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Yong Hu, Christopher K. Kepler, Todd J. Albert, Zhen-shan Yuan, Wei-hu Ma, Yong-jie Gu and Rong-ming Xu

Object

The aims of this study were to evaluate a large series of posterior C-1 lateral mass screws (LMSs) to determine accuracy based on CT scanning findings and to assess the perioperative complication rate related to errant screw placement.

Methods

Accuracy of screw placement was evaluated using postoperative CT scans obtained in 196 patients with atlantoaxial instability. Radiographic analysis included measurement of preoperative and postoperative CT scans to evaluate relevant anatomy and classify accuracy of instrumentation placement. Screws were graded using the following definitions: Type I, screw threads completely within the bone (ideal); Type II, less than half the diameter of the screw violates the surrounding cortex (safe); and Type III, clear violation of transverse foramen or spinal canal (unacceptable).

Results

A total of 390 C-1 LMSs were placed, but 32 screws (8.2%) were excluded from accuracy measurements because of a lack of postoperative CT scans; patients in these cases were still included in the assessment of potential clinical complications based on clinical records. Of the 358 evaluable screws with postoperative CT scanning, 85.5% of screws (Type I) were rated as being in the ideal position, 11.7% of screws (Type II) were rated as occupying a safe position, and 10 screws (2.8%) were unacceptable (Type III). Overall, 97.2% of screws were rated Type I or II. Of the 10 screws that were unacceptable on postoperative CT scans, there were no known associated neurological or vertebral artery (VA) injuries. Seven unacceptable screws erred medially into the spinal canal, and 2 patients underwent revision surgery for medial screws. In 2 patients, unilateral C-1 LMSs penetrated the C-1 anterior cortex by approximately 4 mm. Neither patient with anterior C-1 penetration had evidence of internal carotid artery or hypoglossal nerve injury. Computed tomography scanning showed partial entry of C-1 LMSs into the VA foramen of C-1 in 10 cases; no occlusion, associated aneurysm, or fistula of the VA was found. Two patients complained of postoperative occipital neuralgia. This was transient in one patient and resolved by 2 months after surgery. The second patient developed persistent neuralgia, which remained 2 years after surgery, necessitating referral to the pain service.

Conclusions

The technique for freehand C-1 LMS fixation appears to be safe and effective without intraoperative fluoroscopy guidance. Preoperative planning and determination of the ideal screw insertion point, the ideal trajectory, and screw length are the most important considerations. In addition, fewer malpositioned screws were inserted as the study progressed, suggesting a learning curve to the technique.

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Editorial

Scarring after spinal cord injury

Michael G. Fehlings and Gregory W. J. Hawryluk

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Xing Wu, Jin Hu, Liangfu Zhou, Ying Mao, Bojie Yang, Liang Gao, Rong Xie, Feng Xu, Dong Zhang, Jun Liu and Jianhong Zhu

Object

Mesenchymal stem cells (MSCs) have been shown to migrate toward tumors, but their distribution pattern in gliomas has not been completely portrayed. The primary purpose of the study was to assay the tropism capacity of MSCs to gliomas, to delineate the pattern of MSC distribution in gliomas after systemic injection, and to track the migration and incorporation of magnetically labeled MSCs using 1.5-T magnetic resonance (MR) imaging.

Methods

The MSCs from Fischer 344 rats were colabeled with superparamagnetic iron oxide nanoparticles (SPIO) and enhanced green fluorescent protein (EGFP). The tropism capacity of MSCs was quantitatively assayed in vitro using the Transwell system. To track the migration of MSCs in vivo, MR imaging was performed both 7 and 14 days after systemic administration of labeled MSCs. After MR imaging, the distribution patterns of MSCs in rats with gliomas were examined using Prussian blue and fluorescence staining.

Results

The in vitro study showed that MSCs possessed significantly greater migratory capacity than fibroblast cells (p < 0.001) and that lysis of F98 glioma cells and cultured F98 cells showed a greater capacity to induce migration of cells than other stimuli (p < 0.05). Seven days after MSC transplantation, the SPIO–EGFP colabeled cells were distributed throughout the tumor, where a well-defined dark hypointense region was represented on gradient echo sequences. After 14 days, most of the colabeled MSCs were found at the border between the tumor and normal parenchyma, which was represented on gradient echo sequences as diluted amorphous dark areas at the edge of the tumors.

Conclusions

This study demonstrated that systemically transplanted MSCs migrate toward gliomas with high specificity in a temporal–spatial pattern, which can be tracked using MR imaging.

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Rong Hu, Jianjun Zhou, Chunxia Luo, Jiangkai Lin, Xianrong Wang, Xiaoguang Li, Xiuwu Bian, Yunqing Li, Qi Wan, Yanbing Yu and Hua Feng

Object

A glial scar is thought to be responsible for halting neuroregeneration following spinal cord injury (SCI). However, little quantitative evidence has been provided to show the relationship of a glial scar and axonal regrowth after injury.

Methods

In this study performed in rats and dogs, a traumatic SCI model was made using a weight-drop injury device, and tissue sections were stained with H & E for immunohistochemical analysis. The function and behavior of model animals were tested using electrophysiological recording and the Basso-Beattie-Bresnahan Locomotor Rating Scale, respectively. The cavity in the spinal cord after SCI in dogs was observed using MR imaging.

Results

The morphological results showed that the formation of an astroglial scar was defined at 4 weeks after SCI. While regenerative axons reached the vicinity of the lesion site, the glial scar blocked the extension of regrown axons. In agreement with these findings, the electrophysiological, behavioral, and in vivo MR imaging tests showed that functional recovery reached a plateau at 4 weeks after SCI. The thickness of the glial scars in the injured rat spinal cords was also measured. The mean thickness of the glial scar rostral and caudal to the lesion cavity was 107.00 ± 20.12 μm; laterally it was 69.92 ± 15.12 μm.

Conclusions

These results provide comprehensive evidence indicating that the formation of a glial scar inhibits axonal regeneration at 4 weeks after SCI. This study reveals a critical time window of postinjury recovery and a detailed spatial orientation of glial scar, which would provide an important basis for the development of therapeutic strategy for glial scar ablation.