The eventual aims of this thesis were threefold. The first was to investigate the patterns of impairments suffered by prosopagnosic subjects, measuring both reaction times and errors, with conclusions being drawn about the heterogeneity of the neurological disorder. Three prosopagnosic subjects were tested on a number of face processing tasks, investigating facial identity matching, facial expression matching and the perception of eye gaze direction. They were found to have different patterns of impairments, reflecting the different causes of their prosopagnosia. The second aim was to investigate cerebral hemispheric asymmetry in normal subjects for both face processing and word processing. Using split- field tachistoscopic presentation of visual stimuli, facial identity matching and facial expression matching were tested, followed by making syntactical judgements for words and finally reading words out loud. No hemispheric differences were found for facial identity or facial expression matching, except where the faces to be matched only comprised internal features, when a right hemisphere advantage was found. The majority of the word processing studies elicited a left hemispheric superiority. It was also shown that words were recognised more easily when they contained fewer syllables, and were more common and familiar to the reader. The third aim of the thesis was to test two additional subjects, who had been shown, on the basis of PET imaging, to have reversed cerebral asymmetry, specifically right hemispheric activity for linguistic tasks. These subjects were tested on the facial identity matching and word processing tasks. No hemispheric advantage for face processing was found, but either a right hemisphere advantage or no hemispheric advantage was found for both of them for word processing, whereas on the same tasks control subjects showed a significant left hemisphere advantage. As a result of this finding, it is suggested that one of the word tasks could possibly be used for further clarification when the results of the WADA test, used for assessing the language dominance of epileptics prior to surgery, are unclear. Alternatively, the results of such a task could be correlated with the results of PET and MRI scans to further investigate hemispheric asymmetry in a quantitative way, thus using converging evidence from both experimental psychological and neurological methods.

Prosopagnosia is defined as a profound deficit in facial identification which can be either acquired due to brain damage or is present from birth, i.e. congenital. Normally, faces and objects are processed in different parts of the inferotemporal cortex by distinct cortical systems for face vs. object recognition, an association of function and location. Accordingly, in acquired prosopagnosia locally restricted damage can lead to specific deficits in face recognition. However, in congenital prosopagnosia faces and objects are also processed in spatially separated areas. Accordingly, the face recognition deficit in congenital prosopagnosia can not be solely explained by the association of function and location. Rather, this observation raises the question why and how such an association evolves at all. So far, no quantitative or computational model of congenital prosopagnosia has been proposed and models of acquired prosopagnosia have focused on changes in the information processing taking place after in icting some kind of \damage" to the system. To model congenital prosopagnosia, it is thus necessary to understand how face processing in congenital prosopagnosia differs from normal face processing, how differences in neuroanatomical development can give rise to differences in processing and last but not least why facial identification requires a specialized cortical processing system in the first place. In this work, a computational model of congenital prosopagnosia is derived from formal considerations, implemented in artificial neural network models of facial information encoding, and tested in experiments with prosopagnosic subjects. The main hypothesis is that the deficit in congenital prosopagnosia is caused by a failure to obtain adequate descriptions of individual faces: A predisposition towards a reduced structural connectivity in visual cortical areas enforces descriptions of visual stimuli that lack the amount of detail necessary to distinguish a specific exemplar from its population, i.e. achieve a successful identification. Formally recognition tasks can be divided into identification tasks (separating a single individual from its sampling population) and classification tasks (partitioning the full object space into distinct classes). It is shown that a high-dimensionality in the sensory representation facilitates individuation (\blessing of dimensionality"), but complicates estimation of object class representations (\curse of dimensionality"). The dimensionality of representations is then studied explicitly in a neural network model of facial encoding. Whereas optimal encoding entails a \holistic" (high-dimensional) representation, a constraint on the network connectivity induces a decomposition of faces into localized, \featural" (low-dimensional) parts. In an experimental validation, the perceptual deficit in congenital prosopagnosia was limited to holistic face manipulations and didn't extend to featural manipulations. Finally, an extensive and detailed investigation of face and object recognition in congenital prosopagnosia enabled a better behavioral characterization and the identification of subtypes of the deficit. In contrast to previous models of prosopagnosia, here the developmental aspect of congenital prosopagnosia is incorporated explicitly into the model, quantitative arguments for a deficit that is task specific (identification) - and not necessarily domain specific (faces) - are provided for synthetic as well as real data (face images), and the model is validated empirically in experiments with prosopagnosic subjects.

