皮质下缺血性血管性痴呆的诊断和治疗

皮质下缺血性血管性痴呆主要以小血管疾病为病因,包括腔隙状态、关键部位梗死性痴呆和Binswanger综合征,临床上表现为皮质下综合征和认知障碍.积极诊断和治疗皮质下缺血性血管性痴呆有助于降低老年人认知障碍的发病风险.     

皮质下缺血性血管性痴呆患者胼胝体和扣带回弥散张量成像改变与认知功能障碍的相关性

目的应用磁共振弥散张量成像技术探讨皮质下缺血性血管性痴呆(subcortical ischemic vascular dementia,SIVD)患者胼胝体和扣带回弥散张量参数改变与认知功能的关系。方法选择2015年7月~2016年6月在济宁医学院附属医院神经内科住院的老年SIVD患者60例(SIVD组),年龄匹配的健康体检者40例(对照组),采用测定感兴趣区弥散张量参数的方法,计算平均弥散系数(ADC)和各向异性分数(FA),比较2组纤维束完整性及与简易智能状态检查量表(mini-mental state examination,MMSE)的关系。结果与对照组比较,SIVD组胼胝体膝部ADC明显升高(1.081±0.210 vs 0.966±0.080,P=0.036),FA明显降低(0.636±0.079 vs 0.713±0.067,P=0.003),而2组胼胝体压部ADC和FA比较,差异无统计学意义(P0.05)。SIVD组左右侧扣带回ADC明显升高,FA明显降低,差异有统计学意义(P0.05,P0.01)。胼胝体膝部、左侧扣带回及右侧扣带回FA与MMSE评分呈正相关(r=0.511,r=0.469,r=0.457,P0.05),而胼胝体压部FA与MMSE评分不相关(r=0.364,P0.05)。结论胼胝体和扣带回弥散张量改变有助于SIVD患者认知功能障碍的早期预防及治疗。     

静息态功能磁共振在皮质下缺血性血管性认知损害中的应用

皮质下缺血性血管病(subcortical ischemic vascular disease, SIVD)被认为是引起血管性认知损害(vascular cognitive impairment, VCI)的最重要和常见的原因。若能早期发现皮质下缺血性血管性认知损害(subcortical ischemic vascular cognitive impairment, SIVCI)或皮质下血管性认知损害(subcortical vascular cognitive impairment, sVCI)患者,会使血管性痴呆(vascular dementia, VaD)在发生之前得到识别甚至逆转其进程成为可能。最近的研究显示,静息态功能磁共振(resting-state fMRI, rsfMRI)有可能为 SIVCI 的诊断提供客观依据。文章对 rsfMRI 在 SIVCI 诊断中的应用进行了综述。     

皮质下缺血性血管性痴呆功能磁共振研究进展

<正>血管性痴呆(VD)在老年期痴呆中发生率居第二位,是由脑血管性疾病导致脑组织损害所引起的智能及认知功能障碍的总称[1],其中又以皮质下缺血性VD(SIVD)亚型为主[2]。随着年龄的增长,缺血性脑卒中的发病率呈几何倍数增长[3],而常规的影像学检查手段不足以对与SIVD相关的脑卒中患者给予及时准确的诊断,因此SIVD的发生率也呈明显增加趋势。VD是一种可预防的、可逆的痴呆类型,因此早期诊断及积极防治意     

磁共振波谱在血管性痴呆中的应用

血管性痴呆（vascular dementia,VaD）是老年人群中最常见的痴呆类型之一,其发病率仅次于阿尔茨海默病。目前,对VaD的诊断主要依据患者的临床表现、神经影像学以及神经心理学量表检查,尚缺乏敏感性和特异性较高的代谢指标。磁共振波谱是一种无创性检测活体组织能量和代谢变化的技术,近年来越来越多地应用于VaD患者...     

皮质下缺血性脑血管病

皮质下缺血性脑血管病是血管性认知功能障碍中最常见的亚型之一.文章就其发病机制、神经心理学表现、影像学改变及生物学标记物等方面的研究进展进行了综述.     

非痴呆型血管性认知障碍

作为痴呆的早期阶段,非痴呆型血管性认知障碍(vascular cognitive impairment no dementia,VCI-ND)成为近年来的研究热点,有效识别VCI-ND对于预防痴呆和降低痴呆发病率具有重要的临床意义.文章对VCI-ND的神经心理学、神经影像学、生物学标记物以及预防和治疗等方面的研究进展进行了综述.     

