血管性痴呆，防重于治

什么是血管性认知功能损害 按照目前最新的定义，血管性认知功能损害是指由血管性因素引起或与之相关的认知功能障碍。简单地说就是由脑卒中、高血压、糖尿病、动脉粥样硬化、心脏病等疾病引起或同时伴随的认知功能损害。     

高血压病人的健康指导

高血压是中老年人的常见病、多发病，它可引起心、脑、肾等器官功能的损害。将患者的血压控制在正常或接近水平，对延缓高血压引起的病理变化，延长患者生命，减轻痛苦是非常重要的。因此，高血压病人的自我保健意识非常重要，护理工作者应从以下几方面给予指导。     

脑卒后抑郁患者的观察及心理护理体会

随着对脑卒患者研究的日益深入，人们逐渐认识到脑卒后伴发的情感障碍已成为严重影响脑卒后患者肢体功能、认知功能和社会功能的主要因素之一，其中脑卒后抑郁是脑卒后最为常见的情感障碍，这是由于脑卒后导致的持续性的情感低落，兴趣减退为核心症状的心境障碍。脑卒患者由于抑郁情绪导致注意力，学习和执行功能，淡漠减退，缺乏主动性，不利于患者肢体功能残疾和认知损害的恢复，严重影响患者的预后和生活质量，甚至增加病死率，重症患者可伴有自杀观念甚至自杀行为。据本院调查，每年服药自杀的患者中，80％的患者患有精神抑郁症。     

痴呆的药物治疗

痴呆(dementia)是由于脑功能障碍而产生的获得性和持续性智能障碍综合征。智能损害包括不同程度的记忆、语言、视空间功能、人格异常及认知(概括、计算、判断、综合和解决问题)能力的降低，患者常常伴有行为和情感的异常，这些功能障碍导致病人日常生活、社会交往和工作能力的     

卒中后认知功能损害的演变及治疗进展

脑卒中是我国中老人群最主要的死亡原因之一.卒中可导致神经功能缺损、行为、情感障碍外,认知功能损害很常见.认知功能损害是卒中复发的重要危险因子,使血管性痴呆发生的风险增高并影响病人的康复.研究卒中后认知功能损害的特征,以及病程中的演变轨迹及其相关影响因素,给予针对性干预及治疗,以减少及延缓认知损害的发生.该文对卒中后认知功能损害的演变及治疗进展进行综述.     

治高血压先分清三六九等

血压长期升高会使得患者的心、脑、肾的很多结构和功能发生改变,出现多种高血压并发症。心、脑、肾这些器官称为高血压的靶器官。血压越高,心、脑、肾的损害越严重,这已是医务人员和患者的共识。 由于高血压患者会出现一系列的器官损害,因此治疗高血压的目的就是为了保护患者心、脑、肾。高血压患者出现心、脑、肾的损害程度是医师决定治疗方案的重要依据。     

高血压病人遵医行为调查及护理对策

高血压病是常见的心血管疾病，除了可引起高血压本身的症状外，长期高血压还可成为多种心血管疾病的重要危险因素，并影响心、脑、肾的功能，最终可导致这些器官的功能衰竭。原发性高血压诊断一旦确立，通常需要终身治疗，通过非药物及药物治疗，使血压降至正常范围，以防止或减少心、脑、肾的并发症，降低病死率和病残率。遵医行为是指病人求医后其行为与临床医嘱的符合程度，为遵循医嘱的行为活动。高血压病人遵医程度的高低直接影响其疾病的预后与转归。     

TCD检测高血压病对防治脑血管病的意义

目的：应用TCD技术（经颅多普勒超声）探讨高血压对颅内动脉的影响及损害程度。方法：对500例临床诊断为高血压病患者进行TCD常规检测，观察其脑底动脉血流动力学变化并进行分析。结果：高血压病对脑动脉损害明显，且不同年龄、不同病程其结果也不尽相同。结论：TCD检测有助于对高血压患者的脑动脉功能状态进行观察与评价，有助于脑血管疾病的预防。     

自拟杞远汤治疗缺血性卒中后轻度认知功能障碍临床观察

脑血管疾病是神经系统的常见病和多发病,随着人口的老龄化,高血压、糖尿病、冠心病、脑卒中的发病率呈逐年的上升趋势。并且脑卒中的患者有将近一半伴认知功能障碍,轻度认知功能障碍是患者脑功能高级损害的表现之一,不仅给社会和家庭带来沉重的负担,也严重影响患者的生活质量。有研究发现,如果发生卒中后认知功能障碍不能正确及时的得到处理,则有可能发展到卒中后痴呆,成为血管性认知障碍的一个亚型［1］,笔者采用养阴化痰法联合多奈哌齐治疗轻度认知功能障碍患者40例,观察患者认知功能的改善程度,为治疗脑卒中认知功能障碍积累更多临床经验,为以后的研究提供基础,报告如下。     

