Objective To investigate the prevalence and influencing factors of cognitive impairment in patients with temporal lobe epilepsy (TLE). Methods Total 58 patients with TLE admitted to Shenzhen People's Hospital from May 2017 to January 2026 were enrolled. Montreal Cognitive Assessment (MoCA) was used to evaluate cognitive function. Univariate and multivariate Logistic regression analyses were performed to identify risk factors for comorbid cognitive impairment in TLE patients. Receiver operating characteristic (ROC) curves were plotted to evaluate predictive efficacy of these factors for cognitive impairment. Results A total of 58 patients were divided into a cognitive impairment group (MoCA score<26, n=42) and a normal cognitive function group (MoCA score≥26, n=16). Logistic regression analysis showed that education level of junior high school or below (OR=4.788, 95%CI: 1.298-17.664; P=0.019) and the use of≥2 kinds of antiepileptic seizure medicine (ASM; OR=5.421, 95%CI: 1.032-28.482, P=0.046) were risk factors for cognitive impairment in patients with TLE. ROC curve showed that area under the curve (AUC) for education level of junior high school or below, the use of≥2 kinds of ASM, and their combination in predicting cognitive impairment were 0.701 (95%CI: 0.547-0.855, P=0.019), 0.676 (95%CI: 0.530-0.821, P=0.040) and 0.774 (95%CI: 0.639-0.908, P=0.001), respectively. The corresponding sensitivities were 71.40%, 47.60% and 83.30%, and the specificities were 68.70%, 87.50% and 62.50%, respectively. The predictive performance of the combined indicator was superior only to that of using≥2 kinds of ASM (Z=2.426, P=0.015). Conclusions Patients with TLE have a high risk of comorbid cognitive impairment, which is influenced by factors such as education and the kinds of ASM.

ABSTRACTBackground and aimsRhynchophylline (RHY) can alleviate some cognitive flexibility impairment and stereotyped behavior for attention‐deficit hyperactivity disorder (ADHD) and Tourette syndrome (TS) patients as one of a key extract and an active ingredient in Ningdong granule (NDG), which is a Traditional Chinese medicine (TCM) preparation widely used in the treatment of ADHD and TS children in China; however, the underlying mechanism is not well understood. Therefore, this study aimed to evaluate how RHY alleviates hyperactivity and cognitive flexibility impairment while inhibiting inflammatory responses in mice that partly lack dopamine transporter protein (DAT− mice).MethodsMale DAT− mice were randomly divided into the RHY group (n = 8) and administered RHY (30 mg/kg) in the DAT− group (n = 8) and administered saline (i.p., 10 mL/kg) in wild‐type (WT) mice as the WT control group (n = 8). Hyperactivity and cognitive flexibility impairment were evaluated by the open field test (OFT) and the Morris water maze (MWM) test. The levels of the inflammatory factors of tumor necrosis factor‐α (TNF‐α) and interleukin‐1β (IL‐1β) in cortical homogenates were tested by enzyme‐linked immunosorbent assays (ELISA) after 8 weeks of treatment with RHY. In vitro, primary microglia and astrocytes extracted from the cortices of DAT− neonatal mice and WT neonatal mice were treated with lipopolysaccharide (LPS) (1 mg/mL) to induce neuroinflammatory responses and with RHY (20 mM) for 48 h. The levels of the inflammatory factors TNF‐α, IL‐1β, inducible nitric oxide synthase (iNOS), and cyclooxygenase‐2 (COX2) in the culture medium were measured at 6 h, 24 h, and 48 h after treatment with LPS and RHY.ResultsRHY ameliorated hyperactivity and cognitive flexibility impairment in DAT− mice and inhibited the expression of the inflammatory factors TNF‐α, IL‐1β, iNOS, and COX‐2 in microglia and astrocytes in vitro, and also inhibited the expression of TNF‐α and IL‐1β in cortical homogenates after 8 weeks of treatment.ConclusionRHY improved hyperactivity and cognitive flexibility impairment through inhibiting inflammatory responses in DAT− mice.

