SUBCORTICAL INFARCTION, CORTICAL METABOLISM, AND DEMENTIA

脑卒中患者的痴呆是一种常见但异质性的疾病 这通常很难诊断，病理生理学上也很模糊。 该项目旨在阐明皮质下 腔隙性脑梗死可能会导致认知障碍和痴呆， 磁共振成像（MRI）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（CMRgic）和神经心理学测试。 在 为了解决这个潜在的问题的异质性， 人口，它将使用相对较大的痴呆性中风样本 患者，并将其重点限制在没有皮质 梗塞 共有105名受试者，45名SIVD患者和20名非痴呆患者， 正常对照，非痴呆腔隙性脑梗死患者，和 老年痴呆症患者。 主要变量为1）rCMRgic， 通过高分辨率多层PET扫描仪测量，2）尺寸，数量， 以及通过定量磁共振测量的腔隙的位置 成像，和3）遗忘率的神经心理学测量， 联想语义启动、注意力和抽象推理。 将针对5个具体目标对数据进行分析： 1. 为了验证皮质下腔隙性梗死的假设， 产生痴呆与全身性皮质代谢减退有关。 2. 研究骨陷窝作为皮质代谢减退的预测因子， 痴呆 骨陷窝的位置、大小和数量与骨密度的关系 将研究皮质CMRglc和痴呆。 它是假设 皮质CMRgic最有可能减少，痴呆症是 可能存在严重皮质下额叶梗死 电路，并且优势半球的病变更多 非优势半球的结果。 3. 研究区域CMRgic（rCMRgic）与 与皮层下梗塞有关的痴呆。它是假设 痴呆症的风险在三种特定的 rCMRgic的模式。 4. 为了验证三种特定的 神经心理学损伤可以在痴呆症中识别， 皮质下陷窝 5. 为了测试，结合联合项目'31 P和1H 皮质下缺血性血管性痴呆的光谱成像及 阿尔茨海默氏病（项目2，PI M。Weiner）的假设， SIVD中代谢减少是传入神经阻滞的结果， 通过测量皮质N-乙酰-天冬氨酸（a 神经元密度的推定标志物）和rCMRgic。

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.