NEUROIMAGING AND STROKE REHABILITATION PROGNOSIS

描述（研究者摘要）：本项目研究了 脑影像学对脑卒中恢复期预后的评估 血流和光谱成像方法如何将 量化结构，血管和神经代谢异常后， 中风 这具有潜在的意义，可以提供一个基于 生理测量，用于患者管理和康复 战略，包括使用促进与补偿 康复技术。 主要重点是确定 脑卒中半暗带活动减少的神经联系不能成分，定义为 梗死区以外的区域神经代谢活动减少 不是由于血液动力学血管限制，可能是由于 中风的传入神经阻滞效应 由于非- 梗塞的神经组织确定了受影响的大脑的数量， 回收潜力，假设容量定量 神经机能不能的发生率与脑卒中的恢复预后高度相关。 神经连接不能的成分将通过测定 脑组织血流量减少，超过测量值 解剖梗死面积。 这种过度的体积（这不是由于 缺血）被认为是由于代谢的反应性降低 精神分裂症 复合性神经机能不能引起的神经代谢变化 和局部缺血也将被研究。 将进行T1和T2 MRI， 解剖学上确定梗死区以外的脑体积， 定位半影 一种参考系统方法， 将利用解剖与功能成像的相关性。 将进行脑SPECT和4.1特斯拉NMR光谱成像（MRSI）。 进行以确定扩展的血管和代谢状态， 笔划半影。 这些测量将在70 脑血管病患者和30名对照者提供独立的 测量r-CBF、r-CBF储备反应性和局部代谢 通过1-H和32-P光谱反映的活性。 缺血或任何 将通过Tc-99 m HMPAO确定血管对恢复的限制 SPECT测量静息r-CBF和r-CBF对乙酰唑胺的反应性 应力 任何病灶性质的确证性生化证据 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，无机磷酸盐， ATP和磷酸肌酸。 这些措施将共同提供一种方法， 识别和量化中风影响的可恢复成分。 所有 功能，解剖和代谢神经成像程序将是 以2周、6周、6个月和1年的时间间隔进行 中风后 神经、行为和认知状态评估 将在相同的时间间隔进行。 一年后的成果 将中风与时间上获得的成像参数进行比较 评估哪些参数提供最准确的预后， 复苏

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.