Hereditary transthyretin amyloidosis (ATTR) is an autosomal dominant disease characterized by amyloid fibril deposition. The TTR c.148G > T mutation (V30L) in ATTR is rarely reported, and its biochemical properties are unknown. Seven patients and two asymptomatic carriers from two unrelated families diagnosed with V30L variant of ATTR were included. Data on clinical manifestations, laboratory examination, electrophysiology, ophthalmological corneal confocal microscopy (CCM), pathology and molecular biological experiments was collected and analyzed. Most patients initially experienced paresthesia, with varying degrees of peripheral neuropathy, autonomic dysfunction, and cardiac involvement. Nerve conduction studies showed extensive motor and sensory nerve involvement in upper and lower limbs. CCM revealed reduced corneal nerve density and fiber length. Sural nerve biopsies indicated loss of myelinated nerve fibers, with neurogenic patterns in gastrocnemius muscle biopsies. Asymptomatic carriers had nearly normal electrophysiology but mild reductions in corneal nerve fiber density and length. Sural nerve biopsies in carriers showed mild reductions in small myelinated nerve fibers. V30L mutation impaired thermodynamic and kinetic stability of the mutant protein. Plasma TTR tetramer concentration was lower in ATTR V30L patients compared to healthy donors. Small molecule stabilizers failed to exhibit satisfactory inhibition on fibril formation of V30L mutation in vitro. This study highlights the multisystem involvement in ATTR V30L patients, including neuropathy and cardiac issues. Both patients and carriers showed abnormalities in nerve conduction, corneal microscopy, and pathology. The V30L mutation impaired protein stability and reduced plasma TTR tetramer levels. Small molecule stabilizers were ineffective, indicating a need for alternative treatments.

Distal hereditary motor neuropathies (dHMN) are a group of heterogeneous diseases and previous studies have reported that the compound heterozygous recessive MME variants cause dHMN. Our study found a novel homozygous MME variant and a reported compound heterozygous MME variant in two Chinese families, respectively. Next-generation sequencing and nerve conduction studies were performed for two probands. The probands in two families presented with the muscle weakness and wasting of both lower limbs and carried a c.2122 A > T (p.K708*) and c.1342 C > T c.2071_2072delinsTT (p.R448* p.A691L) variant, respectively. Prominently axonal impairment of motor nerves and slight involvement of sensory nerves were observed in nerve conduction study. Our study reported a “novel” nonsense mutation and a missense variant of autosomal recessive late-onset dHMN and reviewed reported MME variants associated with dHMN phenotype.

This study reported a case of MELAS syndrome presenting as the initial imaging characteristics of Fahr’s syndrome with “near” sudden unexpected death in epilepsy (SUDEP) and lateralized periodic discharges (LPD). The patient, a young boy, experienced loss of consciousness 2 days prior, which was followed by two limb and facial convulsions. He was later found in cardiac arrest during hospitalization, but regained consciousness gradually after receiving cardiopulmonary resuscitation and tracheal intubation. The patient exhibited short stature, intellectual disability, poor sports abilities, and academic performance since childhood, but had no family history. Emergency head computed tomography (CT) revealed high density calcification in bilateral caudate nucleus, lentiform nucleus, thalamus, and dentate nucleus with evidence of an acute process. The patient was transferred to the neurology department where he continued to recover consciousness, though he experienced dysarthria, left limb hemiplegia, and hemiparesthesia. Changes in head magnetic resonance imaging (MRI) findings were noted at admission, 1 month later, and 6 months later. LPD were observed in his video electroencephalogram. The CT urography indicated a narrow left ureteropelvic junction with left hydronephrosis, which was suggestive of ureteropelvic junction obstruction. Ultimately, a diagnosis of near-SUDEP was suspected in this patient, indicating a rare case of MELAS syndrome with near-SUDEP and LPD. The gene tests results revealed the presence of the mitochondrial DNA A3243G mutation, leading to the final diagnosis of MELAS syndrome. This case expands the clinical disease spectrum of the MELAS syndrome.

