Feng Shen, Bin Zhou, Quan Li, Ming Li, Zhiwei Wang, Qiang Li and Bo Ran
The object of this study was to review the effectiveness in treating severe and rigid scoliosis with posterioronly spinal release combined with derotation, translation, segmental correction, and an in situ rod-contouring technique.
Twenty-eight patients with severe and rigid scoliosis (Cobb angle > 70° and flexibility < 30%) were retrospectively enrolled between June 2008 and June 2010. The average age of the patients was 17.1 years old (range 12–22 years old), 18 were female, and 10 were male. Etiological diagnoses were idiopathic in 24 patients, neuromuscular in 2 patients, and Marfan syndrome in 2 patients. All patients underwent posterior spinal release, derotation, translation, segmental correction, and an in situ rod-contouring technique. The scoliosis Cobb angle in the coronal plane, kyphosis Cobb angle, apex vertebral translation, and trunk shift were evaluated preoperatively and postoperatively.
The average operative time was 241.8 ± 32.1 minutes and estimated blood loss was 780.5 ± 132.6 ml. The average scoliosis Cobb angle in the coronal plane was corrected from 85.7° (range 77°–94°) preoperatively to 33.1° (range 21°–52°) postoperatively, with a correction ratio of 61.3%. The average kyphosis Cobb angle was 64.5° (range 59°–83°) preoperatively, which was decreased to 42.6° (range 34°–58°) postoperatively, with a correction ratio of 33.9%. After an average of 24 months of follow-up (range 13–30 months), no major complications were observed in these patients, except screw pullout of the upper thoracic vertebrae in 2 patients and screw penetration into the apical vertebrae in 1 patient.
Posterior spinal release combined with derotation, translation, segmental correction, and an in situ rod-contouring technique has proved to be a promising new technique for rigid scoliosis, significantly correcting the scoliosis and accompanied by fewer complications.
Jinqian Liang, Ran Ding, Sooyong Chua, Zheng Li and Jianxiong Shen
The safety of spinal fusion has been poorly studied in children with surgically corrected congenital cardiac malformations (CCMs). The objective of this study was to evaluate the safety of spinal fusion in patients with CCMs following cardiac surgery.
A retrospective study was conducted on 32 patients with scoliosis who received surgical treatment for their CCMs (CCM group). Sixty-four age- and sex-matched patients with scoliosis and normal hearts who received spinal fusion served as the control group. These 2 groups were compared for demographic distribution, blood loss, transfusion requirements, and incidence of postoperative complications.
The ages, curve pattern distributions, and number of levels fused were similar between the 2 groups before spinal fusion. Overall, a total of 7 patients in the CCM group (21.9%) and 5 (7.8%) in the control group had documented postoperative complications. The perioperative allogenic blood transfusion rate and mean red blood cell transfusion requirement in the CCM group were significantly higher than those found in patients in the control group (68.7% vs 28.1%, respectively, p = 0.000; and 2.68 ± 2.76 units/patient vs 0.76 ± 1.07 units/patient, respectively, p = 0.011). In the CCM group, a preoperative major curve magnitude ≥ 80° was the most accurate indicator of an increased risk for a major complication (p = 0.019), whereas no statistically significant correlation was noted between postoperative complications and age, type of congenital heart disease, operative duration, and estimated blood loss during the operation and transfusion.
Spinal fusion subsequent to prior cardiac surgery is relatively safe and effective in correcting the spinal deformity for patients with scoliosis and surgically corrected CCMs. A preoperative major curve magnitude ≥ 80° may be a risk factor in predicting postoperative complications in scoliotic patients with surgically corrected CCMs.
Feng Yan, Gary Rajah, Yuchuan Ding, Yang Hua, Hongqi Zhang, Liqun Jiao, Guilin Li, Ming Ren, Ran Meng, Feng Lin and Xunming Ji
Symptomatic intracranial hypertension can be caused by cerebral venous sinus stenosis (CVSS) and cerebral venous sinus thrombotic (CVST) stenosis, which is usually found in some patients with idiopathic intracranial hypertension (IIH). Recently, at the authors’ center, they utilized intravascular ultrasound (IVUS) as an adjunct to conventional venoplasty or stenting to facilitate diagnosis and accurate stent placement in CVSS.
The authors designed a retrospective review of their prospective database of patients who underwent IVUS-guided venous sinus stenting between April 2016 and February 2017. Clinical, radiological, and ophthalmological information was recorded and analyzed. IVUS was performed in 12 patients with IIH (9 with nonthrombotic CVSS, 3 with secondary stenosis combined with CVST) during venoplasty through venous access. The IVUS catheter was used from a proximal location to the site of stenosis. Post-stenting follow-up, including symptomatic improvement, stent patency, and adjacent-site stenosis, was assessed at 1 year.
Thirteen stenotic cerebral sinuses in 12 patients were corrected using IVUS-guided stenting. No technical or neurological complications were encountered. The IVUS images were excellent for the diagnosis of the stenosis, and intraluminal thrombi were clearly visualized by using IVUS in 3 (25%) of the 12 patients. A giant arachnoid granulation was demonstrated in 1 (8.3%) of the 12 patients. Intravenous compartments or septations (2 of 12, 16.7%) and vessel wall thickening (6 of 12, 50%) were also noted. At 1-year follow-up, 10 of 12 patients were clinically symptom-free in our series.