间充质干细胞(MSCs)是一种多能干细胞.近来研究发现,MSCs分泌的外泌体具有促进神经细胞再生、调节免疫反应、促进血管生成等多种功能.本文主要综述MSCs源外泌体在神经系统疾病中的研究进展,以期探讨出其在神经系统疾病的治疗方面发挥的重要作用.

BACKGROUND AND PURPOSE:The present study analyzed the relationship between circulating trimethylamine N-oxide (TMAO) levels and stroke severity in diabetic patients with acute ischaemic stroke. A further aim was to investigate whether higher TMAO levels were associated with platelet aggregation and glycemic variability.METHODS:This was a cross-sectional analysis of 108 patients with type 2 diabetes mellitus (DM) undergoing acute ischaemic stroke and 60 healthy controls. Fasting plasma TMAO was measured using high-performance liquid chromatography with online electrospray ionization tandem mass spectrometry.RESULTS:Plasma TMAO levels of patients with acute ischaemic stroke were significantly higher than those of healthy controls. Amongst stroke patients, 50 were defined as undergoing mild stroke, and their plasma TMAO levels were lower compared to those with moderate to severe stroke. Platelet aggregation and mean amplitude of glycemic excursions were both correlated with plasma TMAO levels and these relationships remained significant in multiple linear regression analyses. Moreover, in streptozotocin-induced diabetic rats fed a diet enriched with choline to increase TMAO synthesis, platelet aggregation was significantly increased in the DM + choline and fluctuating DM (FDM) + choline groups compared to the control group. This increase was abolished in rats receiving oral antibiotics, which markedly reduced plasma TMAO levels. Importantly, compared with the DM + choline group, the FDM + choline group displayed significantly elevated TMAO levels and higher platelet aggregation.CONCLUSIONS:Our results demonstrated that higher plasma TMAO levels were associated with stroke severity and suggested a novel link between plasma TMAO levels and glycemic variability in diabetic patients with acute ischaemic stroke.

Introduction: Anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis, a serious neurological autoimmune disorder caused by autoantibodies with diverse clinical manifestations, may simultaneously onset with antimyelin oligodendrocyte glycoprotein (MOG) demyelination after recurrent central nervous system (CNS) demyelination. Case Report: We present a case of anti-NMDAR encephalitis combining with anti-MOG CNS demyelination following recurrent CNS demyelination. A 38-year-old man admitted to hospital developed epileptic seizures following recurrent episodes of cross-sensory disturbance and dizziness. Magnetic resonance imaging (MRI) showed a demyelinating lesion in the right brainstem initially. Despite a good response to methylprednisolone pulse therapy at the beginning, the patient still had relapses and progression after corticosteroid reduction or withdrawal. Then brain MRI discovered new serpentine lesions involving extensive cerebral cortex on his second relapse. Repeat autoantibodies test indicated cerebrospinal fluid (CSF) NMDAR antibodies coexisted with MOG-Abs simultaneously, suggesting the diagnosis of anti-NMDAR encephalitis with anti-MOG CNS demyelination. Results: After a definite diagnosis, the patient was treated with mycophenolate mofetil (MMF) and corticosteroid. He was discharged after his symptoms ameliorated. No neurological sequels remained, and there were no effects on his activities of daily living after 6 months of immunoregulatory therapy of MMF and corticosteroid. Conclusion: For individuals with recurrent CNS demyelination, especially combining with cortical encephalitis, repeated detection of autoantibodies against AE, and demyelination in CSF/serum can be helpful to enable a definite early diagnosis. For patients who suffer from anti-NMDAR encephalitis combining with anti-MOG CNS demyelination, second-line immunotherapy is recommended when first-line treatment such as steroids, intravenous immunoglobulin G (IVIG) and plasma exchange has been proven ineffective to prevent the relapse of disease.

