[Clinical feature and pathophysiology of compression myelopathy]

In treating compressive lesions to the spinal cord, it is essential to understand underlying pathophysiology which causes compression myelopathy. When the spinal cord is compressed by static lesions, such as very slowly expanding extramedullary benign tumors, function of the white matter remains unaffected till later stage. Even in advanced cases, in which the function has been markedly affected, the function recovers remarkably following to surgical removal of the lesion. These phenomena have been proved by neurophysiological and clinical evidence. In cases with spondylotic myelopathy, dynamic factors, such as hyperextension of the neck, play more important role than the size of bony spurs, herniated discs or ossified posterior longitudinal ligament. In these cases, function of the white matter is more easily affected than in cases with static compression. The gray matter is more vulnerable than the white matter. In cases which exhibit slow finger opening, it was proved that the interneuronal connection was affected. In cases with myelopathy caused by overstretch mechanism, main lesion is limited to the gray matter. Based on several experimental works, it was suggested that venous engorgement probably is the main cause which affects the gray matter.