目的 对比分析应用移动卒中单元(MSU)行院前静脉溶栓与常规静脉溶栓对急性缺血性卒中(AIS)的治疗效果.方法 回顾性连续纳入曲靖市第一人民医院神经内科2022 年2 月至2022 年12 月行静脉溶栓的AIS患者.收集患者的一般资料及临床资料,包括年龄、性别、吸烟史、高血压病、糖尿病、高脂血症、既往卒中史、心房颤动史、发病时间、静脉溶栓时间、基线美国国立卫生研究院卒中量表(NIHSS)评分、静脉溶栓后48h症状性颅内出血、静脉溶栓后7 d NIHSS评分、静脉溶栓后90d改良Rankin量表(mRS)评分、静脉溶栓后90d死亡及静脉溶栓过程中是否发生任何过敏反应或其他系统出血等.应用MSU进行院前静脉溶栓的AIS患者为MSU溶栓组,院内阿替普酶静脉溶栓(普通急救车入院或自行来院)的AIS患者为常规溶栓组.观察终点指标包括时间指标、疗效指标和安全性指标.时间指标为发病至静脉溶栓时间;疗效指标为静脉溶栓后7 d NIHSS评分、90 d mRS评分;安全性指标包括静脉溶栓后48h症状性颅内出血、静脉溶栓过程中发生任何过敏反应或其他系统出血及静脉溶栓后90d患者死亡.结果 共纳入151 例应用阿替普酶行静脉溶栓的AIS患者,其中男94 例(62.3%),女57 例(37.7%),年龄39～86 岁,中位年龄为67(58,77)岁.MSU溶栓组50 例,常规溶栓组101 例.两组患者一般资料中年龄、性别、高血压病、高脂血症、心房颤动、吸烟史、卒中史及基线NIHSS评分差异均无统计学意义(均P＞0.05),糖尿病史差异有统计学意义(P =0.024).MSU溶栓组发病至静脉溶栓时间较常规溶栓组明显缩短[93.0(64.5,136.5)min比153.0(118.5,193.5)min,Z =-5.058,P＜0.01].MSU溶栓组溶栓后7 d NIHSS评分低于常规溶栓组[1.0(0.0,3.0)分比2.0(1.0,4.0)分,Z=-2.464,P=0.013],且静脉溶栓后90 d mRS评分较常规溶栓组低[0.0(0.0,0.5)分比0.0(0.0,1.0)分,Z =-2.037,P =0.042].两组静脉溶栓后48h症状性颅内出血发生率及90d内病死率差异均无统计学意义(均P＞0.05).两组患者静脉溶栓过程中均未出现过敏及其他系统出血.结论 基于MSU的AIS院前静脉溶栓可以显著缩短发病至静脉溶栓时间,对改善患者神经功能和提高临床疗效具有一定的作用.

Objective The over-age phenomenon of simple febrile seizures (SFS) was found during the epidemic in COVID-19, but there was no clear explanation, especially in China. This study aimed to analyze the clinical and auxiliary examination features of SFS in children infected with the coronavirus disease 2019 (COVID-19). Methods In total, 78 patients with SFS in the Department of Pediatric and Neurology of Qujing First People's Hospital were enrolled and divided into the COVID-19-positive group (case group) and the COVID-19-negative group (control group). The clinical characteristics, auxiliary examinations, and risk factors were analyzed. Results There were significant differences in age stratification between the two groups. The proportion of children aged over 5 years old in the case group (47.4%) was higher than that of the control group (5%) ( p < 0.0001). In terms of sex distribution, the proportion of males in the case group was higher than that in the control group (71.1% vs. 50%), but the difference was not statistically significant ( p = 0.0678). For blood cell analysis, the values of white blood cells (WBC), lymphocytes (LY), and monocytes (MN) in the case group were significantly lower than those in the control group ( p < 0.01). Serum electrolyte analysis showed the greatest difference in blood sodium. The proportion of hyponatremia in the case group was higher than that in the control group (36.8% vs. 17.5%), but the difference did not reach statistical significance ( p = 0.0745). A multivariate logistic regression analysis showed that the history of FS was a independent protective factors for SFS in children with COVID-19 (OR = 0.115, p = 0.009), and age was an independent risk factor for SFS in children with COVID-19 (OR = 1.042, p = 0.001). Conclusion Age distribution, sex a previous history of FS and hyponatremia were different between children with and without COVID-19 in SFS. The history of FS was an independent protective factors for SFS in children with COVID-19.

