Bowers Dawn, Miller Kimberly, Bosch Wendelyn, Gokcay Didem, Pedraza Otto, Springer Utaka, Okun Michael
Clinical & Health Psychology, College of Public Health and Health Professions, University of Florida, Gainesville, Florida 32601, USA.
J Int Neuropsychol Soc. 2006 Nov;12(6):765-73. doi: 10.1017/S135561770606111X.
In humans, the neural circuitry underlying facial expressions differs, depending on whether facial expressions are spontaneously (i.e., limbic, subcortical) or voluntarily initiated (i.e., frontal cortex). Previous investigators have suggested that the "masked face" of Parkinson's disease involves spontaneous, but not intentional, facial expressions. In contrast, we hypothesized that intentional facial expressions may be slowed (bradykinetic) and involve less movement, in much the same way that other intentional movements are affected by Parkinson's disease. To test this hypothesis, we used sophisticated computer imaging techniques to quantify dynamic facial movement. Relative to controls, Parkinson patients had reduced facial movement (entropy) and were significantly slowed in reaching a peak expression (i.e., bradykinesia). These findings are consistent with the view that the basal ganglia play a role in affecting intentional facial movements. This possibly occurs because of diminished efficiency and/or activation of face representation areas in the frontal cortical regions (i.e., motor, premotor, and supplementary motor area) or because of movement-based suppression secondary to dopaminergic reduction in frontostriatal pathways. Taken together, the characterization of Parkinson's disease as a model system for the neuroanatomic dissociation between voluntary and spontaneous expressions may be unjustified.
在人类中,面部表情背后的神经回路有所不同,这取决于面部表情是自发产生的(即边缘系统、皮层下)还是由意志引发的(即额叶皮层)。先前的研究人员认为,帕金森病的“面具脸”涉及自发的而非刻意的面部表情。相比之下,我们推测,刻意的面部表情可能会变慢(运动迟缓)且涉及的动作较少,这与帕金森病影响其他刻意动作的方式大致相同。为了验证这一假设,我们使用了先进的计算机成像技术来量化动态面部运动。与对照组相比,帕金森病患者的面部运动(熵)减少,达到峰值表情的速度明显减慢(即运动迟缓)。这些发现与基底神经节在影响刻意面部动作中起作用的观点一致。这可能是由于额叶皮层区域(即运动区、运动前区和辅助运动区)中面部表征区域的效率和/或激活降低,或者是由于额纹状体通路中多巴胺能减少继发的基于动作的抑制。综上所述,将帕金森病描述为自愿和自发表情之间神经解剖学分离的模型系统可能是不合理的。