Although the visual system is perhaps the most well understood system in the human brain, the precise organization of the neural system whose activity gives rise to higher order functions like visual recognition remains unknown. Furthermore, the manner in which damage involving this system relates to deficit, or the extent to which other factors modulate this relationship is unknown. Building on prior research in this laboratory and elsewhere, which has related focal brain damage to deficits in visual recognition pertaining to particular categories of stimuli, the present study examined both the specificity of lesion-deficit associations, and the relation between damage to the neural systems subserving visual recognition and the severity of a patient's impairment. In the first part, I employed a novel method to address the specificity of visual recognition impairments in relation to the categories of faces, animals, fruits/vegetables and tools/utensils. By using voxelwise logistic regression to parse out variance that could be attributed to deficits across multiple categories, I was able to identify areas that were uniquely predicted by impairment in a single category. In the second part, I examined the relation between the extent of damage in these "category-specific" regions and the severity of the recognition impairment in the same four categories, as well as potential modulating effects from various demographic (e.g., sex, handedness), neuropsychological (e.g., premorbid intellectual functioning, visual-spatial and visuoperceptual ability), and lesion (e.g., age at onset, time elapsed since onset, extent of damage in other ROIs, lesion size) variables. The findings indicated that the largest factor accounting for performance in the recognition of these entities was the extent of damage in the respective category-specific regions. However, within each of the categories, there were additional factors that were also associated with performance, which helped explain some of the additional variance in recognition performance that could not be explained by extent of damage alone. With regard to the latter, I found that damage in certain category-specific regions was related to the severity of deficit across multiple categories, thereby reinforcing the notion of relative specialization within the visual system.

Dissertação (Mestrado em Engenharia Elétrica) - Centro Universitário FEI, São Bernardo do Campo, 2018

Thesis (Ph.D.)--York University, 2008. Graduate Programme in Psychology. / Typescript. Includes bibliographical references (leaves 228-251). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:NR39024

Current models of face perception suggest independent processing of identity and expression, though this distinction is still unclear. Using converging methods of psychophysics and functional magnetic resonance imaging (fMRI) in healthy and patient populations we assessed the relationship between these two perceptual processes. First, using perceptual aftereffects, we explored the neural representations underlying identity and expression. The expression aftereffect only partially transferred across different identities, suggesting adaptation within identity-invariant and identity-dependent expression representations. Contrarily, the identity aftereffect fully transferred across different expressions. This asymmetry cannot be explained through low-level adaptation. The identity-dependent component of the expression aftereffect relies on adaptation to a coherent expression, not low-level features, in the adapting face. Thus adaptation generating the expression aftereffect must occur within high-level representations of facial expression. Second, using fMRI adaptation, we examined identity and expression sensitivity in healthy controls. The fusiform face area and posterior superior temporal sulcus showed sensitivity for both identity and expression changes. Independent sensitivity for identity and expression changes was observed in the precuneus and middle superior temporal sulcus respectively. Finally, we explored identity and expression perception in a neuropsychological population. Selective identity impairments were associated with inferior occipitotemporal damage, not necessarily affecting the occipital or fusiform face areas. Impaired expression perception was associated with superior temporal sulcus damage, and also with deficits in the integration of identity and expression. In summary, psychophysics, neuroimaging and neuropsychological methods all provide converging evidence for the independent processing of identity and expression within the face network. However, these same methods also supply converging evidence for a partial dependence of these two perceptual processes: in the expression aftereffect, the functional sensitivities of the FFA and pSTS, and identity deficits observed in a patient with primarily impaired expression perception and a spared inferotemporal cortex. Thus, future models of face perception must incorporate representations or regions which independently process identity or expression as well as those which are involved in the perception of both identity and expression.

Current models of face perception suggest independent processing of identity and expression, though this distinction is still unclear. Using converging methods of psychophysics and functional magnetic resonance imaging (fMRI) in healthy and patient populations we assessed the relationship between these two perceptual processes. First, using perceptual aftereffects, we explored the neural representations underlying identity and expression. The expression aftereffect only partially transferred across different identities, suggesting adaptation within identity-invariant and identity-dependent expression representations. Contrarily, the identity aftereffect fully transferred across different expressions. This asymmetry cannot be explained through low-level adaptation. The identity-dependent component of the expression aftereffect relies on adaptation to a coherent expression, not low-level features, in the adapting face. Thus adaptation generating the expression aftereffect must occur within high-level representations of facial expression. Second, using fMRI adaptation, we examined identity and expression sensitivity in healthy controls. The fusiform face area and posterior superior temporal sulcus showed sensitivity for both identity and expression changes. Independent sensitivity for identity and expression changes was observed in the precuneus and middle superior temporal sulcus respectively. Finally, we explored identity and expression perception in a neuropsychological population. Selective identity impairments were associated with inferior occipitotemporal damage, not necessarily affecting the occipital or fusiform face areas. Impaired expression perception was associated with superior temporal sulcus damage, and also with deficits in the integration of identity and expression. In summary, psychophysics, neuroimaging and neuropsychological methods all provide converging evidence for the independent processing of identity and expression within the face network. However, these same methods also supply converging evidence for a partial dependence of these two perceptual processes: in the expression aftereffect, the functional sensitivities of the FFA and pSTS, and identity deficits observed in a patient with primarily impaired expression perception and a spared inferotemporal cortex. Thus, future models of face perception must incorporate representations or regions which independently process identity or expression as well as those which are involved in the perception of both identity and expression.

