老年人脑梗死156例临床分析

目的:探讨老年人脑梗死的病因,危险因素及临床特点。方法:回顾性分析156例老年患者的临床资料并进行统计学分析。结果:动脉硬化是老年人脑梗死最常见的病因。脑梗死主要的危险因素有高血压、高血脂、吸烟、家族史等。男性发病率明显高于女性。结论:尽早明确老年脑梗死的病因,积极预防各种危险因素,给予充分的治疗可有效减少其发生。     

不同治疗方式在老年股骨粗隆间骨折中的对照分析

目的:比较分析不同治疗方式对老年股骨粗隆间骨折的治疗效果。方法:回顾性分析152例老年股骨粗隆间骨折患者的临床资料,保守治疗组24例;手术治疗组128例,其中人工股骨头置换23例、外固定架23例、髓内固定28例(包括股骨近端髓内钉(proximal femoral nail,PFN)、Gamma钉等)、动力髋螺钉(dynamic hip screw,DHS)26例、股骨近端锁定钢板(the locking compress plate,LCP)28例。对各种治疗方式的相关指标进行比较分析。结果:手术治疗组患者卧床时间和并发症发生率均显著优于保守治疗组(t=8.045,7.583,8.673,8.023,8.672,X2=9.124,4.809,6.603,4.276,14.444,P0.05);各手术组之间比较:各组卧床时间无显著差异(F=0.241,P0.05),外固定架组和LCP组手术时间、切口长度、出血量及术后引流量均显著优于其余各组(P0.05);保守组术后Harries评分低于手术组。结论:手术治疗老年股骨粗隆间骨折可获得满意疗效,且并发症较少;外固定架创伤较小,LCP和人工股骨头置换术后疗效较好,其中LCP可作为优先考虑方案。     

肱骨近端锁定接骨板结合抗骨质疏松药物治疗老年骨质疏松性肱骨近端粉碎性骨折的疗效观察

目的:探讨肱骨近端锁定接骨板(LPHP)结合抗骨质疏松药物治疗老年骨质疏松性肱骨近端粉碎性骨折(OP-CFPH)的疗效价值。方法:抽选我院2012年1月-2014年2月收治的45例老年OP-CFPH患者,采用随机分层法分为对照组(n=22例,采用三叶形普通钢板治疗)和观察组(n=23例,采用LPHP+入院后抗骨质疏松治疗),比较两组手术参数、术后肩关节Neer评分及并发症发生率的差异。结果:观察组手术时间、术中出血量、术后引流量及术后骨折愈合时间均显著低于对照组的,组间差异具有统计学意义(P0.05);观察组术后肩关节Neer评分优良率明显高于对照组(P0.05);术后观察组并发症发生率低于对照组,但比较差异无统计学意义(P0.05)。结论:LPHP联合抗骨质疏松治疗老年OP-PHF具有创伤小、疗效好的优点,有利于骨折愈合,是目前治疗该类骨折一种理想的方法。     

创伤性椎体骨折行椎体成形术后复发的危险因素评估

目的：对创伤性椎体骨折患者使用椎体成形术治疗后可能再次引起骨折的多个因素进行评估。方法：选取本院收治的经皮椎 体成形术（Percutaneous vertebroplasty,PVP）或经皮椎体后凸成形术（Percutaneous kyphoplasty,PKP）治疗的患者161 例,其中再次 发生骨折的患者113 例（131 椎）,根据治疗方法（PVP 或PKP）和再次发生骨折的部位（手术椎体或非手术椎体）不同,将患者分成 A1 和A2（再发骨折部位是手术椎体）、B1 和B2（骨折部位为非手术椎体）、C1 和C2（手术椎体和非手术椎体）以及D 组（未再次 发生骨折）共七组,A1,B1,C1 三组使用PVP,A2,B2,C2三组使用PKP,记录各组患者可能导致再发骨折风险的因素并和D组比 较,分析PVP或PKP治疗后椎体再次发生骨折的高危因素。结果：患者身高、体重、年龄等一系列因素之间的差异没有统计学意 义（P>0.05）;而骨水泥注入的体积在再发骨折患者和D 组之间差异有统计学意义（P<0.05）;椎间盘骨水泥是否渗透和是否使用抗 骨质疏松药物治疗的差异有统计学意义（P<0.05）;再发骨折患者和D 组患者25-(OH)D 的浓度之间的差异有统计学意义（P<0. 05）。多因素Logistic 分析显示,椎间盘水泥渗透、低浓度的25-(OH)D 和未使用抗骨质疏松药物治疗是椎体成形术治疗后复发骨 折的危险因素（P<0.05）。结论：PVP或PKP治疗后椎体再次发生骨折的三个危险因素是椎间盘骨水泥渗透、较低的25-(OH)D 浓 度和未使用抗骨质疏松药物治疗。     

经肌间隙微创内固定术与传统椎弓根螺钉内固定术治疗胸腰椎骨折的疗效比较

目的：比较经肌间隙和传统切开椎弓根内固定治疗胸腰椎骨折的临床疗效和安全性。方法：选取我院2010 年1 月-2014 年 12 月收治的胸腰椎骨折患者120例,分为微创手术组和开放手术组。观察并对比两组患者的手术时间、术中出血量、住院时间及 术后恢复情况。结果：两组患者的手术时间比较差异无统计学意义（P>0.05）。与开放手术组比较,微创组患者术中出血量显著减 少、住院时间明显缩短,差异具有统计学意义（P<0.05）。与手术前比较,两组患者术后Cobb 角及伤椎高度均明显改善,差异具有 统计学意义（P<0.05）,但两组间比较差异无统计学意义（P>0.05）;两组患者术后JOA 评分均显著降低,差异具有统计学意义（P<0. 05）,但两组间比较差异无统计学意义（P>0.05）。结论：经肌间隙微创内固定术与传统椎弓根螺钉内固定术均能较好的复位固定胸 腰椎骨折,但经肌间隙微创内固定术具有创伤小、术中出血少、功能恢复快、住院周期短等优势,值得临床推广应用。     

