Neumann Dawn, McDonald Brenna C, West John, Keiski Michelle A, Wang Yang
Department of Physical Medicine and Rehabilitation, Rehabilitation Hospital of Indiana, Indiana University School of Medicine, 4141 Shore Drive, Indianapolis, IN, 46254, USA.
Department of Radiology and Imaging Sciences, Indiana University Center for Neuroimaging, Indiana University School of Medicine, 355 W. 16th St., GH Suite 4100, Indianapolis, IN, 46202, USA.
Brain Imaging Behav. 2016 Jun;10(2):569-80. doi: 10.1007/s11682-015-9415-3.
The neurobiological mechanisms that underlie facial affect recognition deficits after traumatic brain injury (TBI) have not yet been identified. Using functional magnetic resonance imaging (fMRI), study aims were to 1) determine if there are differences in brain activation during facial affect processing in people with TBI who have facial affect recognition impairments (TBI-I) relative to people with TBI and healthy controls who do not have facial affect recognition impairments (TBI-N and HC, respectively); and 2) identify relationships between neural activity and facial affect recognition performance. A facial affect recognition screening task performed outside the scanner was used to determine group classification; TBI patients who performed greater than one standard deviation below normal performance scores were classified as TBI-I, while TBI patients with normal scores were classified as TBI-N. An fMRI facial recognition paradigm was then performed within the 3T environment. Results from 35 participants are reported (TBI-I = 11, TBI-N = 12, and HC = 12). For the fMRI task, TBI-I and TBI-N groups scored significantly lower than the HC group. Blood oxygenation level-dependent (BOLD) signals for facial affect recognition compared to a baseline condition of viewing a scrambled face, revealed lower neural activation in the right fusiform gyrus (FG) in the TBI-I group than the HC group. Right fusiform gyrus activity correlated with accuracy on the facial affect recognition tasks (both within and outside the scanner). Decreased FG activity suggests facial affect recognition deficits after TBI may be the result of impaired holistic face processing. Future directions and clinical implications are discussed.
创伤性脑损伤（TBI）后面部表情识别缺陷背后的神经生物学机制尚未明确。本研究利用功能磁共振成像（fMRI），旨在：1）确定在面部表情处理过程中，有面部表情识别障碍的创伤性脑损伤患者（TBI-I）相对于没有面部表情识别障碍的创伤性脑损伤患者和健康对照（分别为TBI-N和HC），大脑激活是否存在差异；2）确定神经活动与面部表情识别表现之间的关系。在扫描仪外进行面部表情识别筛查任务以确定分组；表现低于正常成绩分数一个标准差以上的TBI患者被归类为TBI-I，而成绩正常的TBI患者被归类为TBI-N。然后在3T环境中进行fMRI面部识别范式。报告了35名参与者的结果（TBI-I = 11，TBI-N = 12，HC = 12）。对于fMRI任务，TBI-I组和TBI-N组的得分显著低于HC组。与观看打乱面部的基线条件相比，面部表情识别的血氧水平依赖（BOLD）信号显示，TBI-I组右侧梭状回（FG）的神经激活低于HC组。右侧梭状回活动与面部表情识别任务（在扫描仪内外）的准确性相关。FG活动降低表明TBI后面部表情识别缺陷可能是整体面部处理受损的结果。讨论了未来的方向和临床意义。
