Attention and Masking in Schizophrenia Laurence Lalanne, André Dufour, Olivier Després, and Anne Giersch Background: Patients with schizophrenia are known to be impaired in masking tasks, but the mechanisms underlying their deficits are still elusive. Our study was intended to examine attentional effects, which have a known impact on masking in healthy volunteers but have only rarely been explored in relation to masking in patients. Methods: We compared focused versus divided attention in 18 control subjects and 18 patients using forward and backward masking tasks. In the conventional masking task, subjects had to locate one target among four possible locations. Presentation of one target allows attention to be focused, in contrast with the divided attention task in which two targets were presented either in the same hemifield or different hemifields. Results: Our results reproduce patients’ deficits in forward and backward masking tasks but only when one target is presented. We show that control subjects benefit from focused attention, much more so than patients. Furthermore, patients’ performance is identical to that of control subjects in backward masking when targets are presented across hemifields. This performance equalization was checked to ensure it was not due solely to the redundancy of signals (two vs. one). We achieved this by comparing performance when two targets were presented in the same vs. across hemifields, the latter yielding a greater redundancy gain. Conclusions: From the results, it is unlikely that redundancy can account for the whole pattern of results, which suggest instead that attention deficits play a role in backward masking impairments in patients. Key Words: Backward masking, divided attention, focused atten- tion, forward masking, redundancy gain, schizophrenia P atients with schizophrenia consistently display deficits in vi- sual masking tasks (1–4). This particular deficit is related nei- ther to intellectual deterioration (5) nor to neuroleptics (6,7). Several authors have proposed that it reflects vulnerability to schizophrenia (8,9) and has an impact on social outcome (10). These results suggest it reveals a key impairment in patients, hence the need to gain a better understanding of its underlying mechanisms and significance. The role of attention has been shown repeatedly in respect of backward masking (11), and attention impairments have been widely described in patients with schizophrenia (12,13). However, the impact of attention on masking paradigms has rarely been explored in patients. In our study, we wished to determine the extent to which patients with schizophrenia were still impaired when their attention could not be focused on a single target, and we controlled for a possible confounding factor, the redundancy gain. In visual masking paradigms, a target (usually a letter or symbol) is presented briefly in quick succession with a mask. The subject is instructed to identify or localize the target, the visibility of which is lessened by the mask. The mask is displayed either before or after the target (forward or backward masking tasks). Mask and target are separated by a stimulus onset asynchrony (SOA), the duration of which is manipulated. Patients with schizophrenia need larger asynchronies between target and mask to reach a performance level equivalent to control subjects (1–4). Mechanisms that are proposed as an explanation for the impairment in patients are derived from theories that account for masking in healthy volun- teers. Masking is a phenomenon traditionally attributed to interac- tions between neural visual channels known as “transient” and “sustained” channels (14 –18). The transient channel responds to stimulation quickly and briefly and conveys information of low spatial and high temporal frequency, that is, transient and global information. In contrast, the sustained channel responds more slowly and to high spatial frequencies and underlies stimulus iden- tification and fine-scale analysis. These systems correspond, respec- tively, to the magnocellular and parvocellular visual pathways and interact in complex ways, depending on the type of masking pro- cedure. Backward masking in healthy volunteers is usually believed to involve both integration and interruption mechanisms. Integra- tion is defined as a fusion between the target and the mask relying on the integration of the sustained activities elicited by both stim- uli, and it occurs primarily at short SOAs (maximal between 0 and 30 msec). Interruption, on the other hand, is believed to occur at lon- ger SOAs (maximal between 50 to 100 msec), when the transient information conveyed by the mask “interrupts” the sustained pro- cessing of the target, thus reducing its visibility (11,14). On this basis, several hypotheses, not mutually exclusive, have been proposed to explain schizophrenia patients’ impairments in backward masking. One influential hypothesis, based on studies that evaluated the detection of low versus high spatial frequency information, suggests a deficit at the level of the transient channel (6,19), which, if impaired, would mean target processing would not be interrupted as efficiently. Consequently, the first stimulus would persist longer and would be merged with the mask via integration mechanisms (20). However, this hypothesis alone may not be enough to explain the entire pattern of deficits observed in patients during masking tasks. Rassovsky et al. (21) used meta- and paracon- trast to show that masking deficits are still observed in patients even when the mask location does not overlap with the target location, such that mask and target cannot be fused in space. Effects observed in metacontrast and paracontrast are explained by “ob- ject substitution,” which might also account for the deficits ob- served in patients. It is a theory based on common views of visual perception, in which object identification requires not only feedfor- From U666 (LL, AG), National Institute for Health and Medical Research; Department of Psychiatry I (LL, AG), University Hospital of Strasbourg; Mixt Unit of Research UMR7237 (AD, OD), National Center for Scientific Research, Laboratory of Imaging and Cognitive Neurosciences, Univer- sity of Strasbourg, Strasbourg, France. Address correspondence to Anne Giersch, M.D., Ph.D., INSERM U666; Centre Hospitalier Régional Universitaire de Strasbourg, Département de Psy- chiatrie I, Hôpital Civil, 1, Place de l’Hôpital, F-67091 Strasbourg, Cedex, France. E-mail: giersch@alsace.u-strasbg.fr. Received May 27, 2011; revised Sep 1, 2011; accepted Sep 10, 2011. BIOL PSYCHIATRY 2012;71:162–168 0006-3223/$36.00 doi:10.1016/j.biopsych.2011.09.018 © 2012 Society of Biological Psychiatry