脑梗死急性期MRI表现与发展为血管性痴呆的关系

目的 探讨脑梗死急性期患者的MRI表现与发展为血管性痴呆(VD)的关系.方法 对卒中半年以上的患者,根据简易精神状态检查量表(MMSE)、临床痴呆评定量表(CDR)评分分为VD组及脑卒中后无痴呆(SWD)组,并回顾性分析两组在卒中急性期的MRI资料.结果 VD组中额叶皮质下、颞叶皮质下、内囊前肢、内囊膝部、尾状核及丘脑梗死的发生率明显高于SWD组(P<0.05～0.01);梗死灶≥3个部位的患者显著多于SWD组(P<0.05);3级脑白质疏松(LA)发生率(35.0%)明显高于SWD组(10.0%)(P<0.05). VD组放射冠及基底节的LA发生率明显高于SWD组(P<0.05).VD组与SWD组间脑萎缩的线性指标海马钩回间距及侧脑室体部宽度指数的差异有统计学意义(P<0.05～0.01).结论 额叶及颞叶皮质下、内囊前肢及膝部、尾状核和丘脑梗死者,且梗死灶≥3个,并出现3级LA,放射冠、基底节的LA,以及海马钩回间距、侧脑室体部宽度指数可作为发展为VD的预测指标.     

缺血性脑卒中后血管性痴呆的MRI特征研究

目的研究急性缺血性脑卒中后血管性痴呆的MRI特点,探讨急性缺血性脑卒中与血管性痴呆的相关性,为指导临床治疗提供帮助。方法选取124例缺血性脑卒中患者,检查后发现血管性痴呆的缺血性脑卒中患者(实验组)66例,非血管性痴呆患者(对照组)58例。经头颅MRI检查后,比较2组患者的脑梗死发生部位、数目、大小。结果 2组患者的年龄、饮酒和吸烟时间、并发高血压、心脏病几率相比差异无统计学意义(P0.05)。但实验组患者的病程较长、患糖尿病几率以及卒中次数明显高于对照组(P0.05)。对照组患者的语言即刻记忆、时间定向、语言复述、言语表达和图形描述等评分与实验组相比差异无统计学意义(P0.05)。但实验组注意和计算、短程记忆评分明显低于对照组(P0.05)。对照组患者中小梗死较为常见,实验组患者梗死部位主要发生在额叶和丘脑,以大梗死发病较多,明显高于对照组(P0.05)。结论额叶、丘脑等是缺血性脑卒中后血管性痴呆的主要梗死部位以大中梗死较为常见,与年龄、卒中次数等密切相关。     

血管性痴呆危险因素及影像学特征

目的探讨血管性痴呆危险因素及影像学特征。方法对我院2014-02—2015-10收治的80例血管性痴呆患者的影像学资料进行回顾性分析,总结归纳血管性痴呆的危险因素及影像学特征。结果文化程度越低、月收入2 500元、夫妻关系一般、居住地位于农村、健康教育2次及以下、具有高血压史患者发生血管性痴呆的几率较高。80例患者均经MRI检查确诊,脑出血14例,脑梗死66例。临床表现:智能障碍80例,记忆力减退71例,不同程度肢体障碍59例,表情冷漠53例,行为异常21例,假性延髓性麻痹25例,语言功能障碍13例,小便失禁19例,感觉障碍11例。影像学表现:脑萎缩71例,脑白质疏松63例,大小不一的单一或多发的梗死灶67例(其中单灶性梗死13例,多灶性梗死54例)。梗死灶部位:基底节区、脑叶、丘脑、内囊、脑干、小脑;脑出血病灶分别位于丘脑、基底节、额叶等。结论血管性痴呆危险因素包括高血压、糖尿病史、心脏病史、高脂血症等,临床要加强危险因素防治,采用药物、心理康复的综合治疗方法积极对患者进行干预,提高患者的生活质量。     

多发性脑梗塞痴呆40例临床报告

本文报告了多发性脑梗塞痴呆（MID）40例，其中轻度24例占60％，中度13例占32．5％，重度3例占7．5％。头颅CT扫描发现梗塞灶112个，平均2.8个，梗塞部位以基底节、皮质下白质、丘脑、内囊多发性脑梗塞多见。基底节梗塞产生痴呆者病灶较皮质下梗塞者面积小。痴呆程度与梗塞数目、脑萎缩明显相关。     

