Varieties of Functional Deficits in Prosopagnosia

Abstract

Prosopagnosia is a neurologically based deficit characterized by the inability to recognize faces of known individuals in the absence of severe intellectual, perceptual, and memory impairments. The nature of the underlying disturbance was investigated in three patients in an attempt to identify the structural and functional levels at which the processing of faces breaks down, the relation between prosopagnosia and associated deficits, and the specificity of the prosopagnosic disturbance. The breakdown of face processing resulted from unilateral damage in different cerebral structures of the right hemisphere in the three patients, and it involved different functional levels of face processing, but all three patients displayed perceptual impairments of unequal severity. In one patient (R.M.), the deficit encompassed all perceptual operations on faces, including matching identical views of the same faces, but it did not extend to all categories of objects characterized by a close similarity among their instances; the second patient (P.M.) exhibited a less severe perceptual impairment but was unable to derive the configurational properties from a facial representation and to extract its physiognomic invariants; the third patient (P.C.) had not lost the capacity to differentiate faces on the basis of their configurations but could not associate a facial representation with its pertinent memories. Associated deficits were present in each patient but differed depending on the anatomofunctional locus of the breakdown, although all patients were impaired at recognizing noncanonical views of objects that they readily recognized when shown from a conventional viewpoint. However, performance dissociation within patients and double dissociation between patients suggest that these associated deficits are not necessary concomitants of prosopagnosia.

Normal acquisition of expertise with greebles in two cases of acquired prosopagnosia

“…Results from neuropsychological studies suggest face processing may dissociate from long-term object expertise. After brain lesions causing prosopagnosia, WJ acquired a flock of sheep and became capable of recognizing sheep faces better than normal controls and scored best among a group of sheep farmers (46), whereas RM retained his superior ability to recognize car makes and models (47). Florence and another acquired prosopagnosic could successfully discriminate bodies, a category that generates substantial inversion effects and is relatively wellmatched to faces in terms of visual exposure and perceptual experience (48).…”

Longer fixation duration while viewing face images

“…Yin, 1969;Valentine 1988;Rossion and Gauthier 2002), a visual preference for facelike stimuli in human neonates (Johnson and Morton 1991;see also Turati et al 2002), and selective impairments of face and object recognition in neurological patients (prosopagnosia and visual agnosia) (e.g. Sergent and Signoret 1992;Farah 1996;Moscovitch et al 1997). Recordings of human event-related potentials showed a different topography to face (including human and animal faces) and non-face object or scene stimuli in the N170 time window (e.g.…”

“…Elecrtophysiology and brain imaging studies further suggested a distinct neuroanatomical region in cerebral cortex associated with the cortical processing of faces (face-selective neurons in monkey inferotemporal cortex, fusiform face area in human cortex) (e.g. Sergent et al 1992;McCarthy et al 1997;Tanaka 1997;Tsao et al 2003). However, this view is recently challenged by some brain imaging studies suggesting that faces are processed by a domain-general system for fine-grained, exemplar-level object perception but probably at different level of recognition or different degree of perceptual expertise (Gauthier et al 1999(Gauthier et al , 2000Tarr and Cheng 2003).…”

Impaired face and body perception in developmental prosopagnosia

“…When prosopagnosia occurs in normal adults as a consequence of brain damage, it is most often associated with lesions in the occipito-temporal brain regions (1)(2)(3)(4)(5)(6). In other cases, there is no evidence of brain damage, and the exact etiology of face recognition deficits is unknown (7)(8)(9).…”