Pain
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The ability of a painful stimulus to suppress pain in another, remote area (DNIC) has been intensely studied. However, the effect of the distance between the two painful stimuli and the attentional factors during the measurement of pain perception received minimal treatment. We evaluated the effect of these factors on DNIC and on the interaction between DNIC and spatial summation (SS) of pain. ⋯ However, the instruction to summate attenuated DNIC and the DNIC instruction attenuated SS of pain. Attention to the conditioning stimulus induced a stronger DNIC than attention to the test stimulus (p<0.001). We conclude that (1) DNIC and SS of pain appear to be antagonistic processes. (2) DNIC is affected by the distance between two noxious stimuli and to a lesser extent, by attention. (3) The interaction between DNIC, SS and attention is complex and reflects the role of sensory-cognitive integration in pain perception.
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A novel cell-cell signaling by microglial transmembrane TNFα with implications for neuropathic pain.
Neuropathic pain is accompanied by neuroimmune activation in dorsal horn of spinal cord. We have observed that in animal models this activation is characterized by an increased expression of transmembrane tumor necrosis factor α (mTNFα) without the release of soluble tumor necrosis factor α (sTNFα). Herein we report that the pain-related neurotransmitter peptide substance P (SP) increases the expression of mTNFα without the release of sTNFα from primary microglial cells. ⋯ In order to evaluate the biological function of uncleaved mTNFα, we transfected COS-7 cells with a mutant full-length TNFα construct resistant to cleavage by TACE. Coculture of COS-7 cells expressing the mutant TNFα with microglial cells led to microglial cell activation indicated by increased OX42 immunoreactivity and release of macrophage chemoattractant peptide 1 (CCL2) by direct cell-cell contact. These results suggest a novel pathway through which the release of SP by primary afferents activates microglial expression of mTNFα, establishing a feed-forward loop that may contribute to the establishment of chronic pain.
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The conscious perception of somatosensory stimuli is thought to be located in the contralateral cerebral cortex. However, recent human brain imaging investigations in the spinal system report bilateral primary somatosensory cortex (SI) activations during unilateral noxious stimuli and that this ipsilateral spinal representation may be independent of transcallosal connections. In the trigeminal system, there is primate evidence for an ipsilateral somatosensory pathway through the thalamus to the face SI. ⋯ We found that both muscle and cutaneous noxious stimuli, from injections of hypertonic saline into the right masseter or overlying skin, evoked bilateral increases in signal intensity in the region encompassing the ventral posterior thalamus as well as the face region of SI and SII. In contrast, innocuous unilateral brushing of the lower lip evoked a strict contralateral ventroposterior thalamic activation, but bilateral activation of SI and SII. These data indicate that, in contrast to innocuous inputs from the face, noxious information ascends bilaterally to the face SI through the ventroposterior thalamus in humans.
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Co-existing algogenic conditions in two internal organs in the same patient may mutually enhance pain symptoms (viscero-visceral hyperalgesia). The present study assessed this phenomenon in different models of visceral interaction. ⋯ In patients' subgroups, symptoms were also re-assessed after treatment of each condition or after no treatment. (a) CAD+Gs presented more numerous/intense angina/biliary episodes and more referred muscle chest/abdominal hyperalgesia than CAD or Gs; cardiac revascularization or cholecystectomy also reduced biliary or cardiac symptoms, respectively (0.001