Objective: To describe the clinical features, laboratory data, treatment, and outcomes of anti-N-methyl-D-aspartate (NMDAR) encephalitis in Chinese patients. Methods: This retrospective study included hospitalized patients definitively diagnosed with anti-NMDAR encephalitis and positive for anti-NMDAR antibodies in the cerebrospinal fluid (CSF) in Shenzhen People's hospital, between November 2015 and February 2020. The clinical manifestation, laboratory data, treatments and outcomes were collected retrospectively. Patients were followed up for more than 1 year. Results: The study included 31 patients (15 men, 48.4%) with a median age of 31 years (in terquartile range 21-48). The most common clinical presentations were psychosis (n = 23, 74.2%), seizures (n = 20, 64.5%), and memory impairment (n = 20, 64.5%). Total magnetic resonance imaging abnormalities were found in 11 patients (35.5%), with the medial temporal and frontal lobes as the most commonly involved. Abnormal electroencephalogram was observed in 16 patients (51.6%). Five out of 31 patients (19.5%) were diagnosed as neoplasm, including five females with ovarian teratoma and one male with a central nervous system tumor. Multiple immune antibodies, including anti-SSA antibody in four patients (15.4%), anti-Ro52 antibody in four (15.4%), antinuclear antibody (ANT) in four (15.4%), anti-thyroglobulin antibodies (TGAb) in five (17.2%), and thyroid peroxidase antibodies (TPOAb) in three (10.3%) were present. All patients received first-line immunization therapy (intravenous immunoglobulin, glucocorticoids, or plasmapheresis alone or combined), and only two patients (7.3%) received second line immunization therapy (rituximab). Mechanical ventilation was more necessary in women (37.5%) than in men (6.7%) (p = 0.04), and 29 (93.5%) had favorable clinical outcomes. At more than 12 months of follow-up, the median modified Rankin Scale score decreased from 4 to 0. Conclusions: Patients with anti-NMDAR encephalitis in China had high rates of psychosis and seizures, with low rates of underlying neoplasms. A higher proportion of female patients required mechanical ventilation. Complications with other positive autoimmune antibodies were a common clinical symptoms of anti-NMDAR encephalitis. Majority of the patients obtained satisfactory outcomes in combination with early first-line and long-term immunization therapy.

目的:探讨表皮生长因子受体(EGFR)抑制剂PD168393对体外氧糖剥夺/复氧(OGD/R)诱导的血脊髓屏障(BSCB)损伤的保护作用及其可能的机制.方法:体外培养大鼠来源的脊髓微血管内皮细胞和混合胶质细胞,应用transwell培养体系建立体外BSCB模型;将培养的细胞分为3组:对照组(正常培养)、损伤组(OGD/R处理)和治疗组(OGD/R后给予10 nM PD168393干预).损伤组和治疗组复氧3 h、6 h和12 h后,应用荧光素渗漏实验及内皮细胞跨膜电阻值(TEER)测定来评估各组BSCB通透性变化;应用免疫荧光、Western Blot技术检测各组内皮细胞间紧密连接蛋白ZO-1、Occludin表达的差异;应用ELISA法检测各组细胞分泌致炎因子白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)和诱导型一氧化氮合酶(iNOS)的差异.结果:损伤组在各个时间点的荧光素渗漏量均高于对照组(均P<0.05),而治疗组荧光素渗漏量均低于损伤组(均P<0.05);损伤组TEER值显著低于对照组(均P<0.01),而治疗组TEER值显著高于损伤组(均P<0.05);损伤组紧密连接蛋白ZO-1和Occludin的表达量低于对照组(均P<0.05),而治疗组ZO-1和Oc-cludin的表达量较损伤组显著提高(均P<0.05);损伤组分泌的致炎因子IL-6、iNOS、TNF-α均显著高于对照组,治疗组在各时间点致炎因子IL-6、iNOS、TNF-α的分泌均低于损伤组(均P<0.05).结论:EGFR抑制剂PD168393有助于维持OGD/R损伤后BSCB的完整性;其机制可能与抑制致炎因子的表达及减少BSCB紧密连接蛋白的破坏有关.

