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NSB II > Spinal Cord/Cauda Equine Diseases > Flashcards

Spinal Cord/Cauda Equine Diseases Flashcards

1
Q

who are the 2 classic examples of breeds affected by cervical spondylomyelopathy/Wobblers?

A
  1. danes
    -tend to be younger
    -osseous-associated: articular processes, cranial-mid cervical
    -cranial cervical (C1-C5)
  2. dobies;
    -tend to be older
    -disc associated
    -caudal cervical (C5-C7)
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2
Q

what are the 3 key players of cervical spondylomyelopathy/Wobblers?

A
  1. dorsal: ligamentum flavum
  2. dorsolateral: articular processes
  3. ventral: IVD, dorsal longitudinal ligament, vertebral body
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3
Q

describe pathology of osseous associated cervical sponylomyelopathy

A

dorsolateral compression or dorso-ventral flattening of articular process joint and joint capsule and ligamentum flavum; often of multiple joints and the worst dominates clinical signs

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4
Q

describe pathology of disc associated cervical spondylomyelopathy

A

hypertrophy

extend hurt

dyanmic bc worse or better in different positions (FILL IN MORE)

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5
Q

give signalment of cervical spondylomyelopathy

A
  1. large to giant breeds
  2. doberman: middle to older, caudal cervical
  3. great dane: young, mid-caudal cervical, stenosis
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6
Q

describe treatment/prognosis of cervical spondylomyelopathy

A
  1. conservative: (same conservative tx for all neuro things)
    -corticosteroids OR NSAIDs
    -exercise restriction (at least 4 weeks)
    -analgesics: gabapentin
  2. surgical: decompressive surgeries are only options for spinal cord
    -hesitate if a lot of gliosis (might not be reversible)
    -ventral slot +/- add screws in vertebral bodies and acrylic to hold in neutral position/prevent joint movement hoping for a bony ankylosis over time to create stimulus for fibrosis
    -+/- efficacy because may put more stress on vertebrae cranial and cause them to have pathology
  3. variable prognosis: months to years
    -no difference between conservative versus surgical
    -survival times mean/median (approx 3-4 years)
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7
Q

describe degenerative lumbosacral stenosis

A
  1. compression of nervous tissue structures at LS articulation
    -cauda equina (L7, S1-S3, and spinal nerves)
  2. L7 nerve root is most commonly affected
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8
Q

describe most common culprit for degenerative lumbosacral stenosis

A
  1. german shepherd (or any large breed)
  2. middle to older aged
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9
Q

describe clinical signs of degenerative lumbosacral stenosis

A

variable!
1. pain is most common
2. paresis
3. lack of tail tone
4. urinary/fecal incontinence
5. pseudohyperreflexia: lack of caudal thigh muscles to inhibit the “kick” of patellar reflex, so looks like crazy patellar! but will lack withdrawal!
6. gait:
-crouched stance
-overflexion of hock, stifle, and CF joints
-short strided

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10
Q

what are the players in degenerative lumbosacral stenosis?

A
  1. dorsal: ligamentum flavum
  2. lateral: articular processes
    3, vent

same as cervical spondylomyelosis

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11
Q

describe diagnosis of degeneratice limbosacral stenosis?

A
  1. plain radiographs:
    -DJD articular processes
    -subluxation
    -ventral spondylosis
    -not incredible but good start and to differentiate from orthopedic disease!!
  2. MRI: same idea as dynamic/doberman cervical spondylomyelosis
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12
Q

describe treatment/prognosis of degenerative lumbosacral stenosis

A
  1. conservative: can apply steroids via epidural! to avoid systemic side effects
  2. surgical:
    laminectomy and discectomy +/- stabilization with screws and acrylic
  3. variable prognosis
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13
Q

describe the history and clinical signs and signalment of degenerative myelopathy

A

history:
1. slow, insidious onset (6-18 months)
2. chronic progressive
3. non-painful paraparesis

clinical signs:
1. slowly progressing paraparesis
2. T3-L3 myelopathy
3. occasional loss of patellar reflex

signalment:
1. highest incidence in boxer, then german shepherd, corgis rly only small breed affected with much significance
-any large breed dog
2. middle to older but really just older age
-older than 5 years, mean 9 years

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14
Q

describe diagnosis of degenerative myelopathy (4 plus a bonus 5th)

