Shinkei Kenkyu no Shinpo Volume 37, Issue 2 (April 1993)

Clinicopathology of cervical spondylotic myelopathy. Keiro ONO 1 , Keiju FUJIWARA 2 1Department of Orthopaedic Surgery, Osaka University Medical School 2Department of Orthopaedic Surgery, Hoshigaoka Kohsei-Nenkin Hospital pp.245-258
Published Date 1993/4/10
  • Abstract
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The principal etiology of cervical spondylotic myelopathy was diffuse compression of the spinal cord caused by spondylotic protrusion, especially at the von Luschka joints. Developmental canal stenosis (anteroposterior canal diameter <13mm) and dynamic instability (retrolisthesis and/or anterior listhesis of the vertebrae) were two major factors responsible for the increased severity of myelopathy. In cadaver specimens with this condition, a decrease in the transverse area of the spinal cord and the compression ratio (the ratio of the anteroposterior to the lateral cord diameter) was observed, and both parameters showed good correlation with the severity of cord degeneration. A cross-sectional study of the spinal cord revealed that the white matter was more vulnerable to mechanical compression than the gray matter. Secondary to the lateral columns, the dorsal columns suffered from mild to moderate compression. The lateral columns include the corticospinal and spinotharamic tracts, and involvement of these tracts produced spastic paralysis and disturbance of pain and temperature sensation below the level of the lesion. Regardless of involvement of the dorsal column, position and vibratory sensation were relatively well preserved. Spongy degeneration, demyelination, gliosis, and ascending or descend-ing Wallerian degeneration were characteristic findings in these columns. Anterior horn cell loss or infarction of the gray matter was associated with severe compression. Finally, even when the entire lateral and dorsal columns were destroyed, the anterior columns were spared. However, in a patient diagnosed as cervical spondylotic amyotrophy, unusual pathological changes were found ; despite com-plete infarction of the gray matter extending over several segments, the white matter was well preserved. The neurological picture before death was characterized by muscle wasting in both forearms and hands without spastic paralysis, which corresponded to the pathological findings.

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37巻2号 (1993年4月)
電子版ISSN 1882-1243 印刷版ISSN 0001-8724 医学書院