An in vivo animal study to examine the influence of pre-existing or concurrent spinal canal stenosis (SCS) on the functional recovery after spinal cord injury (SCI).
To clarify whether spinal cord compression before or after SCI results in less favorable neurological recovery.
The influence of spinal cord compression on the neurological recovery after SCI remains unclear.
We created mice with SCS using an extradural spacer before or after producing SCI and statistically analyzed the correlation between the extent of SCS and neurological outcomes. The extent of SCS was calculated by micro-computed tomography, and the spinal cord blood flow (SCBF) was measured serially with laser Doppler flowmetry. Molecular and immunohistochemical examinations were performed to evaluate the neovascularization at the site of cord compression.
Spacer placement (<300 μm) alone in the control mouse resulted in no neurological deficits. Even with spacer placement that caused asymptomatic SCS, the functional recovery after SCI was progressively impaired as spacer sizes increased in the mice with SCS co-occurring with SCI, whereas no significant impact was observed in the mice with pre-existing SCS, irrespective of the spacer sizes. The SCBF progressively decreased immediately after SCS was produced, but it fully recovered at the later time points. Angiogenesis-related genes were upregulated, and neovascular vessels were observed after producing the SCS. We found that concurrent SCS resulted in a significant reduction and impaired the subsequent recovery of the SCBF, whereas pre-existing SCS did not affect the hemodynamics of the spinal cord after SCI.
The dynamic reduction of the SCBF occurring immediately after spinal cord compression is a significant factor that impairs the neurological recovery after SCI, whereas pre-existing SCS is not always an impediment due to the potentially restructured SCBF.
In this study, we demonstrated that the neurological recovery after spinal cord injury was impaired by concurrent spinal canal stenosis but not by pre-existing spinal canal stenosis. This result was associated with the differences in the hemodynamics of the spinal cord: the spinal cord blood flow decreased immediately after spinal cord compression but recovered thereafter as a result of the neovascularization and restructuring that occurred under asymptomatic compression.
†Advanced Medical Initiatives, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan
*Spinal Injuries Center, Fukuoka, Japan.
Address correspondence and reprints requests to Seiji Okada, MD, PhD, Department of Advanced Medical Initiatives, Graduate School of Medical Sciences, Kyushu University, Maidashi, Higashi-ku, Fukuoka 812-8582, Japan; E-mail: email@example.com
Acknowledgment date: May 13, 2011. Revision date: December 26, 2011. Acceptance date: February 6, 2012.
The manuscript submitted does not contain information about medical device(s)/drug(s).
Grant funds were received in support of this work from The Japanese Ministry of Education, Culture, Sports, Science and Technology, and research foundation from the General Insurance Association of Japan, and Zenkyoren.
No benefits in any form have been or will be received from a commercial party related directly or indirectly to the subject of this manuscript.