The commentaries on our target article have raised important issues about central neuroplasticity and its role in persistent pain states. Some suggest that central neuroplasticity plays nothing more than a minor role in persistent pain, while others argue that persistent pain depends critically on peripheral inputs for its maintenance. Some stress that persistent pain relies to a large extent on changes in the brain and on centrifugal inputs from brain to spinal cord, whereas others argue that it depends on alterations in inhibitory as well as excitatory systems. We attempt to address each of the commentators' points, while defending our position that central neuroplasticity is critical to pathological persistent pain states.