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We examined a stroke patient (HWS) with a unilateral lesion of the right medial ventral visual stream, involving the right fusiform and parahippocampal gyri. In a number of object recognition tests with lateralized presentations of target stimuli, HWS showed significant symptoms of hemiagnosia with contralesional recognition deficits for everyday objects. We further explored the patient's capacities of visual expertise that were acquired before the current perceptual impairment became effective. We confronted him with objects he was an expert for already before stroke onset and compared this performance with the recognition of familiar everyday objects. HWS was able to identify significantly more of the specific (“expert”) than of the everyday objects on the affected contralesional side. This observation of better expert object recognition in visual hemiagnosia allows for several interpretations. The results may be caused by enhanced information processing for expert objects in the ventral system in the affected or the intact hemisphere. Expert knowledge could trigger top–down mechanisms supporting object recognition despite of impaired basic functions of object processing. More importantly, the current work demonstrates that top–down mechanisms of visual expertise influence object recognition at an early stage, probably before visual object information propagates to modules of higher object recognition. Because HWS showed a lesion to the fusiform gyrus and spared capacities of expert object recognition, the current study emphasizes possible contributions of areas outside the ventral stream to visual expertise.

We aimed at investigating social disability and its cerebral correlates in frontotemporal dementia (FTD). To do so, we contrasted answers of patients with early-stage FTD and of their relatives on personality trait judgment and on behavior prediction in social and emotional situations. Such contrasts were compared to control contrasts calculated with answers of matched controls tested with their relatives. In addition, brain metabolism was measured in patients with positron emission tomography and the [18F]fluorodeoxyglucose method. Patients turned out to be as accurate as controls in describing their relative's personality, but they failed to predict their relative's behavior in social and emotional circumstances. Concerning the self, patients were impaired both in current personality assessment and in prediction of their own behavior. Those two self-evaluation measures did not correlate. Only patients' anosognosia for social behavioral disability was found to be related to decreased metabolic activity in the left temporal pole. Such results suggest that anosognosia for social disability in FTD originates in impaired processing of emotional autobiographical information, leading to a self-representation that does not match current behavior. Moreover, we propose that perspective-taking disability participates in anosognosia, preventing patients from correcting their inaccurate self-representation based on their relative's perspective.

Agnosia, the impairment in object and face recognition despite intact vision and intelligence, is one of the most intriguing and debilitating neuropsychological deficits. The goal of this study was to determine whether S.M., an individual with longstanding visual agnosia and concomitant prosopagnosia, can be retrained to perform visual object recognition and, if so, what neural substrates mediate this reacquisition. Additionally, of interest is the extent to which training on one type of visual stimulus generalizes to other visual stimuli, as this informs our understanding of the organization of ventral visual cortex. Greebles were chosen as the stimuli for retraining given that, in neurologically normal individuals, these stimuli can engage the fusiform face area. Posttraining, S.M. showed significant improvement in recognizing Greebles, although he did not attain normal levels of performance. He was also able to recognize untrained Greebles and showed improvement in recognizing common objects. Surprisingly, his performance on face recognition, albeit poor initially, was even more impaired following training. A comparison of preand postintervention functional neuroimaging data mirrored the behavioral findings: Face-selective voxels in the fusiform gyrus prior to training were no longer so and were, in fact, more Greeble-selective. The findings indicate potential for experience-dependent dynamic reorganization in agnosia with the possibility that residual neural tissue, with limited capacity, will compete for representations.

Recent research suggests that the hippocampus is not needed for the maintenance and recovery of extensively used environments learned long ago. Instead, a network of neo-cortical regions differentially supports memory for location-navigation knowledge and visual appearance of well-known places. In this study, we present a patient, S. B., who was diagnosed with probable Alzheimer's disease long after retiring from his 40 years as a taxi driver in downtown Toronto, a place that he has visited rarely, if ever, in the last decade. His performance was compared to that of two other retired taxi drivers, L. R., who developed encephalitis after retirement, and I. L., who is without neurological illness, and a group of eight healthy control participants who were never taxi drivers but all of whom worked or lived in downtown Toronto until at least 10 years ago. Despite S. B.'s widespread atrophy, which has affected mainly his hippocampus and part of his occipitotemporal cortex, he performed at least as well as all other participants on remote memory tests of spatial location and mental navigation between well-known Toronto landmarks. Unlike the comparison populations, however, he was unable to discriminate between the appearances of landmarks that he had visited frequently in his many years as a taxi driver from unknown buildings. This profound deficit extended to famous world landmarks but not to famous faces and does not appear to be semantic in nature. These findings add further support to the claim that the hippocampus is not necessary for mental navigation of old environments and suggest that expertise is not sufficient to protect against landmark agnosia.

