老年性痴呆的诊断

老年性痴呆 ( AD)在临床上是潜隐性起病、缓慢进行性加重的痴呆 ,无可致痴呆的全身性和脑部疾病的临床和实验室证据 ,且无提示局灶性脑损害的、局灶性神经系统定位体征突然发生的病史。病理上主要累及前脑基底、海马和大脑皮层 ,以神经元丧失、老年斑、神经纤维缠结、细胞外淀粉样蛋白沉积、淀粉样血管病为特征。病因上可由 1、14、19和 2 1号染色体或其他可能因子突变所致 ,为多源性 ,故常有临床变异 ,严重影响了 AD临床诊断的准确性。肯定的诊断有赖于临床和病理研究的结合。1　临床诊断AD的发病危险因素为年龄、家族史、颅脑外伤等。…     

老年性痴呆的治疗进展

老年性痴呆是导致老年人认知功能持续减退的最常见的疾病,目前该病唯一应用的治疗方法是用胆碱酯酶抑制剂。随着对AD分子和细胞病理生理的进一步了解,又发展了医一些新的治疗方法,如分泌酶抑制剂、过渡金属元素螯合剂、HMG-CoA还原酶抑制剂和B淀粉样蛋白疫苗等。本文综述了近几年来的老年性痴呆治疗方面的进展。     

老年性痴呆的治疗

老年性痴呆 ( AD)是一种常见的中枢神经变性疾病 ,由于原因未明和发病机制不清 ,目前尚无特异性治疗方法。临床上采用对症治疗、生物学治疗和对因治疗。生物学治疗包括神经介质替代疗法、神经营养因子、促神经细胞代谢药、神经细胞保护剂及神经移植。目前 ,对症治疗和生物学治疗是 AD治疗的主要方法。1　现行治疗方法评价1.1　对症治疗　各种精神症状如嗜睡、抑制、焦虑、攻击行为甚至成为植物人在 AD中常见 ,治疗中选择各种抗精神病药物是合理的。但是绝大部分抗精神病药物都有副作用 ,甚至使病情恶化。控制精神症状首先试用非药物疗法 …     

老年性痴呆的治疗进展

近年来随着对认知障碍分子学机制的认识不断深入,针对不同病理环节的治疗药物已经进入不同的临床阶段。主要的进展有如下几个方面。1胆碱能活化疗法 研究报道,前脑基底部发出至大脑皮质和海马的胆碱能神经通路的病变导致痴呆。已知这些通路与注意力、学习能力、记忆力及其他认知过程有关。     

益智胶囊治疗老年性痴呆30例的临床观察

老年性痴呆属祖国医学“痴呆”的范畴 ,轻者可见神情淡漠、寡言少语、反应迟钝、善忘等 ,重者表现为终日不语 ,或闭门独居 ,或口中喃喃 ,言辞颠倒或举动不经等。该病的主要病因是肾精亏损 ,髓海不足。笔者运用益智胶囊补肾益髓 ,填精养神治疗老年性痴呆 30例 ,临床疗效满意 ,现报告如下。1　临床资料1.1　 一般资料　 30例均为门诊患者 ,其中男 18例 ,女 12例 ,其中 5 0～ 5 9岁 13例 ,6 0～ 6 9岁 10例 ,70～ 79岁 7例 ,病程 2个月～ 5年。轻度痴呆 15例 ,中度痴呆 14例 ,重度痴呆 1例。依据《中药新药治疗老年性痴呆的临床研究指导原则》…     

海马回钩间距检测对早期诊断老年性痴呆的临床意义

目的对高危人群颅脑ＣＴ进行海马回钩间距的检测,有助于老年性痴呆的早期的发现。方法应用颅脑ＣＴ测量了海马回钩间距及海马回钩间距比、结果　健康组的海马回钩间距平均值为 ２０．２２±２． ２３ ｍｍ,海马回钩间距比为 １７． ６８±１, ８４％与轻度异常 组（２５．０８±２．７３ ｍｍ、２１．６２±１． ５５％）相比较,具有非常显著差异（Ｐ＜０．００１）、轻度异常组与痴呆前期组（２９． ４８±３． ３０ ｍｍ、２４．５３±２．２９％）相比较亦具有非常显著差异（Ｐ＜０．０１）。结论老年性痴呆临床前期就有海马回萎缩,使海马回钩间距扩大并随病程进展而增宽,有利于早期发现老年性痴呆。     

