Visual masking has been traditionally viewed in terms of the interaction between 2 key visual channels that form the basis for complex visual processing. The 2 channels are known by the anatomically based terms “parvocellular and magnocelluar” pathways or by the functionally based terms “sustained and transient” channels. The parvocelluar pathway has slower tonic responses related to stimulus identification, and the magnocelluar pathway is characterized by faster phasic responses relevant to stimulus onset, offset, and location. The 2 pathways convey visual information in parallel until they reach the level of primary visual cortex. The parvocelluar pathway is thought to provide input predominantly to the ventral “what” visual cortical areas and the magnocelluar pathway predominantly to the dorsal “where” visual cortical areas. According to this model, the parvocellular activity elicited by a stimulus conveys detailed information that is critical for identifying it, and the magnocelluar activity provides more rapid information that is needed to locate it. The visual masking effect can result from disruption of the parvocellular target information by either the magnocelluar or parvocelluar activity elicited by mask, depending on the particular paradigm.1
For example, backward masking through the interruption mechanism can occur when the parvocelluar activity of a target is interrupted by the magnocelluar activity of a mask.
Previous behavioral studies, including our own work, suggested a key role of the magnocelluar pathway in the visual masking deficits in schizophrenia.6,7,25
However, more recent studies of neural mechanisms of visual masking in schizophrenia with brain imaging methodologies present a more complex picture. One prominent theory about visual masking32
proposes that masking occurs when gamma range (30−70 Hz) activity in the parvocelluar pathway is disrupted by a mask. This theory raises the question of whether EEG-assessed gamma activity in schizophrenia is associated with visual masking performance. In 2 studies,12,33
schizophrenia patients showed reduced event-related gamma compared to controls during a backward masking task. They also failed to show a pattern seen in healthy controls of lateralized gamma activity in the right hemisphere. Patients with schizophrenia and controls did, however, show comparable event-related gamma activities when the target was presented without a mask. These findings suggest that aberrant gamma activity is related to visual masking performance in schizophrenia, but it remains unclear whether abnormal gamma activity is a primary cause of the masking impairment.
In a series of imaging studies, we examined the neural correlates of visual masking in schizophrenia with fMRI.34–36
Studies in healthy individuals have implicated the lateral occipital complex (LO) as a key brain area for detection of masked targets.37
For example, in healthy individuals, LO has shown sensitivity to the masking effect: ie, increased activation with increasing duration between target and mask.38
More generally, LO has been linked to object processing. The exact mechanism through which is it is linked to object processing is not known but may be related with the ability to segregate figure from background.39
Recently, we examined neural mechanisms associated with backward masking deficits in schizophrenia, primarily focusing on 3 key visual processing regions of interests (ROIs): LO, the human motion-sensitive area (hMT+) and the retinotopic area.34
We identified 3 key visual processing ROIs using independent functional localizer tasks.40
Among these 3 ROIs, we found sensitivity to the masking effect in both LO and hMT+, but not in the retinotopic areas, meaning that the activation in LO and hMT + increased as the target became more visible. Furthermore, the masking effect was more pronounced in LO than in hMT+, illustrating the expected role of LO in visual masking. Importantly, while both schizophrenia patients and controls showed increased LO activation as the masking effect became weaker, patients showed overall decreased LO activation compared to controls across all the SOAs. Outside the 3 ROIs, both schizophrenia patients and controls showed comparable sensitivity to the masking effect in several regions, including posterior cingulate cortex and inferior parietal lobule. These findings suggest that the blunted activation of LO during visual processing may be the neural basis for the visual masking deficit in schizophrenia. However, the blunting was seen across levels of visibility and so probably contributes to visual processing problems more generally, and not just limited to visual masking. In a separate study, we found that unaffected siblings of schizophrenia patients did not show blunted LO activation.35
Hence, blunted LO activation during a visual masking task might be a disease-specific factor, rather than a vulnerability marker.
In a subsequent study, we used the psychophysiological interaction (PPI) approach to further examine whether schizophrenia patients showed abnormal functional coupling between LO and other brain regions that are associated with visual perception.36
PPI examines how the functional connectivity with an a priori specified region changes in the presence of cognitive or perceptual task demands. We found that, compared to controls, schizophrenia patients showed altered dynamic coupling with LO in several high-level cortical areas including the left precuneus, left inferior frontal, and superior frontal gyri as a function of target visibility in the backward masking task. Note that we did not observe generally reduced coupling with LO in schizophrenia; patients only showed altered coupling with LO as target visibility was manipulated. Patients with schizophrenia, therefore, appeared to have altered (not overall reduced) dynamic coupling between LO and other cortical regions when processing visual information.
One limitation of these studies of fMRI and visual masking is that they all used the same type of target stimuli—a square with a gap on one side. The task was for the subject to identify which side had a gap (see figure 1). Hence, it is not known whether other types of masking paradigms would have yielded the same pattern of results. However, it is reassuring that our findings regarding LO activation during visual masking are consistent with findings from studies with healthy individuals that used more complex visual stimuli.