Neuropsychological studies with patients suffering from prosopagnosia have provided the main evidence for the hypothesis that the recognition of faces and objects rely on distinct mechanisms. Yet doubts remain, and it has been argued that no case demonstrating an unequivocal dissociation between face and object recognition exists due in part to the lack of appropriate response time measurements (Gauthier et al., 1999). We tested seven developmental prosopagnosics to measure their accuracy and reaction times with multiple tests of face recognition and compared this with a larger battery of object recognition tests. For our systematic comparison, we used an old/new recognition memory paradigm involving memory tests for cars, tools, guns, horses, natural scenes, and houses in addition to two separate tests for faces.Developmental prosopagnosic subjects performed very poorly with the face memory tests as expected. Four of the seven prosopagnosics showed a very strong dissociation between the face and object tests. Systematic comparison of reaction time measurements for all tests indicates that the dissociations cannot be accounted for by differences in reaction times. Contrary to an account based on speed accuracy tradeoffs, prosopagnosics were systematically faster in nonface tests than in face tests. Thus, our findings demonstrate that face and nonface recognition can dissociate over a wide range of testing conditions. This is further support for the hypothesis that face and nonface recognition relies on separate mechanisms and that developmental prosopagnosia constitutes a disorder separate from developmental agnosia.

A common notion is that object perception is a necessary precursor to scene perception. Behavioral evidence suggests, however, that scene perception can operate independently of object perception. Further, neuroimaging has revealed a specialized human cortical area for viewing scenes that is anatomically distinct from areas activated by viewing objects. Here we show that an individual with visual form agnosia, D.F., who has a profound deficit in object recognition but spared color and visual texture perception, could still classify scenes and that she was fastest when the scenes were presented in the appropriate color. When scenes were presented as black-and-white images, she made a large number of errors in classification. Functional magnetic resonance imaging revealed selective activation in the parahippocampal place area (PPA) when D.F. viewed scenes. Unlike control observers, D.F. demonstrated higher activation in the PPA for scenes presented in the appropriate color than for black-and-white versions. The results demonstrate that an individual with profound form vision deficits can still use visual texture and color to classify scenes—and that this intact ability is reflected in differential activation of the PPA with colored versions of scenes.

A dissociation between the ability to recognize misoriented objects and to determine their orientation has been reported in a small number of patients with vascular lesions. In this article, we describe a 57-year-old man with probable Alzheimer's disease who shows the same dissociation. Neuro-imaging findings indicated marked hypometabolism in the posterior cortical regions, particularly the postero-superior parietal lobes. Clinically, the patient had good object recognition accompanied by severely impaired spatial abilities. The experimental investigations comprised a variety of tasks in which he identified misoriented objects, evaluated the orientation of single objects, or discriminated the orientation of simultaneously presented items. Results revealed that his object recognition was independent of orientation and was largely mediated by salient features. With respect to orientation judgements, the patient displayed a profound inability to judge the orientation of nonupright objects, but remarkably intact (though largely implicit) knowledge of the upright orientation. Strikingly, his orientation judgements were also more accurate for upside-down objects than for other orientations (i.e., 90°). We interpret these results as evidence that judgements about object orientation are facilitated when the orientation of the principal axis of the object matches that of an internal representation. We propose that the inability to determine other orientations may be due to the failure of an “axis-finding” mechanism implemented in the posterior parietal lobes, that translates between object-centered and eye-centered coordinates appropriate for guiding visual scanning.

Visual agnosia is a neuropsychological syndrome characterized by a failure of object identification. Apperceptive agnosia, an object identification deficit caused by damage to early perceptual processes, has been explained by appealing to both damaged early sensory processes and to damaged preattentive grouping processes. Which of these two explanations best accounts for the behavior of these patients? We present results from two experiments designed to distinguish rival theoretical accounts of apperceptive agnosia. In our studies, we attempted to simulate apperceptive agnosia in neurologically intact subjects. Sensory-deficit accounts of the syndrome predict that degrading visual processing would make normal subjects perform like patients; grouping-deficit accounts predict that removing perceptual organization cues from visual displays would make normal subjects perform like patients. We were able to simulate the behavior of an apperceptive agnosic patient by removing perceptual organization cues, consistent with a grouping-deficit account of this syndrome. The implications for understanding both apperceptive agnosia and normal visual functioning are discussed.

Prosopagnosia is a neurological syndrome in which patients cannot recognize faces. Kecently it has been shown that some prosopagnosics give evidence of "covert" recognition: they show greater autonomic responses to familiar faces than to unfamiliar ones, and respond differently to familiar faces in learning and interference tasks. Although some patients do not show covert recognition, this has usually been attributed to an "apperceptive" deficit that impairs perceptual analysis of the input. The implication is that prosopagnosia is a deficit in access to, or awareness of, memories of faces: the inducing brain injury does not destroy the memories themselves. We present a case study that challenges this view. LH suffers from prosopagnosia as the result of a closed head injury. He cannot recognize familiar faces or report that they are familiar, nor answer questions about the faces from memory, though he can (1) recognize common objects and subtly varying shapes, (2) match faces while ignoring irrelevant information such as emotional expression or angle of view, (3) recognize sex, age, and like-ability from faces, and (4) recognize people by a number of nonfacial channels. The only other categories of shapes that he has marked trouble recognizing are animals and emotional expressions, though even these impairments were not as severe as the one for faces. Three measures (sympathetic skin response, pupil dilation, and learning correct and incorrect names of faces) failed to show any signs of covert face recognition in LH, though the measures were sensitive enough to reflect autonomic reactions in LH to stimuli other than faces, and face familiarity in normal controls. Thus prosopagnosia cannot always be attributed to a mere absence of awareness (i.e., preserved information about faces whose output is disconnected from conscious cognitive processing), to an apperceptive deficit (i.e., preserved information about faces that cannot be accessed due to improperly analyzed perceptual input), or to an inability to recognize complex or subtly varying shapes (i.e., loss or degradation of shape memory in general). We conclude that it is possible for brain injury to eliminate the storage of information about familiar faces and certain related shapes.

