annulus
Innervation of AF
- Only the outer third is innervated
What is the largest avascular structure in the body?
- L7-S1 disc
Pathophysiology of disc disease Hansen Type I - what happens to the nucleus pulposus?
- Dehydration!
- Nuclear degeneration (loss of glycosaminoglycans, increased collagen, and hyaline cartilage formation)
Signalment for Hansen Type I disc disease
- Chrondrodystrophic breeds (Dachshund, Mini Poodles, etc.)
- Any miniaturized breed
- Younger patients (2-7 years of age), but can be as young as 1 year or geriatric
Most common locations for Type I Disc Extrusions?
- Thoracolumbar region (T11-L4)
- T12-T13 and T13-L1 account for 50% of all disc extrusions from Type I
Why do you rarely see Type I Disc Extrusions between T2-T10?
- Intercaptial ligament runs from each rib head and provides extra support
Where are cervical herniations most common with Type I?
- C2-C3 most common
- C4-C5
- C3-C4
Diagnosis of Hansen Type I?
- Neuro examination
- Most often localizing to either T3-L3 or cervical myelopathies
- Imaging (Radiographs to rule out fracture, MRI)
What can you observe with Type I disc extrusion on radiographs?
- Cannot diagnose disc extrusion but can help rule out tumors and fractures
- Cross sectional imaging helpful
Does a mineralized disc on a radiograph tell you it’s the offending disc?
- Not necessarily!
- It tells you that they have intervertebral disc disease but not necessarily a Type I disc extrusion
Type I disc disease: Protrusion or extrusion?
- Extrusion
Why does the NP usually extrude dorsally?
- Annulus is thinner dorsally
Conservative or medical management for Type I Disc extrusion?
What is the most important part of treatment?
- Strict rest for 6 weeks (MOST IMPORTANT): no more than 5 minute walks on a leash
- Pain control (Tramadol, Codeine, Gabapentin, Fentanyl patch, NSAIDs or steroids)
- +/- some rehab activity
Surgical treatment for Type I disc extrusion - when to do?
- If they can’t walk or are non-ambulatory
- Still need conservative management post-operatively
- If people want to jump to surgery, you still have to be careful due to the risk of fracture from removing bone
What are the two types of surgery that can be used to treat Type I Disc extrusions?
- Hemilaminectomy vs ventral slot
What determines prognosis for Type I Disc Extrusion?
- Is the patient deep pain positive or deep pain negative?
Prognosis if deep pain positive**
- 90-95%
- They may not be exactly the same as before surgery, but they will be able to walk again
Prognosis if deep pain negative?
- 50% with surgery if within the first 24 hours
- <5% within 48 hours
Long term goals after surgery for Type I disc extrusion?
- Ambulation!
Type II Disc disease: what is it termed?
- Protrusion
Signalment of Type II Disc disease?
- Larger breed dogs in general
Course of disease with Type II Disc disease
- Often chronic history
Underlying pathogenesis with Type II Disc disease
- Annular degeneration and subsequent protrusion
- Degenerative changes in the nucleus pulposus as well
Diagnosis of Type II Disc protrusion
- MRI
Prognosis of Type II DIsc Protrusion
- More guarded
- Slow or prevent improvement
- Chronic disease so the changes have already happened
What are the two options for Type II Disc protrusion?
- Surgical vs medical treatment
- Surgery is expensive and doesn’t guarantee that it will make the patients better
With Type II Disc protrusion, does it tend to be only at one site or multiple sites?
- Multiple sites in general
Signalment of dogs with lumbosacral disease
- Middle aged to older dogs
- Large breeds (but GSD predisposed)
Pathophysiology of lumbosacral disease
- Type II Degeneration of L7-S1 IVD and protrusion compresses the nerve roots
- Instability of l7 vertebrae relative to S1
- Soft tissue proliferation
- Synovial cysts from articular facets as well
- Vascular compromise of spinal nerves
- Osteochondrosis
- Presence of vertebral anomalies (e.g. transitional vertebrae)
Clinical signs of lumbosacral disease
- Only pelvic limbs are affected
- Paraparesis
- Crouched gait in rear
- Decreased withdrawals and caudal muscle atrophy
- May have normal patellar reflexes or hyperreflexia
- Decreased anal tone
- Change in tail carriage, pain when lifting tail (more reluctant to go up stairs or jump into the car)
- Incontinence (might be the only sign)
Which nerve is primarily responsible for weight bearing in the hind limb?
