Introduction

Despite the many advances in the pathophysiology and treatment of pain, chronic pain still remains elusive to treat. Once the pain problem has exceeded the acute and subacute stage, peripheral factors seem to loose their importance and central changes become much more important (Sandkühler, 2000; Ji et al., 2003). One major factor that seems to contribute to chronicity are memory traces that occur as a consequence of ongoing and/or very intense pain and that are enhanced by learning processes designed to imprint and consolidate these pain-related memory traces. In this chapter we will review the evidence on plastic changes along the neuraxis and their relationship to pain in humans and then delineate treatment approaches that are designed less towards analgesia but more towards reversing maladaptive plasticity with the hypothesis that this would consequently also reduce chronic pain and extinguish pain memories.

Pain and plasticity

Chronic musculoskeletal pain

In the last two decades our understanding of the modifiability of the primary sensory and motor areas of the brain has greatly changed (see Chapters 6–8 of Volume 1). Animal models have shown that long-lasting and/or intense states of pain (e.g., when an inflammation is present) lead to the sensitization of spinal cord neurons (e.g., Sandkühler, 2000) as well as an altered representation of the painful area in the brainstem (Tinazzi et al., 2000), thalamus (Vos et al., 2000) and cortex (Benoist et al., 1999). In chronic pain patients both perceptual and cerebral hyperreactivity to tactile or noxious stimuli have been observed. For example, Kleinböhl et al.