canis - Articles
Spinal cord: concussion
Synonym(s): Spinal cord trauma, spinal cord contusion
Introduction
- Spinal trauma is a common cause of spinal cord dysfunction in dogs and cats.
- Spinal trauma can occur either from exogenous or endogenous spinal injury.
- Cause: exogenous trauma, type I or type II intervertebral disk herniation, acute non-compressive nucleus pulposus disk extrusion.
- Signs: depend on severity of inciting trauma.
- Autodestructive mediators come into play within minutes of trauma and persist for several days.
- Treatment: high dose methylprednisolone succinate.
- Prognosis: guarded - other life-threatening injuries may be present if exogenous trauma involved.
Presenting signs
- Combination of upper motor neuron (UMN), and/or lower motor neuron (LMN), signs.
Acute presentation
- Always acute presentation; slow progressive lesions cause cord degeneration not contusive injury.
Breed/Species predisposition
- Chondrodystrophic breeds predisposed to type I disk disease Intervertebral disk: type 1 herniation.
- Large breeds with predisposition to fibrocartilagenous embolism Fibrocartilaginous embolism.
Special risks
- If the animal is struggling to move it should be immediately restrained.
- This can be accomplished by firmly taping the animal to a rigid back-board or similar structure.
- If a thoracolumbar vertebral trauma is suspected, the animal can be secured with white tape placed over the scapular and femoral trochanter regions.
- If a cervical injury is suspected, the head should be additionally secured.
- Any rigid surface that is movable can be used to support the spine during manipulations and movement:
- A board 8-10 " in width, 4-5' in length and 3/4-1" in thickness works well.
- Handles can be attached to make it easier to move the board from flat surfaces such as floors.
- It is also helpful to record the weight of the board.
- With this information, an accurate bodyweight can then be recorded on the animal even after it has been immobilized.
- Sedation or anesthesia result in loss of voluntary paraspinal muscle contraction and unstable vertebral segments may be more likely to subluxate.
- If caused by external trauma investigate for other life-threatening injuries.
Pathogenesis
Etiology
- Automobile trauma.
- Fall.
- Trauma from falling object.
- Projectile missile damage, eg gunshot.
- Depending upon the position of the animal, the type of force, area of impact and the inherent strengths and weaknesses of the vertebral column, exogenous spinal injury may result in spinal cord concussion.
- Endogenous trauma: disk herniation or acute non-compressive nucleus pulposus extrusion Spinal cord: acute non-compressive nucleus pulposus extrusion.
Specific
- Chondrodystrophic breeds predisposed to type I disk disease.
- Large breeds with a higher incidence of fibrocartilagenous embolism.
Pathophysiology
- Because the spinal cord is encircled by a rigid, inelastic bony encasement (vertebrae), and because of relatively soft texture of spinal parenchyma, any change in canal diameter results in spinal cord injury.
- Mechanical injury to nervous tissue (especially axons), results in physiologic or morphologic disruption of nervous impulses.
- Ultimately, numerous pathophysiological consequences may evolve including ischemia, hemorrhage, alterations in spinal cord blood flow and edema.
- These secondary events lead to a self-perpetuating process of damage to the spinal cord that often is equally, if not more, detrimental to the spinal cord than the initial mechanical injury (second injury theory).
- Detrimental events are initiated by the mechanical insult, which causes the release of neurotransmitters, damage to glial and neuronal membranes and damage to the local vasculature → energy failure and increased cell membrane permeability → cascade of events including destruction of the microvascular bed → reduction in perfusion of the injured area → increase in intracellular calcium concentration → free radical production → expanding zone of cellular necrosis and apoptosis.
- Inciting agent → inflammatory reaction in cord (swelling, hemorrhage, edema) → autodestructive process in nerve tissue that exacerbates initial damage → increased intracord pressure → transmitted centripetally into the grey matter → high metabolic requirement of injured tissue may not be met.
- Severe cases will also have necrosis of surrounding white matter.
- May also get primary demyelination of white matter → impaired impulse conduction but with axonal preservation.
- Mediators: free radicals, free fatty acids, arachidonic acid metabolites, endogenous opioids and monoamines.
- Other metabolic changes: loss of calcium from and accumulation of potassium in the extracellular space, loss of high energy phosphates, lactic acidosis, reduced intracellular pH.
- Severe cord contusion may → ascending syndrome Diffuse progressive myelomalacia.
Timecourse
- Acute onset.
- Majority of secondary damage occurs within 24 hours of injury and, although cellular apoptosis continues for weeks to months, it is not common for clinical signs of deterioration to be evident much beyond 72 hours following injury.
Diagnosis
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Treatment
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