Mechanism of destructive pathologic changes in the spinal cord under chronic mechanical compression.
METHODS
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.


OBJECTIVE
To clarify the mechanism of destructive pathologic changes in the spinal cord under chronic mechanical compression.


BACKGROUND
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.
Yamaura
Ichiro
I
Department of Orthopaedic Surgery, Faculty of Medicine, Kagoshima University, Kagoshima, Japan. yamaura@med6.kufm.kagoshima-u.ac.jp
Yone
Kazunori
K
Nakahara
Shinji
S
Nagamine
Tomonori
T
Baba
Hisatoshi
H
Uchida
Kenzo
K
Komiya
Setsuro
S
D000368:Aged; D000818:Animals; D017209:Apoptosis; D053148:Caspase 3; D020169:Caspases / Q000096:biosynthesis; D002452:Cell Count; D002908:Chronic Disease; D004195:Disease Models, Animal; D006801:Humans; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D008297:Male; D051379:Mice; D008817:Mice, Mutant Strains; D009333:Neck; D009457:Neuroglia / Q000473:pathology; D009474:Neurons / Q000473:pathology; D017887:Ossification of Posterior Longitudinal Ligament / Q000150:complications* / Q000473:pathology; D013116:Spinal Cord / Q000378:metabolism / Q000473:pathology*; D013117:Spinal Cord Compression / Q000209:etiology* / Q000473:pathology*; D013314:Stress, Mechanical
C505407:CASP3 protein, human; C505409:Casp3 protein, mouse; D053148:Caspase 3; D020169:Caspases