- Femoral nerve
- Means that if you have a true L4-L6 lesion, they are likely non-ambulatory
Diagnosis of lumbosacral disease
- Neurological exam
- Imaging (radiographs, CT, MRI*****)
Discogram
- Needle into L7 and inject contrast into the disc
Treatment for lumbosacral disease
- Medical/conservative
- Rest
- STeroids
- Pain control
- Surgical (dorsal laminectomy)
Prognosis for Type II lumbosacral disease
- Not as favorable as with type I
- Depends on what clinical signs are present (e.g. urinary incontinence, pain)
- Goal is to alleviate pain
Which surgery is used for lumbosacral disease?
- Dorsal laminectomy
What is cervical spondylomyelopathy called?
- Wobbler’s syndrome
Who gets cervical spondylomyelopathy?
- Large/giant breed dogs
- Dobies and Great danes predisposed
What are the two forms of cervical spondylomyelopathy? Who tends to get which type?
- Disc associated (middle aged dogs, Dobies)
- Osseous form (younger giant breeds
Who gets disc associated CSM?
- Dobies
Pathophysiology of disc associated CSM?
- Disc protrusion (Hansen type II)
Vertebral canal stenosis
- Torsion in the caudal cervical spine
- Disc protrusion in the caudal cervical spine
Where does disc associated CSM tend to occur?
- C5-C6 or C6-C7 disc spaces
Who gets osseous associated CSM?
- Young adult giant breeds
Pathophysiology of osseous associated CSM?
- Kind of like the lumbosacral disease in Great Danes
- Some disc compression but more like instability
- New bone formation and new ligaments and joints
Signalment and history suggestive of CSM
- Dobies and other large breeds typically older (<3 years)
- Giant breeds typically younger
- Chronic/progressive history
Neurologic exam for CSM
- All four limbs affected = tetraparesis and ataxia of all limbs
- Patients may have a two engine gait (C6-T2)
- Typically LMN in thoracic limb
- UMN to PL
- Cervical hyperesthesia (pain)
Diagnosis of CSM
- Radiographs to look for osseous change
- Advanced imaging required - MRI preferable to CT
What does hyperintensity on MRI mean?
- Edema nad inflammation or scar formation
- Hard to tell, and the prognosis differs quite a bit (scar can’t heal; edema and inflammation can)
- Steroid trials may help determine if surgery would be helpful or not
Treatment for CSM
- Medical/conservative (Avoid neck leads in addition to other notes)
- Surgical (multiple approaches)
Treatment goals for CSM
- Slow/delay, possibly stop disease progression
Prognostic indicators for CSM
- Non-ambulatory on presentation = poor prognosis
- Probably would never get ambulatory
History/signalment of degenerative myelopathy
- Chronic, progressive disease over a period of months
- Older dogs (typically >5 years); GSD, Corgi, Chesapeake Bay Retriever
What causes degenerative myelopathy?
- SOD1 mutation
- ROS scavenger –> axon and myelin loss in the spinal cord
What’s another name for degenerative myelopathy?
- Amyotrophic Lateral Sclerosis (Lou Gehrig disease)
Breeds predisposed to degenerative myelopathy
- German Shepherd dog
- Corgi
- Chesapeake Bay Retriever
Neurologic findings with degenerative myelopathy
- Often starts as a T3-L3 myelopathy but can present as L4-S1
- Don’t rule out in a GSD
- Chronic/progressive within a few months
- Non-painful disease
Progression of degenerative myelopathy
1: UMN paraparesis
2: Nonambulatory paraparesis to paraplegia (+/- urinary and fecal incontinence)
3: LMN paraplegia to thoracic limb paresis
4: LMN tetraplegia and brain stem signs
Diagnosis of degenerative myelopathy
- Histopathology (postmortem)
- Antemortem is a diagnosis of exclusion; genetic test available
Genetic test for degenerative myelopathy
- How many copies do they have?
- At risk, affected, not affected
- At risk is more likely to develop
- Not affected is unlikely but not possible
Prognosis for degenerative myelopathy
- Poor
- Often non-ambulatory within 6-12 months from onset of clinical signs
- Rehabilitation may somewhat delay progression to a non-ambulatory state
- Will progress to thoracic limbs and brainstem if the patient isn’t euthanized
