Neurological recovery is impaired by concurrent but not by asymptomatic pre-existing spinal cord compression after traumatic spinal cord injury

Kensuke Kubota, Hirokazu Saiwai, Hiromi Kumamaru, Kazu Kobayakawa, Takeshi Maeda, Yoshihiro Matsumoto, Katsumi Harimaya, Yukihide Iwamoto, Seiji Okada

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

STUDY DESIGN. 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). OBJECTIVES. To clarify whether spinal cord compression before or after SCI results in less favorable neurological recovery. SUMMARY OF BACKGROUND DATA. The influence of spinal cord compression on the neurological recovery after SCI remains unclear. METHODS. 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. RESULTS. 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. CONCLUSION. 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.

Original languageEnglish
Pages (from-to)1448-1455
Number of pages8
JournalSpine
Volume37
Issue number17
DOIs
Publication statusPublished - Aug 1 2012

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Spinal Stenosis
Spinal Cord Compression
Spinal Canal
Spinal Cord Injuries
Spinal Cord
Fetal Blood
Laser-Doppler Flowmetry

All Science Journal Classification (ASJC) codes

  • Orthopedics and Sports Medicine
  • Clinical Neurology

Cite this

Neurological recovery is impaired by concurrent but not by asymptomatic pre-existing spinal cord compression after traumatic spinal cord injury. / Kubota, Kensuke; Saiwai, Hirokazu; Kumamaru, Hiromi; Kobayakawa, Kazu; Maeda, Takeshi; Matsumoto, Yoshihiro; Harimaya, Katsumi; Iwamoto, Yukihide; Okada, Seiji.

In: Spine, Vol. 37, No. 17, 01.08.2012, p. 1448-1455.

Research output: Contribution to journalArticle

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abstract = "STUDY DESIGN. 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). OBJECTIVES. To clarify whether spinal cord compression before or after SCI results in less favorable neurological recovery. SUMMARY OF BACKGROUND DATA. The influence of spinal cord compression on the neurological recovery after SCI remains unclear. METHODS. 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. RESULTS. 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. CONCLUSION. 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.",
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AU - Kubota, Kensuke

AU - Saiwai, Hirokazu

AU - Kumamaru, Hiromi

AU - Kobayakawa, Kazu

AU - Maeda, Takeshi

AU - Matsumoto, Yoshihiro

AU - Harimaya, Katsumi

AU - Iwamoto, Yukihide

AU - Okada, Seiji

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N2 - STUDY DESIGN. 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). OBJECTIVES. To clarify whether spinal cord compression before or after SCI results in less favorable neurological recovery. SUMMARY OF BACKGROUND DATA. The influence of spinal cord compression on the neurological recovery after SCI remains unclear. METHODS. 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. RESULTS. 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. CONCLUSION. 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.

AB - STUDY DESIGN. 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). OBJECTIVES. To clarify whether spinal cord compression before or after SCI results in less favorable neurological recovery. SUMMARY OF BACKGROUND DATA. The influence of spinal cord compression on the neurological recovery after SCI remains unclear. METHODS. 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. RESULTS. 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. CONCLUSION. 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.

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