Abnormal face identity coding in the middle fusiform
gyrus of two brain-damaged prosopagnosic patients
Citation for published version (APA):
Steeves, J., Dricot, L., Goltz, H. C., Sorger, B., Peters, J. C., Milner, A. D., Goodale, M. A., Goebel, R., &
Rossion, B. (2009). Abnormal face identity coding in the middle fusiform gyrus of two brain-damaged
prosopagnosic patients. Neuropsychologia, 47(12), 2584-2592.
https://doi.org/10.1016/j.neuropsychologia.2009.05.005

Document status and date:
Published: 01/01/2009
DOI:
10.1016/j.neuropsychologia.2009.05.005
Document Version:
Publisher's PDF, also known as Version of record
Document license:
Taverne
Please check the document version of this publication:
• A submitted manuscript is the version of the article upon submission and before peer-review. There can
be important differences between the submitted version and the official published version of record.
People interested in the research are advised to contact the author for the final version of the publication,
or visit the DOI to the publisher's website.
• The final author version and the galley proof are versions of the publication after peer review.
• The final published version features the final layout of the paper including the volume, issue and page
numbers.
Link to publication

General rights
Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright
owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these
rights.
• Users may download and print one copy of any publication from the public portal for the purpose of private study or research.
• You may not further distribute the material or use it for any profit-making activity or commercial gain
• You may freely distribute the URL identifying the publication in the public portal.
If the publication is distributed under the terms of Article 25fa of the Dutch Copyright Act, indicated by the “Taverne” license above,
please follow below link for the End User Agreement:
www.umlib.nl/taverne-license
Take down policy
If you believe that this document breaches copyright please contact us at:
repository@maastrichtuniversity.nl
providing details and we will investigate your claim.

Download date: 12 Apr. 2024

Neuropsychologia 47 (2009) 2584–2592

Contents lists available at ScienceDirect

Neuropsychologia
journal homepage: www.elsevier.com/locate/neuropsychologia

Abnormal face identity coding in the middle fusiform gyrus of two
brain-damaged prosopagnosic patients
Jennifer Steeves a,∗ , Laurence Dricot b , Herbert C. Goltz c , Bettina Sorger d , Judith Peters d ,
A. David Milner e , Melvyn A. Goodale f , Rainer Goebel d , Bruno Rossion b,∗∗
a

Centre for Vision Research, Department of Psychology, York University, Toronto, Canada
Center for Neuroscience, University of Louvain, Belgium
Department of Ophthalmology and Vision Sciences, University of Toronto, Toronto, Canada
d
Faculty of Psychology and Neuroscience, Maastricht University, Maastricht, The Netherlands
e
Cognitive Neuroscience Research Unit, Durham University, Durham, UK
f
CIHR Group for Action and Perception, The University of Western Ontario, London, Canada
b
c

a r t i c l e

i n f o

Article history:
Received 6 November 2008
Received in revised form 4 May 2009
Accepted 10 May 2009
Available online 18 May 2009
Keywords:
Face perception
Face recognition
Prosopagnosia
Fusiform gyrus
Inferior occipital cortex
fMRI
FFA
OFA
LOC

a b s t r a c t
We report a functional magnetic resonance imaging (fMRI) adaptation study of two well-described
patients, DF and PS, who present face identity recognition impairments (prosopagnosia) following braindamage. Comparing faces to non-face objects elicited activation in all visual areas of the cortical face
processing network that were spared subsequent to brain damage. The common brain lesion in the two
patients was in the right inferior occipital cortex, in the territory of the right “occipital face area” (‘OFA’),
which strengthens the critical role of this region in processing faces. Despite the lesion to the right ‘OFA’,
there was normal range of sensitivity to faces in the right “fusiform face area” (‘FFA’) in both patients,
supporting a non-hierarchical model of face processing at the cortical level. At the same time, however,
sensitivity to individual face representations, as indicated by release from adaptation to identity, was
abnormal in the right ‘FFA’ of both patients. This suggests that the right ‘OFA’ is necessary to individualize
faces, perhaps through reentrant interactions with other cortical face sensitive areas. The lateral occipital
area (LO) is damaged bilaterally in patient DF, who also shows visual object agnosia. However, in patient
PS, in whom LO was spared, sensitivity to individual representations of non-face objects was still found
in this region, as in the normal brain, consistent with her preserved object recognition abilities. Taken
together, these observations, which fruitfully combine functional imaging and neuropsychology, place
strong constraints on the possible functional organization of the cortical areas mediating face processing
in the human brain.
© 2009 Elsevier Ltd. All rights reserved.

1. Introduction
Despite its apparent simplicity, deriving a full percept of an
individual face is one of the most complex tasks performed by
the human visual system. Lesion studies (e.g., Damasio, Damasio,
& Van Hoesen, 1982; Sergent & Signoret, 1992), intracranial
recordings (Allison et al., 1994) and functional neuroimaging investigations (e.g., Haxby, Hoffman, & Gobbini, 2000; Sergent, Ohta, &

∗ Corresponding author at: Centre for Vision Research, Department of Psychology,
York University, 4700 Keele St., Toronto, ON M3J 1P3, Canada.
Tel.: +1 416 736 2100x20452; fax: +1 416 736 5814.
∗∗ Corresponding author at: Unité Cognition & Développement, Université
Catholique de Louvain, 10 Place du Cardinal Mercier, 1348 Louvain-la-Neuve, Belgium. Tel.: +32 10 478788; fax: +32 10 472774.
E-mail addresses: steeves@yorku.ca (J. Steeves), bruno.rossion@uclouvain.be
(B. Rossion).
0028-3932/$ – see front matter © 2009 Elsevier Ltd. All rights reserved.
doi:10.1016/j.neuropsychologia.2009.05.005

MacDonald, 1992) of the human brain have shown that this function
relies primarily on a network of areas located in the occipitotemporal cortex. Functional magnetic resonance imaging (fMRI) studies in
particular have shown that a subset of these areas present a strong
preferential response to faces, including the so-called “fusiform face
area” (‘FFA’, e.g., Kanwisher, McDermott, & Chun, 1997) in the middle fusiform gyrus, the “occipital face area” in the inferior occipital
cortex (‘OFA’, e.g., Gauthier et al., 2000), as well as an area located in
the posterior part of the superior temporal sulcus (pSTS; e.g., Puce,
Allison, Gore, & McCarthy, 1995). These three bilateral areas, which
show a strong right hemisphere advantage, are thought to form the
core system for normal face perception (Haxby et al., 2000; Ishai,
2008).
In an attempt to further clarify the functional neuroanatomy
of face perception, a few fMRI studies (Marotta et al., 2001;
Rossion et al., 2003; Steeves et al., 2006) have measured neural
responses to pictures of faces in neurological patients suffering

