پروزوپاگنوزیا اکتسابی به عنوان یک اختلال خاص چهره: رد کردن کلی شباهت بصری

Abstract Prosopagnosia is classically defined as a disorder of visual recognition specific to faces, following brain damage. However, according to a long-standing alternative view, these patients would rather be generally impaired in recognizing objects belonging to visually homogenous categories, including faces. We tested this alternative hypothesis stringently with a well-documented brain-damaged prosopagnosic patient (PS) in three delayed forced-choice recognition experiments in which visual similarity between a target and its distractor was manipulated parametrically: novel 3D geometric shapes, morphed pictures of common objects, and morphed photographs of a highly homogenous familiar category (cars). In all experiments, PS showed normal performance and speed, and there was no evidence of a steeper increase of error rates and RTs with increasing levels of visual similarity, compared to controls. These data rule out an account of acquired prosopagnosia in terms of a more general impairment in recognizing objects from visually homogenous categories. An additional experiment with morphed faces confirmed that PS was specifically impaired at individual face recognition. However, in stark contrast to the alternative view of prosopagnosia, PS was relatively more impaired at the easiest levels of discrimination, i.e. when individual faces differ clearly in global shape rather than when faces were highly similar and had to be discriminated based on fine-grained details. Overall, these observations as well as a review of previous evidence, lead us to conclude that this alternative view of prosopagnosia does not hold. Rather, it seems that brain damage in adulthood may lead to selective recognition impairment for faces, perhaps the only category of visual stimuli for which holistic/configural perception is not only potentially at play, but is strictly necessary to individualize members of the category efficiently.

Introduction Can recognition of faces be selectively impaired following brain damage, leaving object recognition abilities intact? This question has been of interest to neurologists, cognitive neuropsychologists and cognitive neuroscientists in general at least ever since Bodamer (1947) coined the term “prosopagnosia” to refer to “the selective disruption of the perception of faces, one's own face as well as those of others, which are seen but not recognized as faces belonging to a particular owner” ( Bodamer, 1947, English translation by Ellis & Florence, 1990, p. 83). Providing evidence for a face-specific disorder following brain damage is important because it would apparently support the view that faces are processed specifically, and thus that at least some aspects of face processing could be studied in relative isolation with respect to general visual object recognition. In his definition of prosopagnosia, Bodamer (1947) further stated that “the disorder appears in varying strengths and together with the most different forms of agnosia, but can be separated from these from the outset” (Ellis & Florence, 1990, p. 83). Yet, despite the accumulation of cases of acquired prosopagnosia reported over the years, this important issue of domain-specificity remains largely unclear and debated (e.g., Barton, 2008, Blanc-Garin, 1984, Damasio et al., 1982, Farah et al., 1995, Gauthier et al., 1999, McNeil and Warrington, 1993 and Riddoch et al., 2008). One major reason for this lack of clarification is that, unfortunately, most cases of prosopagnosia1 reported in the literature have not been formally tested to assess their object recognition abilities. A second reason for which this issue of domain-specificity is still debated is that a careful look at reports of some prosopagnosic patients who apparently presented with normal object recognition reveals in fact that some of these cases of “face-specific disorders” also present with object recognition impairments (e.g., FW, QL & WA, Bruyer et al., 1983 and Whiteley and Warrigton, 1977; WJ, McNeil and Warrington, 1991 and McNeil and Warrington, 1993; RM, PM & PC, Sergent & Signoret, 1992; PHD, Eimer & McCarthy, 1999). Unfortunately, most of these reports of cases of acquired prosopagnosia provide insufficient information regarding the patient's object processing abilities, and/or can be criticized for methodological limitations in testing these object recognition abilities. Considering these limitations, a brief but extensive overview of the neuropsychological literature nevertheless points to 13 prosopagnosic patients, who could potentially be considered as presenting with a face-specific recognition impairment (see Table 1). However, in reality, demonstrating that a brain-damaged patient's impairment is truly restricted to face recognition has proved problematic, for several reasons. First, one cannot be certain that the patient reported in a given study would be able to recognize all visually complex objects, as only a limited amount of object categories can be tested in a given study. Second, ideally, evidence for normal face and abnormal object recognition would have to be found within the same task, of equal difficulty for faces and nonface objects. Third, in order to assess the validity of a claim for a face-specific processing impairment, some may expect that the patient always performs as well as normal observers for processing nonface objects. However, low-level vision is rarely intact in cases of prosopagnosia following brain damage (e.g., upper visual field defects, achromatopsia, … see Hécaen and Angelergues, 1962, Meadows, 1974, Barton et al., 2004 and Bouvier and Engel, 2006). Even though such low-level defects cannot explain the face recognition impairments in prosopagnosia ( De Haan, Heywood, Young, Edelstyn, & Newcombe, 1995), they may affect the patients’ object recognition performance in any given task. Moreover, selective attention, memory, or response planning may also be affected by brain damage in such cases, possibly worsening any performance of the patient in a given task. Fourth, in the same vein, potential cases of selective acquired prosopagnosia may be requested to perform as fast as normal observers at object recognition tasks performed equally well ( Gauthier et al., 1999). However, irrespective of their face recognition impairment, brain-damaged patients may be slowed down in complex perceptual, cognitive and motor tasks, or be less confident about their judgment, and their response times may increase proportionally with every operation that they have to perform (see Benton, 1986). Fifth, and perhaps less importantly, some authors have pointed out that normal object recognition performance of the prosopagnosic patient should not be accountable by alternative strategies such as matching identical images that are physically identical for instance (e.g., Riddoch et al., 2008).

. Conclusions In three delayed matching experiments in which visual similarity between the target and a distractor was manipulated parametrically, we demonstrated that the brain damaged prosopagnosic patient PS was able to discriminate objects from visually homogenous categories: novel 3D geometric shapes manipulated on single or multiple dimensions, morphed common objects, and morphed photographs of a highly homogenous familiar category (cars). In all experiments, the prosopagnosic patient showed normal performance and speed, and there was no evidence of a steeper increase of error rates and RTs with increasing levels of visual similarity. These data rule out an account of acquired prosopagnosia in terms of a more general impairment in discriminating objects from visually homogenous categories. Rather, it seems that brain damage in adulthood may lead to selective recognition impairment for faces, perhaps the only category of visual stimuli for which holistic/configural perception is required to individualize members of the category.