目的 本研究旨在探究云南滇东北地区吉兰-巴雷综合征(GBS)患者临床特点,以期为该地区GBS提供临床诊治依据.方法 本研究回顾性分析2018年2月-2022年10月曲靖市第一人民医院神经内科GBS住院患者的临床资料,患者主要来自中国滇东北地区.本研究也对中国近年报道的各地区GBS临床特点进行对比.结果 本研究共回顾性纳入112例符合条件的患者,其中AIDP 49例,AMAN 33例,本组患者春冬两季较高发,以春季为主(38例,33.9%),AIDP多见于冬季(15例,30.6%),AMAN多见于春季(14例,42.4%).GBS患者的中位发病年龄为56岁(范围:8～83岁),在60～69岁年龄达到峰值.男女患病比为1.60(69∶43),上呼吸道感染(25例,22.3%)和肠胃炎(14例,12.5%)为最常见的前驱感染事件.AIDP为最常见的亚型(49例,51.6%),AIDP与AMAN两组在发病年龄、前驱感染事件、初始症状、临床表现、脑脊液蛋白水平、治疗效果等方面无统计学差异(P＞0.05).12例患者(10.7%)在疾病高峰时需要机械通气,机械通气组患者颅神经受累比例,尤其是吞咽困难患者比例较非机械通气组更高(75.0%vs 32.0%,P=0.0081).中国南部、东部及大理地区、滇东北地区GBS患者主要以上呼吸道感染为主要前驱事件(22%～35%),而北方地区胃肠炎比例较高(24%).AMAN为中国北部(40%)和东部(35%)的主要GBS亚型,而AIDP为中国南部(49%)的主要亚型.结论 GBS存在地区差异,滇东北地区GBS亚型仍以脱髓鞘型为主;患者发病年龄以60～69岁男性为主,呈现双峰分布特点;胃肠道和呼吸道感染仍是本地区GBS的主要前驱事件.颅神经受累,尤其是球部肌肉受累与机械通气风险可能相关.

目的 通过研究急性缺血性脑卒中血运重建前后与预后不良有关的影响因素,以期为临床医师预测患者预后提供更多的生物学标志物.方法 收集2020年12月至2021年10月昆明医科大学附属曲靖医院神经内科及神经介入科收治的急性缺血性脑卒中并接受血运重建治疗(包括静脉溶栓、机械取栓切除术或者2者均行)的患者179例,根据3个月后mRS评分分为预后良好组(mRS＜3分)和预后不良组(mRS≥3分).比较2组患者的一般资料、临床检验指标、血运重建前后NLR值、NIHSS评分等,并进一步分析预后不良组患者的独立危险因素.结果 (1)预后良好与预后不良2组患者的甘油三酯、总胆固醇、C反应蛋白、入院的NIHSS评分、中性粒细胞数及百分比、淋巴细胞数及百分比、NLR值及血运重建后8h的白细胞、中性粒细胞数及百分比、淋巴细胞数与百分比、NLR值,差异具有统计学意义(P＜0.05);(2)多因素Logistic回归分析,入院NIHSS评分(OR=1.123,95％CI 1.065～1.184,P＜0.05)是AIS患者血运重建后3个月预后不良的独立危险因素,临床诊断分界值为11;(3)NLR值比较:预后不良组血运重建前后的NLR值均高于预后良好组,差异有统计学意义(P＜0.05),AIS患者血运重建后NLR值较血运重建前升高,差异有统计学意义(P＜0.05).结论 入院时的NIHSS评分是AIS血运重建患者发病3个月不良预后的独立危险因素.AIS患者血运重建前后NLR变化具有上升趋势,预后不良组血运重建前后的NLR高于预后良好组,但并非AIS患者血运重建3个月后不良预后的独立危险因素.

