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S&S - Exam 2 > SA myelopathies > Flashcards

SA myelopathies Flashcards

1
Q

Describe Schiff-Sherrington phenomena

A

Acute, severe lesion T3-L3; in lateral recumbency, px is flaccid in PLs and increased tone in TLs. When standing, px can use TLs fairly normal.

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2
Q

Where in the spinal cord is shock typically observed? What signs occur?

A

T3-L3 myelopathy; FLACCID paralysis in limbs caudal to lesion

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3
Q

What does each type function in?

Large, myelinated fibers:
Intermediately sized, myelinated fibers:
Small, central, un-myelinated fibers:

A

Large, myelinated fibers = proprioception (majority)

Intermediately sized, myelinated fibers = motor (middle)

Small, central, un-myelinated axons = nociception info (least)

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4
Q

Where in the body are the most common sources of pain / neurological deficits (5)?

A

Discs
Meninges
Muscles
Periosteum
Nerve Roots

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5
Q

What are examples of primary spinal cord injuries that cause compression, contusion, and increase spinal cord tissue pressure?

What are examples of secondary spinal cord injuries that further provoke cellular dysfunction and necrosis in tissues where primary injury has occurred?

A

Primary
- disc herniation; vertebral luxation; vascular injury (hemorrhage)

Secondary
- ischemia, neuroinflammation, excitotoxicity, edema

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6
Q

What breeds are most susceptible to IVDE (Type I) vs IVDP (Type II)?

A

IVDE = Chondrodystrophic dogs (short-legged dogs)

IVDP = Older, large-breed, non-chondrodystrophic dogs

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7
Q

Where is the genetic mutation of breeds most susceptible to IVDE?

A

chromosome 12 (CFA-12) = short legs + early chondroid metaplasia

beagles, frenchies, cocker spaniels; dachshunds, corgi, basset, pekinese

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8
Q

Describe pathophysiology of IVDE

A

Typically in the thoracolumbar region (T3-L3):
nucleus pulposus herniates dorsally –> tears through annulus fibrosis –> nucleus pulposus then abnormally sits in vertebral canal –> spinal cord becomes compressed

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9
Q

How is IVDE most commonly diagnosed? What method is not used for a definitive dx?

A

MRI or CT

Rads and CSF (b/c not very specific) not used for definitive dx

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10
Q

What is Extensive Epidural Hemorrhage Subtype?

A

When nucleus pulposus herniates dorsally, it tears the blood vessels running in the epidural space –> causes secondary hemorrhage

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11
Q

What is seen on images of IVDE?

A

mineralized disc material in the vertebral canal

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12
Q

When is it appropriate for the IVDE pt to be medically managed as a tx plan?

A

When pt is ambulatory, non-ambulatory with good motor function, responds well to tx

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13
Q

Stella: DX, TX, PROGNOSIS + RISKS

A

INTERVERTEBRAL DISC EXTRUSION (IVDE)
This specific case: Medical Management (suggest sx b/c non-ambulatory, but ō declined)
- Strict, prolonged (4-6 weeks) rest (to allow tear in annulus to heal)
- Analgesics (NSAIDs)

Prognosis:
- can do very well, but relapse is common. Pt MAY decline.

Risk = progressive myelomalacia developing

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14
Q

Barney’s dx, tx plan and prognosis?

A

Dx = IVDE

Tx = Surgical Management
- MRI or CT + surgery

Prognosis
- good-to-excellent (depending on grade)
- lower prognosis if pt is paraplegic and deep pain is negative

Risk = progressive myelomalacia developing (~10%)

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15
Q

Ascending-Descending Myelomalacia (Progressive Myelomalacia)
- Pathogenesis
- Risk Factors
- Clinical Signs
What is the prognosis / tx?

A
  • Severe progressive spinal cord disease, 2º to injury (IVDE, Type 1 / Hansen’s -> CHONDRODYSTROPHIC dogs!)
    Occurs within first 48-72 hrs post injury (jumping, landing, etc.)
    .
  • RFs: IVDE, lumbar injury
  • Pain, loss of abdominal tone, cranial progression of panniculus reflex, loss of PL reflexes and tone (as the disease progresses), eventually loss of TL function.
  • Tx = euthanasia
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16
Q

What is IVDP? What is the tx / prognosis?

A

Chronic progression; Protrusion of annulus fibrosis into vertebral canal; “cobble stone street”

Tx = medical mgmt. or sx; prognosis depends on grade of severity

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17
Q

What are the non-degenerative IVDD?

