NEURO IMAGING & STROKE REHABILITATION PROGNOSIS

本项目研究脑成像在脑部疾病中的作用 评价脑血流和核磁共振对卒中康复预后的影响 光谱成像方法可以分离和定量结构， 中风后的血管和神经代谢异常。这有 潜在的意义在于提供合理的、生理学的基础 用于患者管理和康复策略的衡量标准， 包括使用设施与补偿性康复 技巧。主要的重点是确定精神错乱 中风半暗带活动减少的组成部分，定义为 梗死灶外局部神经代谢活性降低 由于血液动力学血管的限制，可能是由于 中风的辨证作用。因为这笔钱 非脑梗塞神经组织识别受影响的脑组织的数量 有复苏的潜力，它被假设为 失语的量化将与中风高度相关 恢复预后。失语部分将通过以下方式识别 测定血流减少的脑组织体积，即 超过测量的解剖梗塞大小。过度的 容量(不是由于缺血)被推定是由于 失语引起的新陈代谢反应性减退。神经代谢 由分裂和缺血合并引起的变化也将是 学习。将进行T1和T2磁共振检查，以确定 脑梗塞外的解剖定位半影区。 脑SPECT和4.1T核磁共振波谱成像(MRSI)将 以确定患者的血管和代谢状态 延长的中风半暗带。这些测量将在#年进行 为脑血管疾病患者和30名对照组提供 R-CBF、r-CBF储备和反应性的独立衡量标准，以及 ~1H和~(31)P核磁共振反映的区域代谢活性 光谱学。缺血或任何血管对恢复的限制将 用99mHM-PAO SPECT测定静息r-CBF和 R-CBF对乙酰唑胺应激的反应性。确凿的， R-CBF局灶性减少性质的生化证据 活性将来自于MRSI测量的乳酸、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。总而言之，这项措施将提供一种方式来识别 并对中风努力的可恢复成分进行量化。 所有功能、解剖和代谢性神经成像程序 将以两周、六周、六个月和一年的时间进行 中风后的间歇期。神经、行为和认知状态 将在相同的时间间隔内进行评价。结果合二为一 卒中后一年将与临时获得的成像进行比较 参数来评估哪些参数提供了最准确的 恢复的预后。还将对以下项目进行初步评估 功能恢复可能涉及通过以下方式重新学习的程度 与分辨率相比，未受中风影响的大脑区域 在受影响的区域出现精神错乱。

This project investigates the role of cerebral imaging in prognosis of stroke recovery by evaluating how blood flow and NMR spectroscopic imaging methods can separate and quantify structural, vascular, and neuro-metabolic abnormalities post-stroke. This has potential significance to provide a rational, base on physiological measurements, for patient management and rehabilitation strategies, including the use of facilities 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 differentiation effects of the stroke. Since the amount of non-infarcted neural tissue identifies the amounts 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. The 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 studies. T1 and T2 MRI will be conducted to determine the volume of brain outside the infarction to anatomically localize the penumbra. Brain SPECT and 4.1T 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 cerebrovascular disease patients and 30 controls to provide independent measures of r-CBF, r-CBF reserve and reactivity, and regional metabolic activity as reflected by 1H and 31P NMR spectroscopy. Ischemia or any vascular constraints on recovery will be determined via Tc-99m HM-PAO 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 measure will provide a way to identify and quantitate recoverable components of stroke efforts. 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. A preliminary evaluation will also be made of the extent to which recovery of function may involve relearning by brain regions not affected by the stroke, as compared the resolution of diaschisis in the affected region.