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1247 December 2013 D EVELOPMENTS in neuroimaging over the past 2 decades have given us remarkable insight into the living human central nervous system. Whether the information is neurochemical, structural, or functional, a range of central nervous system disorders will undoubtedly benefit from an improved scientific understanding of the mechanistic changes that occur in vivo and over time as the condition develops or improves. The next challenge for neuroimaging is to deliver statistically robust information at an individual level, rather than group-averaging neural responses. This allows identified mechanisms with their concomitant neuroimaging markers to be related to your patient and their particular set of symptoms, possibly even providing measures that predict treatment response. The study in this month’s issue by Harris et al.1 moves us forward in understanding individual patient responses to analgesics and highlights how brain imaging can be used to distinguish drug from placebo effects in patients. Acute and chronic pain is one area where dramatic strides in our understanding of mechanisms have occurred. Functional imaging is a powerful tool that allows us to measure how the brain is processing and modulating nociceptive inputs to produce pain perceptions—a “behind the scenes” measure distinct from but obviously related to subjective descriptions of pain—a process that occurs subsequently. The relationship between the underlying neuroimaging measures and subsequent ratings and behavior is by no means a simple one. Many factors contribute to pain ratings, which irrespective of the nociceptive input or even the presence of strong analgesics mean divergences, and more complex relationships can occur between what subjects report and measured regional brain activity.2 This has tremendous value if you are careful with interpretation and do not consider or limit brain imaging as simply a surrogate measure of rating, as is sometimes purported. Other measures, say structural or neurochemical, might also provide clues as to the underlying mechanisms sustaining a chronic pain state or how the condition itself is changing the brain—all have value. One approach to test the clinical relevance of any of these measures is to treat the patient, say pharmacologically, and see how they change relative to definitive-standard clinical measures. However, given the differences in sensitivity of behavioral and neuroimaging measures alongside the complex relationship between brain processing of nociceptive inputs and subjective pain ratings, it is possible that a treatment can change structure, function, or neurochemistry in the absence of a significantly altered pain rating. That likelihood is why I find the study by Harris et al.1 published here so fascinating. Alongside identifying neuroimaging markers that correlate with baseline clinical pain scores and that are modulated by drug but not placebo, they also show results where the scenario just described occurs: that observation raises some interesting questions. Using a small cohort of female patients with fibromyalgia (14 and 17 for different neuroimaging measures) and a double-blind two-period cross-over study of pregabalin (dose escalation to 450 mg/day for 14 days, with maintained fixed dose of 450 mg/day for last 3 days) and placebo (using same regime), neurochemical, brain functional connectivity, and brain activity to pressure pain were collected in four separate imaging visits (preand posttreatment for the two arms) to “Seeing” How Our Drugs Work Brings Translational Added Value