青年缺血性卒中患者脑小血管病总负荷的危险因素分析

目的 探讨青年缺血性卒中患者脑小血管病（cerebral small vessel disease,CSVD）总负荷的危险因素。 方法 回顾性纳入2016年1月-2020年10月于首都医科大学附属北京朝阳医院神经内科连续收治的 青年急性缺血性卒中患者。通过MRI评估腔隙、脑白质高信号、扩大的血管周围间隙及脑微出血四种 CSVD影像学标志物,对所有患者的CSVD总负荷进行评分,并根据该评分将患者分为0分组、1分组、2 分组及3～4分组。采用有序logistic回归分析青年缺血性卒中患者CSVD总负荷评分的危险因素。 结果 共纳入272例患者,平均39.55±5.19岁,男性230例（84.6%）。其中0分组146例（53.7%）,1 分组71例（26.1%）,2分组40例（14.7%）,3～4分组15例（5.5%）。单因素分析结果显示,不同CSVD 总负荷评分组年龄、高血压、肌酐水平差异有统计学意义。有序logistic回归分析显示,增龄（OR 1.110, 95%CI 1.048～1.175）和高血压（OR 2.649,95%CI 1.537～4.559）是CSVD总负荷评分的独立危险因素。 结论 增龄和高血压是青年缺血性卒中患者CSVD总负荷评分的独立危险因素。     

血管周围间隙在脑小血管病中的研究进展

血管周围间隙（perivascular spaces，PVS）是脑小血管周围充满液体的潜在腔隙。扩大的血 管周围间隙（enlarged perivascular spaces，ePVS）已成为脑小血管病（cerebral small vessel diseases，CSVD） 公认的影像标志物之一。PVS的量化依赖于MRI，难点在于ePVS与腔隙灶的鉴别。PVS被证明与年龄、 高血压、其他CSVD影像学标志物、认知功能损害、全身性炎症相关，但仍缺乏较为长期的、针对不同 人群的队列研究。研究ePVS与CSVD病程的关系，有助于临床上对CSVD的早期发现和风险预测。     

脑小血管病病理生理机制研究进展

脑小血管病（cerebral small vessel disease,CSVD）是由于不同原因的脑小血管或微小血管发 生病理改变后导致的疾病,是临床上引起血管性认知功能障碍（vascular cognitive impairment,VCI）的 重要病因。充分认识CSVD的发生、发展,将为预防VCI提供可能。本文从脑小血管病的病理生理机制 的研究进展进行综述,以期为临床实践提供思路。     

脑小血管病总负荷与记忆力下降老年患者认知功能、脑萎缩及脑灌注的相关性

目的 探索脑小血管病（cerebral small vessel disease，CSVD）总负荷与记忆力下降老年患者认知功能、 脑萎缩及脑灌注的关系。 方法 回顾性纳入2015年12月-2017年12月同济医院神经内科门诊及记忆减退专病门诊主诉记忆力 下降患者，收集一般资料及影像学信息，进行认知评估、CSVD总负荷评分、全脑及各脑叶脑萎缩评分， 计算脑血流（cerebral blood flow，CBF）值。采用Spearman相关分析CSVD总负荷评分与认知功能、脑萎 缩及CBF的关系。 结果 共纳入200例，平均年龄69.16±9.44岁，男性99例（49.5%）。CSVD总负荷与MoCA评分呈负相 关（r =-0.202，P =0.004）；与全脑（r =-0.234，P =0.001）、额叶（r =-0.252，P <0.001）、顶叶（r =- 0.253，P <0.001）、枕叶（r =-0.224，P =0.001）CBF呈负相关；CSVD负荷与全脑（r =0.313，P <0.001）、 额叶（r =0.393，P＜0.001）及顶叶（r =0.237，P =0.001）的脑萎缩评分呈正相关。 结论 CSVD总负荷越高，认知功能越差、脑灌注越低、脑萎缩越严重。     

脑小血管病总负荷与中老年癫痫患者认知功能的相关性

目的 探讨中老年癫痫患者脑小血管病（cerebral small vessel disease,CSVD）总负荷以及单个CSVD影像标志物与认知功能的关系。      

血管周围间隙在脑小血管病中的研究进展

血管周围间隙（perivascular spaces,PVS）是脑小血管周围充满液体的潜在腔隙。扩大的血
管周围间隙（enlarged perivascular spaces,ePVS）已成为脑小血管病（cerebral small vessel diseases,CSVD）
公认的影像标志物之一。PVS的量化依赖于MRI,难点在于ePVS与腔隙灶的鉴别。PVS被证明与年龄、
高血压、其他CSVD影像学标志物、认知功能损害、全身性炎症相关,但仍缺乏较为长期的、针对不同
人群的队列研究。研究ePVS与CSVD病程的关系,有助于临床上对CSVD的早期发现和风险预测。     

