So far we have reviewed nearly 50 infant NIRS studies, many of which fall short of answering the questions that motivated their authors. Findings across studies are remarkably consistent and inconsistent at the same time. They are consistent in finding some channels that are activated by suprathreshold stimuli, but this is hardly surprising – surely there is some region of cortex that responds to just about any stimulus. The most important question one can ask about NIRS findings from infants is: what have we learned that we didn't know already from other measures? That is, what is the “value-added” of NIRS for studies of infant perception, cognition, and language? The answer, unfortunately, is rather modest. Almost all infant NIRS studies are largely confirmatory and fail to clarify the underlying neural mechanism, beyond specifying its regional selectivity.
Consider evidence that NIRS activations show hemisphere lateralization. If brain area X is activated by stimulus Y, and this regional selectivity mirrors what is present in adults, does this imply a similar functional role for area X? The problem with such an interpretation – that there is developmental continuity of regional brain function – is that hemodynamic responses are slow. Thus, they could reflect feed-forward activation (processing the stimulus), feedback activation (sending information from somewhere else), or some combination of the two (comparing inputs and stored representations). One clear way of overcoming this interpretive limitation is to present a stimulus that can only
activate certain NIRS channels because of known anatomical constraints, but this research strategy, as noted earlier, is extremely rare in the literature (see Minagawa-Kawai, Cristia & Dupoux, 2011
, for a developmental theory of lateralization).
A similar concern can be raised about stimulus specificity in a given brain region. Typically conclusions about stimulus specificity are weak – brain area X is activated by stimulus Y but not (or less so) by stimulus Z. But how specific is this pattern of activation – what stimuli other than Y activate area X, and what stimuli other than Z fail to activate area X? Clearly, there is a need to move away from 2-stimulus designs and focus on multiple levels along a particular stimulus dimension to get a better handle on the linking hypothesis between NIRS activation and underlying psychological processes. As noted by Aslin and Fiser (2005)
, when only two levels along a stimulus dimension are used, and one observes an increase (or decrease) in a dependent measure (e.g., NIRS activation), it is often concluded that the relevant NIRS activation indicates a brain region that represents that stimulus dimension. But if so, one would expect a third level along that stimulus dimension to show a further increase (or decrease) in activation. If that does not happen, then it calls into question the validity of the conclusion about what the NIRS activation means. In other words, it may be less important to know whether a given brain area is activated by a stimulus than to know that a change
in a stimulus is correlated with a change
in NIRS activation. This is because the assumption that brain areas are independent is very unlikely, leading to substantial “cross talk” across areas. The challenge here is to understand how these interactions among brain areas are organized, and to differentiate such interactions from measurement errors stemming from systemic hemodynamic responses.
Finally, developmental questions are rarely asked in infant NIRS studies or in any neuroimaging modality (see Karmiloff-Smith, 2010
). Rather, a single age is often the target of a given study, which makes comparisons across studies difficult because of variations in stimuli, testing designs, probe placements, criteria for data rejection, signal processing, and statistical analysis. The best studies begin with robust behavioral evidence that ability X is absent at age 1 and present at age 2. Then one can ask if NIRS activation emerges between age 1 and age 2. If so, then it is seductive to conclude that the emerging NIRS activation mediates that behavioral change. But of course this correlation does not confirm causality. Moreover, if there is no change in neural activation between ages 1 and 2, then it suggests either an insensitive neural measure or a non-localist mechanism responsible for the developmental change.
There is a caveat to the foregoing picture of NIRS as a technique that has so far under-achieved on its promise of revealing brain mechanisms of infant development. One can view neural signals – ERP, MEG, fMRI, NIRS – as merely dependent measures and not as brain-specific per se. If one's goal is to find some measure of detection, discrimination, or learning, and NIRS provides such a reliable signal, then it has potential utility in answering questions about when during development an underlying process is present. Of course, the presence of a neural response does not necessarily imply that it is functional in supporting perception or influencing behavior. A reliable neural signal may be necessary but not sufficient to enable a neural network to rise above some critical threshold required to support behavior. If NIRS signals were more reliably present at a given age than any other dependent measure, and/or NIRS signals were easier to record from infants than these other measures, then it would be a clear win to use NIRS even with weak linking hypotheses between neural signals and behavior.