Spine trauma: Difference between revisions
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# Pathophysiology | |||
| Injury Phase | Time Relative to Primary Injury | Key Processes and Events | | | Injury Phase | Time Relative to Primary Injury | Key Processes and Events | | ||
| --- | --- | --- | | | --- | --- | --- | | ||
| Immediate | <2 hours | | | Immediate | <2 hours || | ||
| Early acute | <48 hours | | | Early acute | <48 hours | | ||
Revision as of 13:12, 3 February 2024
- Pathophysiology
| 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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