13 research outputs found

    Association of Spinal Alignment Correction With Patient-Reported Outcomes in Adult Cervical Deformity: Review of the Literature

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    Objective Adult cervical deformity (ACD) is a debilitating spinal condition that causes significant pain, neurologic dysfunction, and functional impairment. Surgery is often performed to correct cervical alignment, but the optimal amount of correction required to improve patient-reported outcomes (PROs) are not yet well-defined. Methods A review of the literature was performed and Fisher z-transformation (Zr) was used to pool the correlation coefficients between alignment parameters and PROs. The strength of correlation was defined according to the following: poor (0 <r ≤ 0.3), fair (0.3 < r ≤ 0.5), moderate (0.5 < r ≤ 0.8), and strong (0.8 < r ≤1). Results Increased C2–7 sagittal vertical axis was fairly associated with increased Neck Disability Index (NDI) (pooled Zr=0.31; 95% confidence interval [CI], -0.03 to 0.58). Changes in T1 slope minus cervical lordosis poorly correlated with NDI (pooled Zr=-0.04; 95% CI, -0.23 to 0.30). Increased C7–S1 was poorly associated with worse EuroQoL 5-Dimension (pooled Zr=-0.22; 95% CI, -0.36 to -0.06). Correction of horizontal gaze did not correlate with legacy metrics. Modified Japanese Orthopedic Association correlated with C2-slope, C7–S1, and C2–S1. Conclusion Spinal alignment parameters variably correlated with improved health-related quality of life and myelopathy after corrective surgery for ACD. Further studies evaluating legacy PROs, Patient-Reported Outcomes Measurement System, and ACD specific instruments are needed for further validation

    Novel Technique for C1–2 Interlaminar Arthrodesis Utilizing a Modified Sonntag Loop-Suture Graft With Posterior C1–2 Fixation

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    Objective Conventional techniques for atlantoaxial fixation and fusion typically pass cables or wires underneath C1 lamina to secure the bone graft between the posterior elements of C1–2, which leads to complications such as cerebrospinal fluid (CSF) leak and neurological injury. With the evolution of fixation hardware, we propose a novel C1–2 fixation technique that avoids the morbidity and complications associated with sublaminar cables and wires. Methods This technique entails wedging and anchoring a structural iliac crest graft between C1 and C2 for interlaminar arthrodesis and securing it using a 0-Prolene suture at the time of C1 lateral mass and C2 pars interarticularis screw fixation. Results We identified 32 patients who underwent surgery for atlantoaxial with our technique. A 60% improvement in pain-related disability from preoperative baseline was demonstrated by Neck Disability Index (p<0.001). There were no neurologic deficits. Complications included 2 patients CSF leaks related to presenting trauma, 1 patient with surgical site infection, and 1 patient with transient dysphagia. The rate of radiographic atlantoaxial fusion was 96.8% at 6 months, with no evidence of instrumentation failure, graft dislodgement, or graft related complications. Conclusion We demonstrate a novel technique for C1–2 arthrodesis that is a safe and effective option for atlantoaxial fusion

    Deficiency of thrombospondin-1 reduces Th17 differentiation and attenuates experimental autoimmune encephalomyelitis

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    Transforming growth factor beta (TGF-beta) plays a role both in the induction of Treg and in the differentiation of the IL-17-secreting T cells (Th17) which drive inflammation in experimental autoimmune encephalomyelitis (EAE). We investigated the role that thrombospondin-1 (TSP-1) dependent activation of TGF-beta played in the generation of an encephalitic Th17 response in EAE. Upon immunization with myelin oligodendrocyte glycoprotein peptide (MOG(35-55)), TSP-1 deficient (TSP-1(null)) mice and MOG(35-55) TCR transgenic mice that lack of TSP-1 (2D2.TSP-1(null)) exhibited an attenuated form of EAE, and secreted lower levels of IL-17. Adoptive transfer of in vitro-activated 2D2.TSP-1(null) T cells induced a milder form of EAE, independent of TSP-1 expression in the recipient mice. Furthermore, in vitro studies demonstrated that anti-CD3/anti-CD28 pre-activated CD4+ T cells transiently upregulated latent TGF-beta in a TSP-1 dependent way, and such activation of latent TGF-beta was required for the differentiation of Th17 cells. These results demonstrate that TSP-1 participates in the differentiation of Th17 cells through its ability to activate latent TGF-beta, and enhances the inflammatory response in EAE. (C) 2009 Elsevier Ltd. All rights reserved.U.S. National Institutes of Health (NIH)National Institute of Allergy And Infectious Diseases (NIAID/NIH), MAID[1F32AI066677-01]Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)CAPES[4499-05-0
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