血管性痴呆的CT与SPECT对比研究

目的 :通过 CT和 SPECT检查了解血管性痴呆和非痴呆脑血管病患者的不同影象表现 ,评价两者诊断价值。方法 :选择符合 DSM- 4有关血管性痴呆的诊断标准的患者 45例和非痴呆脑血管病患者 30例 ,完成 CT,SPECT检查。结果 :VD患者 SPECT阳性检出率高出 CT,CT以半卵圆中心 ,基底节 ,丘脑多发性病灶 ,双侧或 /和左半球病灶 ,大容积 ,大多伴有脑萎缩改变 ,SPECT表现以区域性脑灌注减低或缺损 ,皮质额颞顶叶大片状放射缺损多见 ,少部分表现弥漫性放射分布稀疏 ,在检查脑血流灌注障碍方面 SPECT较 CT敏感。结论 :CT,SPECT检查结合有助于 VD的诊断。     

脑梗死MRI表现与患者认知功能障碍及抑郁关系的研究

目的 探讨脑梗死患者认知功能障碍及抑郁与病变部位的关系.方法 经MRI证实的脑梗死患者81例,按部位划分为丘脑组、内囊-基底节组、小脑组、脑干组,另选MRI表现正常者30例作为对照组.采用简易智力状态试验（MMSE）和哈金斯基缺血指数量表（HIS）及汉密顿抑郁量表（HAMD）量表进行测试,对所得结果进行统计学分析.结果 丘脑组、内囊-基底节组、小脑组、脑干组与对照组相比智能下降显著;内囊-基底节组HAMD得分明显高于对照组;左侧梗死组的HAMD得分与对照组相比具有显著性差异;左右两侧病灶组相比,左侧组智能明显低于右侧,两组抑郁得分无显著性差异;抑郁组的智能显著低于非抑郁组.结论 丘脑、内囊-基底节、小脑、脑干部位的梗死导致血管性痴呆,其中左侧病灶组和抑郁组患者更易发生痴呆;内囊-基底节病变组及左侧梗死患者更易患卒中后抑郁.     

血管性痴呆与脑梗塞部位及促发因素相关性探讨

本文报道24例血管性痴呆(其中基底节6例、丘脑7例、内囊6例、左皮层大面积及皮质下基底节4例,左侧额叶1例)。多发性梗塞灶19例,单发性梗塞灶5例,梗塞灶少者1个,多者8个,平均为4个梗塞灶。1年内复发者12例,2～3年复发10例,5年以上复发2例,其中2次以上发病占90%。所有血管性痴呆全部有脑萎缩,且呈中央性萎缩。并就脑梗塞部位,反复发作性及多灶性梗塞、脑萎缩等成因相互关系进行探讨。     

磁共振扩散张量成像在缺血缺氧脑病患儿中的临床应用

目的探讨磁共振扩散张量成像(DTI)在缺血缺氧脑病患儿中的应用价值。方法前瞻性纳入2016-12—2018-12于河南中医药大学第一附属医院行MRI头颅平扫及DTI检查的年龄2岁患儿40例,所有患儿在围生期均有缺氧缺血脑病史,根据最终随访结果分为脑瘫组及非脑瘫组各20例。测量双侧大脑脚、内囊前肢、内囊膝部、内囊后肢、半卵圆中心、皮质脊髓束、下纵束、丘脑后辐射、额叶白质、顶叶白质、胼胝体膝部、胼胝体体部及胼胝体压部的FA值。结果 2组间双侧大脑脚、内囊后肢、半卵圆中心、皮质脊髓束、下纵束、丘脑后辐射、顶叶白质、胼胝体膝部、胼胝体体部、胼胝体压部FA值差异均有统计学意义(P0.05),而双侧内囊前肢、内囊膝部、额叶白质FA值差异无统计学意义(P0.05)。结论 DTI可以定量评估缺血缺氧脑病患儿的损伤程度,有助于早期评估病情及预测预后。     

