Spine trauma

Pathophysiology

Injury Phase	Time Relative to Primary Injury	Key Processes and Events
Immediate	<2 hours	Primary mechanical injury (severing of axons) Gray matter hemorrhage and ischemia Microglial activation Release of pro-inflammatory factors (IL-1β, TNFα, IL-6)
Early acute	<48 hours	Vasogenic and cytotoxic edema ROS production, lipid peroxidation Glutamate-mediated excitotoxicity Continued hemorrhage, ischemia, and necrosis Neutrophil invasion Peak BSCB permeability Early demyelination (oligodendrocyte death) Neuronal death Axonal swelling Systemic events (systemic shock, spinal shock, hypotension, hypoxia)
Subacute	<14 days	Macrophage infiltration Initiation of astroglial scar (reactive astrogliosis) BSCB repair and resolution of edema
Intermediate	<6 months	Continued formation of glial scar Cyst formation Lesion stabilization
Chronic	>6 months	Prolonged Wallerian degeneration Persistence of spared, demyelinated axons Potential structural and functional plasticity of spared spinal cord tissue

| Injury Phase | Time Relative to Primary Injury | Key Processes and Events | | --- | --- | --- | | Immediate | <2 hours || | Early acute | <48 hours |

- Vasogenic and cytotoxic edema - ROS production, lipid peroxidation - Glutamate-mediated excitotoxicity - Continued hemorrhage, ischemia, and necrosis - Neutrophil invasion - Peak BSCB permeability - Early demyelination (oligodendrocyte death) - Neuronal death - Axonal swelling - Systemic events (systemic shock, spinal shock, hypotension, hypoxia)

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| Subacute | <14 days |

- Macrophage infiltration - Initiation of astroglial scar (reactive astrogliosis) - BSCB repair and resolution of edema

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| Intermediate | <6 months |

- Continued formation of glial scar - Cyst formation - Lesion stabilization

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| Chronic | >6 months |

- Prolonged Wallerian degeneration - Persistence of spared, demyelinated axons - Potential structural and functional plasticity of spared spinal cord tissue

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