血管性痴呆的药物干预

痴呆被公认为是继心血管病、肿瘤和脑血管病后老年人第四位最常见的病死原因。随着脑血管病发病率的增加,血管性痴呆已成为老年期痴呆的主要类型之一,同时与阿尔茨海默病相比,血管性痴呆是有可能预防和有希望治疗的痴呆类型。因此本文对血管性痴呆的药物干预进行综述。     

血管性痴呆危险因素的探讨

痴呆系指意识清楚情况下脑部器质性病变所致的持久性智能衰退综合征,可由多种疾病引起。我国属脑血管病高发病区,且血管性痴呆又是一种常见而某些功能障碍可逆的疾病。因此,积极探索引起血管性痴呆的危险因素及早期治疗,对防治脑血管病及血管性痴呆具有积极意义。我科自1986年12月～1989年1月共收治45岁以上脑梗塞住院病人264例,其中22例为血管性痴呆(8.33%)。本文重点讨论引起血管性痴呆的可能因素。     

H型高血压与血管性痴呆

脑血管病是我国首位死亡原因。我国脑卒中年死亡人数200多万,在导致脑卒中发生的可控因素中,高血压和同型半胱氨酸升高位居前列,二者在导致脑卒中的发生上具有协同作用,而缺血性脑卒中是导致血管性痴呆的重要病因。我国学者将伴有同型半胱氨酸升高的高血压定义为＂H型高血压＂。我国原发性高血压患者中约有75%为H型高血压。血管性痴呆是指由各类脑血管病所致的痴呆综合征,是继阿尔茨海默病之后第二常见的痴呆。高血压和高同型半胱氨酸血症可引起认知功能障碍,进而导致血管性痴呆的发生,且待患者达血管性痴呆的诊断标准时,常已错过重要的早期干预治疗阶段,故在认知功能明显损害之前就发现并进行干预是非常重要的。现对H型高血压和血管性痴呆的关系做一综述。     

血管性痴呆诊断与治疗

血管性痴呆(VD)是指因脑血管疾病所致的智能及认知功能障碍的临床综合征,是老年性痴呆最常见的类型之一,是仅次于阿尔茨海默病(AD)造成老年性痴呆的第2位原因.VD是由血管因素和脑血管病相关因素共同作用的结果[1],它与脑血管病的发生密切相关,脑血管病患者中痴呆发生率是26%,是无脑血管病者的5.8倍.VD预后相对较好,治疗途径广泛,且在一定程度上可以进行预防.     

血管性痴呆与血管性认知障碍

由于传统痴呆定义的束缚,目前的血管性痴呆诊断标准不能发现非痴呆的认知障碍,也难以与混合性痴呆相区别,更不能促进血管性痴呆的防治。用血管性认知障碍的概念则可以涵盖所有与血管危险因素和脑血管病变有关的各种程度的认知障碍,促进早期识别和早期干预。     

血管性痴呆与血管性认知障碍

由于传统痴呆定义的束缚，目前的血管性痴呆诊断标准不能发现非痴呆的认知障碍，也难以与混合性痴呆相区别，更不能促进血管性痴呆的防治。用血管性认知障碍的概念则可以涵盖所有与血管危险因素和脑血管病变有关的各种程度的认知障碍，促进早期识别和早期干预。     

法舒地尔联合康复训练治疗脑梗死后血管性痴呆

目前,血管性痴呆尚无特效治疗,临床上多采用改善脑循环、促智药物及预防脑血管病复发药物,使其认知障碍尽可能保持稳定,针对性地康复训练对血管性痴呆的恢复具有一定的促进作用。盐酸法舒地尔属于新型的Rho激酶抑制剂,能够舒张血管平滑肌,改善缺血区血流量,有助于改善炎症反应,对血     

血管性认知损害的筛查工具与早期诊断

血管性认知损害(vascular cognitive impairment,VCI)是由脑血管病危险因素(如高血压、心脏病、糖尿病和高血脂等)、明显(如脑梗死和脑出血等)或不明显的脑血管病(如白质疏松和慢性脑缺血等)引起的从轻度认知障碍到痴呆的综合征[1,2].目前较为统一的意见是VCI包括3个内容[3～6]:非痴呆型血管性认知损害 (vascular cognitive impairment,no dementia,VCIND)、血管性痴呆(vascular dementia,VD )、AD伴血管病变(即混合性痴呆,mixed AD/VD).与血管性痴呆相比,其内涵有了扩展,认知障碍不强调记忆力损害,只要有某些认知领域的功能下降,即使没有记忆力减退,仍然可定性为认知障碍;同时,"血管性"不特指脑出血或梗死,还包括各种可能影响脑功能的心脑血管病变.     

