Sometimes, ground-breaking studies don’t get the attention they deserve – even from experts in the field. One great example of this is an elegant study by Nieuwenhuis et al. from CABN in 2003; in it, they conclusively demonstrate why a particular event-related potential – the negative-going frontocentral deflection at around 200ms following stimulus onset, aka the “N2″ – reflects the detection of response conflict, and not the demand to inhibit a response.
This would seem to be a tough distinction to demonstrate – after all, the demand to inhibit something would be expected to strongly covary with response conflict. This is true of the canonical N2 paradigm, the Go/NoGo task, in which an N2 is elicited on infrequent “NoGo” trials in the context of far more-frequent trials that require a response (“Go” trials). Nieuwenhuis et al simply reversed the probabilities – that is, they made the “Go” trials infrequent and “NoGo” trials much more common. In this case, “Go” trials involve conflict between responding and the dominant behavior (which is the act of not responding!), but no response inhibition.
The results demonstrated that the N2 was elicited by the infrequent trial type, regardless of whether it involved stopping a dominant response or merely initiating a response. This consistent with the idea that the N2 reflects the detection of conflict, independent of whether a dominant response must be inhibited. Moreover, source localization techniques identified that the neural generator of the N2 was in the anterior cingulate cortex, regardless of whether it was elicited by infrequent Go or infrequent NoGo trials. The anterior cingulate has been modeled computationally as a conflict monitor, which is conceptually consistent with these observations. This contrasts with other areas, primarily those in the lateral frontal cortex, which are currently thought to be more crucial for response inhibition.
The authors did notice that infrequent NoGo trials elicited a larger N2 than infrequent Go trials – an asymmetry that might suggest the N2 reflects a combination of conflict monitoring and inhibition-related functions. To the contrary, the authors argue that the task instructions to respond as quickly as possible made conflict greater on the infrequent NoGo trials than the infrequent Go trials. This assumption seems all the more plausible given that the source of these two N2s was essentially identical, arguing against some kind of mechanistically distinct function for the two event-related potentials.
Where the paper really shines is in a discussion of how darn sensible this argument really is N2. Just a few examples:
1) If the N2 were responsible for conflict monitoring but not response inhibition, an enhanced N2 would be expected to infrequent trials that involve no overt behavior – indeed, that’s been previously observed.
2) If the N2 were responsible for conflict monitoring but not response inhibition, then a reduced N2 should be observed on trials in which the previous trial was of the same type. This was observed in the current study as well one published previously.
3) If the N2 were responsible for response inhibition, it would be expected to have a source in the lateral prefrontal cortex, rather than the anterior cingulate (which has been associated with primarily evaluative functions in a variety of previous research).
Case closed? Not quite, for unclear reasons. Many of those who cite this study in fact do so while arguing for an inhibitory explanation of the N2 – seemingly unaware that the study they’ve cited refutes their position. This is not a fluke study: the conclusion that the N2 is not specific to response inhibition has also been reached independently, including a 2004 study by Donkers & Boxtel, as well as a 2006 study by Azizian et al. Unless one redefines response inhibition to include all situations in which capacities like conflict monitoring might be necessary, including those where there is no response to inhibit (and what is response inhibition when there’s no response to inhibit?)… it seems pretty inaccurate to consider the N2 as reflecting response inhibition.