SUBCORTICAL INFARCTION, CORTICAL METABOLISM, AND DEMENTIA

卒中患者的痴呆是一种常见但不同类型的疾病 这通常很难诊断，而且在病理生理学上也很模糊。 该项目试图阐明大脑皮质下 腔隙性脑梗塞可导致认知障碍和痴呆 磁共振成像(MRI)以量化腔隙的特征，高 分辨率正电子发射断层扫描(PET)测量大脑 葡萄糖代谢率(CMR)和神经心理测试。在……里面 为了处理这个潜在的有问题的异构性 人群中，它将使用相对较大的痴呆中风样本 患者，并将其重点限制在没有皮质证据的病例 脑梗塞。 共有105名受试者，45名SIVD患者，以及20名非痴呆者， 正常对照组、非痴呆性腔隙性脑梗塞患者和 阿尔茨海默病患者。主要变量有：1)rCMRic AS 由高分辨率多层PET扫描仪测量，2)大小，数量， 以及通过定量磁共振测量的腔隙位置 成像，以及3)健忘率的神经心理学测量， 联想语义启动、注意力和抽象推理。 数据将根据5个具体目标进行分析： 1.检验皮质下腔隙梗死的假设 产生痴呆症与全身性皮质代谢不足有关。 2.研究腔隙作为皮质低代谢的预测因子和 痴呆症。空隙的位置、大小和数量与 将研究皮质CMRglc和痴呆症。据推测， 皮质CMR能最有可能减少，痴呆症是 可能出现严重的额叶皮质下梗塞 环路，优势半球的病变更多 因此，非优势半球的那些。 3.研究区域CMR能(rCMR能)与 与皮质下梗塞相关的痴呆症。据推测， 当存在三种特定的疾病时，患痴呆症的风险会增加 RCMR基因的模式。 4.检验三种特定模式的假设 痴呆症患者有神经心理障碍 皮质下陷窝。 5.结合联合项目‘31P和1H’进行测试 皮质下缺血性血管性痴呆的光谱成像及临床意义 阿尔茨海默病“(项目2，Pi M.Weiner)，假设 SIVD的代谢减少是去传入的结果，而不是 通过测量皮质N-乙酰天冬氨酸(A) 神经元密度的假定标记物)和rCMR在共享样本中。

Dementia in patients with stroke is a common but heterogeneous condition that is often difficult to diagnose and pathophysiologically obscure. This project seeks to clarify the mechanisms through which subcortical lacunar infarction may lead to cognitive impairment and dementia by using magnetic resonance imaging (MRI) to quantify features of lacunes, high resolution positron emission tomography (PET) to measure cerebral metabolic rates for glucose (CMRgic) and neuropsychological tests. In order to deal with the potentially problematical heterogeneity of this population, it will use a relatively large sample of demented stroke patients, and restrict its focus to cases without evidence of cortical infarction. A total of 105 subjects, 45 SIVD patients, and 20 each of non-demented, normal controls, non-demented lacunar infarction patients, and Alzheimer's disease patients. The major variables are 1) rCMRgic as measured by a high resolution multislice PET scanner, 2) size, number, and location of lacunes as measured by quantitative magnetic resonance imaging, and 3) neuropsychological measures of rate of forgetting, associative semantic priming, attention, and abstract reasoning. The data will be analyzed with respect to 5 specific aims: 1. To test the hypothesis that subcortical lacunar infarcts which produce dementia are associated with generalized cortical hypometabolism. 2. To study lacunes as predictors of cortical hypometabolism and dementia. The relation of location, size, and number of lacunes to cortical CMRglc and dementia will be studied. It is hypothesized that cortical CMRgic is most likely to be diminished and that dementia is likely to be present with infarction of critical subcortical frontal circuits, and that lesions of the dominant hemisphere are more consequential that those of the non-dominant hemisphere. 3. To study the relationship between regional CMRgic (rCMRgic) and dementia associated with subcortical infarction. It is hypothesized that the risk of dementia is elevated in the presence of three specific patterns of rCMRgic. 4. To test the hypothesis that three specific patterns of neuropsychological impairments can be identified in dementia with subcortical lacunes. 5. To test, in conjunction with the allied project '31P and 1H Spectroscopic Imaging of Subcortical Ischemic Vascular Dementia and Alzheimer's Disease' (Project 2, PI M. Weiner), the hypothesis that reduced metabolism in SIVD is the result of deafferentatioin but not of neuronal drop out by measureing both cortical N-acetyl-aspartate (a putative marker of neuronal density) and rCMRgic in a shared sample.