Altered Blood Flow Distribution in the Rat Spinal Cord under Chronic Compression

In Brief Study Design. Sham-operation–controlled animal study to assess alterations in blood flow in the spinal cord in a chronic compression model. Laboratory investigation. Objective. Cervical myelopathy is a common cause of disability in elderly patients. Hypothesis was made that ischemia subsequent to the spinal cord compression plays an important role in the pathogenesis of the spinal cord dysfunction. This study was undertaken to assess alterations in the blood flow of the spinal cord under chronic compression in a rat model. Summary of Background Data. Histologic study of spinal cord from patients with spondylotic myelopathy showed ischemic tissue changes. Experimentally, spinal cord hypoperfusion in combination with chronic spinal cord compression induced myelopathy in dogs. We previously showed that chronic compression of the spinal cord in rats produces gradual deterioration of mobility of the animals accompanied by cord tissue degeneration compatible with ischemic changes. Methods. Chronic compression of the cervical spinal cord was implemented by implantation of a thin urethane polymer sheet under the C5–C6 laminae, which expands by absorbing tissue water over 48–72 hours. The control group underwent sham operation. Twelve weeks later, blood flow to the C3–C4 and C5–C6 spinal cord segments were measured by fluorescent microsphere methods. Results. In the control group, the blood flow in the C5–C6 segment was larger than C3–C4 segment. In the compression group, the blood flow in the C5–C6 was significantly reduced compared to the C3–C4 segment. Conclusion. Under chronic focal spinal cord compression, there was a decrease of the blood flow in the compressed segment in comparison to the rostral segment. Our data are compatible with the hypothesis that alteration in the spinal cord blood flow contributes to pathogenesis of myelopathy. Focal spinal cord blood flow was measured using fluorescent microspheres, in a rat chronic spinal cord compression model which reproduces delayed onset of motor dysfunction and underlying neuronal loss, Twelve weeks after implementing compression, the flow to the compressed segment was significantly reduced as compared to that without compression.