目的 明确表皮生长因子(epidermal growth factor receptor,EGFR)抑制剂奥希替尼治疗脊髓损伤(spinal cord injury,SCI)的最佳时机.方法 将60只大鼠随机分为6组(每组10只):损伤对照组(injury组)和5个奥希替尼治疗组:0天组(0d组)、1天组(1d组)、3天组(3d组)、5天组(5d组)、7天组(7d组).建立大鼠脊髓损伤模型后,奥希替尼治疗组分别于术后即刻、术后1d、3d、5d、7d给予奥希替尼进行干预,损伤对照组使用溶剂(生理盐水)作为对照.应用BBB评分量表于术后1d及术后每周评估各组大鼠行为学的改变,每天记录各组残余尿量;术后14 d,各组随机选择5只大鼠处死,取脊髓组织,应用Western blot技术检测GAP-43的表达.结果 (1)0d组、1d组和3d组大鼠的后肢运动功能评分(BBB评分)明显优于5d组、7d组和injury组(P＜0.05),0d组、1d组和3d组无明显差异(P＞0.05);(2)0 d组、1d组和3d组大鼠残余尿量明显少于其他各组(均P＜0.05),0d组、1d组和3d组无明显差异(P＞0.05);(3)大鼠脊髓损伤后14d,0d组、1d组和3d组的GAP-43表达量明显高于其他各组(分别P ＜0.05,P＜0.01),0d组、1d组和3d组无明显差异(P＞0.05).结论 EGFR抑制剂奥希替尼治疗大鼠脊髓损伤的最佳时机是脊髓损伤后0h～72 h.

Objective: Anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis is an acute form of encephalitis of autoimmune etiology. We aimed to evaluate the risk factors that predicted the need for mechanical ventilation during the acute phase of anti-NMDAR encephalitis through an analysis of the clinical characteristics and biochemical test results of the patients with anti-NMDAR encephalitis.Methods: In this retrospective study, patients who primarily presented with anti-NMDAR encephalitis and exhibited anti-NMDAR antibody positivity in the cerebrospinal fluid (CSF) between November 2015 and February 2020 were included. Data on the clinical characteristics, biochemical test results, and treatment methods selected for the patients were collected for the analysis of factors predicting the need for mechanical ventilation.Results: Thirty-one patients with a median age of onset of 31 years (inter-quartile range: 21–48 years) were included in this study, of which 15 were male (48.4%). Psychosis (23, 74.2%), seizures (20, 64.5%), and memory deficit (20, 64.5%) were the most common clinical manifestations. At admission, 17 patients (54.8%) presented with pyrexia, of which 12 (38.7%) had a body temperature ≥38°C, and six patients (19.4%) presented with central hypoventilation. All patients received first-line therapy (glucocorticoids, intravenous immunoglobulin, or plasmapheresis alone or combined), whereas two patients (6.5%) received rituximab, a second-line agent, as well. Seven patents required mechanical ventilation. Results of univariate logistic regression analysis revealed that body temperature ≥38°C [odds ratio (OR) = 18, 95% confidence interval (CI): 1.79–181.31, P < 0.05] and central hypoventilation at admission (OR = 57.50, 95% CI: 4.32–764.89, P < 0.05) were the risk factors for mechanical ventilation. Multivariate logistic regression analysis showed that central hypoventilation at admission was the only risk factor predicting the need for mechanical ventilation.Conclusion: Central hypoventilation at admission is a key risk factor for mechanical ventilation during hospitalization in patients with anti-NMDAR encephalitis.

