Abstract
Acquired prosopagnosia, the inability to recognize familiar faces, is a rare neurological syndrome that is heterogeneous in both its behavioral deficits and anatomic lesions. One point of reported variability is the presence of impaired expression processing in addition to the impairments in identity processing. We studied the perception of identity and expression in four prosopagnosic patients and asked whether the behavioral findings correlated with data from functional magnetic resonance imaging (fMRI).
We investigated identity and expression processing with an oddity task containing separate identity and expression tests which were equated for level of difficulty in a group of 16 healthy controls. With fMRI, we used a functional localizer to identify damaged and intact face-selective brain regions. Last, we designed an fMRI adaptation study to obtain measures of identity and expression adaptation in the face-selective regions of each subject.
The oddity task showed impaired perceptual processing of identity in three patients, including two with anterior temporal lesions sparing the fusiform face area (FFA), occipital face area (OFA), and superior temporal sulcus (STS). This task also demonstrated clear dissociations in identity and expression impairments, with these three subjects showing normal discrimination of changes in expression, all of whom also had an intact right STS. Despite their difficulties recognizing the identity of faces, adaptation effects for identity were still observed in the OFA of all four patients, but not in the right FFA of the two patients with this area intact. Adaptation effects for expression were observed only in the right STS of the two patients with damage restricted to the anterior temporal lobes.
We conclude that expression can be relatively preserved in prosopagnosic patients with lesions sparing the STS, and that identity adaptation in the OFA does not index processes sufficient on their own to predict normal perceptual sensitivity to facial identity.
This work was supported by operating grants from the Canadian Institutes of Health Research (MOP-77615, MOP-85004), the National Institute for Mental Health (1R01 MH069898), and the Economic and Social Research Council (RES-061-23-0040). CJF was supported by a Canadian Institutes for Health Research Canada Graduate Scholarship Doctoral Research Award and a Michael Smith Foundation for Health Research Senior Graduate Studentship. GI was supported by the Alzheimer Society of Canada and the Michael Smith Foundation for Health Research. JJSB was supported by a Canada Research Chair and a Senior Scholarship from the Michael Smith Foundation for Health Research.