皮质下缺血性血管性认知功能障碍的静息态功能磁共振研究

目的探讨静息态功能磁共振低频振幅(ALFF)的分析方法在皮质下缺血性血管性认知功能障碍中的价值。方法选择49例缺血性脑小血管病患者经临床痴呆量表评分后,分为血管性痴呆(VaD)组10例,非痴呆型血管性认知功能障碍(VCIND)组20例,认知功能正常为对照组19例。分别采集高分辨率结构像和静息态功能磁共振数据,通过ALFF分析方法计算并对比3组患者脑功能活动的改变。观察VaD组ALFF统计脑图与认知量表评分的相关性。结果与对照组比较,VaD组内侧前额叶、后扣带回及双侧颞叶脑区ALFF明显降低,额中回、额上回、顶下小叶脑区ALFF明显升高,VCIND组内侧前额叶ALFF明显降低,左侧顶叶及颞中回ALFF明显升高(P<0.05);与VCIND组比较,VaD组后扣带回/楔前叶、左侧小脑区ALFF明显降低,双侧额叶、颞叶及前扣带回明显升高(P<0.05);回归灰质体积后,VaD组ALFF统计脑图与多个临床量表评分存在相关性(P<0.05)。结论血管性认知功能障碍患者存在以执行功能障碍为主的多个领域的认知功能障碍,其认知功能障碍可能与额叶-皮质下环路受损有关,ALFF在血管性认知功能障碍及其早期诊断中有重要价值。     

阿尔茨海默氏病与血管性痴呆的智能障碍及MRI对比分析

将128例痴呆患者分别为阿尔茨海默氏病(AD)组56例和血管性痴呆(VD)组72例,两组均应用长谷川氏痴呆评定量表检查法、简易精神状态检查法(MUSE)、Kohs立方体组合测验(Kohs测验)检查法测查,并与加以比较研究.发现AD多慢性起病,VD多急性起病,呈阶梯性病程,常伴有高血压和卒中史;头颅MRI显示AD患者以广泛皮质萎缩且以双侧海马明显萎缩为主,VD患者多为局灶异常.VD组的长谷川氏、MMSE测验分数都显著高于AD组.提示MRI用于鉴别诊断AD和VD的方式值得在临床推广.     

皮质下缺血性血管病患者同型半胱氨酸与认知功能障碍的关系

目的探讨皮质下缺血性血管病(SIVD)患者同型半胱氨酸(Hcy)与轻度血管性认知功能障碍(MVCI)的相关性。方法将120例SIVD患者按照蒙特利尔认知评估量表(MOCA)评定的认知功能程度的不同,分为MVCI组(56例)和非MVCI组(64例),检测Hcy、叶酸、VitB_(12)水平,MVCI组患者治疗3个月后,再进行MOCA评分及上述指标检测,并进行分析。结果 MVCI组血浆Hcy水平明显高于非MVCI组;血清叶酸、VitB_(12)水平显著低于非MVCI组(P0.01)。Hcy水平与年龄呈正相关,与MOCA评分呈负相关(P0.01)。结论 Hcy可能是SIVD患者发生MVCI的独立危险因素,叶酸、VitB_(12)缺乏,间接引起Hcy增高,是导致MVCI的重要影响因素。     

Motor cortex hyperexcitability in subcortical ischemic vascular dementia

To study whether in subcortical ischemic vascular dementia (SIVD) the changes of motor cortex excitability are due to the dementing process or to the cerebrovascular lesions, we examined 20 SIVD patients, 20 patients with subcortical ischemic disease without dementia (SIDWD) and 20 control subjects who underwent transcranial magnetic stimulation (TMS). Motor threshold (MT), amplitudes of motor evoked potentials (MEPs) and silent period (SP) were considered. MT in SIVD patients (32.7 ± 2.6%) was significantly lower (p < 0.001) than in SIDWD patients (47.9 ± 3.4%) and in controls (49.1 ± 4.2%). MEP amplitude was larger in SIVD patients (6.8 ± 1.7 mV) than in the other groups (5.7 ± 1.9 mV and 5.2 ± 1.8 mV, p < 0.02). Motor cortex excitability is enhanced in SIVD. Our data, taken together with previous results in Alzheimer disease (AD), indicate that motor cortex hyperexcitability is a common finding in different dementing illnesses.     