肺栓塞的诊断进展

肺栓塞诊断较困难,生前确诊率不高,本文就本病近年来有关诊断方面的资料作一综述。     

乳腺癌影像学诊断进展

文献报道，近年来乳腺癌的发病率及病死率均呈上升趋势。现就乳腺癌的影像学诊断进展综述如下。     

肝硬化诊断的进展

自八十年代初期以来肝纤维化血清标志物的测定陆续应用于临床,对肝硬化的诊断带来了重大进展。各种影象学检查的发展尤其多普勒超声检查对门脉高压症的诊断意义较大。本文重点介绍这两方面的有关内容。 肝纤维化血清标志物 肝硬化形成之前肝纤维化,随着肝细胞坏死、塌陷,纤维化由汇管区伸入肝小叶内,逐渐形成假小叶,始诊断为肝硬化。众所周知     

胆管癌的影像学诊断进展

胆管癌是一种胆道常见恶性肿瘤,临床上出现症状较晚,早期诊断困难,而且由于胆管癌所处的解剖位置特殊及其向周围组织、血管、神经浸润的特点,外科根治性切除率低,预后较差。近年来,胆管癌的发病率与死亡率逐年上升,寻求有效的     

Impediments to timely diagnosis of Alzheimer's disease in African Americans

The purpose of this study was to identify early patterns of care for Alzheimer's disease (AD) in a cohort of African-American patients and their caregivers presenting at an inner city clinic and a suburban memory assessment clinic. Caregivers (N=79) of patients diagnosed with probable AD were interviewed. Data were collected about the delay from noticing first AD signs until recognition that a problem existed and delay from problem recognition until first physician consultation. Patients and caregivers had lower educational status, and patients had been diagnosed more recently at the inner city clinic than at the suburban clinic, although MMSE scores of patients at the two clinics did not differ; median delays in caregivers' recognizing a problem and in consulting a physician were also similar across clinics. Delay was as long as 7 years between noticing symptoms and problem recognition and between problem recognition and physician consultation. Although patients attending the suburban clinic were more likely to have previously seen a physician than those attending the inner city clinic, they were no more likely to have received a prior diagnosis of AD. Lack of physician contact is likely to be widespread in families caring for African Americans with AD. Physician consultation is more characteristic of more highly educated families but may not yield a correct diagnosis for the patient. Intensive efforts are needed to connect African-American families with physicians and to achieve more timely diagnosis of AD to enable families to understand the illness, plan for patient safety, and make long-term plans.     

扩瞳试验在Alzheimer病诊断中的意义

目的　探讨扩瞳试验在Alzheimer病 (AD)诊断中的意义。　方法　在滴入 0 0 1%托吡卡胺 7～ 10min后 ,用双侧瞳孔红外线同步记录分析仪自动记录并分析滴药眼的瞳孔直径扩大程度(按对照侧校正 )。共测定AD 5 2例 ,血管性痴呆 (VD) 33例和健康对照 (HC) 5 8例。利用受试者工作特性曲线 (ROC)确定最能明显区别AD与HC的分界线 ,计算敏感度、特异度和Kappa值 ,评估扩瞳试验的诊断价值。　结果　 ,AD患者滴药眼的瞳孔明显扩大 ,与VD或HC差异有极显著性 (P <0 0 1) ,其中以第 18min时的差别最为显著。如以瞳孔扩大 15 %作为分界线 ,敏感度均为 0 81,特异度分别为 0 82和 0 79,Kappa值分别为 0 6 7和 0 6 0。　结论　扩瞳试验可以作为筛选早期AD的一个手段 ,也可在鉴别AD与VD时作参考。     

言语流畅性测验用于帕金森病痴呆与阿尔茨海默病早期诊断的价值研究

约40%的帕金森病患者在疾病过程中会发展成痴呆,称帕金森病痴呆(PDD),相对于其他认知领域的损害,PDD的执行功能破坏尤其严重。阿尔茨海默病(AD)是老年期常见的痴呆。本研究应用3项言语流畅性测验,评估帕金森病痴呆与阿尔茨海默病患者的言语流畅性损害状况、归纳出对AD、PDD早期诊断和鉴别诊断有价值的流畅性指标,并对流畅性测验内部加工机制进行探讨分析。     

