Functional Brain Hyperactivations Are Linked to an Electrophysiological Measure of Slow Interhemispheric Transfer Time after Pediatric Moderate/Severe Traumatic Brain Injury.
Functional Brain Hyperactivations Are Linked to an Electrophysiological Measure of Slow Interhemispheric Transfer Time after Pediatric Moderate/Severe Traumatic Brain Injury.
复制标题
功能性大脑过度激活与儿科中度/重度创伤性脑损伤后半球间传输时间缓慢的电生理学测量有关。
DOI：
10.1089/neu.2019.6532
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发表时间：
2020
影响因子：
4.2
通讯作者：
Asarnow,RobertF
中科院分区：
文献类型：
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作者：
Olsen,Alexander;Babikian,Talin;Dennis,EmilyL;Ellis-Blied,MonicaU;Giza,Christopher;Marion,SarahDeBoard;Mink,Richard;Johnson,Jeffrey;Babbitt,ChristopherJ;Thompson,PaulM;Asarnow,RobertF
在中/重度创伤性脑损伤（msTBI）的功能性磁共振成像（fMRI）研究中，通常观察到任务相关血氧水平依赖（BOLD）激活增加，但这些过度激活的功能相关性以及它们如何与神经元功能的更直接测量相关联仍在很大程度上未知。在这里，我们研究了如何工作记忆负荷（WML）依赖BOLD激活相关的电生理测量半球间转移时间（IHTT）的样本中的18 msTBI患者和26人口统计学匹配的对照从加州大学洛杉矶分校RAPBI（恢复后小儿脑损伤）研究。在功能磁共振成像任务表现高度相似的情况下，一个亚组的TBI患者慢IHTT有更大的BOLD激活与更高的WML比健康对照儿童和一个亚组的msTBI患者正常IHTT。在全TBI样本和对照组中，作为连续变量处理的较慢IHTT也与BOLD过度活化相关。更高的WML依赖性BOLD激活与临床认知性能指数的更好表现相关，这种关联在IHTT缓慢的患者组中更为明显。我们之前的研究表明，一个亚组的儿童患有缓慢IHTT后，小儿msTBI的白色组织不良，长期神经退行性变，认知结果差的风险增加。msTBI后BOLD过度激活可能反映了在神经元信息传递效率低下的背景下支持高阶能力需求认知功能的神经元代偿过程。BOLD过度激活和缓慢IHTT之间的联系增加了这种电生理测量作为有前途的生物标志物的多模式验证。
Increased task-related blood oxygen level dependent (BOLD) activation is commonly observed in functional magnetic resonance imaging (fMRI) studies of moderate/severe traumatic brain injury (msTBI), but the functional relevance of these hyperactivations and how they are linked to more direct measures of neuronal function remain largely unknown. Here, we investigated how working memory load (WML)-dependent BOLD activation was related to an electrophysiological measure of interhemispheric transfer time (IHTT) in a sample of 18 msTBI patients and 26 demographically matched controls from the UCLA RAPBI (Recovery after Pediatric Brain Injury) study. In the context of highly similar fMRI task performance, a subgroup of TBI patients with slow IHTT had greater BOLD activation with higher WML than both healthy control children and a subgroup of msTBI patients with normal IHTT. Slower IHTT treated as a continuous variable was also associated with BOLD hyperactivation in the full TBI sample and in controls. Higher WML-dependent BOLD activation was related to better performance on a clinical cognitive performance index, an association that was more pronounced within the patient group with slow IHTT. Our previous work has shown that a subgroup of children with slow IHTT after pediatric msTBI has increased risk for poor white matter organization, long-term neurodegeneration, and poor cognitive outcome. BOLD hyperactivations after msTBI may reflect neuronal compensatory processes supporting higher-order capacity demanding cognitive functions in the context of inefficient neuronal transfer of information. The link between BOLD hyperactivations and slow IHTT adds to the multi-modal validation of this electrophysiological measure as a promising biomarker.