In order to study face recognition in relative isolation from visual processes that may also contribute to object recognition and reading, we investigated CK, a man with normal face recognition but with object agnosia and dyslexia caused by a closed-head injury. We administered recognition tests of up right faces, of family resemblance, of age-transformed faces, of caricatures, of cartoons, of inverted faces, and of face features, of disguised faces, of perceptually degraded faces, of fractured faces, of faces parts, and of faces whose parts were made of objects. We compared CK's performance with that of at least 12 control participants. We found that CK performed as well as controls as long as the face was upright and retained the configurational integrity among the internal facial features, the eyes, nose, and mouth. This held regardless of whether the face was disguised or degraded and whether the face was represented as a photo, a caricature, a cartoon, or a face composed of objects. In the last case, CK perceived the face but, unlike controls, was rarely aware that it was composed of objects. When the face, or just the internal features, were inverted or when the configurational gestalt was broken by fracturing the face or misaligning the top and bottom halves, CK's performance suffered far more than that of controls. We conclude that face recognition normally depends on two systems: (1) a holistic, face-specific system that is dependent on orientationspecific coding of second-order relational features (internal), which is intact in CK and (2) a part-based object-recognition system, which is damaged in CK and which contributes to face recognition when the face stimulus does not satisfy the domain-specific conditions needed to activate the face system.

Some patients with face agnosia (prosopagnosia) caused by occipitotemporal damage produce discriminatory covert responses to the familiar faces that they fail to identify overtly. For example, their average skin conductance responses (SCRs) to familiar faces are significantly larger than average SCRs to unfamiliar faces. In this study we describe the opposite dissociation in four patients with bilateral ventromedial frontal damage: The patients recognized the identity of familiar faces normally, yet failed to generate discriminatory SCRs to those same familiar faces. Taken together, the two sets of results constitute a double dissociation: bilateral occipitotemporal damage impairs recognition but allows SCR discrimination, whereas bilateral ventromedial damage causes the opposite. The findings suggest that the neural systems that process the somatic-based valence of stimuli are separate from and parallel to the neural systems that process the factual, nonsomatic information associated with the same stimuli.

Information regarding object identity (“what”) and spatial location (“where/how to”) is largely segregated in visual processing. Under most circumstances, however, object identity and location are linked. We report data from a simultanagnosic patient (K.E.) with bilateral posterior parietal infarcts who was unable to “see” more than one object in an array despite relatively preserved object processing and normal preattentive processing. K.E. also demonstrated a finding that has not, to our knowledge, been reported: He was unable to report more than one attribute of a single object. For example, he was unable to name the color of the ink in which words were written despite naming the word correctly. Several experiments demonstrated, however, that perceptual attributes that he was unable to report influenced his performance. We suggest that binding of object identity and location is a limited-capacity operation that is essential for conscious awareness for which the posterior parietal lobe is crucial.

Bálint's syndrome is characterized by visuospatial dysfunction, with failure to attend to multiple objects in space and poor spatial localization manifested as impaired reaching and saccadic targeting. Less investigated in this disorder is perceptual processing along the dimension of time. We studied the performance of a patient with Bálint's syndrome on two oddity paradigms in which she had to indicate which of three objects was different in color, shape, or structure. Her initial difficulty with processing multiple objects present simultaneously in different locations recovered, but she had persistent difficulty processing objects seen sequentially at the same location. Further studies showed that this deficit was not due to impairments in sustained attention or in distributing attention over time, but to impaired processing of temporal sequences. The deficit was also present with auditory stimuli, indicating a multimodal failure of temporal sequencing. These findings show that bilateral parietal lesions affect not only the spatial but also the temporal organization of perception.

Far (extrapersonal) and near (peripersonal) spaces are behaviorally defined as the space outside the hand-reaching distance and the space within the hand-reaching distance. Animal and human studies have confirmed this distinction, showing that space is not homogeneously represented in the brain. In this paper we demonstrate that the coding of space as “far” and “near” is not only determined by the hand-reaching distance, but it is also dependent on how the brain represents the extension of the body space. We will show that when the cerebral representation of body space is extended to include objects or tools used by the subject, space previously mapped as far can be remapped as near. Patient P.P., after a right hemisphere stroke, showed a dissociation between near and far spaces in the manifestation of neglect. Indeed, in a line bisection task, neglect was apparent in near space, but not in far space when bisection in the far space was performed with a projection lightpen. However, when in the far space bisection was performed with a stick, used by the patient to reach the line, neglect appeared and was as severe as neglect in the near space. An artificial extension of the patient's body (the stick) caused a remapping of far space as near space.