不同剂量阿托伐他汀对急性脑梗死患者超敏C反应蛋白S100B蛋白水平及神经功能缺损的影响

目的：观察不同剂量阿托伐他汀对急性脑梗死患者超敏C反应蛋白(hs-CRP)、S100B水平及神经功能的影响,探索大剂量阿托伐他汀对脑梗死急性期治疗的益处。方法选择急性脑梗死患者96例,随机分为治疗组与对照Ⅰ组、对照Ⅱ组。治疗组服用阿托伐他汀40 mg/d,对照Ⅰ组服用阿托伐他汀20 mg/d,对照Ⅱ组服用阿托伐他汀10 mg/d,其余治疗均相同。分别于治疗前及治疗7、14 d后检测患者血清 hs-CRP和S100B水平,评价神经功能缺损程度。结果治疗7 d后,治疗组 hs-CRP水平明显下降(P<0．05),对照Ⅰ、Ⅱ组hs-CRP水平下降均不明显(P>0．05)。治疗组S100B水平较治疗前显著下降(P<0．05),对照Ⅰ、Ⅱ组S100B水平变化不明显(P>0．05)。治疗14 d后,治疗组hs-CRP水平进一步下降(P<0．05),对照Ⅰ、Ⅱ组血清hs-CRP水平有明显下降(P<0．05)。治疗组S100B水平进一步下降(P<0．05),对照Ⅰ组S100B水平较治疗前明显下降(P<0．05),对照Ⅱ组S100B水平变化不明显(P>0．05)。治疗后,3组神经功能缺损情况均较治疗前有不同程度改善(P<0．05),与对照组相比治疗组改善更明显。结论相对20 mg/d、10 mg/d的阿托伐他汀治疗急性脑梗死,40 mg/d的剂量可更明显降低hs-CRP、S100B蛋白水平,改善患者的神经功能缺损,有益于改善患者预后。     

老年人颅内动脉瘤破裂风险因素分析

目的 探讨与老年人(≥60岁)颅内动脉瘤破裂相关的临床及动脉瘤特征的风险因素.方法 回顾性分析2009年1月至2013年1月连续收治的320例≥60岁的颅内动脉瘤患者的临床资料和影像学资料,根据动脉瘤是否破裂分为破裂组和未破裂组,并对两组患者的性别、年龄、血压、吸烟、饮酒、多发动脉瘤、动脉瘤部位、动脉瘤瘤体大小进行单因素和logistic回归多因素分析.结果 单因素分析结果显示,老年人颅内动脉瘤破裂风险与年龄、高血压及动脉瘤瘤体直径相关(P＜0.05),与性别、吸烟、多发动脉瘤、动脉瘤部位不相关(P＞0.05).logistic回归多因素分析结果仍显示老年人颅内动脉瘤破裂风险与年龄、高血压及动脉瘤大小相关(P＜0.05),与性别、吸烟、多发动脉瘤、动脉瘤部位不相关(P＞ 0.05).结论 老年人颅内动脉瘤破裂风险随着年龄的增加而增加,并且与高血压及动脉瘤大小相关.     

高分辨率磁共振成像评估颅内动脉瘤破裂风险研究进展

筛选具有高危的颅内动脉瘤患者并进行针对性地治疗是预防动脉瘤破裂出血、降低其残死致残率的关键。随着影像学的发展,磁共振成像(MRI)越来越多的应用于颅内动脉瘤的评估。本文就近年来国内外高分辨率MRI在评估颅内动脉瘤破裂风险中的研究进展进行综述。     

血管内治疗大脑中动脉动脉瘤的研究进展

大脑中动脉(MCA)动脉瘤的最佳治疗方式仍存在争议。开颅手术夹闭一直是治疗MCA动脉瘤的首选方法,但随着血管内介入技术的进步和器具的改进,血管内治疗MCA动脉瘤的安全性和疗效也有进一步改善,并逐渐成为一种重要治疗方法。本文对MCA动脉瘤血管内治疗新技术及其安全性与疗效进行文献综述,以期为MCA动脉瘤治疗方式选择提供更多证据。     

瑞芬太尼对重型颅脑损伤患者脑氧代谢改善作用

目的 探讨瑞芬太尼对重型颅脑损伤患者脑氧代谢改善作用.方法 选取2011年12月至2013年9月期间云南省西双版纳州人民医院收治的重型颅脑损伤患者84例为研究对象,对患者的临床指标进行回顾性分析.结果 (1)比较2组入选对象麻醉前的各项氧代谢指标,数据比较差异无显著统计学意义;比较2组入选对象麻醉后10 min的氧代谢指标水平,治疗组的CERO2显著高于对照组,治疗组的CjvO2和Da-jvO2显著低于对照组,且数据比较差异有统计学意义(P＜0.05);(2)比较2组入选对象麻醉前的各项血动力指标,数据比较差异无显著统计学意义;比较2组入选对象麻醉后10 min的血动力指标水平,治疗组的Qmean和Wv显著高于对照组,治疗组的DR显著低于对照组,且数据比较差异均具有统计学意义(P＜0.05).结论 在临床针对重型颅脑损伤患者实施麻醉的实践过程中,采用瑞芬太尼的临床整体效果较好,对重型颅脑损伤患者脑氧代谢改善作用明显,是临床实践过程中理想选择方式之一.     