Objectives:Epilepsy is a chronic neurological disorder that is characterized by episodes of seizure.Methods:In this study, patients with status epilepticus in the Intensive Care Unit of the Department of Neurology of Qujing First People's Hospital were collected and treated with levetiracetam injection, continuous bedside EEG monitoring (cEEG) technology, and quantitative EEG (qEEG) technique. The inhibitory effects of different doses of levetiracetam injection and sodium valproate on abnormal discharge, the improvement of clinical symptoms, the incidence of adverse reactions, and prognosis were monitored, analyzed, and compared.Results:Compared with the experimental group of sodium valproate, 1000 mg/d levetiracetam group and 1500 mg/d levetiracetam group had a high probability of successful symptom control and a short control time. The patients had a low recurrence rate and a long recurrence time, and the probability of abnormal discharge in EEG was low.Conclusions:The recording results showed that levetiracetam could significantly inhibit the abnormal discharge of patients. Compared with sodium valproate, high-dose levetiracetam is a drug with a rapid effect, good effect, and long action time.

目的 探讨艾司西酞普兰联合乌灵胶囊在脑梗死恢复期合并抑郁中的应用效果.方法 方便选取该院2019年4月—2020年4月期间共80例脑梗死恢复期合并抑郁患者,随机数表法设为对照组(n=40)以及观察组(n=40),分别开展常规艾司西酞普兰治疗以及艾司西酞普兰联合乌灵胶囊治疗.评价两组患者各项指标水平.结果 治疗后,观察组患者HAMD分值(13.22±2.54)分低于对照组,差异有统计学意义(t=12.720,P<0.05);观察组治疗后IL-6(51.24±6.24)μg/L、IL-23(70.14±8.14)μg/L、TNF-α(75.25±8.24)μg/L、NE(80.87±9.01)ng/L、5-HT(296.32±33.46)μg/L低于对照组的(72.01±9.24)μg/L、(91.34±10.67)μg/L、(98.45±10.76)μg/L、(56.22±5.25)ng/L、(270.45±25.74)μg/L,差异有统计学意义(t=11.782、9.991、10.827、14.950、3.876,P<0.05).结论 对脑梗死恢复期合并抑郁患者开展艾司西酞普兰联合乌灵胶囊治疗,可有效改善患者心理状态以及炎症水平,对改善患者预后有积极意义.

延髓(medulla oblongata)位于脑干下端,连接脑桥和脊髓,是人类的生命中枢,其血供较中脑、脑桥丰富.延髓解剖结构复杂,神经纤维密集,血管血供复杂,发生缺血损害时临床表现复杂多样,且容易累及呼吸中枢导致预后差.延髓梗死分为外侧梗死(lateral medullary infarction,LMI)和内侧梗死(medial medullary infarction,MMI),其中延髓外侧梗死(LMI)为延髓梗死的常见类型,占延髓梗死的75％.延髓梗死的临床表现与梗死部位相关,依据不同梗死部位及出现的不同临床表现命名为各类延髓梗死综合征,其预后差异较大,与血栓形成的部位、侧支循环的建立、临床治疗及并发症均密切相关.近年来随着人们关注度的提升及影像学技术的发展,各类延髓梗死的报道逐渐增多,主要集中于不典型症状、少见延髓综合征及其预后的报道,对指导临床早期诊断、精准定位、个体化评估、治疗及预测预后具有重要意义.为加深对延髓梗死的认识,该文就各延髓梗死综合征的临床特点及预后的研究进展做一综述.

目的 观察阿替普酶辅助治疗急性脑梗死伴心房颤动的临床效果.方法 选取2017年6月-2019年12月于云南省曲靖市第一人民医院住院治疗的发病时间＜4.5 h急性脑梗死伴心房颤动患者49例,患者均在常规治疗的基础上采用阿替普酶治疗.比较治疗前、治疗后2周、3个月美国国立卫生研究院卒中量表(NIHSS)评分和Barthel指数评分,观察患者治疗期间出血发生率.结果 治疗后2周、3个月,49例患者NIHSS评分均低于治疗前,Barthel指数评分均高于治疗前(P＜0.01);治疗期间出现症状性脑出血2例,皮肤黏膜出血1例,出血总发生率为6.12％(3/49),无患者死亡.结论 阿替普酶辅助治疗急性脑梗死伴心房颤动可减少神经功能缺损,提高患者生存质量,安全性较高,可在临床予以推广.