脊柱跳跃型骨折的临床研究进展

脊柱跳跃型骨折指多节段非相邻的椎体骨折(multiple-level noncontiguous spinal fractures,MNSF)。对于非高龄患者,此类骨折通常为暴力性高能量损伤。由于MNSF受伤机制的复杂性,患者的临床表现不尽相同,导致其常发生漏诊或延迟诊断。目前,临床上对于MNSF发病率和损伤原因有很多报道,特别是其致伤机制,也存在很多理论。脊柱跳跃性骨折的治疗需全面考虑,如脊柱的不稳定性、畸形和骨折节段之间正常的椎体数目甚至患者想要减少住院时间的要求等。治疗时应按照各自损伤部位的情况决定治疗方案,强调个体化治疗。需要手术治疗的患者应依据其损伤特点选择相应术式,重建脊柱稳定性。本文主要就近年来MNSF的临床研究进展了进行总结,旨在为MNSF的临床诊疗提供参考。     

医院口腔颌面部骨折患者的临床特征分析及治疗效果调查

目的:调查研究医院口腔颌面部骨折(OMF)患者的临床特征及治疗效果。方法:选取我院2011年2月至2013年2月期间收治的OMF患者135例作为研究对象。对患者临床特征进行全面分析,并根据患者具体情况制定相应治疗方案,分析对比临床疗效情况。结果:患者男女比例为2.14:1,平均年龄为34.6±4.2岁,其中20~30岁所占比例最高,达42.96%。骨折原因主要为交通事故,占45.19%。骨折类型以单纯型下颌骨骨折最高发,占46.67%。切开复位并行钛板钛钉内固定较单纯接受钛钉颌间牵引内固定,前者临床有效率显著高于后者,差异有统计学意义(P0.05)。结论:OMF高发于男性青壮年,主要骨折原因为交通事故,且以单纯型下颌骨骨折类型居多,临床治疗切开复位并行钛板钛钉内固定疗效显著优于单纯接受钛钉颌间牵引内固定。     

Demonstration of aluminum in amyloid fibers in the cores of senile plaques in the brains of patients with Alzheimer’s disease

Aluminum (Al) exposure has been reported to be a risk factor for Alzheimer’s disease (senile dementia of Alzheimer type), although the role of Al in the etiology of Alzheimer’s disease remains controversial. We examined the presence of Al in the Alzheimer’s brain using energy-dispersive X-ray spectroscopy combined with transmission electron microscopy (TEM-EDX). TEM-EDX analysis allows simultaneous imaging of subcellular structures with high spatial resolution and analysis of small quantities of elements contained in the same subcellular structures. We identified senile plaques by observation using TEM and detected Al in amyloid fibers in the cores of senile plaques located in the hippocampus and the temporal lobe by EDX. Phosphorus and calcium were also present in the amyloid fibers. No Al could be detected in the extracellular space in senile plaques or in the cytoplasm of nerve cells. In this study, we demonstrated colocalization of Al and beta-amyloid (Abeta) peptides in amyloid fibers in the cores of senile plaques. The results support the following possibilities in the brains of patients with Alzheimer’s disease: Al could be involved in the aggregation of Abeta peptides to form toxic fibrils; Al might induce Abeta peptides into the beta-sheet structure; and Al might facilitate iron-mediated oxidative reactions, which cause severe damage to brain tissues.     

Age-related changes of Alzheimer's disease-associated proteins in cynomolgus monkey brains

We characterized senile plaques (SPs) immunohistochemically in cynomolgus monkey brains and also examined age-related biochemical changes of Alzheimer's disease (AD)-associated proteins in these brains from monkeys of various ages. In the neocortex of aged monkeys (>20 years old), we found SPs but no neurofibrillary tangles (NFTs). Antibodies against beta-amyloid precursor protein (APP) or apolipoprotein E (ApoE) stained SPs; however, the pattern of immunostaining was different for the two antigens. APP was present only in swollen neurites, but ApoE was present throughout all parts of SPs. Western blot analysis revealed that the pattern of APP expression changed with age. Although full-length APP695 protein was mainly expressed in brains from young monkeys (4-years-old), the expression of full-length APP751 protein was increased in brains from older monkeys (>20 years old). Biochemical analyses also showed that levels of various AD-associated proteins increased significantly with age in nerve ending fractions. Both SP-associated (APP) and NFT-associated proteins (tau, activated glycogen synthase kinase 3beta, cyclin dependent kinase 5, p35, and p25) accumulated in the nerve ending fraction with increasing age; however, we found no NFTs or paired helical filaments of tau in aged cynomolgus monkey brains. This age-related accumulation of these proteins in the nerve ending fraction was similar to that observed in our laboratory previously for presenilin-1 (PS-1). The accumulation of these SP-associated proteins in this fraction may be a causal event in the spontaneous formation of SPs; thus, SPs may be formed initially in nerve endings. Taken together, these results suggest that intensive investigation of age-related changes in the nerve ending and in axonal transport will contribute to a better understanding of the pathogenesis of neurodegenerative disorders such as AD.