Spinal cord injury

Question 1

Define spinal shock

Answer 1

Spinal shock is the transient loss of muscle tone and segmental reflexes caudal to an acute spinal cord injury/ flaccid paralysis of the limbs below the site of
injury

Question 2

What do you clinically see with a T3-L3 injury?

Answer 2

paraparesis, UMN signs and proprioceptive deficits HLs

Question 3

What do you clinically see with spinal cord shock at T3-L3?

Answer 3

flaccid paralysis of the pelvic limbs

Question 4

How can spinal shock be appreciated on physical exam?

Answer 4

It is appreciated on clinical
examination by noting LMN signs (decreased/absent reflexes) in a patient with an otherwise UMN spinal cord localization.
Results of LMN disfunction

Question 5

What is the rate of recovery from spinal shock (how long)?

Answer 5

This typically lasts for 12 hours or less but may be apparent for 12–48 hours (weeks on SACCM)

Question 6

What is myelomalacia?

Answer 6

progressive condition caused by an impaired blood supply to the spinal cord after an injury

Question 7

How can you distinguish between myelomalacia and spinal shock? What carries poorer prognosis?

Answer 7

• Spinal shock reflex deficits are often partial (i.e., absent flexion/
  withdrawal but present tendon reflexes) and may be asymmetric, VS loss of reflexes with myelomalacia tends to be complete in
  both limbs.
• Patients with myelomalacia will not have deep pain perception.
• Patients with spinal shock may also not have deep pain perception,
  depending on the severity of the lesion, but will have improvement of reflexes and tone to be more consistent with an UMN lesion, even if the spinal cord is functionally transected

Question 8

Define primary and secondary injury

Answer 8

Primary injury: event that causes the initial
spinal cord trauma; considered irreversible; traumatic vs nontraumatic; mechanical forces involved = concussion, compression, shear, laceration, distraction, and contusion.

Secondary injury: molecular and biochemical events that occur following the primary injury

Question 9

Describe the different types of IVDD

Answer 9

Hansen type I: rupture of the annulus fibrosus and subsequent extrusion of the degenerated nucleus pulposus into the vertebral canal;
Hansen type II: dorsal protrusion of the annulus fibrosus that causes a progressive compression;
ANNPE/Hansen type III: acute noncompressive
nucleus pulposus extrusion, high-velocity
extrusions that cause contusion of the spinal cord without any obvious persistent compression

Question 10

T1 weighted images are the best to diagnose IVDD on MRI. T/F

Answer 10

F. T2

T1: fat hyperintense, fluid hypointense, contrast enhancing tissues hyperintense

T2: fat and fluid hyperintense. Used for pathologies.

FLAIR (fluid attenuated inversion recovery): fluid is suppressed and becomes hypointense.

STIR (short tau inversion recovery): fat is suppressed. Used in ortho and spinal.

Question 11

How does IVDD look like on x-rays and MRI?

Answer 11

Rads: narrowing or wedging of the disk space, calcified material within the disk space, and narrowing of intervertebral foramen.

MRI: focal hyperintensity
overlying an IVD on T2-weighted images,
narrowed intervertebral space, reduction in volume and signal intensity of the nucleus pulposus on T2-weighted images, and extruded material within the epidural space
dorsal to an affected disk site

Question 12

Describe the three-compartmentmodel
utilized to describe
the anatomy of the vertebrae

Answer 12

Disruptions in any 2 of the 3 compartments will result
in instability.

Dorsal compartment: articular process, dorsal laminae, pedicles, and the
spinous process.

Middle compartment: dorsal longitudinal ligament and the dorsal portion of both the vertebral body and the annulus fibrosus.

Ventral compartment: ventral longitudinal
ligament, nucleus pulposus, and the remaining portions of both the annulus fibrosus and vertebral body.

Question 13

What is the pathophys behind FCE?

Answer 13

Controversial,several hypotheses:

• direct penetration of nucleus pulposus fragments into the spinal cord or its vascular
  system
• chronic inflammatory neovascularization of
  the degenerated intervertebral disk
• embroyonic remnant
  vessels within the nucleus pulposus
• entrance of fibrocartilage into the spinal cord vasculature
• mechanical herniation of nucleus pulposus into the vertebral bone marrow sinusoidal venous channels with retrograde entrance into the basivertebral vein and intervertebral vein plexuses.

Question 14

T/F. Gray matter is more susceptible to ischemic injury than white matter

Answer 14

T.

Question 15

What is gray matter vs white matter?

Answer 15

Gray matter: made up of neuronal cell bodies

White matter: primarily consists of myelinated axons.

In the brain, white matter is found closer to the center of the brain, whereas the outer cortex is mainly grey matter. The reverse is true in the spinal cord, which has a grey matter-lined interior with white matter on the outside.