A
  1. signalment
  2. clinical signs
    -6-12 months: UMN paresis and GP ataxia
    -9-18 months: LMN paresis to paraplegia
  3. exclusion:
    -normal MRI
    -+/- increased protein lumbar CSF
    -not respond to OA treatment
  4. histopathology (post mortem)
  5. DM testing- Missouri
    -controversial genetic testing
    -just one more piece of evidence though, not definitive diagnosis
    -we’re not sure what to do with the test result yet though (not tested on for class)
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15
Q

describe treatment and prognosis of degenerative myelopathy

A

treatment:
1. none proven
2. controlled exercise to help with concurrent OA and maybe keep walking longer

prognosis:
1. poor long term
2. euthanized within 6-12 months

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16
Q

describe pug myelopathy/constrictive myelopathy/arachnoid diverticular

A
  1. T3-L3 myelopathy
  2. chronic; progressive (months)
  3. non painful
  4. OLD PUG
  5. fecal incontinence +/- urinary
    -normal perineal reflex, normal external sphincter and urethral sphincter tone
    -likely due to lack of sensory information getting to brain in time, so reflex part takes over and they go in the house
  6. tail dropped
  7. questionable response to medication

differentials:
1. IVDD: type II/chronic hansen
2. degenerative myelopathy
3. neoplasia

diagnostics:
1. rads of vertebral column
2. MRI: onion bulb/scallion of subarachnoid space; diverticulum of CSF within subarachnoid space
-results in fibrosis/constriction of leptomeninges
-definitive diagnostic tool!

treatment:
1. often irreversible, esp if gliosis
-can try anti-inflammatories but not really helpful
2. surgery:
-short term improvement but most deteriorate back to where they began in a year so discuss with owners if surgery is worth it (not a fix)

17
Q

describe the clinical signs of chiari-like malformation/caudal occipital malformation- also describe signalment

A

clinical signs:
1. cervical pain
2. tetraparesis (C1-C5 vs C6-T2)
3. unusual neurological signs
-scratching at the neck and ears but phantom scratching (foot doesn’t touch skin)
4. scoliosis

signalment:
1. cavalier king charles spaniel!! most common
2. any toy breed though

18
Q

describe the pathophysiology of caudal occipital malformation

A
  1. obstruction of CSF flow out of the foramen magnum causes syrinx formation in the spinal cord
    -syrinx is buildup of fluid within spinal cord
  2. scoliosis: dissection of syrinx through dorsal grey matter takes out sensory stuff on one side, animal turns to the other direction
  3. scratching: also due to same reason as scoliosis
19
Q

describe diagnosis of caudal occipital malformation

A
  1. MRI is the only way to diagnose!!
    -approx 70% of cavalier king charles spaniels have some degree of abnormality
20
Q

describe treatment of caudal occipital malformation

A
  1. medical: try first!
    -decrease CSF flow/production: omeprazole, acetozolamide
    -symptomatic: pain control if painful or scratching (gabapentin, pregabalin)
  2. surgery:
    -remove the obstruction
    -re-establish CSF
    -procedures: foramen magnum decompression, dorsal laminectomy C1, durotomy
21
Q

describe prognosis of caudal occipital malformation

A
  1. medical therapy: unknown/variable
  2. surgery: 60-80% improvement with a good possibility of recurrence
22
Q

describe the anatomy of the atlanto-axial region

A
  1. joint between C1 and C2
  2. dens: ventral process of C2, separate ossification center (sometimes never ossifies!); ligaments attach here
  3. 4 ligaments:
    -transverse
    -alar
    -apical (2)
23
Q

describe signalment and clinical signs and diagnostics of atlanto-axial subluxation

A

signalment:
1. toy breeds: yorkie!, chihuahua, poodle, pomeranian
2. no sex predilections
3. young age of onset (1-3 years)
-not enough time to have a degenerate nucleus that herniated
4. usually present after a little bit of trauma (jump off, bump into; lack of ossification allows rupture of ligaments or breaking of dens)

clinical signs: relatively sudden
1. cervical pain
2. C1-C6 myelopathy

diagnostics:
1. plain radiographs!
-lateral view most important

24
Q

describe treatment and prognosis of atlanto-axial subluxation

A

treatment:
1. surgical: preferred
-dorsal fixation
-ventral fixation

  1. medical:
    -cervical splinting to allow for some fibrosis
    -cage rest
    -big babushka wrap, some dogs don’t tolerate, but good less expensive option

prognosis:
1. independent of fixation: 60-80% improvement
2. depends on
-age: better when younger
-neurologic status

