It is generally agreed that considerable amounts of low-level sensory processing of visual stimuli can occur without conscious awareness. On the other hand, the degree of higher-level visual processing that occurs in the absence of awareness is as yet unclear. Here, event-related potential (ERP) measures of brain activity were recorded during a sandwich-masking paradigm, a commonly used approach for attenuating conscious awareness of visual stimulus content. In particular, the present study used a combination of ERP activation contrasts to track both early sensory-processing ERP components and face-specific N170 ERP activations, in trials with versus without awareness. The electrophysiological measures revealed that the sandwich masking abolished the early face-specific N170 neural response (onset at ~170 ms post-stimulus), an effect that paralleled the abolition of awareness of face stimuli. Furthermore, however, the masking appeared to render a strong attenuation of earlier feed-forward visual sensory-processing signals. This early attenuation presumably resulted in insufficient information being fed into the higher level visual system pathways specific to object category processing, thus leading to unawareness of the visual object content. These results support a coupling of visual awareness and neural indices of face processing, while also demonstrating an early low-level mechanism of interference in sandwich masking.
The extent of visual perceptual processing that occurs in the absence of awareness is as yet unclear. Here we examined event-related-potential (ERP) indices of visual and cognitive processes as awareness was manipulated through object-substitution masking (OSM), an awareness-disrupting effect that has been hypothesized to result from the disruption of reentrant signaling to low-level visual cortical areas. In OSM, a visual stimulus array is briefly presented that includes a parafoveal visual target denoted by a cue, typically consisting of several surrounding dots. When the offset of the target-surrounding cue dots are delayed relative to the rest of the array, a striking reduction in the perception of the target image surrounded by the dots is observed. Using faces and houses as the target stimuli, we found that successful OSM reduced or eliminated all the measured electrophysiological indices of visual processing stages after 130 ms post-stimulus. More specifically, when targets were missed within the masked condition (i.e., on trials with effective OSM that disrupted awareness), we observed fully intact early feed-forward processing up through the visual extrastriate P1 ERP component peaking at 100 ms, followed by reduced low-level activity over the occipital pole 130–170 ms post-stimulus, reduced ERP indices of lateralized shifts of attention toward the parafoveal target, reduced object-generic visual processing, abolished object-category-specific (face-specific) processing, and reduced late visual short-term-memory processing activity. The results provide a comprehensive electrophysiological account of the neurocognitive underpinnings of effective OSM of visual-object images, including evidence for central roles of early reentrant signal disruption and inadequate visual attentional deployment.
Recent studies suggest that amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) lie on a single clinical continuum. However, previous neuroimaging studies have found only limited involvement of temporal lobe regions in ALS. To better delineate possible temporal lobe involvement in ALS, the present study aimed to examine changes in functional connectivity across the whole brain, particularly with regard to extra-motor regions, in a group of 64 non-demented ALS patients and 38 healthy controls. To assess between-group differences in connectivity, we computed edge-level statistics across subject-specific graphs derived from resting-state functional MRI data. In addition to expected ALS-related decreases in functional connectivity in motor-related areas, we observed extensive changes in connectivity across the temporo-occipital cortex. Although ALS patients with comorbid FTD were deliberately excluded from this study, the pattern of connectivity alterations closely resembles patterns of cerebral degeneration typically seen in FTD. This evidence for subclinical temporal dysfunction supports the idea of a common pathology in ALS and FTD.
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