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1.
Cerebral small-vessel alterations play a central role in determining lesions of subcortical structures and eventually may lead to cognitive impairment. Small-vessel diseases are classified according to the pathological viewpoint. The most important ones are the changes in small arteries and arterioles caused by prolonged hypertension. These small-vessel changes may result in ischemic damage to the brain parenchyma and blood-barrier alterations. Both mechanisms are thought to contribute to the occurrence of white-matter changes and lacunar infarcts. Modern magnetic resonance techniques such as diffusion, perfusion, and spectroscopy may allow the in vivo study of the pathophysiology of small-vessel diseases and the consequences on the brain parenchyma.  相似文献   

2.
Alzheimer disease and cerebrovascular pathology: an update   总被引:27,自引:0,他引:27  
Summary. Recent epidemiological and clinico-pathologic data suggest overlaps between Alzheimer disease (AD) and cerebrovascular lesions that may magnify the effect of mild AD pathology and promote progression of cognitive decline or even may precede neuronal damage and dementia.Vascular pathology in the aging brain and in AD includes: 1. cerebral amyloid angiopathy (CAA) with an incidence of 82–98% often associated with ApoEε2 and causing a) cerebral mass hemorrhages (around 70%, mainly in the frontal and parieal lobes), b) multiple or recurrent microhemorrhages (15%), and c) ischemic (micro-)infarcts or lacunes (around 20%). The frequency of these lesions increases with the severity of CAA and shows no correlation with that of senile amyloid plaques. CAA, significantly more frequent in patients with cerebral hemorrhages or infarcts than in aged controls, is an important risk factor for cerebrovascular lesions in AD. 2. Microvascular changes with decreased density and structural abnormalities causing regional metabolic and blood-brain barrier dysfunctions with ensuing neuronal damage. In large autopsy series of demented aged subjects, around 80% show Alzheimer type pathology, 20–40% with additional, often minor vascular lesions, 7–10% “pure” vascular dementia, and 3–5% “mixed” dementia (combination of AD and vascular encephalopathy). AD cases with additional minor cerebrovascular lesions have significantly more frequent histories of hypertension or infarcts than “pure” AD patients. Vascular lesions in AD include cortical microinfarcts, subcortial lacunes, white matter lesions / leukoencephalopathy, small hemorrhages and corticosubcortical infarcts, while in mixed type dementia multiple larger or hemispheral infarcts are more frequent. Small infarcts in AD patients have no essential impact on global cognitive decline which mainly depends on the severity of Alzheimer pathology, but in early stage of AD they may influence and promote the development of dementia. Recent studies showed lower density of plaques and tangles in brains with cerebrovascular lesions, and similar severity of dementia was related to fewer AD lesions in brains with than in those without small vascular lesions. Further studies will help to elucidate the risk factors and impact of cerebrovascular lesions on the development and progression of dementia in AD. Received November 2, 2001; accepted January 16, 2002  相似文献   

3.
T Yanagihara 《Clinical neurology》1999,39(12):1197-1199
The vast majority of senile dementia consists of Alzheimer's disease and vascular dementia. However, there appear to be geographic differences in the world in the ratio of these two disorders and the types of vascular dementia prevalent in the regions: multi-infarct dementia, lacunar infarct dementia or Binswanger disease. Partly because of those factors, there have been considerable confusions in the classification and diagnostic criteria of vascular dementia. In order to clarify the confusions, it is necessary to recognize the presence of both dementias caused by multiple infarcts as the results of atherothrombosis and embolism, and those caused by multiple lacunar infarcts and periventricular white matter ischemic lesions. Since the clinical manifestations of different types of vascular dementia may be different, it is also necessary to establish the diagnostic criteria which is applicable to all different types of vascular dementia. In order to comprehend the clinicopathologic characteristics of vascular dementia, it is always necessary to analyze the location of arterial occlusion and the mechanism leading to the arterial occlusion.  相似文献   