J. Steeves et al. / Neuropsychologia 47 (2009) 2584–2592

from prosopagnosia—the inability to individualize faces following
brain damage (Bodamer, 1947; Quaglino & Borelli, 1867). A detailed
investigation of patient PS, a rare case of prosopagnosia without
visual object agnosia, showed right hemisphere ‘FFA’ activation
despite a structurally damaged right inferior occipital cortex and
no evidence of right ‘OFA’ activation (Rossion et al., 2003; Sorger,
Goebel, Schiltz, & Rossion, 2007). In a similar vein, this observation of right ‘FFA’ activation without ipsilateral ‘OFA’ was also
recently reported in patient DF (Steeves et al., 2006), who suffers
from visual form agnosia (an inability to recognize objects based
on shape) in addition to prosopagnosia (Milner et al., 1991). This
latter patient has extensive bilateral damage to lateral occipital
cortex and shows no evidence of ‘OFA’ activation in either hemisphere. Taken together, these observations place strong constraints
on the neurofunctional organization of face perception in the normal brain (Rossion, 2008). First, they indicate that the right ‘OFA’
– the common region within the face-preferential cortical network
that is damaged in both patients – must be a critical component
of the face perception network. This observation is corroborated
by a recent retrospective analysis of the overlap of human patient
lesions from structural MRI (Bouvier & Engel, 2006). Second, these
observations suggest that, in contrast to a hierarchical feedforward
model for face perception (Haxby et al., 2000; Ishai, 2008), the ‘FFA’
can be activated without ipsilateral ‘OFA’ inputs, perhaps through
direct functional connections originating from striate and extrastriate cortical areas (Rossion, 2008).
More recent neuroimaging studies of patient PS have shown that
the fMRI signal in the right ‘FFA’, despite showing a normal range of
preferential activation to faces, does not show any evidence of sensitivity to discrimination of individual faces (Dricot, Sorger, Schiltz,
Goebel, & Rossion, 2008; Schiltz et al., 2006). Specifically, the fMRI
response in this area fails to show a larger response for faces of different identities (presented in a block or as pairs of face stimuli)
compared to the presentation of faces of the same identity. This
stands in contrast to the strong effect of a release from adaptation
with fMRI for different face identities that is found in this area in
the normal healthy brain (e.g., Gauthier et al., 2000; Grill-Spector &
Malach, 2001; Schiltz et al., 2006; Winston, Henson, Fine-Goulden,
& Dolan, 2004) or even in patients with congenital prosopagnosia
(Avidan, Hasson, Malach, & Berhmann, 2005). This observation supports the hypothesis that a critical role of the right ‘OFA’ in face
perception is not simply to detect and categorize a stimulus as a
face – a function that is preserved for both PS and DF – but more
importantly to assist in deriving an individual fine-grained face representation, perhaps through reentrant interactions between the
‘FFA’ and the ‘OFA’ (Rossion, 2008; Rossion et al., 2003; Schiltz et
al., 2006).
As a result, this proposal would necessarily predict that face
identity coding – as tested through fMRI adaptation – should also
be impaired in the ‘FFA’ of patient DF. This critical test was the main
goal of the present collaborative study, in which we sought to test
and contrast both patients in an identical face identity adaptation
paradigm. Our objectives were threefold. First, we aimed to replicate the observation of face-preferential activation in the fusiform
gyrus (‘FFA’) in patient DF that had been previously demonstrated
using a block design (Steeves et al., 2006) but in the present experiment using an event-related fMRI paradigm. This paradigm is more
conservative, in that it is less sensitive to potential confounds of
subject’s expectations and attentional biases when compared to
the block design face localizer used previously. Second, we sought
to test the hypothesis that patient DF’s ‘FFA’ in both hemispheres
would show a larger response to faces compared to objects, yet
would be insensitive to differences in face identity unlike normal
controls. Finally, while patient PS has normal object perception
(‘pure prosopagnosia’), DF is profoundly impaired in both face and
object perception, in particular when she has to discriminate indi-

2585

vidual exemplars of the same object class (Humphrey, Goodale,
Jakobson, & Servos, 1994). Hence, given that the ‘FFA’ also shows a
robust response to non-face objects (e.g., Grill-Spector et al., 2006),
we sought to test and compare release from adaptation in fMRI to
both object and face identity in the two patients. Our predictions
were: (1) an absence of adaptation effects for face identity in the
both patients in the FFA and (2) significant adaptation effects for
object identity in patient PS in the right ‘FFA’, but not for patient DF
in either FFA.
Finally, it is important to note that we compare and contrast neuroimaging data from two brain-damaged patients in the
same neuroimaging experiment – patients who have been studied
extensively and characterized previously as single case studies by
independent research groups – and the present work provides a
unique opportunity to strengthen our understanding of the functional neuroanatomy of face and object perception in both the
healthy and neurologically damaged human brain.
2. Materials and methods
2.1. Subjects
Patient DF is a female, 51 years of age at the time of testing, whose neuropsychological profile has been described in detail previously (e.g., Humphrey et al.,
1994; James, Culham, Humphrey, Milner, & Goodale, 2003; Milner et al., 1991;
Servos, Goodale, & Humphrey, 1993). Her primary neurological symptoms are profound visual form agnosia and prosopagnosia. She shows relatively normal static
perimetry in the central visual field up to 30◦ eccentricity but with some upper
right quadrant loss (see Milner et al., 1991). Neuroimaging studies of patient DF’s
brain have been reported in James et al. (2003) and Steeves et al. (2004, 2006).
An extensive description of DF’s behavioural and neural response to face images
is found in Steeves et al. (2006). In brief, however, she is unable to recognize face
identity, gender or emotional expression but she can generally categorize faces and
discriminate faces from objects that she cannot recognize. Patient DF also shows
robust activation for face images within the “FFA”, which is normal in terms of
amplitude and spatial extent, bilaterally, with a block design face/scene localizer
but she does not show face sensitive responses in the inferior occipital cortex (i.e.,
no “OFA”).
Patient PS is a female, 56 years of age at the time of testing, whose neuropsychological profile and brain damage has been described in detail previously (Caldara
et al., 2005; Rossion et al., 2003; Schiltz et al., 2006; Sorger et al., 2007). Her presenting neurological symptom is prosopagnosia and unlike patient DF, she does not
present object recognition difficulties. Patient PS has normal visual fields, with the
exception of a small left paracentral scotoma. The data collected on PS have been
recently reported as a subset of a larger study (Dricot et al., 2008) that tested identity
adaptation to faces with an independent localizer. This independent localizer was
unavailable for patient DF due to limited scanning time and as a result the present
data include a re-analysis of the Dricot et al. (2008) data so that the analysis for
patient DF and PS is exactly the same.
In addition to the two patients, four neurologically intact participants (age:
25–35 years, two female) as well as one age-matched control participant (S5, 56
years of age, female) were tested. While it has been shown that the profile of activation in the right middle fusiform gyrus remains stable across decades (Brodtmann,
Puce, Syngeniotis, Darby, & Donnan, 2003) and therefore perhaps not necessary
to ensure exact age-matching of participants, we also include the data from the
age-matched control.
The patients and the control subjects gave informed written consent prior to
the fMRI experiments. The study conformed to the Declaration of Helsinki and was
approved by the Ethics Committees of the Department of Medicine at the University
of Louvain and the York University Office of Research Ethics. Control subjects and PS
were strongly right-handed according to the Edinburgh Inventory (Oldfield, 1971)
and patient DF is also right handed.
2.2. Stimuli and procedures
Participants viewed three runs of 80 pairs of stimuli during fMRI recordings.
The stimuli were pictures of faces and butterflies as shown in Fig. 1. Thirty-two
face and 32 butterfly images were used in an event-related design. There were
four conditions of interest: two different face identities, two identical face identities, two different butterflies, and two identical butterflies in each pair. Finally,
a fifth condition of a butterfly followed by a face image (or the opposite order
for half of the trials) was used and participants were asked to respond to these
face–object pair trials by pressing a response key. This task was well suited to the
goals of the experiment because it ensured that the participants were attending
to the stimuli, and it was a task that both patients could perform well. [DF has
been shown previously to be able to categorize faces even though she cannot rec-

