The ability to stop a prepared response (reactive inhibition) appears to depend on the degree to which stopping is expected (proactive inhibition). Functional MRI studies have shown that activation during proactive and reactive inhibition overlaps, suggesting that the whole neural network for reactive inhibition becomes already activated in anticipation of stopping. However, these studies measured proactive inhibition as the effect of stop-signal probability on activation during go trials. Therefore, activation could reflect expectation of a stop-signal (evoked by the stop-signal probability cue), but also violation of this expectation because stop-signals do not occur on go trials. We addressed this problem, using a stop-signal task in which the stop-signal probability cue and the go-signal were separated in time. Hence, we could separate activation during the cue, reflecting expectation of the stop-signal, from activation during the go-signal, reflecting expectation of the stop-signal or violation of that expectation. During the cue, the striatum, the supplementary motor complex (SMC), and the midbrain activated. During the go-signal, the right inferior parietal cortex (IPC) and the right inferior frontal cortex (IFC) activated. These findings suggest that the neural network previously associated with proactive inhibition can be subdivided into two components. One component, including the striatum, the SMC, and the midbrain, activated during the cue, implicating this network in proactive inhibition. Another component, consisting of the right IPC and the right IFC, activated during the go-signal. Rather than being involved in proactive inhibition, this network appears to be involved in processes associated with violation of expectations.

It is well known that, typically, saccadic eye movements precede goal-directed hand movements to a visual target stimulus. Also pointing in general is more accurate when the pointing target is gazed at. In this study, it is hypothesized that saccades are not only preceding pointing but that gaze also is stabilized during pointing in humans. Subjects, whose eye and pointing movements were recorded, had to make a hand movement and a saccade to a first target. At arm movement peak velocity, when the eyes are usually already fixating the first target, a new target appeared, and subjects had to make a saccade toward it (dynamical trial type). In the statical trial type, a new target was offered when pointing was just completed. In a control experiment, a sequence of two saccades had to be made, with two different interstimulus intervals (ISI), comparable with the ISIs found in the first experiment for dynamic and static trial types. In a third experiment, ocular fixation position and pointing target were dissociated, subjects pointed at not fixated targets. The results showed that latencies of saccades toward the second target were on average 155 ms longer in the dynamic trial types, compared with the static trial types. Saccades evoked during pointing appeared to be delayed with approximately the remaining deceleration time of the pointing movement, resulting in "normal" residual saccadic reaction times (RTs), measured from pointing movement offset to saccade movement onset. In the control experiment, the latency of the second saccade was on average only 29 ms larger when the two targets appeared with a short ISI compared with trials with long ISIs. Therefore the saccadic refractory period cannot be responsible for the substantially bigger delays that were found in the first experiment. The observed saccadic delay during pointing is modulated by the distance between ocular fixation position and pointing target. The largest delays were found when the targets coincided, the smallest delays when they were dissociated. In sum, our results provide evidence for an active saccadic inhibition process, presumably to keep steady ocular fixation at a pointing target and its surroundings. Possible neurophysiological substrates that might underlie the reported phenomena are discussed.

The pathophysiology of auditory verbal hallucinations (AVH) is largely unknown. Several functional imaging studies have measured cerebral activation during these hallucinations, but sample sizes were relatively small (one to eight subjects) and findings inconsistent. In this study cerebral activation was measured using fMRI in 24 psychotic patients while they experienced AVH in the scanner and, in another session, while they silently generated words. All patients were right handed and diagnosed with schizophrenia, schizo-affective disorder or psychotic disorder not otherwise specified. Group analysis for AVH revealed activation in the right homologue of Broca's area, bilateral insula, bilateral supramarginal gyri and right superior temporal gyrus. Broca's area and left superior temporal gyrus were not activated. Group analysis for word generation in these patients yielded activation in Broca's and Wernicke's areas and to a lesser degree their right-sided homologues, bilateral insula and anterior cingulate gyri. Lateralization of activity during AVH was not correlated with language lateralization, but rather with the degree to which the content of the hallucinations had a negative emotional valence. The main difference between cerebral activity during AVH and activity during normal inner speech appears to be the lateralization. The predominant engagement of the right inferior frontal area during AVH may be related to the typical low semantic complexity and negative emotional content.

The influence of action intentions on visual selection processes was investigated in a visual search paradigm. A predefined target object with a certain orientation and color was presented among distractors, and subjects had to either look and point at the target or look at and grasp the target. Target selection processes prior to the first saccadic eye movement were modulated by the different action intentions. Specifically, fewer saccades to objects with the wrong orientation were made in the grasping condition than in the pointing condition, whereas the number of saccades to an object with the wrong color was the same in the two conditions. Saccadic latencies were similar under the different task conditions, so the results cannot be explained by a speed-accuracy trade-off. The results suggest that a specific action intention, such as grasping, can enhance visual processing of action-relevant features, such as orientation. Together the findings support the view that visual attention can be best understood as a selection-for-action mechanism.

Auditory verbal hallucinations in patients with a psychotic disorder are consistently preceded by deactivation of the parahippocampal gyrus. The parahippocampus has been hypothesized to play a central role in memory recollection, sending information from the hippocampus to the association areas. Dysfunction of this region could trigger inadequate activation of right language areas during auditory hallucinations.

Recent brain imaging studies provided evidence that the brain areas involved with attentional orienting and the preparation of saccades largely overlap, which may indicate that focusing attention at a specific location can be considered as an unexecuted saccade towards that location (i.e. the premotor theory of attention). Alternatively, it may be proposed that attentional orienting is simply relevant for preparing saccades, but the two processes may also be completely unrelated. In two experiments, we examined temporal activation of brain areas by measuring the electroencephalogram. Central cues indicated the likely side (left or right) at which a to-be-attended target would occur, or to which a saccade had to be prepared. Cue direction-related activity was determined, time-locked to cue onset. In addition, in our second experiment, delayed saccades had to be carried out, which allows to focus on processes strongly related to saccade execution. In nearly all tasks, an early directing attention negativity (EDAN), an anterior directing attention negativity (ADAN), and a late directing attention positivity (LDAP) were observed, time-locked to cue onset. Source analyses supported the view that this activity probably originates from areas within the ventral intraparietal sulcus (vIPS) and the frontal eye fields (FEF). The saccade-locked analysis also indicated that the FEF plays an important role in triggering saccades, but the role of vIPS appears to be minimal. The latter finding disfavors the premotor theory of attention, as it suggests that the relation between attention and action is less direct.

No abstract

Spatial working memory entails the ability to keep spatial information active in working memory over a short period of time. To study the areas of the brain that are involved in spatial working memory, a group of stroke patients was tested with a spatial search task. Patients and healthy controls were asked to search through a number of boxes shown at different locations on a touch-sensitive computer screen in order to find a target object. In subsequent trials, new target objects were hidden in boxes that were previously empty. Within-search errors were made if a participant returned to an already searched box; between-search errors occurred if a participant returned to a box that was already known to contain a target item. The use of a strategy to remember the locations of the target objects was calculated as well. Damage to the right posterior parietal and right dorsolateral prefrontal cortex impaired the ability to keep spatial information 'on-line', as was indicated by performance on the Corsi Block-Tapping task and the within-search errors. Moreover, patients with damage to the right posterior parietal cortex, the right dorsolateral prefrontal cortex and the hippocampal formation bilaterally made more between-search errors, indicating the importance of these areas in maintaining spatial information in working memory over an extended time period.