Subcortical vascular dementia (SVaD) without hypertension (HTN) may be a unique subtype of vascular dementia (VaD)

Although HTN is the most important factor in the pathogenesis of SVaD, about 20% of patients with SVaD do not have HTN. We hypothesize that SVaD without HTN may have strong risk factors other than HTN, and the study on this group can elucidate the risk factors for SVaD. We included 332 patients with SVaD from the database of the Clinical Research Center for Dementia of South Korea (CREDOS) study. Among them, 26.2% of patients (87 out of 332) had no history of HTN. We analyzed the differences in risk factors, clinical features, and survival time of SVaD according to HTN. Contrary to our expectations, SVaD without HTN had less known vascular risk factors such as diabetes mellitus (DM), dyslipidemia, and obesity. In addition, SVaD without HTN had different clinical features including less depression, focal neurological signs or symptoms and more features of disinhibition. However, although SVaD without HTN had less known vascular risk factors that can shorten survival times, the survival times did not differ according to the presence of HTN. SVaD without HTN may be a unique subtype of SVaD and can be a target group for studies of unknown risk factors for SVaD.     

Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an inherited autosomal dominant condition characterized by migrane, recurrent stroke, subcortical dementia, and pseudobulbar palsy. It begins with migraine with aura in ～33% of patients. CADASIL is commonly overlooked or misdiagnosed owing to its recent identification. The pathological hallmark of angiopathy is the presence of multiple, small, deep cerebral infarcts, leucoencephalopathy, and nonatherorosclerotic, nonamyloid angiopathy involving mainly small, deep perforating cerebral arteries. Changes also are present in vascular smooth muscle cells and consist in the presence of granular osmiophilic material (GOM). The defective gene in CADASIL is Notch 3, which encodes a large transmembrane receptor. Magnetic resonance imaging shows high intensity signal lesions, often confluent, and areas of cystic degeneration of subcortical white matter and basal ganglia. Diagnostic strategies in CADASIL are matter of discussions because the electron microscopic demonstration of GOM was reported in 100% of symptomatic patients of French authors, but only in 45% of a British study. GOMs are not present in presymptomatic patients.     

Linking Notch signaling to ischemic stroke

Vascular smooth muscle cells (SMCs) have been implicated in the pathophysiology of stroke, the third most common cause of death and the leading cause of long-term neurological disability in the world. However, there is little insight into the underlying cellular pathways that link SMC function to brain ischemia susceptibility. Using a hitherto uncharacterized knockout mouse model of Notch 3, a Notch signaling receptor paralogue highly expressed in vascular SMCs, we uncover a striking susceptibility to ischemic stroke upon challenge. Cellular and molecular analyses of vascular SMCs derived from these animals associate Notch 3 activity to the expression of specific gene targets, whereas genetic rescue experiments unambiguously link Notch 3 function in vessels to the ischemic phenotype.     

Gene therapy for ischemic brain disease with special reference to vascular dementia

Vascular dementia is the second largest cause of dementia in the elderly. There is no effective treatment for cerebral infarction, which is one of the common causes of vascular dementia. In rodent experimental models, gene therapies using growth factors such as brain-derived neurotrophic factor, fibroblast growth factor-2, hepatocyte growth factor, glial cell-line derived neurotrophic factor or vascular endothelial growth factor had beneficial effects on neuroprotection, neurogenesis and/or angiogenesis. Thus, gene therapies can be expected to be useful as new treatments for ischemic diseases, especially for vascular dementia. In clinical trials, gene therapy for vascular dementia still has some problems to be solved, such as the safety and effectiveness of vectors and delivery systems, the timing of treatment, and cell-specific targeting strategies. The most important thing might be the definition of the best combination of these subjects for every target disease.     

老年人缺血性脑卒中后血管性痴呆的危险因素分析

目的:分析老年缺血性脑卒中患者发生血管性痴呆(VD)的危险因素,为临床干预提供参考。方法:选取2014年5月至2017年1月间,我院收治老年缺血性脑卒中患者156例作为研究对象,收集患者一般资料、生活习惯、基础疾病、和脑卒中特征等情况,随访时间至少达6个月,根据随访期间内是否发生VD分为VD组(35例)和非VD组(121例)。单因素分析筛有统计学意义的变量,纳入多因素非条件Logistic回归分析模型,分析影响VD发生的危险因素。结果:156例患者中共35例发生VD,发生率22.4%;单因素分析显示:两组患者间年龄、文化程度、吸烟史、高血压、糖尿病、高脂血症、既往脑卒中病史,多发性脑梗死、大面积脑梗死以及梗死部位情况,差异有统计学意义(P0.05),而性别、体重量指数、饮酒史、合并冠心病情况差异无统计学意义;多因素Logistic分析结果显示年龄≥75岁、高血压病史、糖尿病史、大面积脑梗死以及梗死部位(基底节、额叶)是引起VD的危险因素(P0.05)。结论:老年缺血性脑卒中患者VD发生率相对较高,尤其是伴有基础疾病的高龄老人,当发生大面积梗死以及基底节、额叶梗死时,需要及早干预,预防VD发生。