2586

J. Steeves et al. / Neuropsychologia 47 (2009) 2584–2592
2.4. Data analysis of the imaging experiments
The fMRI signal in the different conditions was compared using BrainVoyager
QX (Version 1.4, Brain Innovation, Maastricht, The Netherlands) applying a General Linear Model analysis. Prior to analysis, the functional data sets were subjected
to a series of preprocessing operations. This preprocessing consisted of linear trend
removal to exclude scanner-related signal drift, temporal high-pass filtering in order
to remove temporal frequencies lower than 3 cycles per run, and a correction for
small interscan head movements using a rigid body algorithm rotating and translating each functional volume in 3D space (Friston, Frith, Turner, & Frackowiak,
1995). In addition to preprocessing, the data from the event-related experiment
were also corrected for the difference between the scan times of the slices. Data
were not smoothed in the spatial domain but were filtered in the temporal domain
(FWHM = 2.8 cycles per second). In order to compare activated brain regions across
subjects, all anatomical images and functional volumes were spatially normalized
(Talairach-transformation; Talairach & Tournoux, 1988). Computed statistical maps
were overlaid on the 3D T1-weighted scans to determine Talairach coordinates for all
relevant activation clusters. Subsequently, the functional data were analyzed using
multiple regression models consisting of predictors, which corresponded to the
particular experimental conditions of the experiment. The predictor time courses
used were computed on the basis of a general linear model (GLM) of the relationship between neural activity and hemodynamic response, assuming a square
wave neural response during phases of visual stimulation (Boynton, Engel, Glover,
& Heeger, 1996). For our two patients and the control subjects, we computed a main
effect to localize the face-preferential areas (faces versus butterflies), and tested
the interaction and simple adaptation effects for each stimulus condition in these
areas. Statistical thresholds were chosen with [q(false discovery rate) < 0.01] with a
minimum of 50 voxel clustering.

3. Results
3.1. Behavioural data during fMRI

Fig. 1. Stimuli and task used in the experiment, with the time line of the presentation
of events shown across the top.

ognize them (Steeves et al., 2006).] Further, this task ensured that the factors of
interest of the study (category effect: faces versus butterflies; adaptation effect:
same versus different identities) would not be contaminated by any decisional
and/or motor processes since the behavioural task was completely orthogonal to
the test factors in the study, and any difference between patients and the controls
could not be attributed to general processing difficulties on the trials of interest.
There were 16 trials per condition per run and the order of conditions was
fully randomized within a run. Within a trial, the first stimulus of a pair was presented for 1000 ms followed by a blank screen for 500 ms and thereafter by the
second stimulus of the pair, which was also presented for 1000 ms (Fig. 1). The pairs
were separated by a fixation cross with a duration of 5000, 6250 or 7500 ms (4–6
functional volumes), and these interstimulus interval (ISI) durations were also fully
randomized. This timing ensured that the onset of distinct events was separated by
at least 6–8 functional volumes (7500–10,000 ms). Randomization of trial order and
of ISI duration further reduced any potential top-down effects of anticipation of the
stimuli.
All images (pictures of faces and butterflies) were presented in the central visual
field in colour and subtended approximately 4◦ of visual angle. Stimuli were spatially
jittered by 40 pixels in X (5%) and 40 pixels in Y (7%) dimensions. The pairs were
displayed in random order with a PC using E-prime 1.1 (PST Inc.) and projected
onto a screen located above the head of the subject and viewed through an angled
mirror.
2.3. Imaging experiments
MR images of brain activity were acquired on all participants using a 3T head
scanner (Siemens Allegra, Siemens AG, Erlangen, Germany), with repeated singleshot echo-planar imaging: echo time (TE) = 50 ms, flip angle (FA) = 90◦ , matrix
size = 64 × 64, field of view (FOV) = 224 mm × 224 mm, slice order descending and
interleaved. Scan parameters were: repetition time (TR) = 1250 ms, 21 slices, slice
thickness = 3.5 mm, no gap between slices, run time length = 11 min, 46 s, 250 ms. A
three-dimensional (3D) T1-weighted data set encompassing the whole brain was
acquired for each subject to provide detailed anatomy (1 mm3 ) using a “modified driven equilibrium Fourier transform” (MDEFT) sequence (scan parameters:
TR = 7.92 ms, TE = 2.4 ms, FA = 15◦ , matrix size = 256 × 256, FOV = 256 mm × 256 mm,
176 slices, slice thickness = 1 mm, no gap, total scan time = 13 min and 43 s).

