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spinal cord injury
from spine fracture/dislocation at speeds greater than 10 ft/s or 7mps or 3ms; lumbar spine fracture at speeds greater than 25 ft/s or 17 mph or 7.5 m/s
primary SCI
occurs at moment of impact, caused by mech forces (compression/contusion/dislocation/hyperextension), results in immediate physical damage to SC tissue
secondary injury
initiated by primary, biochemical/cellular response (schema, hypoxia, inflammation, ionic imbalance (Ca2+ influx), excitotoxicity (glutamate), free radical production, apoptosis); hours to years
cadaveric SCI pros
realistic anatomy and tissue geometry, accurate vertebral cord interactions, allows direct measurement of SC deformation, compression magnitude, injury kinematics
cadaveric SCI cons
no physiological response (no healing, infallamation, blood flow), limited sample size/high variability, ethical/logistics/cost, cannot model secondary fully
Viscous response
Reflects how the SC responds to rate-dependent loading
Calculated used velocity of SC compression during impact
Higher compression velocities → worse neurological outcomes
Reported alongside: max compression, max compression
Estimating SC compression
Cadaveric cervical spine experiments w/ surrogate SC (silicone and barium sulfate), high speed x-ray imaging (1000fps), head-first exile impact simulated using drop tower (impact speed = 3.0 m/s), SC compression measured directly from x-ray image sequences, change in cord cross-section/profile during impact
Atlanto-axial dislocation
produces greater compression; compared to hyperextension injuries, max compression @ 12 ms, compression = transient