Assessing arousal regulation in post-stroke apathy using amantadine and EEG.

项目摘要 这是一个培训奖，以支持戈德法因博士在他的发展成为一个 独立的临床研究者，研究大脑的唤醒系统在 从中风和创伤性脑损伤中恢复过来。觉醒是脑卒中的重要靶点 恢复，因为支持它的大脑系统广泛地激发神经元，从而可以 增强各种损伤的恢复。在此期间，博士。 Goldfine将接受唤醒系统神经科学的正式培训 沿着行为和认知缺陷的量化， 与性唤起障碍有关他还将学习如何使用定量分析， MRI和脑电图（qEEG）用于表征网络上的大脑功能 水平为了支持这项培训，Goldfine博士将开展一个指导研究项目， 中风后冷漠的病理生理学冷漠，也被称为abulia，是一种减少 目标导向的行为超出预期的运动功能障碍，而不是由于 嗜睡。冷漠在中风后很常见（35%的患者）， 残疾更严重，恢复速度更慢，需要机构护理。有 目前没有治疗，冷漠的潜在病理生理学尚不清楚。在这里， 博士Goldfine将测试一个模型，该模型表明目标导向行为的减少可能是由于 大脑的唤醒调节系统-内侧前额叶皮层，前 扣带回和基底神经节与中央丘脑的连接区。他将测试 该模型跨越两个目标：1）通过测量唤醒调节网络的功能， qEEG和血流的MRI测量;以及2）通过确定是否激活了 唤醒调节系统与金刚烷胺改善冷漠。戈德法因博士会先 进行一项横断面研究，比较脑卒中受试者的qEEG和MRI， 与冷漠的对比Goldfine博士将进行一项安慰剂对照试验， 金刚烷胺用于正在接受急性康复治疗的卒中后冷漠患者。 在试验中，将使用横断面研究的qEEG测量值来确定是否 冷漠的消退与唤醒调节功能的改善有关 系统脑卒中后神经元功能障碍的认识提高 从这项工作中获得的冷漠将为科学家和临床医生提供治疗 目标和诊断测试，以改善中风后冷漠患者的结果。

PROJECT SUMMARY This is a training award to support Dr. Goldfine in his development to become an independent clinical investigator studying the role of the brain's arousal systems in recovery from stroke and traumatic brain injury. Arousal is an important target for stroke recovery, as brain systems supporting it excite neurons widely, and can thereby enhance recovery across a wide range of impairments. During this award period, Dr. Goldfine will undertake formal training in the systems neuroscience of arousal mechanisms, along with quantification of behavioral and cognitive deficits typically associated with impaired arousal. He will also learn how to use quantitative analysis of MRI and electroencephalography (qEEG) to characterize brain function at the network level. To support this training, Dr. Goldfine will conduct a mentored research project on the pathophysiology of post-stroke apathy. Apathy, also known as abulia, is a reduction of goal-directed behavior beyond expected from motor dysfunction and not due to somnolence. Apathy is common after stroke (35% of patients) and associated with worse disability, slower rate of recovery, and need for institutional care. There is currently no treatment, and the underlying pathophysiology of apathy is not known. Here, Dr. Goldfine will test a model that reduction of goal-directed behavior can be due to dysfunction of the brain's arousal regulation system - medial prefrontal cortex, anterior cingulate, and connected areas of basal ganglia and central thalamus. He will test the model across two aims: 1) by measuring function of the arousal regulation network using qEEG and an MRI measure of blood flow; and 2) by determining if activation of the arousal regulation system with amantadine improves apathy. Dr. Goldfine will first conduct a cross-sectional study, comparing qEEG and MRI in subjects with stroke with, versus without apathy. Dr. Goldfine will then conduct a placebo-controlled trial of amantadine in subjects with post-stroke apathy who are undergoing acute rehabilitation. In the trial, the qEEG measure from the cross-sectional study will be used to determine if resolution of apathy is associated with improved function of the arousal regulation system. The improved understanding of the neuronal dysfunction underlying post-stroke apathy obtained from this work will provide scientists and clinicians with treatment targets and diagnostic tests to improve outcomes in patients with post-stroke apathy.