REPLY

We appreciate the opportunity to reply to Dr. Sparacia's and Brancatelli's letter about MR images of spinal cord decompression sickness. We did not find the three case reports as Dr. Sparacia described when we wrote our report. We are grateful to Dr. Sparacia for his suggestion regarding our case report. The areas of increased T2 signal intensity in the dorsal columns of the spinal cord is shown to be useful in the diagnosis of the spinal cord decompression sickness. The arterial, venous, and autochthonous theories have been proposed in an attempt to describe the pathophysiologic events that lead to decompression sickness (1, 2). The arterial theory claims that arterial embolization of the microcirculation in the spinal cord and expansion of the bubbles by the assimilation of inert gas from the surrounding tissues finally lead to ischemia and tissue death. The venous theory proposes that bubbles in the spinal epidural venous system activate the clotting factors and platelet aggregation, leading to stagnation and venous obstruction. The autochthonous theory suggests that bubbles within the spinal cord tissue create sufficient local pressure to occlude blood flow, causing anoxic damage and myelin sheath disruption, and the high solubility of nitrogen in myelin with its high fat content leads to further injury of the spinal cord. Our case report, as well as the three cases described by Dr. Sparacia, lend support to the venous theory (3). We emphasized the utility of serial MR imaging for 2 months. Our case contributes to the understanding of the pathophysiologic processes of decompression sickness.