皮质下血管性认知损害危险因素的相关分析

目的 分析皮质下血管性认知损害的相关影响因素.方法 61例符合皮质下缺血性血管病诊断标准患者,经详细的神经心理学测验和临床访谈分为无认知损害组、非痴呆型血管性认知损害组和血管性痴呆组,后两组进一步合并为血管性认知损害组;登记并分析所有患者的社会人口学、血管性危险因素和影像学资料.结果 血管性认知损害总患病率为63.93%(39/61),其中非痴呆型血管性认知损害和血管性痴呆患病率分别为36.07%(22/61)和27.87%(17/61).单因素分析显示:(1)年龄和受教育程度因素比较,血管性痴呆组年龄高于无认知损害组(P=0.029),而受教育程度低于无认知损害组(P=0.022);血管性认知损害组(包括非痴呆型血管性认知损害组和血管性痴呆组)与无认知损害组受试者之间的年龄差异接近统计学意义(t=3.740,P=0.058),但受教育程度低于无认知损害组(t=7.888,P=0.007).(2)血管性认知损害组糖尿病患病率显著高于无认知损害组(P=0.012).(3)皮质下灰质各部位腔隙性梗死灶数目,组间比较差异无统计学意义(均P＞0.05);血管性痴呆组白质梗死灶数目高于无认知损害组(P=0.027),脑白质病变评分高于非痴呆型血管性认知损害组(P=0.001)和无认知损害组(P=0.017),内侧颞叶萎缩评分高于非痴呆型血管性认知损害组(P=0.001)和无认知损害组(P=0.000);血管性认知损害组白质梗死灶数目、脑白质病变评分和内侧颞叶萎缩评分均高于无认知损害组(t=-2.661,P=0.003;t=-2.953,P=0.005;t=-4.712,P=0.000).多因素分析,糖尿病、脑白质梗死和内侧颞叶萎缩同为皮质下血管性认知损害的独立危险因素.结论 皮质下血管性认知损害常见于皮质下缺血性血管病患者,与糖尿病、脑缺血性损伤和退行性变等多种因素有关.     

血管性痴呆的神经影像学进展

痴呆是导致老年人残疾的主要疾病之一。其中有半数的痴呆患者可能是由于脑血管疾病引起或者与之有关。痴呆的诊断仍然以临床表现为主要依据,但是现代神经影像学的发展促进了痴呆临床诊断和治疗研究的深入。血管性痴呆(vasculardementia,VD)为一异源性痴呆综合征,其受以下因素的影响:血管条件、血管相关结构的改变(如脑梗死、脑萎缩、白质病变)和患者个体条件(如年龄、教育、遗传因素)。血管性痴呆有3种主要亚型,即皮质性痴呆(多发梗死性痴呆)、皮质下痴呆(小血管性痴呆)和关键部位梗死性痴呆。皮质性痴呆和关键部位梗死性痴呆常由于大血管…     

Cranial computed tomographic observations in multi-infarct dementia. A controlled study.

BACKGROUND AND PURPOSE: We compared cranial computed tomography findings among 58 multi-infarct dementia index cases and 74 multi-infarct control subjects without cognitive impairment to identify potential determinants of multi-infarct dementia. METHODS: The cranial computed tomography records of acute ischemic stroke patients with a history of multiple cerebral infarcts were compared to determine the number, location, and size of cerebral infarcts; the pattern of infarction; brain volume loss; and the degree of white matter lucency, sulcal enlargement, and ventricular enlargement. Multi-infarct patients were divided into two groups: 1) index cases were defined as those with multi-infarct dementia as defined by the Diagnostic and Statistical Manual of Mental Disorders, edition 3 (DSM-III) criteria; and 2) control subjects were defined as those multi-infarct patients without dementia or multi-infarct dementia according to DSM-III criteria. RESULTS: Overall, multi-infarct index cases had more cerebral infarcts, more cortical and subcortical left hemisphere infarcts, higher mean ventricular volume to brain volume ratio, more extensive enlargement of the body of the lateral ventricles and cortical sulci, and a higher prevalence of white matter lucencies. Among multi-infarct cases and control subjects the most frequent site of infarction was the subcortical region, and the most frequent pattern of infarction was lacunar. Stepwise logistic regression analysis examined cranial computed tomography as well as other factors and showed that level of education, stroke severity, left cortical infarction, and diffuse enlargement of the left lateral ventricle were the best overall predictors of multi-infarct dementia. CONCLUSIONS: Level of education, stroke severity, and left hemisphere infarction may be predictors of multi-infarct dementia.     