All participants performed the behavioural task of indicating across-category trials at ceiling (control means: 95 ± 0.03%),
PS (96%) and DF (100% correct detection but one false alarm).
Patients showed comparable response latencies to each other and
to controls (controls: 595 ± 128 ms; PS: 576 ms; DF: 747 ms) with
t = −0.100, p = 0.463 for PS and t = 1.084, p = 0.17 for DF [modified
t-test (Crawford & Garthwaite, 2002)].
3.2. Neuroimaging results
3.2.1. Whole brain analysis
3.2.1.1. Main effect of category: faces versus objects. The comparison
of face and butterfly images, independent of adaptation effects, led
to significant activation in several high-level visual areas for the
control participants as well as for both patients (Fig. 2). Our group
of normal controls (including the age-matched control) showed significant activation at [p(Bonferroni-corrected) < 0.001] in the right
and left ‘FFA’ (mean Talairach coordinates, right ‘FFA’: 39, −45,
−19; 559 voxels and left ‘FFA’: −39, −43, −19; 777 voxels), and [at
q(FDR) < 0.001] in the right ‘pSTS’ (mean Talairach coordinates, 49,
−44, 12; 77 voxels) and in the right and left ‘OFA’ (mean Talairach
coordinates, right ‘OFA’: 40, −69, −13; 188 voxels and left ‘OFA’:
−40, −66, −16; 101 voxels).
Consistent with previous observations, there was significant
activation [at q(FDR) < 0.001] for faces in the ‘FFA’ and ‘pSTS’ of
the right hemisphere for both patient PS and DF (Talairach coordinates, patient PS: ‘FFA’: 37, −54, −18; 591 voxels and ‘pSTS’: 41,
−49, 14; 37 voxels and patient DF: ‘FFA’: 44, −47, −21; 178 voxels
and ‘pSTS’: 48, −47, −1; 525 voxels) (Fig. 2). These activations were
within the normal range for size and anatomical location as previously reported (PS: Rossion et al., 2003; Sorger et al., 2007; DF:
Steeves et al., 2006). Also consistent with previous work, there was
significant activation in the left ‘FFA’ for patient DF (Talairach coordinates: −36, −48, −19; 434 voxels) and in the left ‘OFA’ for patient
PS [but at p(uncorrected) < 0.045, −31, −81, −17; 30 voxels]. In summary, the missing components of the network of face-preferential
activation in both patients were areas that would have been located

J. Steeves et al. / Neuropsychologia 47 (2009) 2584–2592

2587

Fig. 2. Face-preferential activation in sagittal, coronal and axial slices for each of patients PS, DF and control S1 for the contrast of faces minus butterflies. Right hemisphere
‘FFA’ and left hemisphere ‘OFA’ activation are observed in patient PS while bilateral ‘FFA’ and right ‘pSTS’ activation are seen in patient DF. Control S1 shows bilateral ‘FFA’,
‘OFA’ and right hemisphere ‘pSTS’ activation. Talairach coordinates and cluster sizes are listed in Table 1.

in structurally damaged tissue (Fig. 2). The common lesion site in
the two patients is the right hemisphere ‘OFA’.
3.2.2. ROI-based analysis
3.2.2.1. Adaptation effects for faces. In each of the areas showing
preferential activation for faces, we tested for interactions between
adaptation and category, as well as separately for effects of adaptation for each of the image categories (faces and butterflies).
Adaptation indices were computed using the beta weights of the
general linear model (GLM) analysis [faces index = (different faces
versus same faces)/(different faces + same faces)]. Consistent with
previous findings (Dricot et al., 2008; Schiltz et al., 2006), PS did
not show any evidence of release from adaptation to face identity
in the right ‘FFA’ (t = 1.499; p = 0.1339; Fig. 3), unlike normal participants (t = 3.732; p < 0.0002; Fig. 3). Hence, her middle fusiform
gyrus responds preferentially to a picture of a face, but does not distinguish between different face identities. Strikingly, this absence
of release from adaptation to face identity was also observed for
the first time in the right ‘FFA’ of patient DF (Fig. 3) for which there
was, in fact, a trend toward a pattern of activation opposite that
which was expected (slightly higher signal for pairs of identical
faces than different faces) (t = −1.698, p = 0.09). Thus, the right ‘FFAs’
of the two acquired prosopagnosia patients do not show release
from adaptation to identity, in contrast to the healthy control participants.
Release from adaptation to identity was observed, however, in
other face-preferential areas of the control participants (right ‘OFA’:
t = 2.449, p < 0.0143 and left ‘FFA’: t = 2.414, p < 0.0158) but not in the
left ‘OFA’ (t = 0.594, p = 0.5527) and right pSTS (t = 0.644, p = 0.5194).
In contrast, none of these regions that were intact in either patient

showed such effects. There was no release from adaptation to face
identity for patient PS in the left ‘OFA’ (t = 0.242, p = 0.8089) or
right ‘pSTS’ (t = 0.043, p = 0.9656) nor for patient DF in the left ‘FFA’
(t = −0.967, p = 0.3339) or the right ‘pSTS’ (t = −1.442, p = 0.1494)
(Supplementary Fig. 1).
When comparing patient indices directly to those of controls,
there was a significant difference in the ‘FFA’ for patient DF
(t = −5.07, p = 0.004) and for patient PS (t = −2.48, p = 0.034).

3.2.2.2. Adaptation effects for objects. This absence of release from
adaptation to identity, in particular in the right ‘FFA’ cannot be
attributed to a lower signal overall for the patients, because this
area responds robustly to faces in both patients (Fig. 3). Moreover,
this area (right FFA) shows an identity adaptation effect when contrasting different and identical pictures of butterflies in not only
our control participants (t = 5.281, p < 0.00001; Fig. 3), but also in
patient PS (t = 4.725, p < 0.00001; Fig. 3; see also Dricot et al., 2008).
There was no such effect for patient DF (t = −0.882, p = 0.3778;
Fig. 3).
Release from adaptation to identity for butterflies was observed
in other face-preferential areas of the normal participants including
the right ‘OFA’ (t = 3.040, p < 0.0024), left ‘OFA’ (t = 3.416, p < 0.0006)
and left ‘FFA’ (t = 5.499, p < 0.00001) but not the right pSTS (t = 0.376,
p = 0.7063). For patient PS, release from adaptation was found in
the pSTS (t = 2.787, p < 0.0053) but not in the left ‘OFA’ (t = −0.181,
p = 0.8569) and there was no release from adaptation at all for
patient DF in any of the regions of interest responding preferentially to faces (left ‘FFA’: t = 1.331, p = 0.1833; right ‘pSTS’: t = −2.075,
p = 0.0381) (Supplementary Fig. 1).

