Spinal Injury
Basic Information 
Clinical Presentation
Disease Forms/Subtypes
• Acute SCI: Such as seen after trauma
• Chronic SCI: Chronic phase of acute SCI or chronic or gradual onset of SCI such as seen in cervical vertebral stenotic myelopathy
• Cervical fractures most common
• Foals: C1-C3 and T15-T18 regions most commonly affected
• Adults: Occipital-atlanto-axial region and C5-T1 and caudal thoracic region
Etiology and Pathophysiology
• The severity of SCI is related to the velocity, degree, and duration of impact.
• Cord concussion with transient neurologic deficits is a result of local axonal depolarization and transient dysfunction.
• Permanent paralysis is a result of primary tissue injury followed by spreading of secondary damage.
• Primary damage: Initial mechanical disruption of vasculature and components of the CNS, such as cell bodies (neurons, astrocytes, oligodendrocytes) and axons.
• Secondary damage: A complex cascade of molecular, cellular, and biochemical events that may occur for days to months after the initial insult, resulting in delayed tissue damage and enlargement of the damaged area.
• Systemic alterations such as systemic hypotension further contribute to the tissue damage: Hypoxia, ischemia, infection, breakdown of blood-brain barrier, impaired energy metabolism, altered ionic homeostasis, changes in gene expression, inflammation, and activation or release of autodestructive molecules occur and exacerbate the initial injury.
• Ischemia is exacerbated by spinal cord swelling (hematomas, edema) and cessation of autoregulation of spinal cord blood flow and systemic hypotension.
• Excitotoxicity refers to the deleterious cellular effects of excess glutamate and aspartate. When released, these neurotransmitters activate NMDA (N-methyl-d-aspartic acid) and AMPA (α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate) receptors and lead to release of massive amounts of calcium from intracellular stores. Elevation of intracellular calcium concentrations can trigger a multitude of processes that can lethally alter cellular metabolism, generate free radicals, impair mitochondrial function, cause vascular smooth muscle spasm, and bind phosphates.
• Apoptosis, or programmed cell death, is a slowly spreading form of cell death induced by injury. Apoptosis occurs mostly at the lesion margins and at quite remote distances from the point of impact in areas with degenerating axons that were injured at the original lesion site.
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