4.
There are various types of underlying damage to tissue and vessels in vascular dementia, including (1) single or multiple infarcts that involve association and limbic cortices, (2) small subcortical infarcts disrupting cortico-subcortical circuits, and (3) white matter lesions. The clinical picture of vascular dementia varies, and the role of functional brain imaging of cerebral blood flow and metabolism would be expected to be different among subtypes of vascular dementia. The role and value of functional brain imaging is limited for cortical infarcts; it is very valuable in assessing the impact on cortical function for small subcortical infarcts; and it is probably useful for evaluating white matter lesions, but this needs to be determined in further studies. At least in research of vascular dementia, functional brain imaging criteria should be included for proper patient selection. Careful studies using functional imaging tools in a well-characterized patient population will be needed.  相似文献   

5.
6.
Vascular dementias (VaDs) are the second most common cause of dementia. Cerebrovascular disease (CVD) and stroke relates to high risk of cognitive impairment, but also relate to Alzheimer's disease (AD): Vascular cognitive impairment (VCI) and dementias extend beyond the traditional multi-infarct dementia. Pathophysiology of VaD incorporates interactions between vascular etiologies (CVD and vascular risk-factors), changes in the brain (infarcts, white matter lesions, atrophy), host factors (age, education) and cognition. Variation in defining the cognitive syndrome, in vascular etiologies, and allowable brain changes in current criteria have resulted in variable estimates of prevalence, of groups of subjects, and of the types and distribution of putative causal brain lesions. Should new criteria be developed? Ideally in constructing new criteria the diagnostic elements should be tested with prospective studies with clinical-pathological correlation: replace dogma with data. Meanwhile focus on more homogenous subtypes of VaD, and on imaging criteria could be a solution. Subcortical ischemic vascular disease and dementia (SIVD) incorporate small vessel disease as the chief vascular etiology, lacunar infarct and ischaemic white matter lesions as primary type of brain lesions, subcortical location as the primary location of lesions, and subcortical syndrome as the primary clinical manifestation. It incorporates two clinical entities "Binswanger's disease" and "the lacunar state". AD with VaD (mixed dementia) has been underestimated as a prevalent cause in the older population. In addition to simple co-existence, VaD and AD have closer interaction: several vascular risk factors and vascular brain changes relate to clinical manifestation of AD, and they share also common pathogenetic mechanisms. Vascular cognitive impairment (VCI) is a category aiming to replace the "Alzhemerized" dementia concept in the setting of CVD, and substitute it with a spectrum that includes subtle cognitive deficits of vascular origin, post-stroke dementia, and the complex group of the vascular dementias. As far there is no standard treatment for VaDs, and still little is known on the primary prevention (brain at risk for CVD) and secondary prevention (CVD brain at risk for VCI/VaD). There is no standard symptomatic treatment for VaD. Recently symptomatic cholinergic treatment has shown promise in AD with VaD, as well as probable VaD. Future focus should be directed to the distinct etiological and pathological factors: the vascular and the AD burden of the brain.  相似文献   

7.
Why are stroke patients prone to develop dementia?   总被引:18,自引:0,他引:18  
Stroke patients are more likely to develop dementia than age- and sex-matched controls but the pathogenesis of dementia remains unresolved in most of them. The aim of this review is to determine, from the available literature, the theoretical reasons for a stroke patient to become demented. We found three distinct factors that may explain the occurrence of dementia after a stroke. Firstly, post-stroke dementia may be the direct consequence of the vascular lesions of the brain: this is the most likely cause in patients with normal cognitive functions before a strategic infarct, especially in young patients, in Icelandic-type hereditary amyloid angiopathy and in cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy. Secondly, post-stroke dementia may be due to an associated asymptomatic Alzheimer pathology; the reasons for such an association are that (1) some cases of dementia occurring after a stroke are progressive and Alzheimer’s disease (AD) is the most frequent cause of progressive dementia; (2) age and APOE ɛ 4 genotype are risk factors for both AD and ischaemic stroke; (3) a vasculopathy is often associated with AD. Lastly, white matter changes may also contribute to dementia because they often indicate small-vessel disease and a higher risk of stroke recurrence, and may lead to slight cognitive impairment. Finally, the summation of vascular lesions of the brain, white matter changes, and Alzheimer pathology might lead to dementia, even when each type of lesion, on its own, is not severe enough to induce dementia. Therefore, in patients followed up after a stroke, the term “post-stroke dementia” is probably more appropriate than that of vascular dementia because it includes all possible causal factors. Received: 15 July 1996 Accepted: 19 October 1996  相似文献   