血清生物标志物与脑小血管病关系研究进展

目前认为脑小血管病（cerebral small vessel disease,CSVD）的主要机制是血管内皮损伤,而 炎症和血管内皮损伤密切相关,血清中血管内皮损伤相关标志物及炎性标志物是反映炎症损伤血管 内皮最直接、最简便的方法。关于生物标志物的研究为更深入了解CSVD的发生发展机制提供了重要 的途径。目前多项研究表明炎性及血管内皮损伤相关标志物与CSVD的发生、发展关系密切。另外炎症 与CSVD关系也可能受到人种、遗传等因素的影响。本文就血清中血管内皮相关标志物、炎性标志物与 CSVD不同影像学标志的相关性研究进展进行综述。     

颅内动脉重塑与脑小血管病患者影像学标志物的关系

目的探讨颅内动脉重塑与脑小血管病(CSVD)患者影像学标志物的关系。方法选取2020年1月至2022年5月在郑州大学第二附属医院或新郑市公立人民医院神经内科住院的CSVD患者共156例, 计算其脑动脉重塑(BAR)评分, 将BAR评分≤-1倍标准差的患者定义为颅内动脉缩窄性重塑的个体, BAR评分≥1倍标准差的患者为定义颅内动脉扩张性重塑的个体。对CSVD影像学标志物[脑白质高信号(WMHs)、腔隙、脑微出血、扩大的血管周围间隙和脑萎缩]进行量化, 计算出CSVD总负荷评分并根据评分结果将所有患者分为低负荷组(0～2分, 91例)和高负荷组(3～4分, 65例)。采用单因素分析、二元Logistic回归分析探讨颅内动脉重塑与CSVD各影像学标志物及总负荷的关系, 建立列线图预测模型并绘制受试者工作特征曲线(ROC)以评估颅内动脉重塑对高CSVD总负荷的预测价值。结果颅内动脉扩张性重塑是严重WMHs(OR=3.66, 95%CI 1.38～9.72, P=0.009)、腔隙(OR=3.78, 95%CI 1.17～12.19, P=0.026)、脑萎缩(OR=3.11, 95%CI 1....     

脑小血管病总负荷与记忆力下降老年患者认知功能、脑萎缩及脑灌注的相关性

目的 探索脑小血管病（cerebral small vessel disease,CSVD）总负荷与记忆力下降老年患者认知功能、
脑萎缩及脑灌注的关系。
方法 回顾性纳入2015年12月-2017年12月同济医院神经内科门诊及记忆减退专病门诊主诉记忆力
下降患者,收集一般资料及影像学信息,进行认知评估、CSVD总负荷评分、全脑及各脑叶脑萎缩评分,
计算脑血流（cerebral blood flow,CBF）值。采用Spearman相关分析CSVD总负荷评分与认知功能、脑萎
缩及CBF的关系。
结果 共纳入200例,平均年龄69.16±9.44岁,男性99例（49.5%）。CSVD总负荷与MoCA评分呈负相
关（r =-0.202,P =0.004）;与全脑（r =-0.234,P =0.001）、额叶（r =-0.252,P <0.001）、顶叶（r =-
0.253,P <0.001）、枕叶（r =-0.224,P =0.001）CBF呈负相关;CSVD负荷与全脑（r =0.313,P <0.001）、
额叶（r =0.393,P＜0.001）及顶叶（r =0.237,P =0.001）的脑萎缩评分呈正相关。
结论 CSVD总负荷越高,认知功能越差、脑灌注越低、脑萎缩越严重。     

脑小血管疾病病理机制的研究进展

在过去十年中全球预期寿命大幅增加,与年龄相关性疾病对社会和卫生保健系统造成的挑战愈演愈烈。脑小血管疾病(cerebral small vessel disease,CSVD)是一种增龄性脑微血管病变,其患病率随年龄增长而增加,在50~90岁人群中患病率由5%升至几乎100%,是导致卒中和血管性痴呆的重要血管因素,并与步态障碍和情绪障碍有关。研究表明全球约50%的痴呆症及25%的卒中与CSVD相关,且近年来CSVD的发病率逐年递增并呈多样化,关注CSVD、保护大脑健康成为重中之重。但其潜在的发病机制尚未明确,目前认为CSVD的最关键病理生理机制之一是内皮功能障碍和血脑屏障(BBB)渗漏。本文回顾了CSVD病理学相关文献,并按照CSVD的影像学标志物类型对其病理特征进行综述,其中特别强调了内皮功能障碍在初始发病机制中的作用,以期帮助确定干预的潜在目标,提高小血管疾病患者的风险预测。     

