Pain
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The intensity and submodality of pain are widely attributed to stimulus encoding by peripheral and subcortical spinal/trigeminal portions of the somatosensory nervous system. Consistent with this interpretation are studies of surgically anesthetized animals, demonstrating that relationships between nociceptive stimulation and activation of neurons are similar at subcortical levels of somatosensory projection and within the primary somatosensory cortex (in cytoarchitectural areas 3b and 1 of somatosensory cortex, SI). Such findings have led to characterizations of SI as a network that preserves, rather than transforms, the excitatory drive it receives from subcortical levels. ⋯ These studies demonstrate that an extreme anterior position within SI (area 3a) receives input originating predominantly from unmyelinated nociceptors, distinguishing it from posterior SI (areas 3b and 1), long recognized as receiving input predominantly from myelinated afferents, including nociceptors. Of particular importance, interactions between these subregions during maintained nociceptive stimulation are accompanied by an altered SI response to myelinated and unmyelinated nociceptors. A revised view of pain coding within SI cortex is discussed, and potentially significant clinical implications are emphasized.
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Comparative Study
The effects of prior pain experience on neural correlates of empathy for pain: An fMRI study.
Neuroimaging studies have revealed partially shared neural substrates for both the actual experience of pain and empathy elicited by the pain of others. We examined whether prior pain exposure increased neural activity in the anterior midcingulate cortex (aMCC) and bilateral anterior insula (AI) as a correlate of empathy for pain. Participants (N=64: 32 women, 32 men) viewed pictures displaying exposure to pressure pain (pain pictures) and pictures without any cue of pain (neutral pictures). ⋯ Based on the entire sample, whole brain analyses revealed stronger activation in the retrosplenial cortex, dorsomedial prefrontal cortex, and medial prefrontal cortex in the pain exposure condition. In conclusion, prior pain exposure did not increase, but decreased activity in regions regularly associated with empathy for pain. However, pain experience increased activity in regions associated with memory retrieval, perspective taking, and top-down emotion regulation, which might facilitate empathizing with others.
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Randomized Controlled Trial
Pain as a reward: changing the meaning of pain from negative to positive co-activates opioid and cannabinoid systems.
Pain is a negative emotional experience that is modulated by a variety of psychological factors through different inhibitory systems. For example, endogenous opioids and cannabinoids have been found to be involved in stress and placebo analgesia. Here we show that when the meaning of the pain experience is changed from negative to positive through verbal suggestions, the opioid and cannabinoid systems are co-activated and these, in turn, increase pain tolerance. ⋯ These findings may have a profound impact on clinical practice. For example, postoperative pain, which means healing, can be perceived as less unpleasant than cancer pain, which means death. Therefore, the behavioral and/or pharmacological manipulation of the meaning of pain can represent an effective approach to pain management.
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Multicenter Study
Chronic migraine and chronic tension-type headache are associated with concomitant low back pain: results of the German Headache Consortium study.
The objective of this study was to evaluate the association between low and frequent low back pain and chronic migraine (CM) and chronic tension-type headache (CTTH) in a large, German population-based sample. Headaches were diagnosed according to International Classification of Headache Disorders-2 criteria and categorized according to frequency (episodic 1-14 days/month or chronic ≤15 days/month) and headache type (migraine or TTH). We defined frequent low back pain as self-reported low back pain on ≥15 days/month. ⋯ The odds of having frequent low back pain were between 13.7 (95% CI 7.4-25.3) and 18.3 (95% CI 11.9-28.0) times higher in all chronic headache subtypes when compared to No Headache. Low and frequent low back pain was associated with CM and CTTH. Multiple explanations may contribute to the association of headache and back pain, including the notion that the neurobiology of chronic headache, independent of primary headache type, not only involves the trigeminal pain pathway, but is also a part of abnormal general pain processing.