Degenerative spinal cord diseases Flashcards

1
Q

Where does the vertebral disc sit?

A
  • Between the endplates of the vertebrae
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2
Q

Where does the disc not sit between the endplates of the vertebrae?

A
  • C1 and C2
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3
Q

What are the two structures in the disc?

A
  • Annulus fibrosus (it’s the fibrous outer part)

- Nucleus pulposus (gelatinous structure on the inside)

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4
Q

Compare the blood supply to the AF and NP

A
  • Only blood supply to the outer annulus
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5
Q

Innervation of AF

A
  • Only the outer third is innervated
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6
Q

What is the largest avascular structure in the body?

A
  • L7-S1 disc
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7
Q

Pathophysiology of disc disease Hansen Type I - what happens to the nucleus pulposus?

A
  • Dehydration!

- Nuclear degeneration (loss of glycosaminoglycans, increased collagen, and hyaline cartilage formation)

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8
Q

Signalment for Hansen Type I disc disease

A
  • 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
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9
Q

Most common locations for Type I Disc Extrusions?

A
  • Thoracolumbar region (T11-L4)

- T12-T13 and T13-L1 account for 50% of all disc extrusions from Type I

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10
Q

Why do you rarely see Type I Disc Extrusions between T2-T10?

A
  • Intercaptial ligament runs from each rib head and provides extra support
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11
Q

Where are cervical herniations most common with Type I?

A
  • C2-C3 most common
  • C4-C5
  • C3-C4
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12
Q

Diagnosis of Hansen Type I?

A
  • Neuro examination
  • Most often localizing to either T3-L3 or cervical myelopathies
  • Imaging (Radiographs to rule out fracture, MRI)
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13
Q

What can you observe with Type I disc extrusion on radiographs?

A
  • Cannot diagnose disc extrusion but can help rule out tumors and fractures
  • Cross sectional imaging helpful
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14
Q

Does a mineralized disc on a radiograph tell you it’s the offending disc?

A
  • Not necessarily!

- It tells you that they have intervertebral disc disease but not necessarily a Type I disc extrusion

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15
Q

Type I disc disease: Protrusion or extrusion?

A
  • Extrusion
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16
Q

Why does the NP usually extrude dorsally?

A
  • Annulus is thinner dorsally
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17
Q

Conservative or medical management for Type I Disc extrusion?

What is the most important part of treatment?

A
  • 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
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18
Q

Surgical treatment for Type I disc extrusion - when to do?

A
  • 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
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19
Q

What are the two types of surgery that can be used to treat Type I Disc extrusions?

A
  • Hemilaminectomy vs ventral slot
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20
Q

What determines prognosis for Type I Disc Extrusion?

A
  • Is the patient deep pain positive or deep pain negative?
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21
Q

Prognosis if deep pain positive**

A
  • 90-95%

- They may not be exactly the same as before surgery, but they will be able to walk again

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22
Q

Prognosis if deep pain negative?

A
  • 50% with surgery if within the first 24 hours

- <5% within 48 hours

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23
Q

Long term goals after surgery for Type I disc extrusion?

A
  • Ambulation!
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24
Q

Type II Disc disease: what is it termed?

A
  • Protrusion
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25
Q

Signalment of Type II Disc disease?

A
  • Larger breed dogs in general
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26
Q

Course of disease with Type II Disc disease

A
  • Often chronic history
27
Q

Underlying pathogenesis with Type II Disc disease

A
  • Annular degeneration and subsequent protrusion

- Degenerative changes in the nucleus pulposus as well

28
Q

Diagnosis of Type II Disc protrusion

A
  • MRI
29
Q

Prognosis of Type II DIsc Protrusion

A
  • More guarded
  • Slow or prevent improvement
  • Chronic disease so the changes have already happened
30
Q

What are the two options for Type II Disc protrusion?

A
  • Surgical vs medical treatment

- Surgery is expensive and doesn’t guarantee that it will make the patients better

31
Q

With Type II Disc protrusion, does it tend to be only at one site or multiple sites?