A

Acute Non-Compressive Nucleus Pulpous Extrusion (ANNPE), Hydrated Nucleus Pulpous Extrusion (HNPE)

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18
Q

ANNPE
- etiology
- clinical signs
-tx

A
  • Etiology: secondary to excessive force placed onto disc (vigorous exercise, trauma) -> tear in annulus fibrosis ->small fragment of nucleus pulposus herniates out and causes contusion (bruising) of SC -> peracute signs of spinal cord injury
  • Clinical signs: sudden pain during activity, dog may vocalize (pain only lasts minutes-hours); asymmetric lameness, NO progression of signs after 24-48 hrs

-Tx = analgesics, nursing care

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19
Q

Hydrated Nucleus Pulposus Extrusion (HNPE)
- pathogenesis
- signalement
- clinical signs
- lesion on MRI
-tx

A

Etiology: secondary to excessive force placed onto disc (vigorous exercise, trauma) -> tear in annulus fibrosis -> part of nucleus pulposus herniates out and causes contusion (bruising) and compression of SC -> peracute signs of spinal cord injury, USUALLY CERVICAL MYELOPATHY

  • Clinical signs: sudden pain during activity, dog may vocalize (pain only lasts minutes-hours); asymmetric lameness, NO progression of signs after 24-48 hrs
  • any age, cat/dog
  • MRI: lesion looks like a soaring bird!
    -Tx = analgesics, nursing care
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20
Q

Fibrocartilaginous Embolism (FCE) (Ischemic Myelopathy)?
- Signalement
- Pathogenesis
- Clinical Signs
- Tx

A
  • Mini Schnauzers predisposed; any age, Large-breed dogs
  • Piece of disc (fibrocartilage) embolizes SC vasculature -> blocks blood supply -> neuro signs
  • After running or playing; true pathogen. unknown
  • Peracute weakness, non-progressive after 24 hours. Non-painful spine, asymmetrical (one limb more affected)
  • Tx similar to ANNPE (analgesics, nursing care)
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21
Q

Pathophysiology of Fibrocartilaginous Embolism (FCE) (Ischemic Myelopathy)?

A

Piece of fibrocartilaginous (disc) embolizes the spinal cord vasculature.

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22
Q

ANNPE vs. IIVDE (Intradural / Intramedullary IVD)

A

IIVDE = variant of ANNPE where NON-DEGENERATE DISC RUPTURE in which the disc penetrates the dura and spinal cord (CAUSES COMPRESSION, CONTUSION, ETC.)

23
Q

Signalement and Hx of Degenerative Lumbosacral Stenosis (DLSS)?

A

German Shepherd, Malinois, working dogs; large-breed dogs

Hx: reluctance to jump or use stairs; lumbosacral pain; PL lameness; urinary and fecal incontinence

24
Q

Pathophysiology of Degenerative Lumbosacral Stenosis (DLSS)?

A

Multi-factorial!
IVDP, instability, transitional vertebrae, congenital stenosis, bony and/or soft tissue proliferations

25
Q

Degenerative Lumbosacral Stenosis (DLSS)? treatments?

A

Medical Management
- rest, PO meds
- possibly only short-term solution // prognosis

Surgical Management
- dogs that fail medical mgmt., more severe deficits
- good short term

26
Q

Signalement, hx, clinical signs for Degenerative Myelopathy (DM)? Patho physiology?

A

At least 5y/o, avg 9y/o; German shephers, GSD, corgi, rhodesian, boxer

T3-L3 myelopathy early disease; progressive, non painful

Free radical scavenger (genetic mutation to SOD1); progressive degeneration of white matter of SC (AXONS!)

Similar to ALS in humans (motor axon degeneration)

27
Q

How is a DDx for Degenerative Myelopathy determined? Prognosis?

A

POSTMORTEM – necropsy histo; primarily axonopathy, non-inflamm

FATAL prognosis b/c no tx!

28
Q

Why are both forms (osseous and disc) of Cervical Spondylomyelopathy (CSM) considered to have a DYNAMIC component?

A

CSM associated with NECK –> as CSM-patients’ neck moves, there are differences in the severity of the disease and how they affect the pt

29
Q

What is the signalment for disc-associated CSM? What region of the cervical spinal cord is most frequently affected?

A

Middle-aged, large-breed dogs (dobermans, weimaraners, etc.

Caudal cervical region; C6-C7

30
Q

What is the signalment for osseous-associated CSM? What region of the cervical spinal cord is most frequently affected?

A

Young, giant-breed dogs (great danes, mastiffs, etc.)

Absolute stenosis of vertebral canal

31
Q

Pathogenesis of CSM-OA?

A

Dorsal or lateral bone compresses vertebral canal / SC -> absolute stenosis

32
Q

When is medical management vs. surgery preferred for tx for CSM?

A

Medical Mgmt: mildly affective animals, non-progressive CSM

Sx: severely affected, progressive CSM

33
Q

Signalement for anomalous (congenital) Atlantoaxial Instability (AAI)?

A

Anomalous (congenital) AAI:
- young, small or toy-breed dogs (chihuahuas, yorkies)

34
Q

Atlantoaxial Instability (AAI) affects what region of spinal cord, and presents with what clinical signs?

A

C1-C5 myelopathy, with cervical (neck) pain
-> pain may be intermittent

35
Q

Why should you never perform cervical ventroflexion on a small/toy-breed dog presenting with cervical pain?

