A 24-year-old right-handed woman with a right temporal hematoma showed marked left visual neglect for far but not near space in a variety of tasks systematically given in near and far distance conditions. This case thus provides the dissociation opposite to Halligan and Marshall's patient, who had neglect for near but not far space after a right parietal stroke. Furthermore, although she made rightward errors in bisecting far-distant lines, our patient made smaller opposite leftward errors for near-distant lines. The evidence that unilateral neglect of far and near visual space may exist independently supports a division in the neural systems subserving attention to different compartments of the extrapersonal space in humans.

Patients with anterior limbic lesions, in particular of the posterior orbitofrontal cortex, often act on the basis of memories that do not relate to ongoing reality and justify their behavior with invented stories that can mostly be traced back to real events (spontaneous confabulation). Recent studies demonstrated that the patients fail to suppress activated memory traces that do not pertain to ongoing reality. In the present study, we used a similar paradigm and high-resolution event-related potentials to explore when this suppression happens. Healthy subjects made two runs of a continuous recognition task, composed of the same set of pictures, and were requested to indicate picture recurrences only within the ongoing run. Thus, performance in the first run depends on new learning, whereas the second run requires the ability to realize whether a picture is solely familiar from its occurrence in the previous run ('distracter') or whether it has already appeared in the ongoing second run ('target'). We find that correct rejection (suppression) of currently irrelevant pictures (distracters of run 2) is associated with absent negative deflection of a frontal potential and absence of a specific cortical potential map configuration after 220-300 ms. By contrast, learning and recognition of repeatedly presented information is associated with cortical amplitude modulation after 400-480 ms. These findings indicate that by the time the content of a mental association is recognized and consolidated, its cortical representation has already been adjusted according to whether it relates to ongoing reality or not. This sequence may also explain the ability to distinguish between the memory of a true event and the memory of a thought.

Right hemisphere lesions often lead to severe disorders in spatial awareness and behavior, such as left hemispatial neglect. Neglect involves not only pathological biases in attention and exploration but also deficits in internal representations of space and spatial working memory. Here we designed a new paradigm to test whether one potential component may involve a failure to maintain an updated representation of visual locations across delays when a gaze-shift intervenes. Right hemisphere patients with varying severity of left spatial neglect had to encode a single target location and retain it across an interval of 2 or 3 sec, during which the target was transiently removed, before a subsequent probe appeared for a same/different location judgment. During the delay, gaze could have to shift to either side of the remembered location, or no gaze-shift was required. Patients showed a dramatic loss of memory for target location after shifting gaze to its right (toward their "intact" ipsilesional side), but not after leftward gaze-shifts. Such impairment arose even when the target initially appeared in the right visual field, before being updated leftward due to right gaze, and even when gaze returned to the screen center before the memory probe was presented. These findings indicate that location information may be permanently degraded when the target has to be remapped leftward in gaze-centric representations. Across patients, the location-memory deficit induced by rightward gaze-shifts correlated with left neglect severity on several clinical tests. This paradoxical memory deficit, with worse performance following gaze-shifts to the "intact" side of space, may reflect losses in gaze-centric representations of space that normally remap a remembered location dynamically relative to current gaze. Right gaze-shifts may remap remembered locations leftward, into damaged representations, whereas left gaze-shifts will require remapping rightward, into intact representations. Our findings accord with physiological data on normal remapping mechanisms in the primate brain but demonstrate for the first time their impact on perceptual spatial memory when damaged, while providing new insights into possible components that may contribute to the neglect syndrome.

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Disorders of tactile object recognition (TOR) may result from primary motor or sensory deficits or higher cognitive impairment of tactile shape representations or semantic memory. Studies with healthy participants suggest the existence of exploratory motor procedures directly linked to the extraction of specific properties of objects. A pure deficit of these procedures without concomitant gnostic disorders has never been described in a brain-damaged patient. Here, we present a patient with a right hemispheric infarction who, in spite of intact sensorimotor functions, had impaired TOR with the left hand. Recognition of 2D shapes and objects was severely deficient under the condition of spontaneous exploration. Tactile exploration of shapes was disorganized and exploratory procedures, such as the contour-following strategy, which is necessary to identify the precise shape of an object, were severely disturbed. However, recognition of 2D shapes under manually or verbally guided exploration and the recognition of shapes traced on the skin were intact, indicating a dissociation in shape recognition between active and passive touch. Functional MRI during sensory stimulation of the left hand showed preserved activation of the spared primary sensory cortex in the right hemisphere. We interpret the deficit of our patient as a pure tactile apraxia without tactile agnosia, i.e. a specific inability to use tactile feedback to generate the exploratory procedures necessary for tactile shape recognition.