Patient-reported pain location is diagnostically decisive for some presentations and nearly uninformative for others. The prevailing account treats this as one gradient of diagnostic utility set by anatomical complexity. That explanation conflates three epistemically distinct failures, each with its own mathematics, its own optimal instrument, and its own public-health consequence. In anatomical multiplexing, many structures share one location: a non-identifiable inverse problem. In delocalized amplification - clinically, central sensitization or nociplastic pain - a centrally driven pain-behaviour pattern replaces the peripheral generator: a change of generative model. In referred and atypical displacement, location is hypothesized to shift in a systematic, person-dependent way: a group-conditional bias whose direct evidence is still open. The three are one Bayesian inference problem failing at different nodes - the likelihood, the model class, and the group-conditional prior - with a fourth node at the report itself. The formal development is in a companion paper; this paper states what each model shows and what follows clinically. Re-examination finds that the published "high-utility" accuracy band leans on overstated specificity (Lipton et al., 2003; Bruyninckx et al., 2008; Devillé et al., 2000), so the gradient is real but flatter than drawn. The well-evidenced finding that better detection alone does not improve outcomes when treatment uptake lags is about the care pathway, not perception - a distinction the three-way split makes visible and a single utility number hides. The paper organizes the failures along a why-location-fails axis, distinct from the nociceptive/neuropathic/nociplastic taxonomy (Kosek et al., 2016), and sets out the study that would test the one prediction still open.

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