农村高血压病人药疗依从性及影响因素调查分析

目的：了解农村高血压病人用药依从性及影响因素，为提高药疗依从性提供理论依据。方法：采用问卷调查形式，对上海金山农村200例门诊药疗高血压病人进行依从性和影响因素调查。结果：农村高血压病人的药疗依从性低，仅为6．35％，而影响方面涉及家庭经济、药物因素、疾病认知、医生指导等诸多因素。结论：农村高血压病人药疗依从性急需提高，除了社会、家庭支持以外，医药工作者提高服务理念，加强健康教育，提供多方位详尽咨询和服务成为关键。     

Prospects for prevention and treatment of vascular cognitive impairment

With the aging population and rising prevalence of vascular disease in developed and developing countries, increasing numbers of individuals are at risk of cognitive impairment. Despite the potential of the therapeutics that are currently under investigation, none have yet fulfilled their promise for the prevention and treatment of dementia. The term vascular cognitive impairment (VCI) describes individuals with significant cognitive impairment arising from vascular disease. Risk factors predisposing to stroke correlate with brain changes, cognitive loss and Alzheimer's disease pathology. The volume of the infarcts and white matter changes, silent lacunar infarcts, and global and regional brain atrophy may be imaged non-invasively, targeted as surrogates of the dementia processes and considered parameters to be targeted for interventional strategies. As the greatest chance to prevent cognitive impairment and its progression is by intervening in the early stages or prior to any change, the development of preventative therapeutics is an important strategy. Non-invasive magnetic resonance imaging techniques may help to identify a subgroup of patients in whom infarct prevention, via risk factor control, may be of paramount importance. As the pathophysiology of dementia becomes more fully understood by coupling neuropsychological with neuroimaging, genetic and pathological features, there is the potential for the establishment of diagnostic criteria of the early phase of VCI and the testing of novel interventional strategies.     

Amelioration of recognition memory impairment associated with iron loading or aging by the type 4-specific phosphodiesterase inhibitor rolipram in rats

Increasing evidence indicates that iron deposition in the brain might play a role in cognitive dysfunction associated with neurodegenerative disorders and aging. Previous studies have not examined whether iron-induced memory deficits can be attenuated by acute treatments with memory-enhancing agents. Phosphodiesterase type 4 (PDE4) inhibitors such as rolipram (ROL) ameliorate memory impairments in several rodent models of amnesia and have been proposed as candidate cognitive-enhancing drugs. Here we show that a single posttraining systemic injection of ROL dose-dependently attenuates the impairment of memory for novel object recognition (NOR) in rats given neonatal iron loading, a model of iron-induced cognitive impairment. Posttraining administration of ROL also recovered NOR deficits associated with aging in rats. These findings provide the first evidence that stimulation of an intracellular second messenger signaling pathway can attenuate iron-induced memory impairment, and support the view that PDE4 inhibitors might ameliorate cognitive dysfunction associated with aging and neurodegenerative disorders.     

Cognitive skill learning in healthy older adults after 2 months of double-blind treatment with piribedil

Rationale Cognitive skill learning, as assessed by repeated testing on the Tower of Toronto (TT) task, has been found to be impaired in normal aging. There is evidence that this impairment might be accounted for by the well-documented, age-dependent decline of dopamine D2-like receptor availability.Objectives This study was an investigation of whether the D₂/D₃ dopaminergic agonist piribedil improves cognitive skill learning in older adults.Methods Healthy elderly volunteers were assessed using the TT paradigm. Subjects were evaluated at baseline, and after 2 months of a placebo or piribedil (50 mg daily) treatment in a double-blind, crossover design. Two components of cognitive skill learning were considered—the ability to learn to solve the puzzle and the acquisition of a problem-solving routine.Results Piribedil showed a beneficial effect on the acquisition of a problem-solving routine, depending on the age of subjects, as revealed by solution reliability indexes measures. The effect of piribedil on the ability to learn to solve the puzzle was found to be dependent on the subjects working memory capacities.Conclusions The present results suggest that piribedil is likely to enhance cognitive skill learning in healthy older adults and give further evidence that age-related dopamine decline plays an important role in cognitive impairment occurring in normal aging.     

The Hypertension in the Very Elderly Trial – latest data

Early trials in the field of hypertension focused on adults in their fifties and sixties. However, with the passage of time, a progressive effort has been made to expand the evidence base for treatment in older adults. 2008 saw publication of data from the Hypertension in the Very Elderly Trial which demonstrated significant mortality and morbidity benefits from antihypertensive therapy in octogenarians. More recently, additional data from this cohort has been published suggesting that appropriate anti-hypertensive therapy may lead to a reduction in incident cognitive impairment and fractures, whilst a 1 year open label extension of the main study confirmed many of the original trial findings. This review provides an overview of the Hypertension in the Very Elderly Trial whilst also discursively evaluating the latest data.     