MRI and CSF studies in the early diagnosis of Alzheimer's disease

The main goal of our studies has been to use MRI, FDG-PET, and CSF biomarkers to identify in cognitively normal elderly (NL) subjects and in patients with mild cognitive impairment (MCI), the earliest clinically detectable evidence for brain changes due to Alzheimer's disease (AD). A second goal has been to describe the cross-sectional and longitudinal interrelationships amongst anatomical, CSF and cognition measures in these patient groups. It is now well known that MRI-determined hippocampal atrophy predicts the conversion from MCI to AD. In our summarized studies, we show that the conversion of NL subjects to MCI can also be predicted by reduced entorhinal cortex (EC) glucose metabolism, and by the rate of medial temporal lobe atrophy as determined by a semi-automated regional boundary shift analysis (BSA-R). However, whilst atrophy rates are predictive under research conditions, they are not specific for AD and cannot be used as primary evidence for AD. Consequently, we will also review our effort to improve the diagnostic specificity by evaluating the use of CSF biomarkers and to evaluate their performance in combination with neuroimaging. Neuropathology studies of normal ageing and MCI identify the hippocampal formation as an early locus of neuronal damage, tau protein pathology, elevated isoprostane levels, and deposition of amyloid beta 1-42 (Abeta42). Many CSF studies of MCI and AD report elevated T-tau levels (a marker of neuronal damage) and reduced Abeta42 levels (possibly due to increased plaque sequestration). However, CSF T-tau and Abeta42 level elevations may not be specific to AD. Elevated isoprostane levels are also reported in AD and MCI but these too are not specific for AD. Importantly, it has been recently observed that CSF levels of P-tau, tau hyperphosphorylated at threonine 231 (P-tau231) are uniquely elevated in AD and elevations found in MCI are useful in predicting the conversion to AD. In our current MCI studies, we are examining the hypothesis that elevations in P-tau231 are accurate and specific indicators of AD-related changes in brain and cognition. In cross-section and longitudinally, our results show that evaluations of the P-tau231 level are highly correlated with reductions in the MRI hippocampal volume and by using CSF and MRI measures together one improves the separation of NL and MCI. The data suggests that by combining MRI and CSF measures, an early (sensitive) and more specific diagnosis of AD is at hand. Numerous studies show that neither T-tau nor P-tauX (X refers to all hyper-phosphorylation site assays) levels are sensitive to the longitudinal progression of AD. The explanation for the failure to observe longitudinal changes is not known. One possibility is that brain-derived proteins are diluted in the CSF compartment. We recently used MRI to estimate ventricular CSF volume and demonstrated that an MRI-based adjustment for CSF volume dilution enables detection of a diagnostically useful longitudinal P-tau231 elevation. Curiously, our most recent data show that the CSF isoprostane level does show significant longitudinal elevations in MCI in the absence of dilution correction. In summary, we conclude that the combined use of MRI and CSF incrementally contributes to the early diagnosis of AD and to monitor the course of AD. The interim results also suggest that a panel of CSF biomarkers can provide measures both sensitive to longitudinal change as well as measures that lend specificity to the AD diagnosis.     

Thiamine therapy in Alzheimer's disease

Fursultiamine (TTFD), a derivative of thiamine, at an oral dose of 100 mg/day had a mild beneficial effect in patients with Alzheimer's disease in a 12-week open trial. The improvement could be observed not only in their emotional or other mental symptoms but also in intellectual function. Only mildly impaired subjects showed cognitive improvement. Alzheimer patients' blood levels of thiamine before the trial were within the normal range. No adverse reactions were observed and all patients tolerated the trial well. TTFD could afford an alternate treatment to large doses of thiamine hydrochloride in Alzheimer patients. However, further investigations of the therapeutic implications of thiamine and its possible etiologic clues to Alzheimer's disease are necessary.     

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阿尔茨海默病是最常见的老年认知障碍,本文着重对阿尔茨海默病的治疗研究领域中的热点进行点评,包括Aβ聚集抑制剂、Aβ生成抑制剂、Aβ介导的神经递质抑制剂、Tau介导的神经毒性抑制剂等。对在困境中的AD治疗研究如何进一步深入,提出需要重新审视的问题。     

Apathy in Alzheimer's disease

Apathy, or loss of motivation, is arguably the most common change in behavior in Alzheimer's disease (AD) but is underrecognized. Apathy represents a form of executive cognitive dysfunction. Patients with apathy suffer from decreased daily function and specific cognitive deficits and rely on families to provide more care, which results in increased stress for families. Apathy is one of the primary syndromes associated with frontal and subcortical pathology, and apathy in AD appears to have multiple neuroanatomical correlates that implicate components of frontal subcortical networks. Despite the profound effects of this common syndrome, only a few instruments have been designed to specifically assess apathy, and these instruments have not been directly compared. Assessment of apathy in AD requires clinicians to distinguish loss of motivation from loss of ability due to cognitive decline. Although apathy may be misdiagnosed as depression because of an overlap in symptoms, current research has shown apathy to be a discrete syndrome. Distinguishing apathy from depression has important treatment implications, because these disorders respond to different interventions. Further research is required to clarify the specific neuroanatomical and neuropsychological correlates of apathy and to determine how correct diagnosis and treatment of apathy may improve patient functioning and ease caregiver burden.     