2588

J. Steeves et al. / Neuropsychologia 47 (2009) 2584–2592

Fig. 3. (A) Event-related average time courses within the right ‘FFA’ for patients PS, DF and controls for the four experimental conditions of the study. (B) Histograms with
adaptation indices computed using the beta weights of the general linear model (GLM) analysis [faces index = (different faces versus same faces)/(different faces + same faces)].
AM refers to the age-matched control. The * indicates a significantly different repetition index from controls.

When comparing patient indices directly to those of controls,
there was a significant difference in the ‘FFA’ for patient DF
(t = −6.26, p = 0.002) and but not for patient PS (t = −0.387, p = 0.36).
3.2.2.3. Interaction between adaptation and category. In summary,
identity adaptation effects for both faces and objects were observed
in normal participants in the right ‘FFA’ and in other facepreferential areas (Table 1). For patient PS, identity adaptation
effects were only observed for objects, while for patient DF there
were no adaptation effects for objects or faces. When testing
the interaction between category and adaptation, normal participants showed equally large identity adaptation in the ‘FFA’
for faces and objects (interaction: t = −1.091, p = 0.2755), while PS
showed a larger effect for objects (t = −2.293, p < 0.0219) than for
faces in the right ‘FFA’, and DF did not show identity adaptation for either image category in any of these areas (t = −0.573,
p = 5665).
3.2.2.4. Whole brain conjunction analysis. To strengthen our results,
a whole brain analysis was performed on the control participants
with the conjunction of three contrasts: [((different faces + same
faces) versus (different butterflies + same butterflies)) & (different
faces − same faces) & (different butterflies − same butterflies)]. This
was done using a fixed effects analysis with our five subjects, for
which we found only one significant cluster, corresponding to the

Talairach coordinates of the ‘FFA’ (Fig. 4): 37, −43, −22; 31 voxels, q(FDR) < 0.05. The same analysis did not reveal any activation
for either patient, which is consistent with their absence of adaptation effects for faces in the faces’ ROI analyses. In addition, we
performed a whole brain analysis searching for identity adaptation effects for pictures of faces and butterflies in patient PS and
DF’s brain. Consistent with our most recent findings (Dricot et al.,
2008), we found a significant release from face and object identity
adaptation for PS in an area adjacent to her right inferior occipital lesion, corresponding to the ventral part of the lateral occipital
complex (vLOC, see Dricot et al., 2008) [Talairach coordinates: 50,
−64, −10; 506 voxels at p(uncorrected) < 0.045, t = 3.705, p < 0.0002
for face adaptation and t = 3.206, p < 0.0014 for object adaptation
without an interaction between category and adaptation (t = 0.344,
p = 0.7306); Fig. 5].
This cluster is not specific to faces and responds even more to
objects than to faces [contrast ([different butterflies + same butterflies] versus [different faces + same faces]), t = 2.758, p < 0.0059].
This indicates that patient PS recruits an area that does not respond
preferentially to faces, the vLOC, to differentiate face identities.
Importantly, this effect is not specific to patient PS—when the
vLOC is localized independently in normal observers, this region
also shows a larger response to different exemplars than same
exemplars, irrespective of the category. This has been observed in
several studies with normal observers (Avidan, Hasson, Hendler,

J. Steeves et al. / Neuropsychologia 47 (2009) 2584–2592

2589

Table 1
Talairach coordinates and cluster size in face-preferential areas for controls and patients PS and DF.
Controls

PS

DF

Right
“FFA”

Talairach coordinates
Size [mm2 ; q(FDR) < 0.001]
Face adaptation
Object adaptation

39, −45, −19
559*
Yes
Yes

37, −54, −18
591
No
Yes

44, −47, −21
178
No
No

Left
“FFA”

Talairach coordinates
Size [mm2 ; q(FDR) < 0.001]
Face adaptation
Object adaptation

−39, −43, −19
111*
Yes
Yes

Lesioned

−36, −48, −19
434
No
No

Right
“OFA”

Talairach coordinates
Size [mm2 ; q(FDR) < 0.001]
Face adaptation
Object adaptation

40, −69, −13
188
Yes
Yes

Lesioned

Lesioned

Left
“OFA”

Talairach coordinates
Size [mm2 ; q(FDR) < 0.001]
Face adaptation
Object adaptation

−40, −66, −16
101
No
Yes

−31,−81,−17
30**
No
No

Lesioned

Right
pSTS

Talairach coordinates
Size [mm2 ; q(FDR) < 0.001]
Face adaptation
Object adaptation

49, −44, 12
77*
No
No

41, −49, 14
37
No
Yes

48, −47, −1
525
No
No

*
**

Bonferroni corrected.
p(uncorrected) < 0.045.

Zohary, & Malach, 2002; Grill-Spector et al., 1999; Sayres &
Grill-Spector, 2006), as well as for both faces and objects in individual normal subjects tested with the paradigm used in the
present study, in which the vLOC was localized independently

(Dricot et al., 2008). Hence, the sensitivity to different individual faces in the vLOC of patient PS appears to reflect a residual
rather than a compensatory mode of processing the individual
face.

Fig. 4. (A) Whole brain fixed effects analysis on the control subjects with the conjunction of three contrasts: [(different faces + same faces) versus (different butterflies + same
butterflies) & (different faces versus same faces) & (different butterflies versus same butterflies)]. This revealed only one significant cluster corresponding to the Talairach
coordinates of the ‘FFA’: 37, −43, −22; 31 voxels, q(FDR) < 0.05 [represented at p(uncorrected < 0.001, 105 voxels]. The same analysis did not reveal any activation in either
patient PS or DF. (B) Event-related average time courses for the four experimental conditions in the study.

2590

J. Steeves et al. / Neuropsychologia 47 (2009) 2584–2592

Fig. 5. Event-related average time courses for the four experimental conditions in the study in a whole brain analysis for patient PS with the conjunction of two contrasts:
[(different faces versus same faces) & (different butterflies versus same butterflies)]. Significant release from face identity adaptation was found in patient PS in an area adjacent
to her right inferior occipital lesion, corresponding to the ventral part of the lateral occipital complex [Talairach coordinates: 50, −64, −10; 506 voxels at p(uncorrected) < 0.045].
The same analysis did not reveal any activation in patient DF.

In contrast, there was no evidence for any identity adaptation
effects in patient DF’s brain for faces or butterflies, consistent with
her general visual form agnosia.

