Traumatic spinal cord injury produced by controlled contusion in mouse

Previous work from this laboratory has described a rat spinal cord injury ( SCI) model in which the mid-thoracic spinal cord is subjected to a single r apid and calibrated displacement at the site of a dorsal laminectomy. Injur y is initiated at the tip of a vertical shaft driven by an electromagnetic shaker. Transducers arranged in series with the shaft record the patterns o f displacement and force during the impact sequence. In the present study, this device and the relevant surgical procedures were adapted to produce a spinal contusion injury model in laboratory mice. The signal generator for the injury device has also been converted to a computer-controlled interfac e to permit extension of the model to other laboratories. Mice were subject ed to SCI across a range of severities by varying the amplitude of displace ment and the magnitude of measured preload force on the dural surface. A mo derate injury produced by displacement of 0.5 mm over 25 msec resulted in i nitial paralysis and recovery of locomotion with chronic deficits in hindli mb function. The magnitude of the peak force, impulse, power, and energy ge nerated at impact were correlated with behavioral outcome at 1 day postinju ry, while peak displacement and impulse were the best predictors of behavio ral outcome at 28 days postinjury. The shape of the force recording proved to be a highly sensitive measure of subtle variations in the spinal compart ment that were otherwise difficult to detect in this small species. The res ults demonstrate that the electromagnetic spinal cord injury device (ESCID) can be used to produce a well-controlled contusion injury in mice. The uni que features of controlled displacement and monitoring of the biomechanical parameters at the time of impact provide advantages of this model for redu cing outcome variability. Use of this model in mice with naturally occurrin g and genetically engineered mutations will facilitate understanding of the molecular mechanisms of pathophysiology following traumatic spinal cord in jury.