目的 分析左乙拉西坦注射液对惊厥性癫痫持续状态(CSE)的控制效果及预后,以期在临床推广应用.方法 收集2018年9月至2021年4月曲靖市第一人民医院神经内科重症监护室(NICU)CSE患者80例,按照随机分组原则选取左乙拉西坦组(实验组)40例,丙戊酸钠组(对照组)40例,比较其疗效、不良反应、脑电图变化、Synek分级及预后.结果 左乙拉西坦组有效控制率为77.5％,丙戊酸钠组有效控制率为67.5％,2组无统计学差异(P=0.317).左乙拉西坦组较丙戊酸钠组起效时间更短,2组具有统计学差异(P＜0.05).预后分析:单因素分析显示,症状未得到有效控制、控制成功的时间≥60 min、脑电图有异常放电以及Synek分级和预后不良显著相关,差异有统计学意义(P＜0.05),多因素Logitstic回归分析结果显示,Synek分级与预后呈负相关(β=-3.867,OR＜1),Synek分级较高是预后不良的独立危险因素及预测因素(P＜0.05).结论 左乙拉西坦注射液对CSE的控制更迅速、控制效果更显著,可应用于临床,脑电图分析(脑电图异常放电、Synek分级)可为判断CSE预后提供可靠依据.

目的 观察阿替普酶静脉溶栓联合丁苯酞治疗急性脑梗死的临床效果.方法 选取2017年10月-2019年3月于云南省曲靖市第一人民医院神经内科住院治疗的急性脑梗死患者84例,采用随机数字表法分为联合用药组和常规溶栓组各42例.2组患者均接受控制血糖、血压、血脂,降低颅内压和抗血小板聚集等常规治疗,在此基础上,常规溶栓组使用阿替普酶静脉溶栓治疗,联合用药组在常规溶栓治疗的基础上给予丁苯酞氯化钠注射液治疗.比较2组治疗前、治疗后2周、3个月的美国国立卫生研究院卒中量表(NIHSS)评分和Barthel评分.结果 治疗后2周和3个月,2组患者NIHSS评分均低于治疗前,Barthel评分均高于治疗前,且联合用药组的变化幅度大于联合用药组(P<0.05).结论 阿替普酶静脉溶栓联合丁苯酞注射液治疗可改善急性脑梗死患者的神经功能缺损症状.

Background: As the priority drug for treating acute ischemic stroke (AIS), alteplase is a thrombolytic drug with strong fibrin specificity. It can obviously treat AIS with high safety. However, the validity of its time window is controversial. This study focus on the efficacy and safety of intravenous thrombolysis with alteplase for treating AIS at different time windows. Methods: Retrieval of English database (PubMed, Embase, Web of Science, the Cochrane Library) and Chinese database was conducted (China National Knowledge Infrastructure, WAN FANG, VIP, China Biology Medicine disc) by computers. From the establishment of the database to October 2020, a retrospective study and case-control study on intravenous thrombolysis at different time windows for treating AIS were conducted. Two researchers independently conducted data extraction and quality evaluation of literature on the included studies, and RevMan5.3 was used for Meta-analysis on the included literature. Results: This study aims to evaluate the efficacy and safety of intravenous thrombolysis with alteplase at different time windows for treating AIS by National Institutes of Health Stroke Scale score, modified Rankin Scale rating scale, spontaneous intracerebral hemorrhage incidence rate, All-cause mortality, and so on. Conclusions: This study will provide an evidence-based basis for the clinical efficacy of alteplase for treating AIS by thrombolytic therapy at different time windows. Ethics and dissemination: Private information from individuals will not be published. This systematic review also does not involve endangering participant rights. Ethical approval was not required. The results may be published in a peer-reviewed journal or disseminated at relevant conferences.