4. Discussion
Within the network of occipitotemporal areas that respond preferentially to faces, our two acquired prosopagnosia patients present
a common lesion site encompassing the right ‘OFA’. Each of the
other components of the network was intact either in one of the
patients (left ‘OFA’ for PS; left ‘FFA’ for DF), or in both patients’ brain
(right pSTS and ‘FFA’). The preferential activation for faces in the two
patients was in the normal range in terms of amplitude and spatial
extent, even though the large variability in patterns of activation
in the healthy control participants may mask minor abnormalities
at this level. That is, one can never rule out the possibility that
without the lesions to other face-sensitive regions (e.g., the right
‘OFA’), the level of activation in response to faces in the other components of the network might have been higher in these patients.
Nevertheless, these findings strongly support the notion that, in
addition to the right middle fusiform gyrus (Barton, Press, Keenan,
& O’Connor, 2002), a critical site implicated in prosopagnosia is
located in the inferior occipital cortex in the right hemisphere, in
the vicinity of the right ‘OFA’ (Bouvier & Engel, 2006). Moreover,
these data indicate that the ‘OFA’, whether it is located in the right
or left hemisphere, does not constitute a stage of processing that
necessarily has to precede and send input to the rest of the face

cortical network in order for those higher areas to be activated. This
observation casts doubts on a hierarchical view of face processing,
advocated in several papers (Haxby et al., 2000; Ishai, 2008; see also
Jiang et al., 2006; Pitcher, Walsh, Yovel, & Duchaine, 2008). Rather,
these data support the view that there must be direct connections
from early visual areas that do not show preferential sensitivity to
faces, to the middle fusiform gyrus and possibly the pSTS, leading
to face-preferential responses in those areas (Rossion, 2008).
This hypothesis is not novel, but is reinforced by the present
data and by previous observations made by two groups of independent researchers with these patients. The key observation of the
present study, however, is the lack of release from adaptation to
face identity in the ‘FFA’ of both patients DF and PS. This is consistent with previous findings observed in patient PS (Dricot et
al., 2008; Schiltz et al., 2006). Behaviourally, both patients present
strong impairments at individualizing faces, and they do not show
the release from adaptation to face identity that is observed in the
healthy control participants both in the present experiment and in
numerous other studies (e.g., Gauthier et al., 2000; Grill-Spector
& Malach, 2001). Taken together, this strengthens the notion that
the right ‘OFA’ – the two patients’ common missing region within
the cortical face network – is an integral component of the network for processing face identity (Gauthier et al., 2000), and is
necessary for this function. Its role within this network may not
be to precede the preferential activation for faces at the level of
the FFA but rather its role in face identity processing, in particular
in the right hemisphere, may be to contribute to the refinement
of the face representation, following the initial categorization of a

J. Steeves et al. / Neuropsychologia 47 (2009) 2584–2592

face in the “higher-order” right ‘FFA’ (Rossion, 2008). This reverse
hierarchical view (Hochstein and Ahissar, 2002) of face perception
is consistent with the presence of massive cortical bi-directional
connections (Felleman & Van Essen, 1991) and the hypothesis of
reentrant phasic signaling between areas of visual cortex (Edelman,
1978, 1993). In a similar vein, a number of authors have suggested
that higher level perceptual computations and representations that
require high resolution details, fine geometry and spatial precision may involve lower visual areas through feedback connections
(Bullier et al., 2001; Galuske et al., 2002; Mumford, 1992; Lee et al.,
1998). For the recognition of face identity, refinement in the initial coarse face representation would require the high resolution
details both at the level of the face features and of its configuration
(Sergent, 1986).
Despite presenting a common lesion in the right inferior occipital cortex that is most likely critical in causing their face processing
impairment (Bouvier & Engel, 2006), patients PS and DF do not
present the same neuropsychological profile. While patient DF has
a visual form agnosia, and is unable to recognize common objects
(Milner et al., 1991), patient PS does not present any difficulty in
recognizing objects, whether they have to be identified or discriminated at the basic-level or at more fine-grained categorization levels
(Rossion et al., 2003; Schiltz et al., 2006). Consistent with these
behavioural differences, patient DF has bilateral damage to the lateral occipital area (LO, James et al., 2003), while this region is both
structurally and functionally intact for patient PS (bilateral dorsal
LO and right ventral LO, Sorger et al., 2007). Moreover, patient PS’
area LO shows a larger response to normal shapes compared to
scrambled shapes (Sorger et al., 2007), and it also shows release
from adaptation to the repetition of the same object shape (Dricot
et al., 2008; the present study).
In addition, we note that while patient PS showed a significant
release from adaptation in the right ‘FFA’ to object shapes, patient
DF did not. This is an interesting observation because patient DF
is able to discriminate some non-face stimuli, particularly natural
objects such as fruits and vegetables based on surface properties
such as colour (Humphrey et al., 1994), yet her right ‘FFA’ did not
show release from adaptation in this condition. This suggests that
the positive adaptation effect observed for patient PS in the ‘FFA’
for objects (Dricot et al., 2008) may not be attributable to a simple
release from adaptation driven by colour alone.
Further to these differences in object recognition, the two
patients are not equally strongly impaired with respect to face
processing. Patient DF is severely impaired in individual face discrimination, scoring generally at chance levels (Steeves et al., 2006).
Patient PS, however, is impaired relative to controls but nonetheless
performs well above chance levels in individual face discrimination
tasks (Rossion et al., 2003; Schiltz et al., 2006). Previous studies have
shown that patient PS relies on suboptimal cues to discriminate
and recognize individual faces (e.g., the mouth and lower external
contour; Caldara et al., 2005), and appears to analyze each facial
feature consecutively, in detail, rather than resorting to an efficient
holistic processing of the individual face, as do normal observers
(Orban de Xivry, Ramon, Lefèvre, & Rossion, 2008). The imaging
data for patient PS collected previously (Dricot et al., 2008) and that
in the present study suggest that this sub-efficient, analytical mode
of processing the individual face does not rely on areas responding
preferentially to faces, but may involve more general processes in
the ventral part of the lateral occipital complex.
Another original aspect of the present experiment lies in the
fact that while patient DF’s face-preferential regions in the middle
fusiform gyrus (‘FFA’) were reported previously in a block design
face localizer experiment (Steeves et al., 2006), this is the first time
that this face selective-activation is reported in an ER design, limiting the putative role of top-down influences on the activation of
the ‘FFA’. This is an important observation, since it is known that

