Capacity limitations in working memory (WM) necessitate the need to effectively control its contents. Here, we examined the effect of cabergoline, a dopamine D 2 receptor agonist, on WM using a continuous report paradigm that allowed us to assess the fidelity with which items are stored. We assessed recall performance under three different gating conditions: remembering only one item, being cued to remember one target among distractors, and having to remember all items. Cabergoline had differential effects on recall performance according to whether distractors had to be ignored and whether mnemonic resources could be deployed exclusively to the target. Compared with placebo, cabergoline improved mnemonic performance when there were no distractors but significantly reduced performance when distractors were presented in a precue condition. No significant difference in performance was observed under cabergoline when all items had to be remembered. By applying a stochastic model of response selection, we established that the causes of drug-induced changes in performance were due to changes in the precision with which items were stored in WM. However, there was no change in the extent to which distractors were mistaken for targets. Thus, D 2 agonism causes changes in the fidelity of mnemonic representations without altering interference between memoranda.

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.

We examined priming of visual search by repeated target location or color in two patients with left visual neglect and extinction, following strokes centered on the right inferior parietal lobe. Both patients, like the healthy controls we tested, showed intact priming, with performance speeded when either the location or color of a singleton target was repeated over successive trials in a standard search condition (Experiment 1). This was observed both from and to targets on the contralesional (left) side. Moreover, priming of search was still observed even when a return of fixation back to display-center was required between successive trials (Experiment 2). When briefer displays were used (Experiment 3), the patients often failed to detect left targets. This situation revealed an important dissociation: Whereas location priming only arose from preceding left targets that had been consciously detected, color priming (possibly arising within the intact ventral stream) did not depend on awareness of the preceding target. There was considerable color priming from missed targets. These findings demonstrate relatively intact priming of visual search by color and location in patients with right parietal damage, and also reveal that location priming may differ from color priming in requiring awareness.

Right-hemisphere patients with left neglect often demonstrate abnormal visual search, re-examining stimuli to the right while ignoring those to the left. But re-fixations alone do not reveal if patients misjudge whether they have searched a location before. Here, we not only tracked the eye movements of 16 neglect patients during search, but also asked them to click a response button only when they judged they were fixating a target for the very first time. “Re-clicking” on previously found targets would indicate that patients erroneously respond to these as new discoveries. Lesions were mapped with high-resolution MRI. Neglect patients with damage involving the right intraparietal sulcus or right inferior frontal lobe “re-clicked” on previously found targets on the right at a pathological rate, whereas those with medial occipito-temporal lesions did not. For the intraparietal sulcus patients, the probability of erroneous re-clicks on an old target increased with time since first discovering it; whereas for frontal patients it was independent of search time, suggesting different underlying mechanisms in these two types of patient. Re-click deficits correlated with degree of leftward neglect, mainly due to both being severe in intraparietal cases. These results demonstrate that misjudging previously searched locations for new ones can contribute to pathological search in neglect, with potentially different mechanisms being involved in intraparietal versus inferior frontal patients. When combined with a spatial bias to the right, such deficits might explain why many neglect patients often re-examine rightward locations, at the expense of items to their left.

Visual extinction after right parietal damage involves a loss of awareness for stimuli in the contralesional field when presented concurrently with ipsilesional stimuli, although contralesional stimuli are still perceived if presented alone. However, extinguished stimuli can still receive some residual on-line processing, without awareness. Here we examined whether such residual processing of extinguished stimuli can produce implicit and/or explicit memory traces lasting many minutes. We tested four patients with right parietal damage and left extinction on two sessions, each including distinct study and subsequent test phases. At study, pictures of objects were shown briefly in the right, left, or both fields. Patients were asked to name them without memory instructions (Session 1) or to make an indoor/outdoor categorization and memorize them (Session 2). They extinguished most left stimuli on bilateral presentation. During the test (up to 48 min later), fragmented pictures of the previously exposed objects (or novel objects) were presented alone in either field. Patients had to identify each object and then judge whether it had previously been exposed. Identification of fragmented pictures was better for previously exposed objects that had been consciously seen and critically also for objects that had been extinguished (as compared with novel objects), with no influence of the depth of processing during study. By contrast, explicit recollection occurred only for stimuli that were consciously seen at study and increased with depth of processing. These results suggest implicit but not explicit memory for extinguished visual stimuli in parietal patients.