IVUS is a promising tool with the potential to improve the diagnostic accuracy in IIH, aiding in identification of the types of intracranial venous stenosis, assisting in stent selection, and guiding stent placement. Further study of the utility of IVUS in venous stenting and venous stenosis pathology is warranted.
Xin Zhang, Tamrakar Karuna, Zhi-Qiang Yao, Chuan-Zhi Duan, Xue-Min Wang, Shun-Ting Jiang, Xi-Feng Li, Jia-He Yin, Xu-Ying He, Shen-Quan Guo, Yun-Chang Chen, Wen-Chao Liu, Ran Li and Hai-Yan Fan
Among clinical and morphological criteria, hemodynamics is the main predictor of aneurysm growth and rupture. This study aimed to identify which hemodynamic parameter in the parent artery could independently predict the rupture of anterior communicating artery (ACoA) aneurysms by using multivariate logistic regression and two-piecewise linear regression models. An additional objective was to look for a more simplified and convenient alternative to the widely used computational fluid dynamics (CFD) techniques to detect wall shear stress (WSS) as a screening tool for predicting the risk of aneurysm rupture during the follow-up of patients who did not undergo embolization or surgery.
One hundred sixty-two patients harboring ACoA aneurysms (130 ruptured and 32 unruptured) confirmed by 3D digital subtraction angiography at three centers were selected for this study. Morphological and hemodynamic parameters were evaluated for significance with respect to aneurysm rupture. Local hemodynamic parameters were obtained by MR angiography and transcranial color-coded duplex sonography to calculate WSS magnitude. Multivariate logistic regression and a two-piecewise linear regression analysis were performed to identify which hemodynamic parameter independently characterizes the rupture status of ACoA aneurysms.
Univariate analysis showed that WSS (p < 0.001), circumferential wall tension (p = 0.005), age (p < 0.001), the angle between the A1 and A2 segments of the anterior cerebral artery (p < 0.001), size ratio (p = 0.023), aneurysm angle (p < 0.001), irregular shape (p = 0.005), and hypertension (grade II) (p = 0.006) were significant parameters. Multivariate analyses showed significant association between WSS in the parent artery and ACoA aneurysm rupture (p = 0.0001). WSS magnitude, evaluated by a two-piecewise linear regression model, was significantly correlated with the rupture of the ACoA aneurysm when the magnitude was higher than 12.3 dyne/cm2 (HR 7.2, 95% CI 1.5–33.6, p = 0.013).
WSS in the parent artery may be one of the reliable hemodynamic parameters characterizing the rupture status of ACoA aneurysms when the WSS magnitude is higher than 12.3 dyne/cm2. Analysis showed that with each additional unit of WSS (even with a 1-unit increase of WSS), there was a 6.2-fold increase in the risk of rupture for ACoA aneurysms.
Guang Yang, Zhendong Liu, Lu Wang, Xin Chen, Xiaoxiong Wang, Qi Dong, Daming Zhang, Zhao Yang, Qi Zhou, Jingxian Sun, Linmeng Xue, Xinzhuang Wang, Ming Gao, Lili Li, Ran Yi, Gareev Ilgiz, Jing Ai and Shiguang Zhao
It has been reported that microRNA-195 (miR-195) protects against chronic brain injury induced by chronic brain hypoperfusion. However, neither the expression profile of miR-195 nor its potential role during acute ischemic stroke has been investigated. In this study, the authors’ aim was to verify the mechanism of miR-195 in acute ischemic stroke.
The plasma levels of miR-195 expression were assessed using real-time PCR in 96 patients with acute ischemic stroke, and the correlation with the National Institutes of Health Stroke Scale score was evaluated. In addition, cerebral infarct volume, neurological score, and levels of miR-195 and CX3CL1/CX3CR1 mRNA and protein expression were assessed in mice subjected to middle cerebral artery occlusion (MCAO) with or without intra-cerebroventricular infusion of lentiviral vector. The inflammatory cytokines tumor necrosis factor–α (TNFα), interleukin (IL)–1β, and IL-6 of mouse brains after MCAO and BV2 cells treated with oxygen-glucose deprivation were measured using enzyme-linked immunosorbent assay, and apoptotic proteins were examined by Western blotting. Direct targeting of CX3CL1/CX3CR1 by miR-195 was determined by immunoblotting and dual luciferase assay.
In ischemic stroke patients, miR-195 was significantly downregulated and expression levels of miR-195 in these patients negatively correlated with the National Institutes of Health Stroke Scale score. In mice after MCAO, miR-195 overexpression decreased infarct volume, alleviated neurological deficits, and most importantly, suppressed an inflammatory response. Meanwhile, miR-195 suppressed the expression of the inflammatory cytokines TNFα, IL-1β, and IL-6 in vitro and in vivo. The authors further discovered that both CX3CL1 and CX3CR1 are direct targets of miR-195, but miR-195 exerts neuroprotective roles mainly through inhibiting CX3CR1-mediated neuroinflammation and subsequent neuronal cell apoptosis.
Taken together, these findings suggest that miR-195 promotes neuronal cell survival against chronic cerebral ischemic damage by inhibiting CX3CR1-mediated neuroinflammation. This indicates that miR-195 may represent a novel target that regulates neuroinflammation and brain injury, thus offering a new treatment strategy for cerebral ischemic disorders.