Peterson Matthew F, Zaun Ian, Hoke Harris, Jiahui Guo, Duchaine Brad, Kanwisher Nancy
Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA.
Center for Brain Science, Harvard University, Cambridge, MA, USA.
J Vis. 2019 Aug 1;19(9):7. doi: 10.1167/19.9.7.
Despite extensive investigation, the causes and nature of developmental prosopagnosia (DP)-a severe face identification impairment in the absence of acquired brain injury-remain poorly understood. Drawing on previous work showing that individuals identified as being neurotypical (NT) show robust individual differences in where they fixate on faces, and recognize faces best when the faces are presented at this location, we defined and tested four novel hypotheses for how atypical face-looking behavior and/or retinotopic face encoding could impair face recognition in DP: (a) fixating regions of poor information, (b) inconsistent saccadic targeting, (c) weak retinotopic tuning, and (d) fixating locations not matched to the individual's own face tuning. We found no support for the first three hypotheses, with NTs and DPs consistently fixating similar locations and showing similar retinotopic tuning of their face perception performance. However, in testing the fourth hypothesis, we found preliminary evidence for two distinct phenotypes of DP: (a) Subjects characterized by impaired face memory, typical face perception, and a preference to look high on the face, and (b) Subjects characterized by profound impairments to both face memory and perception and a preference to look very low on the face. Further, while all NTs and upper-looking DPs performed best when faces were presented near their preferred fixation location, this was not true for lower-looking DPs. These results suggest that face recognition deficits in a substantial proportion of people with DP may arise not from aberrant face gaze or compromised retinotopic tuning, but from the suboptimal matching of gaze to tuning.
尽管进行了广泛的研究，但发育性面孔失认症（DP）——一种在没有后天脑损伤情况下出现的严重面孔识别障碍——的病因和本质仍知之甚少。借鉴之前的研究成果，即被认定为神经典型（NT）的个体在面部注视位置上存在显著的个体差异，并且当面孔在该位置呈现时识别效果最佳，我们定义并测试了关于非典型面部注视行为和/或视网膜拓扑面孔编码如何损害DP患者面孔识别的四个新假设：（a）注视信息贫乏的区域；（b）扫视目标不一致；（c）视网膜拓扑调谐较弱；（d）注视位置与个体自身的面部调谐不匹配。我们没有找到支持前三个假设的证据，NT组和DP组始终注视相似的位置，并在面部感知表现上呈现出相似的视网膜拓扑调谐。然而，在测试第四个假设时，我们发现了DP的两种不同表型的初步证据：（a）以面孔记忆受损、典型的面孔感知以及倾向于注视面部上方为特征的受试者；（b）以面孔记忆和感知均严重受损以及倾向于注视面部非常下方为特征的受试者。此外，虽然所有NT组和注视面部上方的DP组在面孔在其偏好的注视位置附近呈现时表现最佳，但注视面部下方的DP组并非如此。这些结果表明，相当一部分DP患者的面孔识别缺陷可能并非源于异常的面部注视或视网膜拓扑调谐受损，而是源于注视与调谐的次优匹配。