2591

the ‘FFA’ can be modulated and activated through top-down processes, for instance through visual imagery of faces (O’Craven &
Kanwisher, 2000) or recognizing the voices of familiar people (von
Kriegstein et al., 2005). In the kind of paradigm used here, the participant does not know in advance which stimulus category will be
presented (pair of faces or objects) and thus anticipatory top-down
processes cannot account for the differential activity observed in
these areas. A further novel aspect of the present study is that we
used a different category for the contrast compared to the previous
study with patient DF (Steeves et al., 2006). Here we define these
areas by contrasting faces with objects while the previous study
contrasted faces with scenes.
In summary, the present study compared functional brain activation in two unique brain-damaged patients who both suffer from
acquired prosopagnosia. The findings strengthen the critical role of
the right inferior occipital cortex, in the vicinity of the right ‘occipital face area’, in acquired prosopagnosia (Bouvier & Engel, 2006;
Sorger et al., 2007). Damage to this region does not prevent overall
face sensitivity within the right middle fusiform gyrus (‘FFA’), thus
arguing against a strict hierarchical view of face processing in the
human brain. However, right ‘OFA’ damage does appear to prevent
the differential sensitivity of the ‘FFA’ to different face identity, suggesting a reentrant role of the right ‘OFA’ in extracting fine-grained
individual representations of faces in the normal brain.
Acknowledgements
This study was supported by grants from the Belgian National
Fund for Scientific Research (FNRS) and a grant ARC 07/12-007 to BR
(Mandat d’Impulsion Scientifique), the Natural Sciences and Engineering Research Council of Canada (NSERC) to JS and the Medical
Research Council (MRC) # G0401090 to AM. We thank two anonymous reviewers for their helpful comments on a previous version
of the paper.
Appendix A. Supplementary data
Supplementary data associated with this article can be found, in
the online version, at doi:10.1016/j.neuropsychologia.2009.05.005.
References
Allison, T., McCarthy, G., Nobre, A., Puce, A., & Belger, A. (1994). Human extrastriate
visual cortex and the perception of faces, words, numbers, and colors. Cerebral
Cortex, 4(5), 544–554.
Avidan, G., Hasson, U., Hendler, T., Zohary, E., & Malach, R. (2002). Analysis of the
neuronal selectivity underlying low fMRI signals. Current Biology, 12, 964–972.
Avidan, G., Hasson, U., Malach, R., & Berhmann, M. (2005). Detailed exploration of
face-related processing in congenital prosopagnosia. 2. Functional neuroimaging
findings. Journal of Cognitive Neuroscience, 17(7), 1150–1167.
Barton, J. J., Press, D. Z., Keenan, J. P., & O’Connor, M. (2002). Lesions of the fusiform
face area impair perception of facial configuration in prosopagnosia. Neurology,
58, 71–78.
Bodamer, J. (1947). Die-Prosop-agnosie. Arch. Psychiatr. Nervenkrankh., 179, 6–54.
English translation by Ellis, H.D. and Florence, M. (1990). Cognitive Neuropsychology, 7, 81-105.
Bouvier, S. E., & Engel, S. A. (2006). Behavioral deficits and cortical damage loci in
cerebral achromatopsia. Cerebral Cortex, 16(2), 183–191.
Boynton, G. M., Engel, S. A., Glover, G. H., & Heeger, D. J. (1996). Linear systems analysis
of functional magnetic resonance imaging in human V1. Journal of Neuroscience,
16, 4207–4221.
Brodtmann, A., Puce, A., Syngeniotis, A., Darby, D., & Donnan, G. (2003). The functional magnetic resonance imaging hemodynamic response to faces remains
stable until the ninth decade. Neuroimage, 20, 520–528.
Bullier, J., Hupe, J. M., James, A. C., & Girard, P. (2001). The role of feedback connections
in shaping the responses of visual cortical neurons. Progress in Brain Research,
134, 193–204.
Caldara, R., Schyns, P., Mayer, E., Smith, M. L., Gosselin, F., & Rossion, B. (2005). Does
prosopagnosia take the eyes out of face representations? Evidence for a defect
in representing diagnostic facial information following brain damage. Journal of
Cognitive Neuroscience, 17(10), 1652–1666.
Crawford, J. R., & Garthwaite, P. H. (2002). Investigation of the single case in neuropsychology: Confidence limits on the abnormality of test scores and test score
differences. Neuropsychologia, 30, 1196–1208.