A

If pt has AAI, cervical ventroflexion can cause worsening clinical signs and even death!

36
Q

What structure missing? How can you tell? What do these findings indicate?

A

Cervical dens –> cranial aspect of C2 is rounded out/smooth (ABNORMAL!) –> –> AAI

37
Q

What worsens the prognosis for medical management tx of Anomalous AAI?

A

High recurrence rate

38
Q

Risks of surgical mangement tx for AAI?

A

Death (putting in pins close to brainstem) and implant infections

39
Q

How do vertebral anomalies develop (block, hemi, wedge, butterfly)?

What SC region is most susceptible? What dog breeds? Are there usually clinical signs? Possible sequela?

A

Bones develop in growing dog -> one of the centers of ossification don’t develop properly -> which center dictates which anomaly forms

T7-T12!
Screwtail breeds (bulldogs), pugs
Typically no clinical signs. MAY cause myelopathy via SC compression!

40
Q

What can this severe vertebral anomaly cause?

A

Image: severe hemi vertebra -> kyphosis -> can cause myelopathy due to SC compression

41
Q

How does spina bifida arise?

A

Deficit in neural tube development.

42
Q

Classic signalment and clinical signs for spinal bifida-myelomeningocele?

A

young english bulldogs, manx cats; LMN signs

43
Q

Signalement, clinical signs and pathophysiology of Caudal Articular Process dysplasia (CAP dysplasia)

A

PUGS
Signs: may causes none; fecal and urinary incontinence

Pathophysiology: congenital vertebral malformation resulting from failure of ossification centers in articular processes of vertebrae -> aplasia (never develops) or hypoplasia (underdeveloped)
–> T10-T13

CT image: A&C = normal, B&D = CAP dysplasia

44
Q

What vertebral anomaly is typically presented with T3-L3 myelopathy?

A

Insidious-onset Caudal Articular Process (CAP) dysplasia

45
Q

Following Pts present with chronic, progressive myelopathy:

Rotweiller: cervical region
Pugs: thoracolumbar region

Dx tests / official dx?
Tx plan:

A

Spinal Arachnoid Diverticulum (SAD)
-> fluid-filled CYST -> CAUSES DILATION in subarachnoid space that causes SC compression

Dx: CT, CT w/ myelogram; MRI

teardrop-shaped dilated subarachnoid
Tx = surgery (open the cyst + drain)

46
Q

Caudal Occipital Malformation Syndrome (a malformation of the skull) causes Chari-like Malformation and/or Syringomyelia in Cavalier King Charles Spaniels. What are the pathophysiologies of the two?

A

Charli-like Malformation: skull too small to accommodate brain -> cerebellum starts to protrude/herniate out of foramen magnum (severe)

Syringomyelia: Fluid dilation of central canal of the SC

47
Q

What category of neoplasia would you see meningiomas and peripheral nerve sheath tumors?

A

Intradural–Extramedullary

must be within this region b/c the dura layer is continuous with the meningeal layer of the brain at the foramen magnum (hole of CNS that connects brain w/ spinal cord)

48
Q

What category of neoplasia would you see osteosarcoma or chondrosarcoma in the vertebrae?

A

Extradural

49
Q

What category of neoplasia would you see gliomas or ependymomas in the spinal cord?

A

Intramedullary

50
Q

Meningomyelitis is typically an _______-caused disease.

A

immune-mediated

(Infectious cause = UNCOMMON FOR MENINGOMYELITIS!)

51
Q

Pathogenesis of discospondylitis? Dx method? Prognosis?

A

Destruction/infection of vertebral endplates pathogens like staph, strep, E. coli, brucella, aaspergillus in large/giant breeds (males > females)

Dx = Radiographs, CBC/Chem, Culture
-> does not typically cause neurological deficits (b/c inflammation is of disk, not SC)

Bacterial: good prog (abx)
Fungal: poorer prog (no abx tx)

52
Q

Make the diagnosis and treatment plan.

Dog < 2 years of age, large-breed dog or beagle with acute (< 1 month duration) cervical pain, lethargy, stiff gait. Normal neuro exam. Marked neutrophilia in CSF analysis, thickened meninges in MRI.

A

Steroid Responsive Meningitis Arteritis (SRMA)

Tx = corticosteroids (immune suppression)

Immune-mediated inflammatory disease of CNS. Immune system causes inflammation of leptomeninges (arachnoid + pia layers) + associated arteries.

53
Q

What condition would you perform an abbreviated neurologic exam, and why? What is the etiology of this condition?

A

Vertebral Fracture/Luxation -> b/c GOAL is to NOT make the Pt any worse (most likely has other injuries occurring)

Etiology = trauma (HBC, fights, etc.)

54
Q

Signalment and clinical signs of Sacrocaudal Luxation (“Tail Pull”). Tx?

A

Outdoor cats of any age; plantigrade stance or paraparesis, paralyzed or flaccid tail

Tx: cage rest + analgesics; tail amp if no recovery

S&S - Exam 2 (16 decks)

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