免疫反应与血管性痴呆

血管性痴呆的发生是一个多因素的过程,其中脑血管病、白质疏松可导致智能损害已得到公认,而近年来发现的阿尔茨海默病样的组织学变化引起了学者们的关注。目前能确定免疫系统及免疫反应在阿尔茨海默病的神经退行性病变中的作用,故炎症因子与血管性痴呆的关系也日益受到重视,为进一步探索血管痴呆的发病机制及治疗途径提供了新思路。     

脑苷肌肽联合尼莫地平治疗血管性痴呆39例

正随着社会经济的发展,科技的进步,人类寿命不断延长,全球人口出现老龄化趋势,痴呆发病率呈逐年上升趋势。其中血管性痴呆是脑血管病后引起的痴呆,包括记忆、语言、视空间功能不同程度受损,人格异常和认知能力降低,常伴行为和情感异常,日常生活、社交和工作能力明显减退。本文采用脑苷肌肽联合尼莫地平治疗血管性痴呆,观察其临床疗效。     

Hypertension and Cognitive Function

Arterial hypertension, cerebrovascular disease, and dementia are related pathologies. This paper has reviewed comparatively the incidence of arterial hypertension and adult-onset dementia disorders. Hypertension is associated with cerebrovascular disease, which is in turn associated with dementia. It is the most important modifiable risk factor for stroke, which is a recognized cause of vascular dementia. In terms of pathophysiology of hypertensive brain damage, several hypotheses were developed, such as that vascular alterations induced by hypertension can induce lacunar or cortical infarcts and leucoaraiosis, that hypertension is responsible for cerebrovascular disease and acts into the contest of a pre-existing subclinic Alzheimer's disease (AD), that hypertension determines neurobiologic alterations (such as β-amyloid accumulation) resulting in neuropathologic damage, and that aging and cerebrovascular risk factors act together to cause cerebral capillary degeneration, mitochondrial disruption, reduced glucose oxidation, and reduced ATP synthesis. The consequence of these alterations are neuronal death and dementia. Macroscopic results of these mechanisms are the so-called white matter lesions (WML), the significance of which is analyzed. Increasing clinical evidence suggests a close relationship between the reduction of elevated blood pressure and countering of both vascular dementia and AD. Antihypertensive treatment probably influences cognitive performances and prevents cognitive function alterations and the development of dementia. It is therefore important to evaluate as soon as possible cognitive functions of hypertensive patients.     

The ACE gene I/D polymorphism is not associated with the blood pressure and cardiovascular benefits of ACE inhibition

The insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene might have consequences for the risks of vascular diseases. We examined the ACE genotype and the effects of a perindopril-based blood pressure-lowering regimen on macrovascular events, dementia, and cognitive decline among hypertensive and nonhypertensive patients with a history of cerebrovascular disease. ACE I/D genotypes were measured in 5688 of 6105 individuals with previous stroke or transient ischemic attack who participated in the PROGRESS trial. The DD genotype was significantly (P<0.0001) less frequent in Asian subjects (Chinese and Japanese, 14.7%) than in non-Asian subjects (32.0%). Controlling for racial background, there were no associations between ACE genotypes and cerebrovascular disease history or cardiovascular risk factors, including baseline blood pressure. The ACE genotype was not associated with the long-term risks of stroke, cardiac events, mortality, dementia, or cognitive decline; neither did the ACE genotype predict the blood pressure reduction associated with the use of the ACE inhibitor perindopril. Similarly, there was no evidence that the ACE genotype modified the relative benefits of ACE inhibitor-based therapy over placebo. This study provides no evidence that in patients with cerebrovascular disease, knowledge of ACE genotype is useful for predicting either the risk of disease or the benefits of perindopril-based blood pressure-lowering treatment.     