左侧丘脑结节动脉梗死患者的认知功能障碍：1例病例报告及文献复习

血管性认知功能障碍目前正逐步成为脑卒中后临床关注的重点。多种机制介导的血管性认知功能障碍是一类异质性疾病,而作为与血管性事件直接相关的重要部位的梗死在其中起着重要作用。左侧丘脑结节动脉梗死所造成的急性认知功能障碍因病变部位较局限,易为临床医生忽略。本文报告1例左侧丘脑结节动脉梗死患者的诊治情况,并就此种重要部位梗死患者的认知功能障碍作一简要介绍。     

芍药苷对D-半乳糖和亚硝酸钠诱导的小鼠认知障碍与神经元变性的改善作用

目的:探讨芍药苷(PF)对D-半乳糖(D-gal)和亚硝酸钠(NaNO2)诱导的衰老小鼠认知障碍与神经元凋亡的改善作用.方法:皮下注射D-gal和NaNO2制备小鼠衰老模型.使用Morris水迷宫检测小鼠空间记忆能力.取小鼠脑组织检测丙二醛(MDA)水平、总超氧化物歧化酶(T-SOD)和谷胱甘肽过氧化酶(GSH-Px)活性.经H&E、TUNEL染色和caspase-3免疫组化染色观察海马神经元损伤、凋亡和caspase-3表达变化.结果:D-gal和NaNO2可诱导小鼠认知功能衰退,海马神经元损伤.给予PF可改善模型鼠认知障碍和海马神经元损伤,减少caspase-3在海马的表达,提高降低的T-SOD、GSH-Px活性,减少升高的MDA含量.结论:PF通过抑制氧化损伤途径改善D-gal和NaNO2诱导的小鼠认知障碍与海马神经元变性.     

Cholinergic activity and amyloid precursor protein processing in aging and Alzheimer's disease

Among the neuropathological features of Alzheimer's disease (AD), are senile plaques and dysfunction of cholinergic neurotransmission are the major hallmarks. Senile plaques are formed by amyloid beta-peptides (Abeta), derived from amyloidogenic processing of a larger protein named amyloid precursor protein (APP). It has been suggested and also proved that cholinergic system plays an important role in the cognitive function of the brain and its deficit correlates well with the cognitive impairment of AD. Aging is the most important risk factor for AD. In normal aging, cholinergic system undergoes degeneration. APP processing changes with aging, probably resulting in higher amyloidogenic products. The current clinical treatments for Alzheimer's disease solely rely on cholinomimetic drugs i.e., acetylcholinesterase inhibitors. Recently, a great effort has been made to seek therapies that could reduce Abeta products by influencing APP processing. Through genetic engineering in cell lines and mice, in vitro and in vivo models for AD studies have been created. Experimental evidence obtained from the studies on these model organisms suggests that activity of cholinergic neurotransmission might have an impact on APP processing. On the other hand, the proteolytic products of APP have also been found able to influence the cholinergic system in both in vitro and in vivo models. To determine whether there exists a reciprocal interaction between cholinergic neurotransmission and APP processing is important for the development of new therapeutic strategies with high efficacy and specificity for AD.     

Women's cognitive and affective health and neuropsychiatry

Recent interest in women's health has focused on the cognitive consequences of aging and hormonal changes. Based on hypotheses about estrogenic effects in the central nervous system (CNS), large-scale clinical trials were designed to address the efficacy of hormone replacement on protection against dementia and cognitive decline. Surprisingly, an absence of risk reduction for dementia and cognitive loss was found and much reanalysis of these findings has focused on timing of hormone replacement. Here we take a broad perspective to address a fuller range of psychological health. Gender differences in other psychiatric conditions including depression and anxiety have been attributed to hormones, and the neurotransmitter systems that are implicated in affective disorders may have an impact on cognitive impairment as well. Hormonal influences on neurotrophic mechanisms, as well as neurotransmitter effects, may be responsible for a breadth of neuropsychiatric conditions, particularly in aging. This review will focus on cognition, mood and anxiety issues among women with an emphasis on changes associated with aging. We will review data on the epidemiology of these entities and examine the biological mechanisms, which may be involved, with an emphasis on those mechanisms that may contribute to the multiple aspects of neuropsychiatry and women's health.     

Relationship of Age to Impulsivity and Decision Making: A Baseline Secondary Analysis of a Behavioral Treatment Study in Stimulant Use Disorders

Because stimulant use disorders remain prevalent across the lifespan, cognition is an important area of clinical care and research focus among aging adults with stimulant use disorders. This secondary analysis of a National Institute on Drug Abuse Clinical Trials Network study suggests that decision making, verbal learning/memory, executive function, and set shifting are important cognitive domains to screen clinically and treat in aging adults with stimulant use disorders. Some suggestions are made on how clinical treatment providers can practically use these results. An important direction for future research is the development of cognitively remediating treatments for impaired cognitive domains in aging adults with stimulant use disorders.     

血管性认知障碍相关关键蛋白的神经保护机制的研究进展

血管性认知障碍主要由脑血管病变引起认知功能损害,其发生发展与神经元存活状态密切相关。多种经典信号通路以及相关蛋白分别从促进突触发生和轴突生长、抑制细胞凋亡、修复氧化DNA损伤和应对氧化应激等方面在血管性认知障碍的防治过程中发挥重要作用。本文就部分信号通路中关键蛋白以及其他相关蛋白对血管性认知障碍的神经保护机制进行概述。