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Face processing models propose a holistic representation of faces in the human brain. Additionally, behavioral studies in healthy individuals indicate a bias towards the eye region of faces, namely a Feature Salience Hierarchy. The exact mechanisms of this feature salience hierarchy are not known. Using behavioral face perception and neuroimaging experiments, we investigated the perceptual mechanisms and the neural correlates of the feature salience hierarchy, and the correlations of the human perceptual performance with the neural signal. Prosopagnosia studies also indicate an asymmetrical loss of the ability to deduce information from the eye region of faces. In a cohort of ten acquired prosopagnosia patients, we investigated and characterized the relationship between the structural brain damage and the behavioral face processing impairments. This dissertation examines the perceptual and neuroanatomical bases of the bias towards the eye region of a face in healthy individuals and the deviation from this bias in relation to the brain lesion locations in acquired prosopagnosia patients. Our findings confirm the dominance of the eyes in feature salience hierarchy in an adaptation aftereffects experiment. Investigation of the neuroanatomical correlates of the feature salience hierarchy shows that the activation pattern in Fusiform Face Area (FFA) correlates with the human perceptual performance, suggesting FFA’s involvement in the feature salience hierarchy demonstrated for the eye region of faces behaviorally. Examination of the eye region processing in prosopagnosia patients shows that both apperceptive and associative variants of prosopagnosia can cause eye region processing deficits, yet apperceptive prosopagnosia patients with inferior occipitotemporal cortex lesions have significantly more severe deficits in eye region processing. Face scanning patterns in a learning and memory task with unlimited viewing times demonstrate that both healthy and prosopagnosic individuals spend more time looking at the upper halves of faces while learning the faces, yet prosopagnosia patients spend significantly longer durations studying the faces. Our investigation of memory for half faces indicate that when presented in isolation, the upper and lower face halves do not have different contributions to face memory in healthy subjects. Prosopagnosia patients are similarly impaired in memory for upper and lower face halves.

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.