Pain
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The Emotional Controls of Nociception (ECON) paradigm involves the presentation of emotionally-charged pictures during which painful stimuli are delivered. Across several ECON studies, unpleasant pictures enhanced pain and nociception, whereas pleasant pictures inhibited pain and nociception. However, at this time it is unknown whether emotional valence (unpleasant, neutral, pleasant) influences the habituation or sensitization of pain responses that occurs within a testing session. ⋯ Mixed effects ANOVAs verified that within-subject changes in pain responses were influenced by stimulus repetition (NFR and SCR habituated, pain ratings sensitized) and emotional valence (responses were highest during unpleasant pictures, intermediate during neutral pictures, and lowest during pleasant pictures). However, habituation/sensitization slopes were unaffected by emotional valence, thus indicating emotional valence modulation was consistently observed throughout the testing session. These results provide additional validation for the ECON paradigm and suggest that the circuit responsible for emotional modulation of pain and nociception is less susceptible to habituation or sensitization than the circuits responsible for responses to suprathreshold shocks.
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Previous studies suggested that areas of the pain matrix of the human brain are recruited by the processing of pain-related environmental cues such as pain-related pictures or descriptors of pain. However, it is still sketchy whether those activations are specific to the pain-relevance of the stimuli or simply reflect a general effect of negative valence or increased arousal. The present study investigates the neural mechanisms underlying the processing of pain-related, negative, positive, and neutral words. ⋯ However, when attention was focused on a foreground task and words were presented in the background (distraction task), we found a decrease in activation within dorsal anterior cingulum (dACC) and a relative increase in activation within the subgenual ventral anterior cingulum (sACC) when processing pain related words compared to other words. Thus, activations to pain-related words are strongly modulated by the attention demands of the task. Most remarkably, the differences in processing pain-related words compared to non-pain-related words are specific to the pain-relevance of the words and cannot simply be explained by their valence or arousal.
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Observing someone else in pain produces a shared emotional experience that predominantly activates brain areas processing the emotional component of pain. Occasionally, however, sensory areas are also activated and there are anecdotal reports of people sharing both the somatic and emotional components of someone else's pain. Here we presented a series of images or short clips depicting noxious events to a large group of normal controls. ⋯ The subjects were scanned while observing static images of noxious events. In contrast with emotional images not containing noxious events the responders activated emotional and sensory brain regions associated with pain while the non-responders activated very little. These findings provide convincing evidence that some people can readily experience both the emotional and sensory components of pain during observation of other's pain resulting in a shared physical pain experience.
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The majority of neuroimaging studies on pain focuses on the study of BOLD activations, and more rarely on deactivations. In this study, in a relatively large cohort of subjects (N=61), we assess (a) the extent of brain activation and deactivation during the application of two different heat pain levels (HIGH and LOW) and (b) the relations between these two directions of fMRI signal change. Furthermore, in a subset of our subjects (N=12), we assess (c) the functional connectivity of pain-activated or -deactivated regions during resting states. ⋯ In contrast to what we observe with the signal increases, the extent of deactivations is greater for LOW than HIGH pain stimuli. The functional dissociation between activated and deactivated networks is further supported by correlational and functional connectivity analyses. Our results illustrate the absence of a linear relationship between pain activations and deactivations, and therefore suggest that these brain signal changes underlie different aspects of the pain experience.
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Extraterritorial spread of sensory symptoms is frequent in carpal tunnel syndrome (CTS). Animal models suggest that this phenomenon may depend on central sensitization. We sought to obtain psychophysical evidence of sensitization in CTS with extraterritorial symptoms spread. ⋯ Proximal spread may represent referred pain. Central sensitization may be secondary to abnormal activity in the median nerve afferents or the consequence of a predisposing trait. Our data may explain the persistence of sensory symptoms after median nerve surgical release and the presence of non-anatomical sensory patterns in neuropathic pain.