Sustained spinal cord compression: part I: time-dependent effect on long-term pathophysiology.

BACKGROUND: The objective of this study is to determine whether there is a relationship between the duration of sustained spinal cord compression and the extent of spinal cord injury and the capacity for functional recovery after decompression. METHODS: Sixteen dogs underwent sustained spinal cord compression for thirty or 180 minutes. The cords were compressed with use of a loading device with a hydraulic piston. A pressure transducer was attached to the surface of the piston, which transmitted real-time spinal cord interface pressures to a data-acquisition system. Somatosensory evoked potentials were monitored during a sixty-minute recovery period as well as at twenty-eight days after the injury. Functional motor recovery was judged throughout a twenty-six-day period after the injury with use of a battery of motor tasks. The volume of the lesion and damage to the tissue were assessed with both magnetic resonance imaging and histological analysis. RESULTS: Sustained spinal cord compression was associated with a gradual decline in interface pressure. Despite this, there was continuous decline in the amplitude of the somatosensory evoked potentials, which did not return until the cord was decompressed. Within one hour after the decompression, the dogs in the thirty-minute-compression group had recovery of somatosensory evoked potentials, but no animal had such recovery in the 180-minute group. Recovery of the somatosensory evoked potentials in the thirty-minute group was sustained over the twenty-eight days after the injury. Motor tests demonstrated rapid recovery of hindlimb motor function in the thirty-minute group, but there was considerable impairment in the 180-minute group. Within two weeks after the injury, balance, cadence, stair-climbing, and the ability to walk up an inclined plane were significantly better in the thirty-minute group than in the 180-minute group. The longer duration of compression produced lesions of significantly greater volume, which corresponded to the long-term functional outcome. CONCLUSIONS: The relatively rapid viscoelastic relaxation of the spinal cord during the early phase of sustained cord compression suggests that there are mechanisms of secondary injury that are linked to tissue displacement. Longer periods of displacement allow propagation of the secondary injury process, resulting in a lack of recovery of somatosensory evoked potentials, limited functional recovery, and more extensive tissue damage.

Sustained spinal cord compression: part II: effect of methylprednisolone on regional blood flow and recovery of somatosensory evoked potentials.

BACKGROUND: The efficacy of methylprednisolone in the treatment of traumatic spinal cord injury is controversial. We examined the effect of methylprednisolone on regional spinal cord blood flow and attempted to determine whether recovery of electrophysiological function is dependent on reperfusion, either during sustained spinal cord compression or after decompression. METHODS: The effects of methylprednisolone therapy on recovery of somatosensory evoked potentials and on spinal cord blood flow were examined in a canine model of dynamic spinal cord compression. Methylprednisolone (30 mg/kg intravenous loading dose followed by 5.4 mg/kg/hr intravenous infusion) or saline solution was administered to thirty-six beagles (eighteen in each group) five minutes after cessation of dynamic spinal cord compression and loss of all somatosensory evoked potentials. After ninety minutes of sustained compression, the spinal cords were decompressed. Somatosensory evoked potentials and spinal cord blood flow were evaluated throughout the period of sustained compression and for three hours after decompression. RESULTS: Seven dogs treated with methylprednisolone and none treated with saline solution recovered measurable somatosensory evoked potentials during sustained compression. After decompression, three more dogs treated with methylprednisolone and seven dogs treated with saline solution recovered somatosensory evoked potentials. Four dogs treated with methylprednisolone lost their previously measurable somatosensory evoked potentials. In the methylprednisolone group, spinal cord blood flow was significantly higher (p < 0.05) in the dogs that had recovered somatosensory evoked potentials than it was in the dogs that had not. Reperfusion blood flow was significantly higher (p < 0.05) in the saline-solution group than it was in the methylprednisolone group. Spinal cord blood flow in the saline-solution group returned to baseline levels within five minutes after decompression. It did not return to baseline levels in the dogs treated with methylprednisolone. CONCLUSIONS: The methylprednisolone administered in this study did not provide a large or significant lasting benefit with regard to neurological preservation or restoration. Methylprednisolone may reduce regional spinal cord blood flow through mechanisms affecting normal autoregulatory blood-flow function.