In search of a reliable electrophysiological marker of oculomotor inhibition of return

Abstract

Inhibition of return (IOR) operationalizes a behavioral phenomenon characterized by slower responding to cued, relative to uncued, targets. Two independent forms of IOR have been theorized: input-based IOR occurs when the oculomotor system is quiescent, while output-based IOR occurs when the oculomotor system is engaged. EEG studies forbidding eye movements have demonstrated that reductions of target-elicited P1 components are correlated with IOR magnitude, but when eye movements occur, P1 effects bear no relationship to behavior. We expand on this work by adapting the cueing paradigm and recording event-related potentials: IOR is caused by oculomotor responses to central arrows or peripheral onsets and measured by key presses to peripheral targets. Behavioral IOR is observed in both conditions, but P1 reductions are absent in the central arrow condition. By contrast, arrow and peripheral cues enhance Nd, especially over contralateral electrode sites.

Does response selection contribute to inhibition of return?

“…Those rather sensory components are followed by some other phasic differences in the ERP between cued and uncued trials that are not unequivocally bound to a distinct component of the underlying wave shapes, often simply called negative differences (Nd;McDonald et al, 1999). In a previous EEG study, we (Wascher & Tipper, 2004) reported that a right parietal Nd around 310 ms appears to be the component most related with the behavioral manifestation of IOR (see also Satel, Hilchey, Wang, Reiss, & Klein, 2014). The posterior maxima of those effects indicate that they can be assigned to sensory or attentional mechanisms.…”

What Neuroscientific Studies Tell Us about Inhibition of Return

“…When cues and targets were both peripheral stimuli and eye movements were made to cues [44], although P1 effects were still observed, the P1 modulation was not correlated with behavioral IOR, unlike the case when the eye movement system was suppressed in this and in the earlier studies. Furthermore, this P1 cueing effect disappeared entirely when there was no repeated peripheral stimulation (i.e., eye movements were made in response to central arrow cues) [45], even though IOR was still observed behaviorally in response to the peripheral targets. Similarly, when the spatiotopic location was dissociated from the retinotopic location with an eye movement between cue and target, greater behavioral inhibition was observed at the spatiotopic location than at the retinotopic location, however cue-related P1 reductions were only observed in the retinotopic and not in the spatiotopic condition [46].…”

“…When this literature was reviewed by Martin-Arevalo et al [43], it was concluded that there was not one single ERP component that could serve as a "marker" for IOR. Although reduction of the early sensory P1 component was often seen in the literature reviewed by Martin-Arevalo et al [43], P1 reductions are an unlikely reflection of IOR because, as was pointed out by Satel and colleagues [44,45], these modulations can occur without IOR and IOR can occur without P1 reductions.…”

“…However, these Nd effects are even more inconsistent than those related to P1. They are not always present and sometimes go in the 'wrong' direction, suggesting that although something is going on in this time range, the Nd component may not be the most appropriate marker for IOR [45].…”

“…A later ERP component in the 220-300 ms post-cue period, the Nd, is also often modulated by cueing in IOR paradigms [43]. In addition to being observed when eye movements are forbidden and there is repeated peripheral stimulation, Nd modulations have also been observed when eye movements were made in response to central arrow cues [45] and at spatiotopic, but not retinotopic locations when an eye movement occurred between cue and target appearance [46]. However, these Nd effects are even more inconsistent than those related to P1.…”