Present state of hemorheology

Hemorheological disturbances are present in more than 50% of cerebrovascular disease (CVD). An inverse relationship between cerebral blood flow (CBF) and viscosity has been established. There also exists an interaction of vessel wall changes, whole blood viscosity, and plasma fibrinogen. The acute ischemic episode is associated with hyperaggregability of the blood platelets, increased blood viscosity, hyperaggregability of the red cells and an increase in plasma fibrinogen. Hemorheological changes to a certain extend may occur not only in CVD but also in senile dementia of Alzheimer type (SDAT) and certain cases of Parkinson's disease. This fact allows to differentiate between idiopathic parkinsonism and Parkinson's disease with high hemodynamic risk.     

Effects of blood pressure lowering with perindopril and indapamide therapy on dementia and cognitive decline in patients with cerebrovascular disease

BACKGROUND: High blood pressure and stroke are associated with increased risks of dementia and cognitive impairment. This study aimed to determine whether blood pressure lowering would reduce the risks of dementia and cognitive decline among individuals with cerebrovascular disease. METHODS: The Perindopril Protection Against Recurrent Stroke Study (PROGRESS) was a randomized, double-blind, placebo-controlled trial conducted among 6105 people with prior stroke or transient ischemic attack. Participants were assigned to either active treatment (perindopril for all participants and indapamide for those with neither an indication for nor a contraindication to a diuretic) or matching placebo(s). The primary outcomes for these analyses were dementia (using DSM-IV criteria) and cognitive decline (a decline of 3 or more points in the Mini-Mental State Examination score). RESULTS: During a mean follow-up of 3.9 years, dementia was documented in 193 (6.3%) of the 3051 randomized participants in the actively treated group and 217 (7.1%) of the 3054 randomized participants in the placebo group (relative risk reduction, 12% [95% confidence interval, -8% to 28%]; P =.2). Cognitive decline occurred in 9.1% of the actively treated group and 11.0% of the placebo group (risk reduction, 19% [95% confidence interval, 4% to 32%]; P =.01). The risks of the composite outcomes of dementia with recurrent stroke and of cognitive decline with recurrent stroke were reduced by 34% (95% confidence interval, 3% to 55%) (P =.03) and 45% (95% confidence interval, 21% to 61%) (P<.001), respectively, with no clear effect on either dementia or cognitive decline in the absence of recurrent stroke. CONCLUSIONS: Active treatment was associated with reduced risks of dementia and cognitive decline associated with recurrent stroke. These findings further support the recommendation that blood pressure lowering with perindopril and indapamide therapy be considered for all patients with cerebrovascular disease.     

祖细胞和干细胞与缺血性疾病的治疗

缺血性疾病是严重危害人类健康的疾病之一,主要包括缺血性脑血管疾病、缺血性心血管疾病、下肢缺血性疾病等。祖细胞和干细胞都是具有自我复制能力的多潜能细胞,在一定条件下,它们可以分化成多种功能细胞。根据干细胞所处的发育阶段分为胚胎干细胞和成体干细胞,虽然胚胎干细胞具有万能分化型功能,但伦理学方面的争议使其研究困难重重,而成体干细胞相较胚胎干细胞,不仅避免了伦理学方面的争议问题,而且无移植后免疫排斥反应。本文主要讨论成体干细胞和祖细胞在缺血性疾病中的应用。近年来,关于祖细胞和干细胞在缺血性疾病中应用的研究日益增多,受到了广泛的关注,为我们提供了一条治疗缺血性疾病的新思路。     