A
  • Multiple sites in general
32
Q

Signalment of dogs with lumbosacral disease

A
  • Middle aged to older dogs

- Large breeds (but GSD predisposed)

33
Q

Pathophysiology of lumbosacral disease

A
  • 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)
34
Q

Clinical signs of lumbosacral disease

A
  • 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)
35
Q

Which nerve is primarily responsible for weight bearing in the hind limb?

A
  • Femoral nerve

- Means that if you have a true L4-L6 lesion, they are likely non-ambulatory

36
Q

Diagnosis of lumbosacral disease

A
  • Neurological exam

- Imaging (radiographs, CT, MRI*****)

37
Q

Discogram

A
  • Needle into L7 and inject contrast into the disc
38
Q

Treatment for lumbosacral disease

A
  • Medical/conservative
  • Rest
  • STeroids
  • Pain control
  • Surgical (dorsal laminectomy)
39
Q

Prognosis for Type II lumbosacral disease

A
  • Not as favorable as with type I
  • Depends on what clinical signs are present (e.g. urinary incontinence, pain)
  • Goal is to alleviate pain
40
Q

Which surgery is used for lumbosacral disease?

A
  • Dorsal laminectomy
41
Q

What is cervical spondylomyelopathy called?

A
  • Wobbler’s syndrome
42
Q

Who gets cervical spondylomyelopathy?

A
  • Large/giant breed dogs

- Dobies and Great danes predisposed

43
Q

What are the two forms of cervical spondylomyelopathy? Who tends to get which type?

A
  • Disc associated (middle aged dogs, Dobies)

- Osseous form (younger giant breeds

44
Q

Who gets disc associated CSM?

A
  • Dobies
45
Q

Pathophysiology of disc associated CSM?

A
  • Disc protrusion (Hansen type II)

Vertebral canal stenosis

  • Torsion in the caudal cervical spine
  • Disc protrusion in the caudal cervical spine
46
Q

Where does disc associated CSM tend to occur?

A
  • C5-C6 or C6-C7 disc spaces
47
Q

Who gets osseous associated CSM?

A
  • Young adult giant breeds
48
Q

Pathophysiology of osseous associated CSM?

A
  • Kind of like the lumbosacral disease in Great Danes
  • Some disc compression but more like instability
  • New bone formation and new ligaments and joints
49
Q

Signalment and history suggestive of CSM

A
  • Dobies and other large breeds typically older (<3 years)
  • Giant breeds typically younger
  • Chronic/progressive history
50
Q

Neurologic exam for CSM

A
  • 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)
51
Q

Diagnosis of CSM

A
  • Radiographs to look for osseous change

- Advanced imaging required - MRI preferable to CT

52
Q

What does hyperintensity on MRI mean?

A
  • 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
53
Q

Treatment for CSM

A
  • Medical/conservative (Avoid neck leads in addition to other notes)
  • Surgical (multiple approaches)
54
Q

Treatment goals for CSM

A
  • Slow/delay, possibly stop disease progression
55
Q

Prognostic indicators for CSM

A
  • Non-ambulatory on presentation = poor prognosis

- Probably would never get ambulatory

56
Q

History/signalment of degenerative myelopathy

A
  • Chronic, progressive disease over a period of months

- Older dogs (typically >5 years); GSD, Corgi, Chesapeake Bay Retriever

57
Q

What causes degenerative myelopathy?

A
  • SOD1 mutation

- ROS scavenger –> axon and myelin loss in the spinal cord

58
Q

What’s another name for degenerative myelopathy?

A
  • Amyotrophic Lateral Sclerosis (Lou Gehrig disease)
59
Q

Breeds predisposed to degenerative myelopathy

A
  • German Shepherd dog
  • Corgi
  • Chesapeake Bay Retriever
60
Q

Neurologic findings with degenerative myelopathy

A
  • 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
61
Q

Progression of degenerative myelopathy

A

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

62
Q

Diagnosis of degenerative myelopathy

A
  • Histopathology (postmortem)

- Antemortem is a diagnosis of exclusion; genetic test available

63
Q

Genetic test for degenerative myelopathy

A
  • 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
64
Q

Prognosis for degenerative myelopathy

A
  • 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