8.
Vascular cognitive impairment, the recent modification of the terminology related to vascular burden of the brain, reflects the all-encompassing effects of vascular disease or lesions on cognition. It incorporates the complex interactions between vascular aetiologies, risk factors and cellular changes within the brain and cognition. The concept covers the frequent poststroke cognitive impairment and dementia, as well as cerebrovascular disease (CVD) as the second most common factor related to dementia. CVD as well as vascular risk factors including arterial hypertension, history of high cholesterol, diabetes or forms of heart disease are independently associated with an increased risk of cognitive impairment and dementia. Traditional vascular risk factors and stroke are also independent factors for the clinical presentation of Alzheimer's disease (AD). In addition to these vascular factors, CVD/strokes, infarcts and white-matter lesions may trigger and modify the progression of AD as the most common cause of neurodegenerative dementia. The main subtypes of previously defined vascular dementia (VaD) include the cortical VaD or multi-infarct dementia also referred as poststroke VaD, subcortical ischaemic vascular disease and dementia or small-vessel dementia and strategic-infarct dementia. Whilst CVD is preventable and treatable, it is clearly a major factor in the prevalence of cognitive impairment in the elderly worldwide.  相似文献   

9.
M G Bousser 《L'Encéphale》1977,3(4):357-372
The incidence of both atherosclerosis and demential increases with age and therefore the terms "cerebral atherosclerosis" or "cerebro-vascular dementia" are commonly used for any mental deterioration in elderly persons. These names depend on the proposition of a gradual narrowing of cerebral arteries as an inevitable accompaniement of ageing which ends in dementia through a progressive reduction of cerebral blood flow. This apparently reasonnable hypothesis has now been shown to be wrong. ;t has been established that first, senile dementia is not due to cerebral atherosclerosis in spite of the frequent coexistence of degenerative and vascular lesions; and secondly, true cerebro vascular dementia results from the destruction of brain tissue following cerebral infarction; hence the proper term is "multi-infarct dementia". This neuronal destruction leads to decrease in cerebral metabolism and blood flow and to intellectual deterioration. The diagnostic criteria are therefore those of cerebral infarcts i.e: arterial hypertension and/or signs of atherosclerosis, sudden onset and/or stepwise progression, and focal neurological signs. If one follow those criteria, multi-infarct dementia accounts for only about 10% of all dementias; if one does not, the diagnosis will continue to be made to the exclusion of other potentially curable causes of dementias. Five clinico-pathological forms can be distinguished according to the size, number and site of the infarcts: lacunar state, large multiple infarcts, watershed infarction, single infarct and Binswanger's encephalopathy. This distinction is always arbitrary because the association of lacunes and large infarcts is very common in multi-infarct dementia. The almost invariable failure of all therapeutic measures once multi-infarct dementia has been established stresses the importance of prevention. This depends on prevention of cerebral infarcts, i.e. on the correction of risk factors amongst which arterial hypertension is by far, the most important. Some cases benefit also from carotid surgery, anticoagulants, and antiplatelet drugs but antihypertensive drugs are the most essential part. It is very likely that if all cases of arterial hypertension are properly treated, the incidence of multi-infarct dementia will decrease greatly.  相似文献   

10.
脑梗死早期智能障碍与脑影像学改变关系分析   总被引:28,自引:0,他引:28  
目的 探讨脑梗死患者智能障碍与脑影像学及其它因素之间的关系。方法 应用韦氏智力量表对经CT证实的 16 6例脑梗死患者进行神经心理学检查。对比分析其智能障碍的发生与性别、年龄、文化程度、脑梗死灶的部位、体积、是否伴发皮层萎缩或皮层下变性影像学结果的关系。结果 92例出现智能障碍 ,其中轻度 46例 ,中度 2 1例 ,重度 2 5例。智能障碍与其梗死体积呈明显正相关 ,与各皮层及皮层下萎缩因子呈明显负相关 ,与文化程度呈明显负相关。结论 智能障碍的发生与梗死体积 ,慢性脑循环障碍所致皮层及皮层下病理改变 ,以及文化程度的差异等多种因素有  相似文献   

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