“Pain Intensity Processing within the Human Brain: A Bilateral, Distributed Mechanism,”

Pain and Neurosensory Mechanisms Branch, National Institutes of Dental Research, National Institutes of Health, Bethesda, Maryland 20892, USA.
Journal of Neurophysiology (Impact Factor: 2.89). 11/1999; 82(4):1934-43.
Source: PubMed


Functional imaging studies of human subjects have identified a diverse assortment of brain areas that are engaged in the processing of pain. Although many of these brain areas are highly interconnected and are engaged in multiple processing roles, each area has been typically considered in isolation. Accordingly, little attention has been given to the global functional organization of brain mechanisms mediating pain processing. In the present investigation, we have combined positron emission tomography with psychophysical assessment of graded painful stimuli to better characterize the multiregional organization of supraspinal pain processing mechanisms and to identify a brain mechanism subserving the processing of pain intensity. Multiple regression analysis revealed statistically reliable relationships between perceived pain intensity and activation of a functionally diverse group of brain regions, including those important in sensation, motor control, affect, and attention. Pain intensity-related activation occurred bilaterally in the cerebellum, putamen, thalamus, insula, anterior cingulate cortex, and secondary somatosensory cortex, contralaterally in the primary somatosensory cortex and supplementary motor area, and ipsilaterally in the ventral premotor area. These results confirm the existence of a highly distributed, bilateral supraspinal mechanism engaged in the processing of pain intensity. The conservation of pain intensity information across multiple, functionally distinct brain areas contrasts sharply with traditional views that sensory-discriminative processing of pain is confined within the somatosensory cortex and can account for the preservation of conscious awareness of pain intensity after extensive cerebral cortical lesions.

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    • ") and is involved in the processing of noxious and innocuous stimuli (Coghill et al., 1999; Davis, 2000; Haase et al., 2009; Kinomuraa et al., 1994) and their subjective appreciation (Brooks et al., 2002). Thus view implies that body awareness and pain perception are interrelated pro- cesses. "
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    ABSTRACT: Although body awareness and pain perception are considered to be parts of the interoceptive system, the relationship between them is unclear. This study examines the association between body awareness and pain habituation, hypothesizing that this association is moderated by pain catastrophizing and mindfulness. Sixty subjects received a mildly aversive electrical stimulus for 60 s, during which they were requested to rate the amount of perceived pain. Complete habituation was indicated by abolition of pain sensation; partial habituation was indicated by a decrease in pain sensation. Individuals who demonstrated complete habituation had lower levels of pain catastrophizing and lower levels of mindfulness. As hypothesized, the association between body awareness and pain habituation was moderated by pain catastrophizing: Among low pain catastrophizers, the higher the body awareness, the stronger the tendency to exhibit complete habituation. Among high pain catastrophizers, the higher the body awareness, the greater the likelihood to present partial habituation.
    Journal of Behavioral Medicine 09/2015; DOI:10.1007/s10865-015-9676-8 · 3.10 Impact Factor
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    • "It is therefore proper to study the brain activity for pain in relation to the stimulus intensity and/or perception magnitudes to functionally differentiate components of the underlying circuitry (Porro et al., 2004). In general, somatosensory cortical areas and anterior cingulate activity seem to track stimulus intensity, whereas lateral prefrontal and posterior parietal regions do not (Bü chel et al., 2002; Coghill et al., 1999; Davis et al., 1997; Peyron et al., 1999). Brain activity related to perceived magnitude of pain is studied less systematically (Baliki et al., 2009; Johnstone et al., 2012; Loggia et al., 2012; Moulton et al., 2012). "
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    ABSTRACT: Recent neuroimaging studies suggest that the brain adapts with pain, as well as imparts risk for developing chronic pain. Within this context, we revisit the concepts for nociception, acute and chronic pain, and negative moods relative to behavior selection. We redefine nociception as the mechanism protecting the organism from injury, while acute pain as failure of avoidant behavior, and a mesolimbic threshold process that gates the transformation of nociceptive activity to conscious pain. Adaptations in this threshold process are envisioned to be critical for development of chronic pain. We deconstruct chronic pain into four distinct phases, each with specific mechanisms, and outline current state of knowledge regarding these mechanisms: the limbic brain imparting risk, and the mesolimbic learning processes reorganizing the neocortex into a chronic pain state. Moreover, pain and negative moods are envisioned as a continuum of aversive behavioral learning, which enhance survival by protecting against threats. Copyright © 2015 Elsevier Inc. All rights reserved.
    Neuron 08/2015; 87(3):474-91. DOI:10.1016/j.neuron.2015.06.005 · 15.05 Impact Factor
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    • "In particular, the anterior cingulate cortex (ACC) and the insula have been found to be activated during attention to pain or expectation of painful stimulation (Peyron et al., 1999; Sawamoto et al., 2000). The ACC is associated with pain affect (Rainville et al., 1997) and subjective pain intensity and unpleasantness (Coghill et al., 1999; Sawamoto et al., 2000), while the insula and the secondary somatosensory cortex (SII) play an important role in the integration of pain for feelings and behavior (Craig, 2002). Especially pain-induced oscillations in the gamma band (>30 Hz), localized in the insula/SII are "
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    ABSTRACT: Attention is an important factor that is able to strongly modulate the experience of pain. In order to differentiate cortical mechanisms underlying subject-driven (i.e., top-down) and stimulus-driven (bottom-up) modes of attentional pain modulation, we recorded electric brain activity in healthy volunteers during painful laser stimulation while spatial attention and stimulus intensity were systematically varied. The subjects' task was to evaluate the pain intensity at the attended finger, while ignoring laser stimuli delivered to the other finger. Top-down (attention) and bottom up (intensity) influences differed in their effects on oscillatory response components. Attention towards pain induced a decrease in alpha and an increase in gamma band power, localized in the insula. Pain intensity modulated delta, alpha, beta and gamma band power. Source localization revealed stimulus driven modulation in the cingulate gyrus (CG) and somatosensory areas for gamma power changes. Our results indicate that bottom-up and top-down modes of processing exert different effects on pain-induced slow and fast oscillatory activities. Future studies may examine pain-induced oscillations using this paradigm to test for altered attentional pain control in patients with chronic pain.
    Frontiers in Human Neuroscience 07/2015; 9:375. DOI:10.3389/fnhum.2015.00375 · 3.63 Impact Factor
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