Publications related to this work

Following brain damage (trauma, stroke ...), some people may present with great difficulties in recognizing familiar faces and encode new faces in memory. This visual recognition impairment does not appear to be due to sensory visual defects or intellectual disorders, and recognition of other people through other modalities, the voice for instance, is preserved. This condition was termed prosopagnosia by Bodamer (1947) and first described by Wigan in 1844, and then Quaglino & Borelli in 1867 (paper translated by Ellis & Florence, 1990).

Cases of acquired prosopagnosia with preserved visual functions are extremely rare, and most cases have also large deficits in object recognition. In fact, the question of whether prosopagnosia can be 'pure' (without object recognition impairments) is still a matter of debate for some authors, even though there are a few cases described in the literature who seem to have normal object recognition (as reviewed by a recent paper in our laboratory, Busigny et al., 2010).

Studying cases of prosopagnosia can be particularly interesting, for two reasons:

1. They can help us understanding better the location and the critical role(s) of the brain areas involved in normal face recognition (see e.g., Rossion et al., 2003; Schiltz et al., 2006; Dricot et al., 2008).

2. The kind of visual cues that they still can or cannot extract and remember on faces may help us understanding better how normal people recognize faces (what kind of information processes are particularly important) (see e.g., Caldara et al., 2005; Van Belle et al., 2010).

Because the patients are extremely rare and all have different associated impairments, we advocate the detailed investigations of single-cases of prosopagnosia rather than group studies of prosopagnosic patients.

For instance, we have been studying a fascinating case of prosopagnosia, PS, who sustained brain damage in 1992 at the age of 41. She has recovered all neuropsychological functions but has a massive prosopagnosia (for a paper in French describing PS' story and summarizing our results, see here). Unlike the majority of cases of prosopagnosia, such as the case NS for instance (Delvenne et al., 2004), PS recognizes objects normally, including living things. She can even discriminate visually similar objects at the individual level (e.g. discriminating two pictures of cars or birds) like normal people, at a normal speed (see Busigny et al., 2010). Unlike many prosopagnosic patients, she is not achromatopsic either, nor does she suffer from topographical agnosia. She has a small left paraccentral scotoma and a lower normal range color discrimination, but these cannot account for her prosopagnosia.

By presenting PS with little information on face pictures sampled randomly over hundreds of trials ('Bubbles', Gosselin & Schyns, 2001), we showed that she suffers from a deficit at extracting information at the level of the eyes of the faces, and mostly relied on the mouth (Caldara et al., 2005). In a later study, we showed using eye movement recordings that PS fixates mainly on the mouth during identification of personally familiar faces, contrary to normal observers, who fixate in the center of the face slightly below the eyes (Orban de Xivry et al., 2008). We believe that this loss of ability to extract diagnostic information at the level of the top part of the face, in particular the eye region, is a dominant aspect of prosopagnosia. Studies of cases of acquired prosopagnosia by others (Bukach et al., 2006; 2008) and on another case of prosopagnosia studied in our laboratory (GG, Busigny et al., 2010) support this view.

We believe that the reason why patients with prosopagnosia following different lesions present the same behavior, relying less on the eyes of faces than normal observers, is because of their inability to perceive faces holistically. This inability to perceive individual faces holistically can be shown through their absence (or reduction) of inversion effect (Busigny & Rossion, 2010), composite and whole-part effects (Ramon et al., 2010; see also Ramon & Rossion, 2010). The rationale here is that the region of the eyes of the face contain a lot of diagnostic information to individualize faces, but this information is distributed among many elements (2 eyes, eyebrows, ...) who have particular relations between them. Hence, the diagnosticity of this area would depend heavily on the integrity of holistic processing.

At the behavioral level, our most recent work use a gaze contingency method to show directly that acquired prosopagnosia is related to a feature-by-feature analysis of individual faces (Van Belle et al., 2010).

At the neural level, our fMRI studies of PS have shown that her main lesion in the right hemisphere destroyed part of the inferior occipital cortex, where preferential processing for faces is usually observed in neuroimaging studies of normal subjects ('occipital face area', 'OFA'), and which appears to be the region most often damaged in cases of prosopagnosia (see Bouvier & Engel, 2006). However, she has a preserved right fusiform gyrus and preferential 'FFA' activation for faces (Rossion et al., 2003), suggesting that in the normal brain the 'FFA' is not dependent on inputs from the posteriorly located 'OFA' in a feedforward model for face processing. Nevertheless, our studies show that PS' 'FFA' does not discriminate between individual faces in line with the behavior of the patient (Schiltz et al., 2006). These findings have been replicated with the visual agnosic patient DF (Steeves et al., 2006; Steeves et al., 2009).

Other studies on the neuro-functional basis of prosopagnosia provides clues about the reasons why PS' deficit is specific for that category: while her main lesion in the right hemisphere destroyed part of the inferior occipital cortex, the lesion spared the ventral and dorsal part of the lateral occipital complex (LOC), as well as parahippocampal areas, where recognition of non-face objects may take place (Sorger et al., 2007; Dricot et al., 2008). That the ventral LOC in the right hemisphere is structurally and functionnally intact is amazing, given the localization of the right hemisphere lesion.

For a review on prosopagnosia with an emphasis on PS' case, see Mayer & Rossion, 2007, or Rossion (2008): La reconnaissance des visages (Cerveau & Psycho, N°25).