Abstract

We have learned much about peripheral or spinal mechanism of pain and hyperalgesia, including the role of sodium channel regulation, inflammatory mediators, cytokines, neurotrophins, and TRP channels as well as spinal sensitization and disinhibition.1 However, this knowledge about pain has not been paralleled by success in treatment of chronic pain disorders such as phantom limb pain or complex regional pain syndromes (CRPS). In these patients pain control is difficult, particularly once initial treatments (whether pharmacologic or invasive) have been unsuccessful. When treatment fails we hypothesize alterations in pain memory or centralized pain or may regard the patients' symptoms as functional or hysterical. The use of these terms usually reflects an unsuccessful attempt to disguise our ignorance. Recently, promising results helping to explain chronic pain syndromes have been published. Functional imaging has found that fundamental changes of somatosensory processing in the brain may underlie both phantom limb pain2 and CRPS.3 …

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