Sporadic vascular dementia as clinical presentation of a new missense mutation within exon 7 of NOTCH3 gene

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a genetic disease characterized by ischemic stroke with early onset, migraine, seizures, and vascular dementia. CADASIL is associated with mutations within NOCT3 gene, mainly clustered in exons 3 and 4. We report a case of CADASIL presenting progressive subcortical dementia in the sixth decade. Neither family history, nor acute ischemic events were present. MRI findings were typical for CADASIL. NOTCH3 analysis disclosed a new missense mutation within exon 7, leading to the substitution of cysteine 366 with a tryptophan (Cys366Trp). Our finding suggests CADASIL diagnosis must be considered in patients with vascular dementia also in absence of stroke-like events and of family history.     

线性法测量皮质下缺血性血管病患者脑萎缩及其与认知损害的相关性分析

目的通过线性法测量皮质下缺血性血管病(SIVD)患者脑萎缩,分析其与认知功能损害的相关性。方法共纳入SIVD组50例,健康对照组50例。所有入组对象均完成一般情况评定、Mo CA量表评估认知功能、头颅MRI检查,线性法进行脑萎缩测量。结果 SIVD组代表脑室系统横径的测量值及脑沟测量值,除桥池宽度外,均较对照组显著增大(P 0. 05)。SIVD组的脑萎缩测量相对值除脑干指数外,均显著高于对照组(P 0. 05)。SIVD组双侧侧脑室两额角间最宽距离、双侧侧脑室额角两侧尾状核头间最小距离、第三脑室宽度、双侧侧脑室腰部外侧壁最小距离与Mo CA评分呈显著负相关(P 0. 05)。SIVD组脑萎缩测量相对值中的额角指数、尾状核指数、哈氏值、第三脑室宽度与视空间能力、计算力、延迟记忆和定向力均呈负相关(P 0. 05)。结论 SIVD患者存在明显的皮质和皮质下萎缩,并与认知功能损害相关。哈氏值、额角指数、尾状核指数、第三脑室宽度可作为SIVD患者脑萎缩的预测指标,提示执行功能/视空间及计算力、记忆力的损害。     

The role of brain infarcts and hippocampal atrophy in subcortical ischaemic vascular dementia

Abstract. We investigated if, in patients with vascular lesions, the variable that best discriminated demented from non–demented patients was the severity of the vascular pathology or the degree of hippocampal atrophy. A total of 39 patients multiple subcortical infarcts, who could be considered as possible vascular dementia with small vessel pathology, with underwent a neuropsychological study and brain magnetic resonance imaging (MRI) DSM IV criteria supported by neuropsychological data were used to distinguish demented from non–demented patients. The MRI study took into account the degree of hippocampal atrophy (hippocampal height and interuncal distance) and the severity of vascular pathology (number of brain infarcts). The distribution of lesions and a factor analysis showed that hippocampal atrophy is a better predictor of dementia than the number of brain infarcts. Multiple subcortical infarcts alone are probably not able to cause clinical dementia but the presence of vascular lesions increases the expression of concomitant Alzheimers disease.     

Is multi-infarct dementia representative of vascular dementias? A retrospective study

Multi-infarct dementia (MID) indicates a dementia disorder primarily caused by multiple cerebral infarcts. Since other pathogenetic mechanisms cause vascular dementia we evaluated clinical, CT scan and CSF neurochemical parameters of 134 MID and 67 PVD (probable vascular dementia) patients. We found no differences with regard to the presence of major risk factors. Only TIA/stroke episodes and focal neurological signs were significantly more frequent in MID than in PVD cases, an anticipable result on the basis of MID definition. CT scan findings showed a prevalence of subcortical with respect to cortical lesions in both groups, with a higher frequency in MID patients. Subjects with deep infarcts more frequently showed TIA/stroke episodes and diabetes mellitus. No differences were detectable in CSF monoamine metabolite levels. We conclude that in the majority of vascular dementias subcortical damage seems to have a major pathogenetic role.     