神经生长液对缺血性脑损伤的保护作用

目的观察神经生长液(NGD)对大鼠实验性脑缺血再灌注损伤的保护作用。方法采用大脑中动脉线栓法建立大鼠局灶性脑缺血再灌注模型,观察NGD对大鼠神经功能的恢复、血清总超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量、梗死体积、病理组织损伤及细胞超微结构改变的影响。结果NGD能改善大鼠的神经功能评分,增加血清SOD活性,降低血清MDA含量,减少梗死体积(P<0.05或0.01)。NGD能改善大鼠局灶性脑缺血再灌注3d后的病理组织学损害及细胞超微结构改变。结论神经生长液对实验性脑缺血再灌注损伤具有保护作用。     

Sex differences in associations between blood lipids and cerebral small vessel disease

Background and aims

Dyslipidemia predicts higher risk of coronary events and stroke and might be associated with cerebral small vessel disease (SVD). Previous studies linking blood lipids and SVD have yielded inconsistent results, which may be attributable to sex differences in lipids metabolism. The aim of this study was to investigate the relationships between blood lipids and SVD in neurologically healthy men and women.

Neoplastic lesions in CADASIL syndrome: report of an autopsied Japanese case

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL) is one of the most common heritable causes of stroke and dementia in adults. The gene involved in the pathogenesis of CADASIL is Notch3; in which mutations affect the number of cysteine residues in its extracellular domain, causing its accumulation in small arteries and arterioles of the affected individuals. Besides the usual neurological and vascular findings that have been well-documented in CADASIL patients, this paper additionally reports multiple neoplastic lesions that were observed in an autopsy case of CADASIL patient; that could be related to Notch3 mutation. The patient was a 62 years old male, presented with a past history of neurological manifestations, including gait disturbance and frequent convulsive attacks. He was diagnosed as CADASIL syndrome with Notch3 Arg133Cys mutation. He eventually developed hemiplegia and died of systemic convulsions. Autopsy examination revealed-besides the vascular and neurological lesions characteristic of CADASIL- multiple neoplastic lesions in the body; carcinoid tumorlet and diffuse idiopathic pulmonary neuro-endocrine cell hyperplasia (DIPNECH) in the lungs, renal cell carcinoma (RCC), prostatic adenocarcinoma (ADC) and adenomatoid tumor of the epididymis. This report describes a spectrum of neoplastic lesions that were found in a case of CADASIL patient that could be related to Notch3 gene mutations.     

Two novel mutations in NOTCH3 gene causes cerebral autosomal dominant arteriopathy with subcritical infarct and leucoencephalopathy in two Chinese families

Objective: To investigate the genetic pathogenic causes of cerebral autosomal dominant arteriopathy with subcritical infarct and leucoencephalopathy (CADASIL) in two Chinese families, to provide the molecular basis for genetic counseling and antenatal diagnosis. Methods: The genetic mutation of gene NOTCH3 of propositus and family members was analyzed in these two CADASIL families by polymerase chain reaction and DNA sequencing technology directly. At the same time, the NOTCH3 gene mutation point of 100 healthy collators was detected, to explicit the pathogenic mutation by function prediction with Polyphen-2 and SIFT. Results: Both propositus of the two families and patients with symptom were all accorded with the clinical features of CADASIL. It was shown by DNA sequencing that the 19^th exon [c. 3043 T > A (p.Cys1015Ser)] in gene NOTCH3 of propositus, 2 patients (II3, III7), and a presymptomatic patient (IV1) in Family I all had heterozygosity missense mutation; and the 3^rd exon [c.316T > G, p. (Cys106Gly)] in gene NOTCH3 of the propositus, a patient (IV3) and two presymptomatic patients (IV5, 6) in Family II all had heterozygosity missense mutation; and no mutations were detected in the 100 healthy collators. It was indicated by analyzing the function prediction that the mutation of [c. 3043 T > A (p.Cys1015Ser)] and [c.316T > G, p. (Cys106Gly)] may both influence encoding protein in NOTCH3. By analysis of the conservatism of mutation point in each species, these two basic groups were highly conserved. Conclusion: The heterozygosity missense mutation of 19^th exon [c. 3043 T > A (p.Cys1015Ser)] and the 3^rd exon [c.316T > G, p. (Cys106Gly)] in NOTCH3 gene are the new pathogenic mutations of CADASIL, and enriches the mutation spectrum of NOTCH3 gene.