维生素E对Alzheimer病模型大鼠的影响

采用ＡｌＣｌ３诱导，建立Ａｌｚｈｅｉｍｅｒ病（ＡＤ）模型大鼠。用维生素Ｅ（ＶＥ）（５ｍｇ／１００ｇ体重·ｄ－１）对ＡＤ模型大鼠进行灌胃治疗。通过行为测试，光镜形态学观察，用免疫细胞化学ＡＢＣ结合图像定量分析的方法，对ＡＤ大鼠行为改变，海马结构ＣＡ１区淀粉样蛋白免疫反应阳性神经元的形态和数目、胞体平均截面积和光密度以及β淀粉样蛋白的沉积变化进行观察。结果显示ＶＥ组大鼠治疗３个月和５个月后，受电击次数和潜伏期较对照组明显减少和延长（Ｐ＜００１），３个月与５个月之间有显著性差异（Ｐ＜００１）；ＶＥ组大鼠海马结构ＣＡ１区淀粉样蛋白免疫反应阳性神经元的形态和数目、胞体平均截面积和光密度值，３个月和５个月较对照组均有明显减少和降低（Ｐ＜００１），３个月和５个月之间也有显著性差异（Ｐ＜００１），β淀粉样蛋白样反应染色减少或消失。说明ＶＥ可以改善ＡＤ模型大鼠的学习记忆，其作用机制是通过抑制和清除海马结构ＣＡ１区β淀粉样蛋白的沉积来实现的，作用效果随治疗时间的延长而更加明显。本实验研究结果为临床应用ＶＥ治疗老年性痴呆提供了形态学依据。     

阿尔茨海默病与血管性痴呆的非认知功能损害

目的　观察阿尔茨海默病与血管性痴呆的患者除认知功能异常外 ,是否存在非认知功能的异常。方法　根据DSM -Ⅳ阿尔茨海默病及血管性痴呆的诊断标准以及CDR的临床痴呆分级标准 ,对神经内科老年记忆障碍专科病房的 2 1例轻中度阿尔茨海默病及 2 5例血管性痴呆患者的非认知功能损害的临床表现进行了观察 ,包括情感反应、行为异常、人格变化及知觉异常。结果　阿尔茨海默病患者的非认知功能损害在情感障碍 (16例 ,76 % )、人格异常 (10例 ,48% )及知觉异常 (6例 ,2 9% )方面 ,明显多于血管性痴呆组 (分别为 10例 ,40 % ;1例 ,4% ;1例 ,4% )。结论　痴呆患者不仅有认知功能的损害 ,还有非认知功能的损害。阿尔茨海默病的非认知功能损害重于血管性痴呆 ,可能与两种痴呆的发病机制不同有关。     

Dementia and Alzheimer's disease incidence in relationship to cardiovascular disease in the Cardiovascular Health Study cohort

OBJECTIVES: To determine whether coronary artery disease, peripheral arterial disease (PAD), or noninvasive markers of cardiovascular disease (CVD) predict the onset of dementia and Alzheimer's disease (AD). DESIGN: Longitudinal cohort study. SETTING: Four U.S. communities. PARTICIPANTS: Men and women (N=3,602) with a brain magnetic resonance imaging (MRI) scan but no dementia were followed for 5.4 years. Participants with stroke were excluded. MEASUREMENTS: Neurologists and psychiatrists classified incident cases of dementia and subtype using neuropsychological tests, examination, medical records and informant interviews. CVD was defined at the time of the MRI scan. Noninvasive tests of CVD were assessed within 1 year of the MRI. Apolipoprotein E allele status, age, race, sex, education, Mini-Mental State Examination score, and income were assessed as potential confounders. RESULTS: The incidence of dementia was higher in those with prevalent CVD, particularly in the subgroup with PAD. The rate of AD was 34.4 per 1,000 person-years for those with a history of CVD, versus 22.2 per 1,000 person-years without a history of CVD (adjusted hazard ratio (HR)=1.3, 95% confidence interval (CI)=1.0-1.7). Rates of AD were highest in those with PAD (57.4 vs 23.7 per 100 person-years, adjusted HR=2.4, 95% CI=1.4-4.2). Results were similar with further exclusion of those with vascular dementia from the AD group. A gradient of increasing risk was noted with the extent of vascular disease. CONCLUSION: Older adults with CVD other than stroke had a higher risk of dementia and AD than did those without CVD. The risk was highest in people with PAD, suggesting that extensive peripheral atherosclerosis is a risk factor for AD.