目的 研究表皮生长因子受体(EGFR)抑制剂奥希替尼对大鼠脊髓损伤(SCI)后血脊髓屏障通透性的影响.方法 60只8周龄雌性SD大鼠(200～250 g)按照随机数字表法分为假手术组(n=20)和SCI模型组(n=40),采用随机数字表法将40只SCI模型大鼠分为损伤组和奥希替尼组,每组20只.奥希替尼组给予浓度为0.4 mg/mL奥希替尼溶液灌胃(2 mL/d),假手术组和损伤组给予生理盐水灌胃(2 mL/d),三组均干预3 d.SCI后3 d测定脊髓组织含水量,Western blot技术检测水通道蛋白-4(AQP-4)表达量,采用伊文思蓝(EB)染料渗漏实验及免疫荧光技术测定脊髓白蛋白含量评估血脊髓屏障通透性变化.采用Basso-Beattie-Bresnahan(BBB)评分评估大鼠运动功能.结果 SCI后3 d奥希替尼组脊髓含水量明显低于损伤组(P<0.05);奥希替尼组AQP-4蛋白表达量明显低于损伤组(P<0.01);奥希替尼组脊髓组织EB染料聚集较损伤组少,EB荧光强度较损伤组弱(P<0.05);奥希替尼组白蛋白免疫荧光强度较损伤组弱.奥希替尼组总体BBB评分高于损伤组(P<0.05).结论 EGFR抑制剂奥希替尼可改善SCI后血脊髓屏障的破坏并减轻脊髓继发性损伤,促进神经功能恢复.

目的 研究表皮生长因子受体(EGFR)抑制剂奥希替尼对大鼠脊髓损伤(spinal cord injury,SCI)后致炎因子、紧密连接蛋白表达及神经功能的影响.方法 将60只SD大鼠随机分为:假手术组、损伤组、奥希替尼组,建立大鼠脊髓损伤模型.造模后3、7 d采用Western blot检测各组大鼠脊髓组织紧密连接蛋白ZO-1、Occludin和致炎因子IL-1β、TNF-α、COX-2、iNOS以及p-EGFR、EGFR蛋白的表达;造模后7 d应用免疫荧光染色及Western blot技术检测各组大鼠脊髓组织GFAP、CD11b的表达;应用Luxol Fast Blue染色评估各组大鼠髄鞘脱失情况,应用BBB评分量表评估大鼠运动功能,应用膀胱残余尿量评估大鼠排尿功能.结果 ①SCI后3、7 d,奥希替尼组致炎因子IL-1β、TNF-α、COX-2、iNOS表达量明显低于损伤组(均P<0.05);②SCI后3、7 d,奥希替尼组紧密连接蛋白ZO-1、Occludin蛋白表达量明显高于损伤组(均P<0.05);③SCI后3、7 d,奥希替尼组EGFR活化较损伤组减少(均P<0.05);④SCI后7 d损伤组GFAP及CD11b表达均明显增加,而奥希替尼组两者表达均较损伤组明显减少(均P<0.05);⑤与损伤组比较,奥希替尼组脊髓组织髄鞘脱失面积明显减少(P<0.05),BBB评分明显升高(P<0.05),残余尿量明显减少(P<0.05).结论 EGFR抑制剂奥希替尼可有效抑制SCI后EGFR活化,降低脊髓组织致炎因子表达,减少紧密连接蛋白缺失,抑制胶质细胞活化,缓解髄鞘脱失,促进神经功能恢复.

Epidermal growth factor receptor (EGFR) activation is involved in blood spinal cord barrier (BSCB) disruption and secondary injury after spinal cord injury (SCI). However, the underlying mechanisms of EGFR activation mediating BSCB disruption and secondary injury after SCI remain unclear. An in vitro model of oxygen and glucose deprivation/reoxygenation (OGD/R) induced BSCB damage and in vivo rat SCI model were employed to define the role of EGFR/p38/NF-kappa B signal pathway activation and its induced inflammatory injury in main cellular components of BSCB. Genetic regulation (lentivirus delivered shRNA and overexpression system) or chemical intervention (agonist or inhibitor) were applied to activate or inactivate EGFR and p38 in astrocytes and microvascular endothelial cells (MEC) under which conditions, the expression of pro-inflammatory factors (TNF-alpha, iNOS, COX-2, and IL-1 beta), tight junction (TJ) protein (ZO-1 and occludin), nuclear translocation of NF-kappa B and permeability of BSCB were analyzed. The pEGFR was increased in astrocytes and MEC which induced the activation of EGFR and p38 and NF-kappa B nuclear translocation. The activation of EGFR and p38 increased the TNF-alpha, iNOS, COX-2, and IL-1 beta responsible for the inflammatory injury and reduced the ZO-1 and occludin which caused BSCB disruption. While EGFR or p38 inactivation inhibited NF-kappa B nuclear translocation, and markedly attenuated the production of pro-inflammatory factors and the loss of TJ protein. This study suggests that the EGFR activation in main cellular components of BSCB after SCI mediates BSCB disruption and secondary in-flammatory injury via the EGFR/p38/NF-kappa B pathway.

