Just reading this new paper by Lucina Uddin and felt like a quick post. It is a nice review of one of my favorite brain networks, the ever present insular cortex and ‘salience network’ (thalamus, AIC, MCC). As we all know AIC activation is one of the most ubiquitous in our field and generally shows up in everything. Uddin advances the well-supported idea that in addition to being sensitive to visceral, autonomic, bodily states (and also having a causal influence on them), the network responds generally to salient stimuli (like oddballs) across all sensory modalities. We already knew this but a thought leaped to my mind; what is the order of causation here? If the AIC responds to and causes arousal spikes, are oddball responses driven by the novelty of the stimuli or by a first order evoked response in the body? Your brainstem, spinal cord, and PNS are fully capable of creating visceral responses to unexpected stimuli. How can we dissociate ‘dry’ oddball responses from evoked physiological responses? It seems likely that arousal spikes accompany anything unexpected and that salience itself doesn’t really dissociate AIC responses from a more general role of bodily awareness. Recent studies show that oddballs evoke pupil dilation, which is related to arousal.
Check out this figure:
Clearly AIC and ACC not only receive physiological input but also can directly cause phsyio outputs. I’m immediately reminded of an excellent review by Markus Ullsperger and colleagues, where they run into a similar issue trying to work out how arousal cues contribute to conscious error awareness. Ultimately Ullsperger et al conclude that we can’t really dissociate whether arousal cues cause error awareness or error-awareness causes arousal spikes. This seems to also be true for a general salience account.
How can we tease these apart? It seems like we’d need to somehow both knock out and cause physiological responses during the presence and absence of salient stimuli. I’m not sure how we could do this – maybe de-afferentiated patients could get us part of the way there. But a larger problem looms also: the majority of findings cited by Uddin (and to a lesser extent Ullsperger) come from fMRI. Indeed, the original Seeley et al “salience network” paper (one of the top 10 most cited papers in neuroscience) and the original Critchley insula-interoception papers (also a top ten paper) is based on fMRI. Given that these areas are also heavily contaminated by pulse and respiration artifacts, how can we work out the causal loop between salience/perception and arousal? If a salient cue causes a pulse spike then it might also cause a corresponding BOLD artifact. It might be that there is a particularly non-artefactual relationship between salient things and arousal but currently we can’t seem to work out the direction of causation. Worse, it is possible the process driving the artifacts themselves are crucial for ‘salience’ computation, which would mean physio-correction would obscure these important relationships! A tough cookie indeed. Lastly, we’ll need to go beyond the somewhat psychological label of ‘salience’ if we really want to work out these issues. For my money, I think an account based on expected precision fits nicely with the pattern of results we see in these areas, providing a computational mechanism for ‘salience’.
In the end I suspect this is going be one for the direct recording people to solve. If you’ve got access to insula implantees, let me know! 😀
Note: folks on twitter said they’d like to see more of the cuff posts – here you go! This post was written in a flurry of thought in about 30 minutes, so please excuse any snarfs!