Search

It has recently been proposed that the face recognition deficits seen in neurodevelopmental disorders may reflect impaired short-term face memory (STFM). For example, introducing a brief delay between the presentation of target and test faces seems to disproportionately impair matching or recognition performance in individuals with Autism Spectrum Disorders. The present study sought to determine whether deficits of STFM contribute to impaired face recognition seen in Developmental Prosopagnosia. To determine whether developmental prosopagnosics exhibit impaired STFM, the present study used a six-alternative-forced-choice match-to-sample procedure. Memory demand was manipulated by employing a short or long delay between the presentation of the target face, and the six test faces. Crucially, the perceptual demands were identical in both conditions, thereby allowing the independent contribution of STFM to be assessed. Prosopagnosics showed clear evidence of a category-specific impairment for face-matching in both conditions; they were both slower and less accurate than matched controls. Crucially, however, the prosopagnosics showed no evidence of disproportionate face recognition impairment in the long-interval condition. While individuals with DP may have problems with the perceptual encoding of faces, it appears that their representations are stable over short durations. These results suggest that the face recognition difficulties seen in DP and autism may be qualitatively different, attributable to deficits of perceptual encoding and perceptual maintenance, respectively., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Introduction: Even though people with congenital prosopagnosia (CP) never develop a normal ability to "overtly" recognize faces, some individuals show indices of "covert" (or implicit) face recognition. The aim of this study was to demonstrate covert face recognition in CP when participants could not overtly recognize the faces., Methods: Eleven people with CP completed three tasks assessing their overt face recognition ability, and three tasks assessing their "covert" face recognition: a Forced choice familiarity task, a Forced choice cued task, and a Priming task., Results: Evidence of covert recognition was observed with the Forced choice familiarity task, but not the Priming task. In addition, we propose that the Forced choice cued task does not measure covert processing as such, but instead "provoked-overt" recognition., Conclusions: Our study clearly shows that people with CP demonstrate covert recognition for faces that they cannot overtly recognize, and that behavioural tasks vary in their sensitivity to detect covert recognition in CP., (Copyright © 2011 Elsevier Srl. All rights reserved.)

It has been reported that congenital prosopagnosics may have a general imagery deficit or an imagery deficit specific to faces. However, much of this evidence is based on self-report questionnaires, rather than experimentally based testing (Grüter et al., 2007, 2009). This study tested face and non-face based imagery in a case series of congenital prosopagnosics, utilising both questionnaire based and forced choice accuracy measures. Our findings indicate that all the prosopagnosics showed impaired face based imagery, which contrasted with normal performance on imagery of objects and colours - a pattern that is consistent with reports of acquired prosopagnosia (Barton, 2008; Michelon and Biederman, 2003). Given all our experimentally based testing indicated face imagery impairments, despite no such problems being seen on self-report questionnaires, we would argue that testing based only on the latter must be interpreted with some caution. Overall, we would advocate that our findings demonstrate a category specific visual imagery impairment in congenital prosopagnosia, such that general imagery skill can be intact in such cases., (Crown Copyright © 2010. Published by Elsevier Srl. All rights reserved.)

While extensive work has examined the role of covert recognition in acquired prosopagnosia, little attention has been directed to this process in the congenital form of the disorder. Indeed, evidence of covert recognition has only been demonstrated in one congenital case in which autonomic measures provided evidence of recognition (Jones and Tranel, 2001), whereas two investigations using behavioural indicators failed to demonstrate the effect (de Haan and Campbell, 1991; Bentin et al., 1999). In this paper, we use a behavioural indicator, an "eye movement-based memory effect" (Althoff and Cohen, 1999), to provide evidence of covert recognition in congenital prosopagnosia. In an initial experiment, we examined viewing strategies elicited to famous and novel faces in control participants, and found fewer fixations and reduced regional sampling for famous compared to novel faces. In a second experiment, we examined the same processes in a patient with congenital prosopagnosia (AA), and found some evidence of an eye movement-based memory effect regardless of his recognition accuracy. Finally, we examined whether a difference in scanning strategy was evident for those famous faces AA failed to explicitly recognise, and again found evidence of reduced sampling for famous faces. We use these findings to (a) provide evidence of intact structural representations in a case of congenital prosopagnosia, and (b) to suggest that covert recognition can be demonstrated using behavioural indicators in this disorder.

We compared six cases of congenital prosopagnosia to unimpaired participants using standardized test batteries, tailor-made experimental paradigms, and clinical questionnaires. Every prosopagnosic participant displayed deficits in recognizing famous faces and retaining novel faces over short periods of time. Other aspects of face perception such as judgment of emotional expression, speech reading and memory for faces and names were impaired to a lesser degree or only in single cases. No evidence was found for general visual deficits or social dysfunctions. Two of our six cases are first order relatives, and a further three report first-order relatives suffering from prosopagnosic symptoms. The results are in line with the idea of a genetic component to congenital prosopagnosia.