2592

J. Steeves et al. / Neuropsychologia 47 (2009) 2584–2592

Damasio, A. R., Damasio, H., & Van Hoesen, G. W. (1982). Prosopagnosia: Anatomic
basis and behavioral mechanisms. Neurology, 32, 331–341.
Dricot, L., Sorger, B., Schiltz, C., Goebel, R., & Rossion, B. (2008). The roles of “face” and
“non-face” areas during individual face perception: Evidence by fMRI adaptation
in a brain-damaged prosopagnosic patient. Neuroimage, 40(1), 318–332.
Edelman, G. M. (1978). Group selection and phasic reentrant signaling: a theory of
higher brain function. In F. O. Schmitt (Ed.), The mindful brain. Cambridge: MIT
Press.
Edelman, G. M. (1993). Neural Darwinism: Selection and Reentrant Signaling in
Higher Brain Function. Neuron, 10, 115–125.
Felleman, D. J., & Van Essen, D. C. (1991). Distributed hierarchical processing in the
primate cerebral cortex. Cerebral Cortex, 1, 1–47.
Friston, K. J., Frith, C. D., Turner, R., & Frackowiak, R. S. (1995). Characterizing evoked
hemodynamics with fMRI. Neuroimage, 2, 157–165.
Galuske, R. A., Schmidt, K. E., Goebel, R., Lomber, S. G., & Payne, B. R. (2002). The role
of feedback in shaping neural representations in cat visual cortex. Proceedings of
the National Academy of Sciences of the United States of America, 99, 17083–17088.
Gauthier, I., Tarr, M. J., Moylan, J., Skudlarski, P., Gore, J. C., & Anderson, A. W. (2000).
The fusiform “face area” is part of a network that processes faces at the individual
level. Journal of Cognitive Neuroscience, 12, 495–504.
Grill-Spector, K., & Malach, R. (2001). fMR-adaptation: A tool for studying the functional properties of human cortical neurons. Acta Psychologica, 107, 293–321.
Grill-Spector, K., Kushnir, T., Edelman, S., Avidan, G., Itzchak, Y., & Malach, R. (1999).
Differential processing of objects under various viewing conditions in the human
lateral occipital complex. Neuron, 24, 187–203.
Grill-Spector, K., Sayres, R., & Ress, D. (2006). High-resolution imaging reveals highly
selective nonface clusters in the fusiform face area. Nature Neuroscience, 9,
1177–1185.
Haxby, J. V., Hoffman, E. A., & Gobbini, I. A. (2000). The distributed neural system for
face perception. Trends in Cognitive Sciences, 4, 223–233.
Hochstein, S., & Ahissar, M. (2002). View from the top: hierarchies and reverse hierarchies in the visual system. Neuron, 36(5), 791–804. Review
Humphrey, G. K., Goodale, M. A., Jakobson, L. S., & Servos, P. (1994). The role of surface
information in object recognition: Studies of a visual form agnosic and normal
subjects. Perception, 23, 1457–1481.
Ishai, A. (2008). Let’s face it: It’s a cortical network. Neuroimage, 40(2), 415–419.
James, T. W., Culham, J., Humphrey, G. K., Milner, A. D., & Goodale, M. A. (2003). Ventral occipital lesions impair object recognition but not objectdirected grasping:
An fMRI study. Brain, 126, 2643–2675.
Jiang, X., Rosen, E., Zeffiro, T., Vanmeter, J., Blanz, V., & Riesenhuber, M. (2006). Evaluation of a shape-based model of human face discrimination using FMRI and
behavioral techniques. Neuron, 50, 159–172.
Kanwisher, N., McDermott, J., & Chun, M. M. (1997). The fusiform face area: A module
in human extrastriate cortex specialized for face perception. Journal of Neuroscience, 17, 4302–4311.
Lee, T. S., Mumford, D., Romero, R., & Lamme, V. A. (1998). The role of the primary
visual cortex in higher level vision. Vision Research, 38, 2429–2454.
Marotta, J. J., Genovese, C. R., & Behrmann, M. (2001). A functional MRI study of face
recognition in patients with prosopagnosia. Neuroreport, 13, 1581–1587.
Milner, A. D., Perrett, D. I., Johnston, R. S., Benson, P. J., Jordan, T. R., Heeley, D. W., et
al. (1991). Perception and action in “visual form agnosia. Brain, 114, 405–428.
Mumford, D. (1992). On the computational architecture of the neocortex II. The role
of cortico-cortical loops. Biological cybernetics, 66, 241–251.
O’Craven, K. M., & Kanwisher, N. (2000). Mental imagery of faces and places activates
corresponding stiimulus-specific brain regions. Journal of Cognitive Neuroscience,
12(6), 1013–1023.

Oldfield, R. C. (1971). The assessment and analysis of handedness: The Edinburgh
inventory. Neuropsychologia, 9, 97–113.
Orban de Xivry, J.-J., Ramon, M., Lefèvre, P., & Rossion, B. (2008). Reduced fixation
on the upper area of personally familiar faces following acquired prosopagnosia.
Journal of Neuropsychology, 2, 245–268.
Pitcher, D., Walsh, V., Yovel, G., & Duchaine, B. (2008). TMS evidence for the involvement of the right occipital face area in early face processing. Current Biology, 17,
1568–1573.
Puce, A., Allison, T., Gore, J. C., & McCarthy, G. (1995). Face-sensitive regions in human
extrastriate cortex studied by functional MRI. Journal of Neurophysiology, 74,
1192–1199.
Quaglino, A., & Borelli, G. (1867). Emiplegia sinistra con amaurosi – guarigione –
perdita totale della percezione dei colori e della memoria della configurazione
degli oggetti. Giornale d’Oftalmologia Italiano, 10, 106–117.
Rossion, B. (2008). Constraining the cortical face network by neuroimaging studies
of acquired prosopagnosia. NeuroImage, 40, 423–426.
Rossion, B., Caldara, R., Seghier, M., Schuller, A.-M., Lazeyras, F., & Mayer, E.
(2003). A network of occipito-temporal face-sensitive areas besides the right
middle fusiform gyrus is necessary for normal face processing. Brain, 126,
2381–2395.
Sayres, R., & Grill-Spector, K. (2006). Object-selective cortex exhibits performanceindependent repetition suppression. Journal of Neurophysiology, 95, 995–1007.
Schiltz, C., Sorger, B., Caldara, R., Ahmed, F., Mayer, E., Goebel, R., et al. (2006).
Impaired face discrimination in acquired prosopagnosia is associated with
abnormal response to individual faces in the right middle fusiform gyrus. Cerebral Cortex, 16(4), 574–586.
Sergent, J. (1986). Microgenesis of face perception. In H. D. Ellis, M. A. Jeeves, F. Newcombe, & A. M. Young (Eds.), Aspects of face processing (pp. 17–33). Dordrecht:
Martinus Nijhoff.
Sergent, J., & Signoret, J. L. (1992). Varieties of functional deficits in prosopagnosia.
Cerebral Cortex, 2, 375–388.
Sergent, J., Ohta, S., & MacDonald, B. (1992). Functional neuroanatomy of face
and object processing. A positron emission tomography study. Brain, 115,
15–36.
Servos, P., Goodale, M. A., & Humphrey, G. K. (1993). The drawing of objects by a visual
form agnosic: Contribution of surface properties and memorial representations.
Neuropsychologia, 31, 251–259.
Sorger, B., Goebel, R., Schiltz, C., & Rossion, B. (2007). Understanding the
functional neuroanatomy of acquired prosopagnosia. Neuroimage, 35(2),
836–852.
Steeves, J. K. E., Humphrey, G. K., Culham, J. C., Menon, R. S., Milner, A. D., & Goodale,
M. A. (2004). Behavioral and neuroimaging evidence for a contribution of color
and texture information to scene classification in a patient with visual form
agnosia. Journal of Cognitive Neuroscience, 16(6), 955–965.
Steeves, J. K. E., Culham, J. C., DuChaine, B. C., Cavina Pratesi, C., Valyear, K., Schindler,
I., et al. (2006). The fusiform face area is not sufficient for face recognition:
Evidence from a patient with dense prosopagnosia and no occipital face area.
Neuropsychologia, 44(4), 596–609.
Talairach, G., & Tournoux, P. (1988). Co-planar stereotaxic atlas of the human brain.
New York: Thieme.
von Kriegstein, K., Kleinschmidt, A., Sterzer, P., & Giraud, A. L. (2005). Interaction of
face and voice areas during speaker recognition. Journal of Cognitive Neuroscience,
17(3), 367–376.
Winston, J. S., Henson, R. N. A., Fine-Goulden, M. R., & Dolan, R. J. (2004). fMRIadaptation reveals dissociable neural representations of identity and expression
in face perception. Journal of Neurophysiology, 92, 1830–1839.