Objectives: miR-199a can regulate autophagy, its underlying mechanisms remain unknown. The purpose of this study was to investigate the mechanisms of miR-199a involved in regulating autophagy in a 1-methyl-4-phenylpyridine (MPP+)-induced in vitro model of PD. Methods: PC12 cells were incubated in MPP+, and the expression levels of miR-199a were bidirectionally regulated via either transfection of an miR-199a mimic or incubation in miR-199a inhibitors. The experimental manipulations were divided into four groups, including the control group, MPP+ group, MPP+ + miR-199a mimic group, and MPP+ + miR-199a inhibitor group. MTT, CCK-8, qRT-PCR, Western blotting and linear correlation analysis were performed to evaluate various experimental indicators. Results: At increasing MPP+ concentrations, the following results were found: the expression levels of miR-199a, phosphorylated AKT and mTOR proteins expression decreased; the expression levels of phosphatase and tensin homologue (PTEN), GSK3 beta, Beclin1, and LC3II increased; PC12 autophagy increased; and cellular viability and survival rates decreased. Transfection of an miR-199a mimic increased miR-199a expression and induced all of the following: the expression levels of PTEN, GSK3 beta, Beclin1, and LC3II decreased; the expression levels of phosphorylated AKT and mTOR proteins expression increased; PC12 autophagy decreased; and cellular viability and survival rates increased. Discussion: In this in vitro study, we found that increasing miR-199a expression in PC12 cells reduced protein levels of Beclin1 and LC3II, decreased autophagy, enhanced cellular viability, increased survival rate, and ameliorated MPP+-induced parkinsonian-like cellular pathologies by targeting pro-autophagic pathways and GSK3 beta to activate PTEN/AKT/mTOR signaling.

Objective To investigate the associated factors and trends of prehospital delay in elderly patients with acute ischemic stroke (AIS).Methods Elderly patients with AIS admitted to the First People's Hospital of Qujing from 2007 to 2017 were enrolled retrospectively.The data of patients was collected from the medical records.Onset-to-door time ＞ 2 h was defined as prehospital delay.The demographic and baseline data were compared between the delay group and the non-delay group.Multivariate logistic regression analysis was used to determine the associated factors for prehospital delay.In addition,the trends of prehospital delay time at the different stages of the study were also analyzed.Results A total of 1 566 patients with AIS aged ≥65 years were enrolled.Their mean age was 75.61 ±6.06 years.The mean time of prehospital delay was 10.83 ± 7.47 h (median time 8.27 h).Multivariatelogistic regression analysis showed that advanced age (odds ratio [OR] 1.271,95％ confidence interval [CI] 1.029-2.896;P =0.039),nocturnal onset (OR 1.413,95％ CI 1.067-3.859;P=0.013),and atypical symptom onset (OR 2.345,95％ CI 1.184-8.126;P=0.029) were independently positively correlated with prehospital delay,while the emergency medical service transport (OR 0.743,95％ CI 0.261-0.998;P =0.010),having medical insurance (OR 0.219,95％ CI 0.015-0.799;P =0.042),and having a bystander at the time of onset (OR 0.618,95％ CI 0.149-0.814;P=0.003) were independently negatively correlated with prehospital delay.At the different stages of the study,January 2007 to October 2010,November 2010 to April 2015,and May 2015 to December 2017,the mean time of prehospital delay was 12.59 ± 7.06 h,10.57 ±7.78 h,and 8.47 ±7.07 h,respectively.They showed a decrease trend,but the difference was not statistically significant.Conclusion Advanced age,nocturnal onset,and atypical symptom onset were the independent risk factors for prehospital delay,while emergency medical service transport,having medical insurance,and having a bystander at the time of onset were the independent protective factors for prehospital delay.The delay time of the elderly patients with AIS is declining year by year,but the improvement is not significant.The delay in seeking timely medical intervention remains an important public health problem.