By means of brain connectomics, structural patterns of the brain nerve cells can be abstracted into a highly complex network, and epilepsy is one of the most common disorders of brain network. Although focal epilepsy (FE) is once thought to be a focal brain disease, current researches have confirmed that extensive changes exist in the FE brain network. With the development of brain connectomics in the field of epilepsy, the brain network characteristics of FE are gradually characterized. In this paper, the recent advance in human brain connectomics of FE is reviewed to summarize the characteristics of FE brain network.

星形胶质细胞(AS)是中枢神经系统(CNS)中最主要的胶质细胞类型,在生理和病理状态下均发挥着复杂而重要的调节作用.AS在CNS中的各种调节功能与其分泌的外泌体密切相关.本文主要对AS源外泌体的研究进展进行综述.

目的 通过研究咽炎消合剂对慢性咽炎大鼠模型咽部粘膜组织中TGF-β1、Smad3 mRNA表达的趋势,阐明咽炎消合剂修复慢性咽炎模型大鼠咽粘膜的作用机制,进一步研究该病的发病机理.方法 选用45只SD大鼠,随机分3组造模:标准慢性咽炎模型组,慢性咽炎模型治疗组,空白对照组.成功造模后进行咽炎消合剂治疗15d,然后对各实验组大鼠粘膜组织病理切片免疫组化检测,以及用Q-PCR检测不同组别中的TGF-β1、Smad3 mRNA的表达情况,对Q-PCR中Ct值进行t检验,按照2-ΔΔCt方法进行计算.结果 一般观测及病理检查显示,慢性咽炎模型建立成功.治疗组比较标准慢性咽炎模型组,咽粘膜组织病理增生情况好转明显,局部炎性细胞的数量减少,血管通透性明显降低.Q-PCR检测显示,模型组及治疗组的TGF-β1、Smad3 mRNA表达要高于空白组(P<0.05),经咽炎消合剂治疗后,治疗组TGF-β1、Smad3 mRNA表达明显低于模型组.结论 咽炎消合剂对慢性咽炎大鼠模型咽粘膜中有TGF-β1/Smad3信号通路具有调控作用,干预了咽粘膜的组织纤维增生及炎性改变,证实了该药物对慢性咽炎治疗的有效性.

目的:了解神经内科住院患者临床流行病学特征,为临床管理和疾病防治提供依据.方法:回顾性分析2014至2018年在我院神经内科住院的14 431例患者资料,描述性统计分析临床特征,采用x2检验、Fisher's精确检验和多元Logistic回归分析探索影响院内感染和死亡的因素.结果:神经内科住院患者以60岁以上老年人为主(72.7％),心脑血管疾病患者占82.6％,入院时93.9％的患者有并发症.日均住院费用均呈逐年上升趋势(P＜0.05).院内感染率及死亡率分别为0.6％和0.3％,有逐年下降趋势(P＜0.05).60岁以上(OR =2.2,95％ CI:1.2 ～4.0)、住院时间为10～14 d(OR =4.4,95％ CI:1.7 ～ 11.4)、住院时间≥15 d(OR =31.9,95％ CI: 12.7 ～80.3)和有过院内手术(OR =2.4,95％ CI:1.3～4.3)的患者发生院内感染的几率更高.60岁以上(OR =4.7,95％ CI:1.4 ～15.5)、非心脑血管疾病(OR =2.1,95％ CI:1.1～4.2)、未开展院内手术(OR =3.0,95％ CI:1.2 ～7.5)和入院并发症≥3种(OR =7.4,95％ CI:2.6～20.9)的患者院内死亡的比例更高.结论:老年人和心脑血管疾病患者是神经内科住院治疗的主要对象;应适当缩短住院时间、注重侵袭性手术患者的感染控制和呼吸系统、泌尿系统等感染高发部位的感染防治;应重视对患者入院并发症的控制,降低院内死亡比例.

