Department of Brain and Cognitive Sciences Massachusetts Institute of Technology Neuropsychology Laboratory Massachusetts General Hospital.
J Cogn Neurosci. 1991 Winter;3(1):25-41. doi: 10.1162/jocn.1991.3.1.25.
Prosopagnosia is a neurological syndrome in which patients cannot recognize faces. Kecently it has been shown that some prosopagnosics give evidence of "covert" recognition: they show greater autonomic responses to familiar faces than to unfamiliar ones, and respond differently to familiar faces in learning and interference tasks. Although some patients do not show covert recognition, this has usually been attributed to an "apperceptive" deficit that impairs perceptual analysis of the input. The implication is that prosopagnosia is a deficit in access to, or awareness of, memories of faces: the inducing brain injury does not destroy the memories themselves. We present a case study that challenges this view. LH suffers from prosopagnosia as the result of a closed head injury. He cannot recognize familiar faces or report that they are familiar, nor answer questions about the faces from memory, though he can (1) recognize common objects and subtly varying shapes, (2) match faces while ignoring irrelevant information such as emotional expression or angle of view, (3) recognize sex, age, and like-ability from faces, and (4) recognize people by a number of nonfacial channels. The only other categories of shapes that he has marked trouble recognizing are animals and emotional expressions, though even these impairments were not as severe as the one for faces. Three measures (sympathetic skin response, pupil dilation, and learning correct and incorrect names of faces) failed to show any signs of covert face recognition in LH, though the measures were sensitive enough to reflect autonomic reactions in LH to stimuli other than faces, and face familiarity in normal controls. Thus prosopagnosia cannot always be attributed to a mere absence of awareness (i.e., preserved information about faces whose output is disconnected from conscious cognitive processing), to an apperceptive deficit (i.e., preserved information about faces that cannot be accessed due to improperly analyzed perceptual input), or to an inability to recognize complex or subtly varying shapes (i.e., loss or degradation of shape memory in general). We conclude that it is possible for brain injury to eliminate the storage of information about familiar faces and certain related shapes.
面容失认症是一种神经综合征，患者无法识别面孔。最近的研究表明，一些面容失认症患者表现出“内隐”识别的证据：他们对熟悉的面孔表现出比不熟悉的面孔更大的自主反应，并且在学习和干扰任务中对熟悉的面孔有不同的反应。尽管有些患者没有表现出内隐识别，但这通常归因于一种“知觉”缺陷，这种缺陷会损害对输入的知觉分析。这意味着面容失认症是一种获取或意识到面孔记忆的缺陷：诱导性脑损伤本身并没有破坏这些记忆。我们提出了一个案例研究，挑战了这一观点。LH 由于头部闭合性损伤而患有面容失认症。他无法识别熟悉的面孔或报告他们熟悉，也无法从记忆中回答有关面孔的问题，尽管他可以 (1) 识别常见物体和微妙变化的形状，(2) 在忽略无关信息（如情绪表达或视角）的情况下匹配面孔，(3) 从面孔中识别性别、年龄和喜欢程度，以及 (4) 通过多种非面部渠道识别人。他唯一标记有问题识别的其他形状类别是动物和情绪表达，尽管这些障碍也不如面孔障碍严重。有三种测量方法（交感皮肤反应、瞳孔扩张和学习面孔的正确和错误名称）未能在 LH 中显示出任何内隐面孔识别的迹象，尽管这些测量方法足够敏感，可以反映 LH 对除面孔以外的刺激的自主反应，以及正常对照者对面孔的熟悉程度。因此，面容失认症不能仅仅归因于缺乏意识（即，有关面孔的信息保存，但与有意识的认知处理输出断开连接）、知觉缺陷（即，由于不正确的知觉输入分析而无法访问有关面孔的信息）或无法识别复杂或微妙变化的形状（即，一般形状记忆的丧失或退化）。我们的结论是，大脑损伤有可能消除有关熟悉面孔和某些相关形状的信息存储。
