Pharmacological plasticity associated with neuropathic pain states

TL;DRAbstract

Chronic pain is a major clinical problem with considerable impact on the quality of life. There is much evidence for plasticity of somatosensory processing in chronic pain states which contributes to variations in the duration, intensity, physiology and pharmacology of these conditions. Brain mapping with positron emission tomography in experimental human studies of pain [1] suggests that different brain areas subserve different components of pain experience [2] and that distinct somatosensory pathways and CNS areas underlie experimental pathophysiological touch evoked pain (allodynia) and physiological pain [3]. The pathology associated with chronic pain states often leads to alterations in both peripheral and central pain systems, with vast implications for the treatment of these conditions. Conventional analgesics, such as the opioids, can have reduced effectiveness in some chronic pain states, in particular some neuropathic pains. The diversity of maladaptive plasticity within peri

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