Abnormalities of cortical thickness,subcortical shapes,and white matter integrity in subcortical vascular cognitive impairment

Subcortical vascular cognitive impairment (sVCI) is caused by lacunar infarcts or extensive and/or diffuse lesions in the white matter that may disrupt the white matter circuitry connecting cortical and subcortical regions and result in the degeneration of neurons in these regions. This study used structural magnetic resonance imaging (MRI) and high angular resolution diffusion imaging (HARDI) techniques to examine cortical thickness, subcortical shapes, and white matter integrity in mild vascular cognitive impairment no dementia (VCIND Mild) and moderate‐to‐severe VCI (MSVCI). Our study found that compared to controls (n = 25), VCIND Mild (n = 25), and MSVCI (n = 30) showed thinner cortex predominantly in the frontal cortex. The cortex in MSVCI was thinner in the parietal and lateral temporal cortices than that in VCIND Mild. Moreover, compared to controls, VCIND Mild and MSVCI showed smaller shapes (i.e., volume reduction) in the thalamus, putamen, and globus pallidus and ventricular enlargement. Finally, compared to controls, VCIND Mild, and MSVCI showed an increased mean diffusivity in the white matter, while decreased generalized fractional anisotropy was only found in the MSVCI subjects. The major axonal bundles involved in the white matter abnormalities were mainly toward the frontal regions, including the internal capsule/corona radiata, uncinate fasciculus, and anterior section of the inferior fronto‐occipital fasciculus, and were anatomically connected to the affected cortical and subcortical structures. Our findings suggest that abnormalities in cortical, subcortical, and white matter morphology in sVCI occur in anatomically connected structures, and that abnormalities progress along a similar trajectory from the mild to moderate and severe conditions. Hum Brain Mapp 35:2320–2332, 2014. © 2013 Wiley Periodicals, Inc .     

Neurotransmitter deficits in a non-multi-infarct category of vascular dementia

Brain tissue from 9 severely demented patients cared for in psychiatric long-term wards and with records of stroke episodes, macroscopic signs of brain infarcts and with no clinical evidence of senile dementia of the Alzheimer type was investigated and compared with control material. The mean volume of the brain infarcts in this vascular dementia group was only 6.8 ml. Pronounced disturbances of the serotoninergic and cholingergic systems were found in subcortical and cortical grey matter. These widespread neurotransmitter changes can hardly be explained by the localized brain infarcts per se, but suggest the existence of another category of vascular dementia. Since the neurotransmitter disturbances were found to be similar to those of Alzheimer's disease and senile dementia of the Alzheimer type, it seems more likely that they indicate a common pathway for dementia disorders than that they serve as markers of different dementia categories.     

Pathogenetic basis of vascular dementia

Vascular dementia (VAD) was studied with reference to pathogenetic aspects, especially the importance of brain infarcts. A VAD diagnosis was chosen when the patients showed dementia in combination with transitory ischemic attacks (TIA), stroke episodes, or other pronounced vascular diseases judged to be causally related to the dementia. Computed tomography (CT) white matter lesions were shown to occur frequently (85%); a pronounced decrease in myelin lipids was common in subcortical white matter; a fronto-subcortical symptom complex was the prevailing clinical pattern; and an overall increased albumin ratio without relation to TIA/stroke was noted, indicating blood-brain barrier (BBB) dysfunction. When infarcts were present, they appeared to be endpoint manifestations of the vascular pathology rather than the cause of the disease. Today, thromboembolism with multiple cerebral infarcts is considered more or less the only pathogenetic substrate of VAD, with multi-infarct dementia (MID) as its clinical counterpart. Our findings suggest that subcortical white matter changes are another important VAD substrate.     

胼胝体和扣带回弥散张量成像改变对皮质下缺血性血管性痴呆患者认知功能障碍的影响

目的应用磁共振弥散张量成像(DTI)技术,探讨皮质下缺血性血管性痴呆(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。方法对60例SIVD患者和40例年龄匹配的非痴呆对照者,采用测定感兴趣区弥散张量参数的方法,比较其纤维束完整性差异及与MMSE的关系。结果 (1)与对照组比较,SIVD组胼胝体膝部、双侧扣带回的FA值显著下降及ADC值显著升高,而胼胝体压部的FA值和ADC值无显著性差异。(2)胼胝体膝部、双侧扣带回的FA值与MMSE评分呈明显正相关。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测。