Spinal cord injury Flashcards
Define spinal shock
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
What do you clinically see with a T3-L3 injury?
paraparesis, UMN signs and proprioceptive deficits HLs
What do you clinically see with spinal cord shock at T3-L3?
flaccid paralysis of the pelvic limbs
How can spinal shock be appreciated on physical exam?
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
What is the rate of recovery from spinal shock (how long)?
This typically lasts for 12 hours or less but may be apparent for 12–48 hours (weeks on SACCM)
What is myelomalacia?
progressive condition caused by an impaired blood supply to the spinal cord after an injury
How can you distinguish between myelomalacia and spinal shock? What carries poorer prognosis?
- 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
Define primary and secondary injury
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
Describe the different types of IVDD
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
T1 weighted images are the best to diagnose IVDD on MRI. T/F
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.
How does IVDD look like on x-rays and MRI?
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
Describe the three-compartmentmodel
utilized to describe
the anatomy of the vertebrae
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.
What is the pathophys behind FCE?
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.
T/F. Gray matter is more susceptible to ischemic injury than white matter
T.
What is gray matter vs white matter?
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.
What area is more commonly affected by FCE according to literature?
caudal lumbar area
What are the main mechanisms involved in secondary spinal cord injury?
- 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
How does excessive release of glutamate and aspartate occur after neuronal injury?
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.
What does activation of glutamate receptors results in?
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
What happen with increased intracell Na?
Increases in the amount of intracellular sodium cause
activation of the Na+-Ca2+ exchanger, resulting in
an increase in neuronal intracellular calcium
What does intracell Ca accumulation lead to?
- 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
What are the mechanisms behind the production of ROS in spinal injury?
ischemia-reperfusion
injury, increased intracellular calcium, glutamate accumulation, and the presence of iron and copper complexes found in petechial hemorrhages
How do ROS cause damage?
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
Describe the biphasi immunologic response that occurs in acute spinal
cord injury.
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
