New Developments in the Understanding and Management of Persistent Pain

Herta Flor PhD


Curr Opin Psychiatry. 2012;25(2):109-113. 

In This Article

Central Changes Related to Learning and Pain

The increase or decrease of sensory input into the brain leads to adaptive changes in the primary sensory and motor areas. For example, in patients with amputations, the map in primary sensorimotor cortex changes in such a manner that input from neighboring areas occupies the region that formerly received input from the now amputated limb.[9] Interestingly, reorganizational changes were only found in amputees with phantom limb pain after amputation but not in amputees without pain. This suggests that nociceptive input may contribute to the changes observed and that the persisting pain might also be a consequence of the plastic changes that occur. Similar observations were made in patients with complex regional pain syndrome.[10•] In addition to functional changes, structural changes have also been related to chronic pain. For example, Gustin et al.[11••] showed gray matter volume reductions in the primary somatosensory cortex, anterior insula, putamen, nucleus accumbens, and thalamus, whereas gray matter volume was increased in the posterior insula in patients with trigeminal neuropathic pain but not in those with temporomandibular disorders. Furthermore, in trigeminal neuropathy patients, magnetic resonance spectroscopy revealed a significant reduction in the N-acetylaspartate/creatine ratio, a biochemical marker of neural viability, in the region of thalamic volume loss. Structural changes have been documented in many types of chronic pain,[12•] but the specificity and the underlying mechanisms have not yet been explored. It has, however, been shown that they change with successful treatment.[13••] Connectivity of large-scale brain networks is also altered in chronic pain and has been associated with pain symptoms.[14•]

But also increased behaviorally relevant input related to nonneuropathic pain leads to changes in the cortical map and other brain regions. This might underlie the changes in functional and structural plasticity seen in many musculoskeletal pain disorders. For example, Diesch and Flor[15] documented changes in primary somatosensory cortex as a consequence of Pavlovian conditioning with painful stimuli. More recent evidence has focused on the affective and cognitive processing of pain and how this might be altered in chronic pain. Spontaneous fluctuations in chronic pain were found to be associated with increased prefrontal activation in chronic pain patients; and it was also shown that chronic pain alters the motivational value of pain; in that chronic pain patients do not attribute the same value to the cessation of acute pain as healthy controls do (cf.[16,17••]). Eck et al.[18•] showed that the mere imagination of painrelated words activated brain regions involved in the affective processing of pain. However, many of the brain activations seen may not be specific for pain but may rather be involved in saliency detection and multisensory processing.[19••,20•]


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