目的 探讨血清同型半胱氨酸(homocysteine,Hcy)水平与重组组织型纤溶酶原激活剂(recombinant tissue plasminogen activator,rt-PA)溶栓治疗急性缺血性脑卒中(acute ischemic stroke,AIS)老老年患者预后的关系.方法 收集符合研究入选标准患者47例,并依据Hcy水平分为Hcy高水平(≥18.54μmol/L)组(A组)24例和Hcy低水平组(<18.54μmol/L)组(B组)23例,分析2组年龄、性别、脑血管疾病危险因素、起病至静脉溶栓时间、血糖、血脂、尿酸、纤维蛋白、血红蛋白、血小板计数、卒中类型和临床结局等指标.所有患者在溶栓治疗24 h后行CT/MRI检查以排除脑出血.采用美国国立卫生研究院卒中量表(National Instituteof Health Stroke Scale,NIHSS)与改良Rankin量表(Modified Rankin Scale,MRS)评估神经功能,以溶栓治疗90 d后MRS评分≥4分为预后不良.分析影响急性缺血性脑卒中溶栓患者预后的危险因素,并计算Hcy预测预后的潜在界值.结果 2组Hcy水平均高于正常,其水平与糖尿病、吸烟、饮酒、尿酸及血红蛋白有关.治疗1周后,Hcy高水平组NIHSS评分明显高于低水平组(P<0.05),且高水平组24 h后症状性出血转化风险增加(P<0.05).治疗3个月后与Hcy低水平组相比,Hcy高水平组MRS评分较低、临床结局较差(P<0.05).Hcy水平和初始NIHSS评分是AIS老老年患者接受rt-PA溶栓治疗预后不良的危险因素,Hcy预测预后不良的潜在最佳界值可能为21.35μmol/L(敏感度78.6％,特异度63.3％).结论 Hcy高水平可能是AIS老老年患者接受rt-PA溶栓治疗预后不良的潜在独立预测因子,最佳界值是21.35μmol/L.

脑微出血是由于脑微小血管病变所致的以脑微小出血为主要影像学表现的脑血管病,与各种神经系统疾病具有相关性.由于脑微出血有时并不会产生相应的临床症状而易被患者忽视,随着时间的推移对患者的生活质量及健康产生严重的影响,现对脑微出血的发病机制、临床意义及检查手段作一综述,以提高临床检出率,并为脑微出血的防治提供临床依据.

The result of ambulatory EEG (AEEG) examination on 168 comatose patients showed that AEEG grading was negatively correlated with Glasgow Coma Scale (GCS) score (r = - 0.995, P = 0.005). More serious the patients' condition was and the deeper coma they were in, the lower GCS score and the higher EEG grade they would got. Among all patients, there were 84 cases with AEEG grade Ⅱ, in whom 74 cases (88.10% ) had favorable prognosis; 26 cases (49.06% ) of 53 cases with grade Ⅲ and 4 cases (12.90% ) of 31 cases with grade Ⅳ - Ⅴ had favorable prognosis. The differences between groups had statistical significance ( χ 2 = 60.565, P = 0.042). AEEG is non-invasive, repeatable and easy to operate, which is in favor of the neurological evaluation and prognosis of patients with coma. DOI: 10.3969/j.issn.1672-6731.2016.10.013

The expression of let-7 family members was differentiated in ischemic stroke (IS), functioning as an important regulating molecular in the pathophysiology of stroke. We hypothesized that genetic polymorphism in the promoters of let-7 family may be associated with the risk of IS. To test this hypothesis, we investigated the association of the rs10877887 and rs13293512 in the promoters of let-7 family with the susceptibility to IS. A hospital-based case–control study was performed. The rs10877887 genotype was determined by using a polymerase chain reaction-restriction fragment length polymorphism assay, and the rs13293512 genotype was determined by using a TaqMan assay. We found that the rs13293512CC genotype was associated with a reduced risk of IS (CC vs. TT: adjusted OR = 0.43, 95 % CI 0.26–0.71; dominant model: adjusted OR = 0.70, 95 % CI 0.49–0.98; recessive model: adjusted OR = 0.45, 95 % CI, 0.28-0.73). Stratification analysis showed that the rs10877887TT carriers had a higher level of total cholesterol compared to rs10877887TC/CC carriers (P = 0.03). Combined analysis showed that the rs10877887TC/CC and rs13293512TC/CC genotypes had a reduced risk of IS risk (adjusted OR = 0.58, 95 % CI 0.36–0.95). Our findings suggest that the rs13293512 polymorphism may be a protective factor for the development of IS.