Current models of face perception suggest independent processing of identity and expression, though this distinction is still unclear. Using converging methods of psychophysics and functional magnetic resonance imaging (fMRI) in healthy and patient populations we assessed the relationship between these two perceptual processes. First, using perceptual aftereffects, we explored the neural representations underlying identity and expression. The expression aftereffect only partially transferred across different identities, suggesting adaptation within identity-invariant and identity-dependent expression representations. Contrarily, the identity aftereffect fully transferred across different expressions. This asymmetry cannot be explained through low-level adaptation. The identity-dependent component of the expression aftereffect relies on adaptation to a coherent expression, not low-level features, in the adapting face. Thus adaptation generating the expression aftereffect must occur within high-level representations of facial expression. Second, using fMRI adaptation, we examined identity and expression sensitivity in healthy controls. The fusiform face area and posterior superior temporal sulcus showed sensitivity for both identity and expression changes. Independent sensitivity for identity and expression changes was observed in the precuneus and middle superior temporal sulcus respectively. Finally, we explored identity and expression perception in a neuropsychological population. Selective identity impairments were associated with inferior occipitotemporal damage, not necessarily affecting the occipital or fusiform face areas. Impaired expression perception was associated with superior temporal sulcus damage, and also with deficits in the integration of identity and expression. In summary, psychophysics, neuroimaging and neuropsychological methods all provide converging evidence for the independent processing of identity and expression within the face network. However, these same methods also supply converging evidence for a partial dependence of these two perceptual processes: in the expression aftereffect, the functional sensitivities of the FFA and pSTS, and identity deficits observed in a patient with primarily impaired expression perception and a spared inferotemporal cortex. Thus, future models of face perception must incorporate representations or regions which independently process identity or expression as well as those which are involved in the perception of both identity and expression. / Medicine, Faculty of / Graduate

Face recognition involves a number of complex cognitive processes, including memory, executive functioning, and perception. A breakdown of one or more of these processes may result in false facial recognition, a memory distortion in which one mistakenly believes that novel faces are familiar. This study examined the cognitive mechanisms underlying false facial recognition in healthy older and younger adults, patients with frontotemporal dementia, and individuals with congenital prosopagnosia. Participants completed face recognition memory tests that included several different types of lures, as well as tests of face perception. Older adults demonstrated a familiarity-based response strategy, reflecting a deficit in source monitoring and impaired recollection of context, as they could not reliably discriminate between study faces and highly familiar lures. In patients with frontotemporal dementia, temporal lobe atrophy alone was associated with a reduction of true facial recognition, while concurrent frontal lobe damage was associated with increased false recognition, a liberal response bias, and an overreliance on "gist" memory when making recognition decisions. Individuals with congenital prosopagnosia demonstrated deficits in configural processing of faces and a reliance on feature-based processing, leading to false recognition of lures that had features in common from study to test. These findings may have important implications for the development of training programs that could serve to help individuals improve their ability to accurately recognize faces.

It is acknowledged that the genre of animated documentary is particularly suited to depicting the subjective point of view (Wells, 1997, Honess Roe, 2013). It has also been suggested that animated documentary may have a tendency toward collaborative working methods (Ward, 2005: 94). This PhD work explores and expands these suggestions and presents the development of a methodology adapted from what has been termed collaborative ethnography (Lassiter, 2005) when using animation to document perceptual brain states. The claim to originality in this thesis lies in the methodological approach taken through the documenting of idiopathic perceptual brain states, previously unrepresented in animation. It involves a shifting of the roles of subject and director to collaborative consultant and facilitator respectively, and differentiates between the recording of an animated document and the creation of an animated documentary . It rejects the sound reliant template of the 'animated interview' (Strøm, 2005: 15) as the dominant model of creating animated documents, which assumes both that the indexical is crucial to documenting, and that this can only be achieved in animation through the use of indexical sound. It agrees with Tom Gunning s argument that Charles Sanders Pierce's original idea of the index as part of an interconnected triad of signs (index, symbol and icon) has been abstracted from its richer signifying context and extracted a simplified version of what Pierce intended it to mean (a trace or impression left by an object) to become a 'diminished concept' (2007:30-1), essentially a short hand coda in this instance for document . The practice in this work challenges this by presenting an alternative; using a collaborative cycle methodology.