25
Q

describe congenital malformations (2)

A
  1. anomalies of vertebra or spinal cord
    -usually incidental findings with no clinical signs
  2. vertebral abnormalities:
    -pugs, bulldogs, boston terriers
    -hemivertebrae
    -block vertebrae
    -manx cat: sacrocaudal dysgenesis (we bred for it, oops)
  3. most common presentation: Spina Bifida L7/meningomyelocele
    -LMN S1-S3
    -when palpate spine, finger goes into a divot
    -tipoff is: “can’t housebreak puppy”
26
Q

what are the first diagnostic steps when you suspect neoplasia? (older dog, chronic progression

A
  1. radiographs of vertebral column
  2. radiographs of thorax (3 view)
    -assess for metastasis
  3. minimum database (CBC., chem, +/- urinalysis)

work most common to least common, outside to inside

27
Q

describe signalment and clinical signs of osteosarcoma

A
  1. older, large breed dogs

clinical signs:
1. variable
2. acute to progressive
3. painful
4. neuro deficits

diagnosis:
1. plain radiographs: lysis of vertebra
2. MRI
3. biopsy

28
Q

describe diagnostic steps when see monoparesis

A
  1. neurological exam!!
  2. minimum database
    -CBC, chem, UA +/- specialized testing based on results
  3. serological tests
  4. electrophysiology: microscopic evaluation
29
Q

describe neoplastic nerve sheath tumors

A
  1. nerve sheath neoplasms
    -unsure of cell of origin
  2. most cases malignant
  3. behave like sarcomas: locally aggressive, rarely metastasize

signalment:
1. older dogs (8-9 years) no breed or sex

history:
chronic, progressive, unilateral limb lameness

clinical signs:
1. unilateral lameness
2. pain in axilla (50%)
3. varying degrees of paresis
4. peripher vs. spinal cord (C6-T2 myelopathy)
5. lame gait but normal ortho exam

diagnosis:
1. strong clinical suspicion: old dog, progressive lame, can’t find ortho disease
2. electrodiagnostics: help support that is a neuro issue; maps out distribution
3. imaging

treatment:
1. surgery:
-amputation: can you get high enough to control?
-laminectomy
2. radiation

prognosis:
1. peripheral group: dies of other disease
2. plexus group:
-MST 11 months
-disease free. interval 6 months
3. root group:
-MST 5 months
-DFI 1 month

30
Q

describe nephroblastoma

A
  1. nephrologic tumor in meninges in young dogs!
  2. come in with T3-L3 myelopathy
  3. RARE
31
Q

describe discospondylitis pathology

A
  1. infection (likely hematogenous spread) of intervertebral disc and adjacent endplates
  2. blood supple to vertebral body ends in capillary beds in region of end plates; disc gets nutrients by diffusion through end plates; blood flow is slow so infection can settle
  3. most common source of infection is UTI
    -but could also be skin, heart valces, mouth
  4. etiology:
    -bacteria: STAPH, strep, E.coli, kelbsiella
    -brucella (ZOONOTIC = ALWAYS TEST FOR IF DOG)
    -fungal: apergillus (common in german shepherds and young dogs with IgA deficiency)
32
Q

describe signalment discospondylitis

A

signalment:
1. medium to giant breed
2. young to middle age
3. more males than females

clinical signs/history:

diagnosis:
1. plain radiographs-end plate lysis
-narrow disc space followed by lysis followed by sclerosis from inside to outside
2. CT/MRI
3. CBC, chem, urinalysis, urine culture
4. BRUCELLA TEST

treatment:
1. antimicrobials (8-12 weeks): ideally based on culture and sensitivity
-for staph:
–cephalosporins
–potentiated penicillins (amoxicillin/clavulonic acid)
2. cage rest
3. analgesics
-NSAIDs or opioids

prognosis:
1. good!
2. worse if serve neuro deficits, resistant bacteria, or fungal disease

33
Q

describe traumatic spinal fractures/luxations

A
  1. most occur at the junction of relatively stable and mobile portions of the vertebral column
    -thoracolumbar junction
    -lumbosacral junction
    -sacrococcygeal junction
    -cervical: C1 and C2 most commonly affected
  2. peracute
34
Q

FCEM

A

fibrocartilaginous embolic myelopathy

NSB II (17 decks)

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