Background and Study Aims Although laminectomy with lateral mass screw fixation (LCSF) is an effective surgical treatment for cervical spondylotic myelopathy (CSM), loss of cervical curvature may result. This study aimed to investigate the effect of cervical curvature on spinal cord drift distance and clinical efficacy. Patients and Methods We retrospectively analyzed 78 consecutive CSM patients with normal cervical curvature who underwent LCSF. Cervical curvature was measured according to Borden's method 6 months after surgery. Study patients were divided into two groups: group A, reduced cervical curvature (cervical lordosis depth 0–7mm; n = 42); and group B, normal cervical curvature (cervical lordosis depth 7–17mm; n = 36). Spinal cord drift distance, laminectomy width, neurologic functional recovery, axial symptom (AS) severity, and incidence of C5 palsy were measured and compared. Results Cervical lordosis depth was 5.1 ± 1.2 mm in group A and 12.3 ± 2.4 mm in group B (p < 0.05). Laminectomy width was 21.5 ± 2.6 mm in group A and 21.9 ± 2.8 mm in group B (p > 0.05). Spinal cord drift distance was significantly shorter in group A (1.9 ± 0.4 vs. 2.6 ± 0.7 mm; p < 0.05). The Japanese Orthopaedic Association (JOA) score significantly increased after surgery in both groups (p < 0.05). Neurologic recovery rate did not differ between the two groups (61.5 vs. 62.7%; p > 0.05). AS severity was significantly higher in group A (p < 0.05). C5 palsy occurred in three group A patients (7.1%) and four group B patients (11.1%), but the difference was not significant (p > 0.05). Conclusion After LCSF, 53.8% of the patients developed loss of cervical curvature. A smaller cervical curvature resulted in a shorter spinal cord drift distance. Loss of cervical curvature was related to AS severity but not improvement of neurologic function or incidence of C5 palsy.
Purpose Investigating the roles of phosphorylated epidermal growth factor receptor (pEGFR) in the recovery of neural function after decompression of CSCI, therefore provide experimental basis for the development of therapeutic strategies and medicines for treating CSCI. Methods A CSCI model was established with a customized device, and was then subjected to spinal decompression. The motor functions were monitored by the Basso, Beattie & Bresnahan(BBB) locomotor rating scale; the number of axonal myelinated fibers was estimated by staining with luxol fast blue (LFB); pEGFR and phosphorylated Akt1 (pAkt1) were detected by Western blot; pEGFR+-NG2+(NG2+ cells are precursor to oligodendrocytes and pAkt1+-NG2+ cells were detected by double-labeling immunefluorescence assay. Results After decompression of CSCI, the BBB scores and the number of myelinated nerve fibers gradually increased with time. Meanwhile, the expression of pEGFR and pAkt1 were up-regulated and the number of pEGFR+-NG2+ and pAkt1+-NG2+ cells increased consistent with the changes of motor functions and the number of myelinated nerve fibers. Whereas, significant decreases in BBB scores, expression level of pAkt1, as well as numbers of myelinated nerve fibers, and pAkt1+-NG2+ cells were observed after inhibition of expression. Conclusions Up-regulated expression of pEGFR can promote recovery of neurological functions in rats with CSCI. This effect is achieved by activation of pAkt1(a downstream signal molecule of pEGFR), which subsequently promotes the proliferation of oligodendrocyte precursor cells (OPCs).
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