Pain
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Neuropathic pain conditions are common after nerve injuries and are suggested to be regulated in part by genetic factors. We have previously demonstrated a strong genetic influence of the rat major histocompatibility complex on development of neuropathic pain behavior after peripheral nerve injury. In order to study if the corresponding human leukocyte antigen complex (HLA) also influences susceptibility to pain, we performed an association study in patients that had undergone surgery for inguinal hernia (n=189). ⋯ This finding was subsequently replicated in the clinical material of patients with lumbar disc herniation (n=258), where carriers of the DQB1*03:02 allele displayed a slower recovery and increased pain. In conclusion, we here for the first time demonstrate that there is an HLA-dependent risk of developing pain after surgery or lumbar disc herniation; mediated by the DRB1*04 - DQB1*03:02 haplotype. Further experimental and clinical studies are needed to fine-map the HLA effect and to address underlying mechanisms.
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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.
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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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Bone cancer pain has a strong impact on the quality of life of patients, but is difficult to treat. Better understanding of the pathogenic mechanisms underlying bone cancer pain will likely lead to the development of more effective treatments. In the present study, we investigated whether inhibition of KCNQ/M channels contributed to the hyperexcitability of primary sensory neurons and to the pathogenesis of bone cancer pain. ⋯ On the contrary, activation of the KCNQ/M channels with retigabine not only inhibited the hyperexcitability of these small DRG neurons, but also alleviated mechanical allodynia and thermal hyperalgesia in bone cancer rats, and all of these effects of retigabine could be blocked by KCNQ/M-channel antagonist XE-991. These results suggest that repression of KCNQ/M channels leads to the hyperexcitability of primary sensory neurons, which in turn causes bone cancer pain. Thus, suppression of KCNQ/M channels in primary DRG neurons plays a crucial role in the development of bone cancer pain.