三叉神经痛经皮球囊压迫术的脑血管并发症——10例报道

目的 探讨三叉神经痛经皮球囊压迫术（percutaneous balloon compression,PBC）并发脑血管病的相关因素,以减少手术相关并发症的发生。方法 回顾性分析辽宁省人民医院2000年12月至2010年12月期间采用PBC治疗三叉神经痛中并发脑血管病患者的临床资料,探讨其发生的原因。结果 在6 759例接受PBC治疗的三叉神经痛患者中,共有10例(0.15％)发生脑血管病,其中动静脉瘘2例;颅内出血5例：急性硬膜下出血2例,脑室出血伴蛛网膜下腔出血2例,脑干少量出血1例;1例在术中穿刺时发生颈内动脉出血而暂时停止手术,2周后再次手术成功;脑梗死2例,均为脑血管病危险人群,治疗3周后病情均有改善,其中1例出院时遗留较严重肢体瘫痪。结论 PBC治疗三叉神经痛安全,脑血管病并发症发生率较低,手术操作和血压变化是发生脑血管病并发症的重要原因。     

外周血干细胞移植治疗冠心病研究进展

干细胞移植治疗冠心病是目前医学研究的热点。本文简要介绍了外周血干细胞治疗冠心病的研究进展,包括外周血干细胞与冠心病发病的关系、外周血干细胞治疗冠心病的方法和效果以及存在的问题和展望。     

Exercise: a potential contributing factor to the relationship between folate and dementia

OBJECTIVES: To investigate whether exercise confounds the relationship between folate and cerebrovascular events, all-cause dementia, and Alzheimer's disease. DESIGN: Prospective cohort study. SETTING: Multiple centers in Canada. PARTICIPANTS: In the Canadian Study of Health and Aging, 466 people reported exercise levels, had folate measurements, and were not demented at baseline. After 5 years, 194 had adverse cerebrovascular events, and 65 had dementia (Alzheimer's disease in 47). MEASUREMENTS: Associations between folate and cerebrovascular outcomes were examined using logistic regression in the presence and absence of exercise and other confounders. RESULTS: Folate was associated with greater risk of Alzheimer's disease (odds ratio (OR)=2.12, 95% confidence interval (CI)=1.01-4.54) and cerebrovascular outcomes (OR=2.05, 95% CI=1.11-3.78) in adjusted analyses before the inclusion of exercise and neared significance with all-cause dementia (OR=1.80, 95% CI=0.94-3.45). After the inclusion of exercise, the association between folate and dementia and Alzheimer's disease was 29% and 25% lower, respectively, and neither association was any longer significant (Alzheimer's disease: OR=1.91, 95% CI=0.89-4.11; all-cause dementia: OR=1.62, 95% CI=0.84-3.15). Exercise was a significant confounder in the relationship between folate and Alzheimer's disease (P=.03) and dementia (P=.003) but not cerebrovascular outcomes (P=.64). Unlike folate, exercise was significantly associated with Alzheimer's disease (OR=0.43, 95% CI=0.19-0.98) and dementia (OR=0.35, 95% CI=0.17-0.72) in adjusted analyses. CONCLUSION: Exercise seems to account for much of the relationship between folate and incident dementia and Alzheimer's disease.     

Are antihypertensive agents protective against dementia? A review of clinical and preclinical data

In the United States, the size of the population of persons aged 65 years or older is expected to double within the next 30 years, resulting in a marked increase in the prevalence of dementia. Hypertension is a risk factor for cognitive impairment and dementia in addition to cerebrovascular morbidity and mortality. The evidence for a connection between high blood pressure in midlife and dementia in late life comes from numerous longitudinal studies. A placebo-controlled, double-blind, randomized trial involving 2,418 patients aged 60 years or older with isolated systolic hypertension demonstrated that active treatment based on the dihydropyridine calcium antagonist nitrendipine with the addition of enalapril, hydrochlorothiazide, or both if needed to control systolic blood pressure to <150 mmHg, significantly reduced not only stroke and cardiovascular complications but also the incidence of vascular dementia and Alzheimer's disease. Several trials of antihypertensive treatment are ongoing to confirm this important finding. The newer dihydropyridine calcium antagonists lacidipine and lercanidipine are effective and well tolerated in the treatment of hypertension. In animal models, these newer agents also have been shown to prevent the progression of hypertensive microvascular damage. Their neuroprotective effects offer possible unique advantages in the management of hypertension.