The discovery of neuroplastic phenomena such as central sensitization of nociception has challenged pain theory to evolve, to encompass unpredictable and unlikely chronic pain states, and to cope with the emerging complexity of the brain. Recently, the proposition that chronic pain is a disease in its own right has gained currency, based upon functional and structural changes in the brain constituting a distinctive pathology. Proponents have expanded the theory to identify "eudynia" ("good" pain) and "maldynia" ("bad" pain).A critical examination of the proposition that chronic pain is a disease was conducted within the framework of evolution of pain medicine theory.Three dominant theories were identified: specificity theory (the "hard-wired" nervous system); neuroplasticity theory (the "soft-wired" nervous system); and pain-as-a-disease. The progression from specificity theory to neuroplasticity theory was based upon empirical evidence and conceptual clarity. The latter theory confronts the uncertainty and the unpredictability of pain, and offers explanations for conditions where ongoing noxious input is not discernible. However, not only does pain-as-a-disease elevate the neurophysiological mechanisms underlying the experience of chronic pain to the status of a disease, but also it conceives of pain as a "thing" that is itself capable of producing an effect. This reasoning is found to be faulty on two grounds: the confusion of pain as a symptom, a cause, and a pathology; and the fallacy that can arise when an interpretation is claimed to be a truth.The proposition that chronic pain is a disease cannot be supported on clinical and pathological grounds, as well as in terms of ways of knowing. The promulgation of "good" and "bad" pain has the potential to obstruct necessary dialogue for advancing the science and treatment of pain. We suggest a way forward to resolve this impasse.