Felis ISSN 2398-2950

Spinal cord: concussion

Synonym(s): Spinal cord trauma, spinal cord contusion

Contributor(s): Agnes Delauche, Laurent Garosi

Introduction

  • Trauma to the spinal cord induces a sequence of pathological events that leads to paralysis, tissue necrosis and cellular apoptosis.
  • 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.
  • Diagnosis: history, signs, CSF analysis, diagnostic imaging.
  • Treatment: high-dose methylprednisolone succinate.
  • Prognosis: guarded - other life-threatening injuries may be present if exogenous trauma involved.

Pathogenesis

Pathophysiology

  • 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, ischemia)   →   autodestructive process in nerve tissue that exacerbates initial damage   →   increased intracord pressure   →   transmitted centripetally into the gray matter   →   high metabolic requirement of injured tissue may not be met.
  • Severe cord concussion may   →   ascending syndrome.
  • Mediators: endogenous opioids Analgesia: opioid, serotonin, glutamate, aspartate, monoamines, free radicals, free fatty acids and arachidonic acid metabolites.
  • 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.

Timecourse

  • 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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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Olby N (2010) The pathogenesis and treatment of acute spinal cord injuries in dogs. Vet Clin Small Anim 40 (5), 791-807 PubMed.
  • Bruce C W, Brisson B A, Gyselinck K (2008) Spinal fracture and luxation in dogs and cats: a retrospective evaluation of 95 cases. Vet Comp Orthop Traumatol 21 (3), 280-284 PubMed.
  • Olby N, Levine J, Harris T et al (2003) Long term functional outcome of dogs with severe thoracolumbar spinal cord injuries: 87 cases (1996-2001). JAVMA 222 (6), 762-769 PubMed.
  • Bagley R S, Cambridge A J, Harrington M L et al (1999) Exogenous spinal trauma - clinical assessment and initial management. Comp Contin Educ Pract Vet 21 (12), 1138-1144 VetMedResource.
  • Shores A (1992) Spinal trauma. Pathophysiology and management of traumatic spinal injuries. Vet Clin North Am Small Anim Pract 22 (4), 859-888 PubMed.
  • Katayama Y, Glisson J D, Becker D P et al (1985) Concussive head injury producing suppression of sensory transmission within the lumbar spinal cord in cats. J Neurosurg 63 (1), 97-105 PubMed.


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