Question 16

What area is more commonly affected by FCE according to literature?

Answer 16

caudal lumbar area

Question 17

What are the main mechanisms involved in secondary spinal cord injury?

Answer 17

• Vascular damage and loss of autoregulation:
• Upregulation of the gene Trpm4 following primary injury= leads to molecular changes including ion entry, oncotic swelling, and neuronal cell death.
• Excessive release of the excitatory neurotransmitters
  aspartate+ glutamate
• Intracellular neuronal calcium accumulation
• Cellular damage from the production of ROS
• The inflammatory response to acute spinal cord injury

Question 18

How does excessive release of glutamate and aspartate occur after neuronal injury?

Answer 18

Excessive release of glutamate and aspartate occurs after neuronal injury due to leakage from damaged neurons and depolarization-induced release.

Hypoxia = no ATP = impaired astrocyte-mediated reuptake of these neurotransmitters from the extracellular compartment.

Question 19

What does activation of glutamate receptors results in?

Answer 19

excess sodium
entry into neuronal cells. Low ATP concentrations from local tissue hypoxia decrease the ability of the Na+-K+ ATPase to pump sodium out of the cell, resulting in sodium accumulation and cytotoxic edema

Question 20

What happen with increased intracell Na?

Answer 20

Increases in the amount of intracellular sodium cause
activation of the Na+-Ca2+ exchanger, resulting in
an increase in neuronal intracellular calcium

Question 21

What does intracell Ca accumulation lead to?

Answer 21

• formation of oxygen-free radical species
  and lipid peroxidative damage
• major factor in apoptosis
  and cell death
• Calcium-mediated activation of
  phospholipase A2 also results in induction of the
  arachidonic acid cascade, leading to the production of inflammatory mediators and further perpetuation of cellular injury

Question 22

What are the mechanisms behind the production of ROS in spinal injury?

Answer 22

ischemia-reperfusion
injury, increased intracellular calcium, glutamate accumulation, and the presence of iron and copper complexes found in petechial hemorrhages

Question 23

How do ROS cause damage?

Answer 23

through lipid peroxidation of lipid rich membranes.
ROS are also involved in oxidative damage to protein and nucleic acids as well as inhibition
of mitochondrial respiration15 that canworsen ischemia

Question 24

Describe the biphasi immunologic response that occurs in acute spinal
cord injury.

Answer 24

First phase: neutrophils recruitment= further free radical production,
direct parenchymal damage by proteolytic enzyme release, and by ischemic damage through capillary plugging.

Secondary phase: macrophage recruitment and migration

Question 25

What proteins have been identified to
increased in concentration and exacerbate secondary injury in dogs with IVDD?

Answer 25

• Myelin basic-protein (MBP): increases >3 nM/mL in the CSF of affected dogs
  has been suggested as a poor prognostic indicator of functional recovery following injury
• matrix metalloproteinase-9 (MMP-9) activity= associated with disruption
  of the spinal cord blood barrier following acute
  injury

Question 26

What are the currently validated scoring systems to assess the neurologic status of patients experiencing spinal cord injury?

Answer 26

• Modified Frankel Score
• 14-Point Motor Score
• Texas Spinal Cord Injury Score

Question 27

What are the principal benefits of corticosteroids in acute spinal injury?

Answer 27

• free-radical scavenging properties
• antiinflammatory
  effects (inhibiting the arachidonic acid cascade via inhibition of the enzyme Phospholipase A2)
• preservation of spinal cord blood flow

Question 28

What is the most studied corticosteroid in acute spinal cord injury and why?

Answer 28

Methylprednisolone due to its free-radical scavenging
effects. These effects were demonstrated to be absent
with both prednisone and dexamethasone.

Question 29

T/F: in a clinical trial, methylprednisolone
was suggested to have beneficial effects if administered
within 24 hours of the initial injury

Answer 29

F: within 8h

Question 30

What could be side effects of therapeutic hypothermia?

Answer 30

bradycardia, hypotension, cardiac arrhythmias,
tissue hypoxia due to shifting of the oxygen–dissociation curve to the left, impairing of the immunologic system,
and coagulation abnormalities

Question 31

How is polyethilen glycole supposed to help with spinal cord injury?

Answer 31

(kinda like sucralfate for GI tract)
Polyethylene glycol is a hydrophilic polymer compound
that is capable of repairing damaged cell membranes.
The mechanism by which polyethylene glycol acts is
through sealing breaks along neuronal cell membranes
that occur as a result of mechanical damage. It is
theorized that exposing neurons to this sealing property spares much of the damaging effects of secondary injury including ion channel abnormalities, exposure to inflammatory mediators, and exposure to ROS.
Was safe in a study of dogs with IVDD given IV