Real-time fMRI applied to pain management

Heather Chapin, Epifanio Bagarinao, Sean Mackey
2012 Neuroscience Letters  
Introduction Modern views conceptualize pain as a brain-based phenomenon [74] [75] [76] . Advances in neuroscience have allowed us to explore how the varieties of pain experience we observe are mediated by the complex relationships between the mind, brain, and body. We have learned that far from activating a single "pain" center in the brain, pain results in widespread activation of multiple cortical and subcortical regions involved in many functions including primary and secondary
more » ... areas (SI, SII), primary motor (MI) and premotor cortices (PMC), supplementary motor area (SMA), basal ganglia, parietal and insular cortices, periaqueductal gray (PAG), rostral ventromedial medulla, hippocampus, amygdala, parahippocampus, anterior cingulate cortex (ACC), and prefrontal cortex (PFC) [108] . Pain experience can be influenced by many cognitive, emotional, and other factors affecting brain function. Indeed, evidence suggests that many of these areas participate in a pain modulatory pathway and can have a significant effect on pain experience [37, 108] . The brain's central role in pain experience is underscored by the growing appreciation that chronic pain involves dysregulation of central pain modulatory systems [82, 86, 107, 122] . A number of studies have revealed that the brains of patients with chronic pain are functionally and structurally altered compared to healthy controls. Alterations in functional connectivity between brain regions have been found in various chronic pain conditions [6, 7, [19] [20] [21] 80 ]. Some of these connectivity changes involve the "default-mode network" [6, 7, 19, 80], a network of areas correlated at rest and thought to be related to internal self-referential processing [48] . Chronic pain has also been associated with structural changes in the brain, showing decreases in gray matter volume in numerous areas including prefrontal cortex [2, 15, 41, 61, 90, 100, 109] , insula [41, 61, 90, 109], brainstem [90, 95], thalamus [2, 96, 100], amygdala [15, 90], ACC [15, 90, 109], posterior cingulate cortex (PCC) [109], cingulate [61], SI [95, 122], MI/PMC [61], posterior parietal cortex [61, 100], superior temporal gyrus [96], and ventral striatum [41]. Chronic pain has also been associated with increases in gray matter volume in prefrontal cortex [96, 100], pregenual ACC [100], basal ganglia [95, 96, 98, 122], cerebellum [96, 122], thalamus [95, 122], inferior frontal gyrus [122], insula [122], brainstem [122], and parahippocampus/hippocampus [98] . While it is difficult to determine the direction of causality with regard to how these changes relate to chronic pain, several recent studies have shown that structural [49, 83, 90, 101] and functional [101] changes were reversible after chronic pain was resolved through successful treatment (e.g., hipreplacement surgery), suggesting that chronic pain leads to these structural changes rather
doi:10.1016/j.neulet.2012.02.076 pmid:22414861 pmcid:PMC3377818 fatcat:zdpepw7rpjbehol6jp7te2oxpe