ABSTRACT
BACKGROUND: Accurate location of the skin incision is helpful to decrease the technical difficulty and save the operative time in anterior cervical spine surgery. Spine surgeons usually use the traditional neck anatomic structures (the hyoid bone, thyroid cartilage, and cricoid cartilage) as landmarks during the surgery. However, the reliability of these landmarks has not been validated in actual practice. OBJECTIVE: To find out which landmark is the most accurate for identifying the cervical levels in anterior cervical spine surgery. METHODS: The lateral flexion and extension radiographs of cervical spine in standing position from 30 consecutive patients from January 2015 to February 2015 were obtained. The cervical vertebral bodies from C2 to C7 were divided equally into 2 segments. The cervical segments corresponding to each of the surface landmarks were recorded on the flexion and extension radiographs, respectively, and the displacement of corresponding cervical segments from the flexion to extension radiographs for each landmark was calculated. RESULTS: Based on the measurements, the main corresponding cervical levels for the mandibular angle were C2 on both of the flexion and extension films, for the hyoid bone were the C3-C4 interspace on flexion film and C3 on extension film, for the thyroid cartilage C5 on both of flexion and extension films, and for the cricoid cartilage C6 on flexion film and C5-C6 interspace on extension film, respectively. The ratios of displacement within 2 segments from flexion to extension were 83.3% (25/30) for mandibular angle, 56.7% (17/30) for hyoid bone, 66.7% (20/30) for thyroid cartilage, and 56.7% (17/30) for cricoid cartilage, respectively. The mean displacement from flexion to extension films were significantly less than 2 cervical segments for the mandibular angle but greater than 2 segments for the other landmarks. Significant differences were found between mandibular angle and the other 3 landmarks for the displacement from flexion to extension. CONCLUSIONS: The angle of mandible was found to be the most accurate landmark for identifying the cervical level, which corresponded to C2 and C2-C3 disc space. The hyoid bone, thyroid cartilage, and cricoid cartilage were not reliable to predict the cervical levels.
Subject(s)
Anatomic Landmarks/diagnostic imaging , Cervical Vertebrae/surgery , Cricoid Cartilage/diagnostic imaging , Hyoid Bone/diagnostic imaging , Thyroid Cartilage/diagnostic imaging , Adult , Anatomic Landmarks/anatomy & histology , Cricoid Cartilage/anatomy & histology , Female , Humans , Hyoid Bone/anatomy & histology , Male , Neck/anatomy & histology , Neck/diagnostic imaging , Radiography , Reproducibility of Results , Thyroid Cartilage/anatomy & histology , Young AdultABSTRACT
It was reported that CXCR4 signaling played an important role in the migration and differentiation of endogenous neural stem cells after spinal cord injury (SCI). However, the molecular mechanism of it is still unclear. Here, we established a model of SCI in rats and AMD3100 was used to treat them. The rats were then sacrificed and the injured spinal cord specimens were harvested. Additionally, the neural stem cells (NSCs) line was culture and treated with AMD3100 in vitro. Results showed the locomotor function of SCI rats was worse after treated with AMD3100. And the expression levels of Nestion in neural stem cells and ß-tubulin in neuron cells were significantly increased in the injured spinal cord, which can be inhibited by the CXCR4 antagonist of AMD3100. Additionally, the expression of ß-catenin and phosphorylase ß-catenin protein was significantly down regulated by AMD3100. In vitro, the NSCs proliferation ability was inhibited and the migration was decreased after treated with AMD3100. Also, the expression of Nestion, ß-tubulin, ß-catenin and phosphorylase ß-catenin protein was significantly decreased in AMD3100 group comparing with untreated group. Taken together, this study suggested that AMD3100 could inhibit the migration and differentiation of endogenous neural stem cells in rats with SCI. The mechanism of it maybe that AMD3100 could down regulate of SDF-1/CXCR4 by targeting ß-catenin signaling pathway.