NeuroImage
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Recent brain imaging studies have shown that the neural substrates underlying the ability to infer and share the feeling of pain of other individuals overlap with the pain matrix that mediates the process of one's own pain. While there has been evidence that the neural activity mediating pain experience is influenced by top-down attention, it remains unclear whether the neural substrates of empathy for pain are modulated by top-down controlled mechanisms. The current work investigated whether the neural correlates of empathic processes of pain are altered by task demand and prior knowledge of stimulus reality. ⋯ However, the neural activities related to pain rating were eliminated when subjects counted the number of hands in the painful stimuli. In addition, the ACC activity associated with empathy for pain was stronger for the pictures than for the cartoons. Our findings indicate that the involvement of the neural substrates underlying pain-related empathy is constrained by top-down attention and contextual reality of stimuli.
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The aim of this study was to differentiate the processing of nociceptive information, matched for pain intensity, from capsaicin-induced hyperalgesic vs. control skin at multiple levels in the trigeminal nociceptive pathway. Using an event-related fMRI approach, 12 male subjects underwent three functional scans beginning 1 h after topical application of capsaicin to a defined location on the maxillary skin, when pain from capsaicin application had completely subsided. Brush and two levels of painful heat (low-Thermal-1 and high-Thermal-2) were applied to the site of capsaicin application and to the mirror image region on the opposite side. ⋯ Thus, trigeminal nociceptive regions showed increased activation in the context of perceptually equal pain levels. Beyond these regions, contrast analyses of capsaicin vs. control skin stimulation indicated significant changes in bilateral dorsolateral prefrontal cortex and amygdala. The involvement of these emotion-related regions suggests that they may be highly sensitive to context, such as prior experience (application of capsaicin) and the specific pain mechanism (hyperalgesic vs. normal skin).
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Whether neural synchronization is engaged in binding of verbal and spatial information in working memory remains unclear. The present study analyzed oscillatory power and phase synchronization of electroencephalography (EEG) recorded from subjects performing a working memory task. ⋯ However, the same effects were not observed in the gamma band. These results suggest that working memory binding involves large-scale neural synchronization at the theta band.
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Following injury and inflammation, pain to light stroking (dynamic mechanical allodynia) might develop at the damaged site (primary area) or in adjacent normal tissue (secondary area). Using fMRI we mapped changes in the spinal trigeminal nucleus (spV), and supraspinal brainstem nuclei following heat/capsaicin-induced primary and secondary dynamic mechanical allodynia in the human trigeminal system. The role of these structures in dynamic mechanical allodynia has not been clarified yet in humans. ⋯ The vlPAG showed decreased activity that inversely correlated with pain ratings during primary allodynia, i.e. the more deactivated the vlPAG the higher the pain intensity (p<0.05, Pearson's correlation). Primary and secondary dynamic mechanical allodynia were also characterized by significant differences involving distinct supraspinal structures mainly involved in pain modulation and including the rostroventromedial medulla, pons reticular formation, dorsolateral PAG, all more active during primary versus secondary allodynia, and the medial reticular formation of the caudal medulla that was more active during secondary versus primary allodynia. These results indicate that the pain modulatory system is involved to a different extent during primary versus secondary mechanical allodynia.
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Cold allodynia, meaning that innocuous cold stimuli become painful, is a characteristic, but enigmatic feature of neuropathic pain. Here, we used functional magnetic resonance imaging (fMRI) and investigated brain activations underlying menthol-induced cold allodynia. 12 healthy volunteers were investigated using a block-design fMRI approach. Firstly, brain activity was measured during application of innocuous cold stimuli (at 5 degrees C above cold pain threshold) and noxious cold stimuli (at 5 degrees C below cold pain threshold) to normal skin of the forearm using a peltier- driven thermostimulator. ⋯ However, comparing cold allodynia and equally intense cold pain conditions, we found significantly increased activations in bilateral dorsolateral prefrontal cortices (DLPFC) and the brainstem (ipsilateral parabrachial nucleus) during cold allodynia. Furthermore, in contrast maps cold allodynia contributed significantly more to activations of the bilateral anterior insula, whereas the contribution to activation of the contralateral posterior insula was equal. It is concluded that cold allodynia activates a network similar to that of normal cold pain but additionally recruits bilateral DLPFC and the midbrain, suggesting that these brain areas are involved in central nociceptive sensitisation processes.