Recent advances in human brain imaging techniques offer an exciting opportunity to examine brain processes in experimental and clinical pain conditions. This has allowed insights into neural correlates of pain and led to a much greater understanding of the pain matrix,191,192 which includes brain structures, such as the anterior cingulate cortex (ACC), insula, frontal cortices, S1, second somatosensory cortex (S2), and amygdala.193
Neural correlates of allodynia have been examined in various conditions, including patients with neuropathic pain, central pain, or experimentally provoked allodynia. However, the existing data are controversial with some suggesting that allodynia is processed differently than nociceptive pain and others suggesting they share a common neural basis. Areas shown to be involved in allodynia include the parietal association cortex,194 medial thalamus, putamen, and prefrontal cortex.195 The ACC, which is almost always activated during acute pain in normal subjects and is involved in the affective (cognitive-evaluative) component of pain, has been differentially associated with processing of allodynia.196197, 198,199 This suggests that A-p-mediated pain may have a unique cortical representation in some situations which may aid further understanding of the phenomenon that is tactile allodynia. The amygdala, which plays an important role in fear-conditioning and affective disorders, such as anxiety and depression,200 is activated by a diverse range of persistent nociceptive stimuli in the rat.201, 202 Evidence suggests a role for the amygdala in the affective-emotional pain response in a rodent model of neuropathy involving GABAergic systems.203 The amygdala has also been linked to spontaneous pain in humans suffering from postherpetic neuralgia.204 Such studies highlight the involvement of a number of brain areas in pain responses in neuropathic pain conditions. However, further work using brain imaging techniques is required before our understanding of such systems is complete.
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