SA myelopathies Flashcards by Kate Karlen

Describe Schiff-Sherrington phenomena

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

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

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What does each type function in?

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

Large, myelinated fibers = proprioception (majority)

Intermediately sized, myelinated fibers = motor (middle)

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

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

Discs
Meninges
Muscles
Periosteum
Nerve Roots

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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?

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

Secondary
- ischemia, neuroinflammation, excitotoxicity, edema

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

IVDE = Chondrodystrophic dogs (short-legged dogs)

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

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

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

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

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Describe pathophysiology of IVDE

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

MRI or CT

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

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What is Extensive Epidural Hemorrhage Subtype?

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

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What is seen on images of IVDE?

mineralized disc material in the vertebral canal

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

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

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Stella: DX, TX, PROGNOSIS + RISKS

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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Barney’s dx, tx plan and prognosis?

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

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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What is IVDP? What is the tx / prognosis?

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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What are the non-degenerative IVDD?

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

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ANNPE
- etiology
- clinical signs
-tx

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

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

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

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

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ANNPE vs. IIVDE (Intradural / Intramedullary IVD)

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

Signalement and Hx of Degenerative Lumbosacral Stenosis (DLSS)?

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

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

Pathophysiology of Degenerative Lumbosacral Stenosis (DLSS)?

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

Degenerative Lumbosacral Stenosis (DLSS)? treatments?

Medical Management - rest, PO meds - possibly only short-term solution // prognosis Surgical Management - dogs that fail medical mgmt., more severe deficits - good short term

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

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)

How is a DDx for Degenerative Myelopathy determined? Prognosis?

POSTMORTEM -- necropsy histo; primarily axonopathy, non-inflamm FATAL prognosis b/c no tx!

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

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

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

Middle-aged, large-breed dogs (dobermans, weimaraners, etc. Caudal cervical region; C6-C7

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

Young, giant-breed dogs (great danes, mastiffs, etc.) Absolute stenosis of vertebral canal

Pathogenesis of CSM-OA?

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

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

Medical Mgmt: mildly affective animals, non-progressive CSM Sx: severely affected, progressive CSM

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

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

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

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

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

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

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

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

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

High recurrence rate

Risks of surgical mangement tx for AAI?

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

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?

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!

What can this severe vertebral anomaly cause?

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

How does spina bifida arise?

Deficit in neural tube development.

Classic signalment and clinical signs for spinal bifida-myelomeningocele?

young english bulldogs, manx cats; LMN signs

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

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

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

Insidious-onset Caudal Articular Process (CAP) dysplasia

Following Pts present with chronic, progressive myelopathy: Rotweiller: cervical region Pugs: thoracolumbar region Dx tests / official dx? Tx plan:

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)

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?

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

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

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)*

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

Extradural

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

Intramedullary

Meningomyelitis is typically an _______-caused disease.

immune-mediated (Infectious cause = UNCOMMON FOR MENINGOMYELITIS!)

Pathogenesis of discospondylitis? Dx method? Prognosis?

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)

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.

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.

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

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.)

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

Outdoor cats of any age; plantigrade stance or paraparesis, paralyzed or flaccid tail Tx: cage rest + analgesics; tail amp if no recovery