Denervation study of synapses of organ of corti of old world monkeys

Fine structural characteristics of synapses in the spiral organ of Corti were examined, with reference to differences between inner and outer haircell systems, and to location of neurons of origin of efferent axons. Surgical interruption of crossed olivocochlear bundle, of vestibular nerve, of facial nerve, and excision of superior cervical ganglia were used to determine the pathways of efferent axons. Interruption of the vestibular nerve near the brainstem results in degeneration of all efferent terminals on outer hair cells. Mid-line lesions at, and caudal to, the facial colliculus result in degeneration of about half of these efferent terminals. Efferent synaptic bulbs to the inner hair-cell system are small, of the order of one micron, and form type 2 junctions with afferent dendrites. They tend to have more large dense-core vesicles (about 80 nm) than the large efferent terminals of the outer hair-cell system, and appear to be the terminals of axons in the habenula perforata, which exhibit varicosities laden with large dense core vesicles. The varicosities are unaffected by excision of the superior cervical ganglia. So far as our material can reveal, it appears that the varicosities in the habenula perforata do not survive vestibular root interruption, nor do the efferent processes in the internal spiral bundle or at the base of inner hair cells. Most interestingly, the afferent processes of the inner hair-cell system, as identified for example by their relation to pre-synaptic bodies in the inner hair cells, are subject to a trans-synaptic reaction after severance of the vestibular root. They undergo a dramatic cytological transformation, characterized by increase of volume, engorgement with microtubules, microfilaments, microvesicles of various sizes, and clusters of lysosomes. Thus, both the efferent and afferent terminals of the inner hair-cell system show marked cytological differences from the corresponding terminals of the outer hair cell system.     

Mechanism of action of tubocurarine on nicotinic cholinoreceptors of neurons of the sympathetic ganglia of rats

Tubocurarine (Tc) effect on membrane currents elicited by acetylcholine (ACh) was studied in isolated superior cervical ganglion neurons of rat using patch-clamp method in the whole-cell recording mode. The "use-dependent" block of ACh current by Tc was revealed in the experiments with ACh applications, indicating that Tc blocked the channels opened by ACh. Mean lifetime of Tc-open channel complex, tau, was found to be 9.8 +/- 0.5 s (n = 7) at -50 mV and 20-24 degrees C. tau exponentially increased with membrane hyperpolarization (e-fold change in tau corresponded to the membrane potential shift by 61 mV). Inhibition of the ACh-induced current by Tc (3-30 microM/1) was completely abolished by membrane depolarization to the level of 80-100 mV. Inhibition of ACh-induced current was augmented at increased ACh doses. It is concluded that the open channel block produced by Tc is likely to be the only mechanism for Tc action on nicotinic acetylcholine receptors in superior cervical ganglion neurons of rat.     

The effect of age of onset of PD on risk of dementia

Background Dementia occurs in the majority of patients with Parkinson’s disease (PD). Late onset of PD has been reported to be associated with a higher risk for dementia. However, age at onset (AAO) and age at baseline assessment are often correlated. The aim of this study was to explore whether AAO of PD symptoms is a risk factor for dementia independent of the general effect of age. Methods Two community-based studies of PD in New York (n = 281) and Rogaland county, Norway (n = 227) and two population-based groups of healthy elderly from New York (n = 180) and Odense, Denmark (n = 2414) were followed prospectively for 3–4 years and assessed for dementia according to DSM-IIIR. All PD and control cases underwent neurological examination and were followed with neurological and neuropsychological assessments. We used Cox proportional hazards regression based on three different time scales to explore the effect of AAO of PD on risk of dementia, adjusting for age at baseline and other demographic and clinical variables. Findings In both PD groups and in the pooled analyses, there was a significant effect of age at baseline assessment on the time to develop dementia, but there was no effect of AAO independent of age itself. Consistent with these results, there was no increased relative effect of age on the time to develop dementia in PD cases compared with controls. Interpretation This study shows that it is the general effect of age, rather than AAO that is associated with incident dementia in subjects with PD. Received in revised form: 22 December 2005     

Limits of deinstitutionalization--perspectives of relatives of psychiatric patients

After a hopeful beginning, the social process of the reintegration of those with severe mental illness has come to a standstill. I am led to wonder whether "the community" really wants to live together with people suffering from severe mental illness, and if so, how closely? As long as the medical treatment of mental illness provided by the general practitioners is fundamentally deficient, as they are not able to prescribe the necessary interventions--such as out-patient psychiatric nursing, and service providers in the out-patient sector are content with offering increasingly intensive forms of care for the less seriously ill at the cost of the Social Welfare System--the reintegration of those with serious mental illness remains an illusion--which is mainly to the benefit of providers of residential care in homes and hostels.     

Summary of legislation of 1935 of interest to the department of Mental Hygiene

Psychiatric Quarterly -