NEUROIMAGING AND STROKE REHABILITATION PROGNOSIS

描述(调查人员摘要)：本项目调查 脑成像对卒中恢复期预后的评估作用 血流和光谱成像方法如何分离和 量化结构、血管和神经代谢异常 卒中。这具有潜在的意义，为我们提供了一个基于 关于生理测量，用于病人管理和康复 战略，包括使用促进性而非补偿性 康复技术。主要的重点是确定 中风半暗带活动减少的失语成分，定义 作为梗塞外局部神经代谢活动的减少 不是由于血液动力学血管受限，而是可能是由于 中风的去传入效应。因为非-的数量 梗塞的神经组织识别受影响的大脑的数量 恢复的潜力，它被假设为体积定量 失语的程度与卒中恢复预后密切相关。 失语症部分将通过测定 脑组织血流量减少，超过测量范围 解剖性脑梗塞面积。这一过量的交易量(这不是由于 缺血)被认为是由于新陈代谢的反应性降低 因为失语。混合性失语所致的神经代谢改变 还将对缺血进行研究。将进行T1和T2磁共振成像以 用解剖学方法确定梗死灶以外的脑体积 本地化半影。一种允许精确的参考系方法 将利用解剖学与功能成像的相关性。 脑SPECT和4.1特斯拉核磁共振波谱成像(MRSI)将 以确定延长的患者的血管和代谢状态 中风半暗带。这些测量将在70分钟内进行 为脑血管疾病患者和30名对照组提供独立 R-CBF、r-CBF储备反应性和区域代谢的测量 ~(32)P和~(1-H)H波谱所反映的活性。缺血或任何 恢复的血管限制将通过~(99m)Tc-HMPAO确定 静息r-CBF和r-CBF对乙酰唑胺反应性的SPECT测量 压力。任何病灶性质的确凿的生化证据 R-CBF活性的降低将来自乳酸的MRSI测量， 胆碱、肌酸、N-乙酰天冬氨酸、谷氨酸、无机磷、 三磷酸腺苷和磷酸肌酸。这些措施将共同提供一种方式来 识别和量化中风效应的可恢复成分。全 功能、解剖和代谢性神经成像程序将 每隔两周、六周、六个月和一年进行一次 中风后。神经、行为和认知状态评估 将以相同的间隔进行。一年后的结果 将卒中与时间上获得的成像参数进行比较 评估哪些参数可提供最准确的预后 恢复。

DESCRIPTION (Investigator's Abstract): This project investigates the role of cerebral imaging in prognosis of stroke recovery by evaluating how blood flow and spectroscopic imaging methods can separate and quantify structural, vascular, and neuro-metabolic abnormalities post- stroke. This has potential significance to provide a rationale, based on physiological measurements, for patient management and rehabilitation strategies, including the use of facilitatory versus compensatory rehabilitation techniques. The primary emphasis is on identifying the diaschisis component of reduced activity in the stroke penumbra, defined as a reduction in regional neurometabolic activity outside the infarct not due to hemodynamic vascular constraints, and presumably due to deafferentation effects of the stroke. Since the amount of non- infarcted neural tissue identifies the amount of affected brain that has potential for recovery, it is hypothesized that volumetric quantitation of diaschisis will be highly correlated with stroke recovery prognosis. The diaschisis component will be identified by determining the volume of brain tissue with reduced blood flow that is in excess of the measured anatomic infarction size. This excessive volume (which is not due to ischemia) is presumed to be due to the reactive reduction of metabolism from diaschisis. Neuro-metabolic changes caused by combined diaschisis and ischemia will also be studied. T1 and T2 MRI will be conducted to determine the volume of brain outside the infarction to anatomically localize the penumbra. A reference system method that permits accurate correlation of anatomic with functional imaging will be utilized. Brain SPECT and 4.1 Tesla NMR spectroscopic imaging (MRSI) will be performed to determine the vascular and metabolic status of the extended stroke penumbra. These measurements will be conducted in 70 cerebrovascular disease patients and 30 controls to provide independent measures of r-CBF, r-CBF reserve reactivity, and regional metabolic activity as reflected by 1-H and 32-P spectroscopy. Ischemia or any vascular constraints on recovery will be determined via Tc-99m HMPAO SPECT measures of resting r-CBF and r-CBF reactivity to acetazolamide stress. Corroborative biochemical evidence for the nature of any focal reductions in r-CBF activity will come from MRSI measures of lactate, choline, creatine, N-acetyl aspartate, glutamate, inorganic phosphate, ATP , and phosphocreatine. Together the measures will provide a way to identify and quantitate recoverable components of stroke effects. All functional, anatomic and metabolic neuroimaging procedures will be conducted at two-week, six-week, six-month, and one year time intervals post-stroke. Neurological, behavioral, and cognitive status evaluations will be conducted at the same intervals. Outcome at one year post stroke will be compared with the temporally obtained imaging parameters to evaluate which parameters provide the most accurate prognosis of recovery.