STUDY DESIGN: A histologic and histochemical study was performed both in the autopsy of a human patient with cervical spinal cord compression caused by ossification of the posterior longitudinal ligament and in a tiptoe-walking Yoshimura mouse model of progressive cervical cord compression. OBJECTIVES: To clarify the mechanism of destructive pathologic changes in the spinal cord under chronic mechanical compression. SUMMARY OF BACKGROUND DATA: Under chronic compression, the spinal cord exhibits destructive changes considered to be causes of profound and irreversible motor paresis. Recently, some investigators have found that apoptosis in acute spinal cord injury induces both secondary degeneration at the site of injury and chronic demyelination of tracts away from the site of injury. However, the mechanism responsible for these destructive spinal cord changes under chronic compression remains unclear. METHODS: The spinal cord was examined histologically, and an attempt was made to detect apoptotic cells using terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling in both the autopsy of a human patient and tiptoe-walking mice exhibiting spinal cord compression. RESULTS: Apoptotic cells were observed in the chronically compressed spinal cord in both the autopsy of a human patient and model mice. In tiptoe-walking mice exhibiting spinal cord compression, descending degeneration in the anterior and lateral columns and ascending degeneration in the posterior column were observed. The distribution of oligodendrocytes with positive results from terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling was similar to that for degeneration of the long tracts. CONCLUSIONS: Spinal cord cell apoptosis may produce destructive changes in the spinal cord under chronic compression, with a resulting irreversible neurologic deficit.
STUDY DESIGN: A histologic and histochemical study was performed both in the autopsy of a humanpatient with cervical spinal cord compression caused by ossification of the posterior longitudinal ligament and in a tiptoe-walking Yoshimura mouse model of progressive cervical cord compression. OBJECTIVES: To clarify the mechanism of destructive pathologic changes in the spinal cord under chronic mechanical compression. SUMMARY OF BACKGROUND DATA: Under chronic compression, the spinal cord exhibits destructive changes considered to be causes of profound and irreversible motor paresis. Recently, some investigators have found that apoptosis in acute spinal cord injury induces both secondary degeneration at the site of injury and chronic demyelination of tracts away from the site of injury. However, the mechanism responsible for these destructive spinal cord changes under chronic compression remains unclear. METHODS: The spinal cord was examined histologically, and an attempt was made to detect apoptotic cells using terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling in both the autopsy of a humanpatient and tiptoe-walking mice exhibiting spinal cord compression. RESULTS: Apoptotic cells were observed in the chronically compressed spinal cord in both the autopsy of a humanpatient and model mice. In tiptoe-walking mice exhibiting spinal cord compression, descending degeneration in the anterior and lateral columns and ascending degeneration in the posterior column were observed. The distribution of oligodendrocytes with positive results from terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling was similar to that for degeneration of the long tracts. CONCLUSIONS: Spinal cord cell apoptosis may produce destructive changes in the spinal cord under chronic compression, with a resulting irreversible neurologic deficit.