Several cognitive processes are involved in task-switching. Using a prosaccade/antisaccade paradigm, we manipulated both the interval available for preparation between the cue and the target and the predictability of trial sequences, to isolate the contributions of foreknowledge, an active switching (reconfiguration) process, and passive inhibitory effects persisting from the prior trial. We tested 15 subjects with both a random and a regularly alternating trial sequence. Half of the trials had a short cue-target interval of 200 ms, and half a longer cue-target interval of 2,000 ms. When there was only a short preparatory interval, switching increased the latencies for both prosaccades and antisaccades. With a long preparatory interval, switching was associated with a smaller latency increase for prosaccades and, importantly, a paradoxical reduction in latency for antisaccades. Foreknowledge of a predictable sequence did not allow subjects to reduce switch costs in the manner that a long preparatory cue-target interval did. In the trials with short preparatory intervals, the effects on latency attributable to active reconfiguration processes were similar for prosaccades and antisaccades. We propose a model in which the passive inhibitory effects that persist from the prior saccadic trial are due not to task-set inertia, in which one task-set inhibits the opposite task-set, but to inhibition of the saccadic response-system by the antisaccade task, to account for the paradoxical set-switch benefit for antisaccades at long cue-target intervals. Our findings regarding foreknowledge show that previous studies used to support task-set inertia may have conflated the effects of both active reconfiguration and passive inhibitory processes on latency. While our model of response-system plasticity can explain a number of effects of dominance asymmetry in switching, other models fail to account for the paradoxical set-switch benefit for antisaccades.

It has been hypothesized that social developmental disorders (SDD) like autism, Asperger's disorder and the social-emotional processing disorder may be associated with prosopagnosic-like deficits in face recognition. We studied the ability to recognize famous faces in 24 adults with a variety of SDD diagnoses. We also measured their ability to discriminate changes in internal facial configuration, a perceptual function that is important in face recognition, and their imagery for famous faces, an index of their facial memory stores. We contrasted their performance with both healthy subjects and prosopagnosic patients. We also performed a cluster analysis of the SDD patients. One group of eight SDD subjects performed normally on all tests of face perception and recognition. The other 16 subjects were impaired in recognition, though most were better than prosopagnosic patients. One impaired SDD subgroup had poor perception of facial structure but relatively preserved imagery, resembling prosopagnosic patients with medial occipitotemporal lesions. Another subgroup had better perception than imagery, resembling one prosopagnosic with bilateral anterior temporal lesions. Overall, SDD subgroup membership by face recognition did not correlate with a particular SDD diagnosis or subjective ratings of social impairment. We conclude that the social disturbance in SDD does not invariably lead to impaired face recognition. Abnormal face recognition in some SDD subjects is related to impaired perception of facial structure in a manner suggestive of occipitotemporal dysfunction. Heterogeneity in the perceptual processing of faces may imply pathogenetic heterogeneity, with important implications for genetic and rehabilitative studies of SDD.

The processing of facial identity and that of facial expression are dissociable in social developmental disorders. Deficits in perceiving facial expression may be related to emotional processing more than face processing. Dissociations between the perception of facial identity and facial emotion are consistent with current cognitive models of face processing. The results argue against hypotheses that the social dysfunction in social developmental disorder causes a generalized failure to acquire face-processing skills.

Direct and indirect covert functions likely share similar mechanisms in patients with apperceptive prosopagnosia and may reflect residual activity in anterior and left hemispheric components of the normal face-processing network. However, face priming may be ineffectual in patients with severely degraded facial memories from anterior temporal damage. This may indicate a difference between residual patterns of face-related activity in associative and apperceptive prosopagnosia.