目的 观察老年脑梗死伴肺部感染患者的临床特点并探讨感染的影响因素.方法 选取146例老年脑梗死患者为研究对象,根据是否发生院内肺部感染分为感染组(31例)和非感染组(115例).分析病原菌构成及耐药情况,采用多因素Logistic回归分析老年脑梗死患者发生院内肺部感染的影响因素.结果 146例老年脑梗死患者中31例发生院内肺部感染,感染率为21.2％.分离致病菌34株,病原菌种类主要为革兰阴性菌(27株,79.4％),以肺炎克雷伯菌、铜绿假单胞菌为主.肺炎克雷伯菌、铜绿假单胞菌均对氨苄西林、左氧氟沙星及环丙沙星耐药性高,对头孢哌酮舒巴坦、亚胺培南较敏感.多因素Logistic回归分析结果显示,合并糖尿病(OR=10.334)、侵入性操作(OR=9.137)、既往肺部疾病(OR=4.440)、球麻痹(OR=7.498)、意识功能障碍(OR=4.976)是老年脑梗死患者发生院内肺部感染的危险因素(P<0.05).结论 老年脑梗死患者发生院内肺部感染率较高,病原菌以革兰阴性菌为主.合并糖尿病、侵入性操作、既往肺部疾病、球麻痹、意识功能障碍是老年脑梗死患者发生院内肺部感染的危险因素.

目的 基于筛查量表,分析中国常染色体显性遗传性脑动脉病伴皮质下梗死和白质脑病(cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy,CADASIL)患者的临床特征.方法 回顾性纳入2012年1月-2019年11月在深圳市人民医院经NOTCH3基因检测确诊的CADASIL患者,行CADASIL筛查量表评分测试其敏感度.检索国内外数据库查找中国CADASIL相关文献,汇总中国患者基于筛查量表各项目的出现频率.将本研究数据(A组)、中国患者文献复习数据(B组)、制订CADASIL筛查量表时使用的原始数据(C组)三组的数据进行比较,总结中国患者的临床特征.结果 本研究1 6例CADASIL患者中,筛查量表的敏感性为68.8％ (11/16).其中出现频率较低的项目分别为伴先兆的偏头痛(0/16,0％)、偏头痛(5/16,31.3％)、情绪精神障碍(5/16,31.3％)、脑白质病变累及颞极(7/16,43.8％)、阳性家族史(其中1代家族史阳性7/16,43.8％;2代家族史阳性4/16,25％);TIA或卒中、认知功能下降/痴呆出现率均在一半以上.A、B、C三组进行比较,偏头痛、伴先兆的偏头痛、认知功能下降/痴呆、脑白质病变、脑白质病变累及颞极、阳性家族史在三组间的出现频率均有统计学差异(均P＜0.05).经两两比较,在伴先兆的偏头痛和阳性家族史两个项目中,A组、B组的出现率均明显低于C组(均P＜0.001);偏头痛、认知功能下降/痴呆、脑白质病变、脑白质病变累及颞极这几项,B组的出现率均低于C组(均P＜0.05).结论 CADASIL筛查量表应用于中国患者的敏感度不高.制定CADASIL筛查量表时使用的原始数据常见的临床症状伴或不伴先兆的偏头痛、脑白质病变累及颞极、可采集到阳性家族史,在中国患者却很低;中国CADASIL患者最常见的临床特征是TIA或卒中.