Pain
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Patients with neuropathic pain syndromes are heterogeneous. They present with a variety of sensory symptoms and pain qualities. The knowledge of these data and etiology-specific differences is important to optimize clinical trial design and to develop more effective drugs. ⋯ All subgroups occur in relevant numbers in both entities but the frequencies differ between PHN and DPN. Since sensory symptoms likely translate into pain-generating mechanisms enrichment for potential treatment responders might be possible in clinical trials by assessing the sensory profiles. Patient-Reported Outcomes can be used to obtain a precise sensory characterization of each patient.
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Deep-brain stimulation (DBS) of the posterior hypothalamus has been shown to be clinically effective for drug-resistant chronic cluster headache, but the underlying mechanism is still not understood. The hypothalamus as an important centre of homeostasis is connected among others to the trigeminal system via the trigeminohypothalamic tract. We aimed to elucidate whether hypothalamic stimulation affects thermal sensation and pain perception only in the clinically affected region (the first trigeminal branch) or in other regions as well. ⋯ Short-term interruption of stimulation did not induce any changes in DBS patients. Clinically relevant differences were found neither between non-stimulated cluster headache patients and healthy controls nor between the affected and the non-affected sides in the chronic cluster headache patients without DBS. These results support the notion that neurostimulation of the posterior hypothalamus is specific for cluster headache and only affects certain aspects of pain sensation.
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NMDA receptors, which are implicated in pain processing, are highly expressed in forebrain areas including the anterior cingulate cortex (ACC). The ACC has been implicated in the affective response to noxious stimuli. Using a combination of immunohistochemical staining, Western blot, electrophysiological recording and formalin-induced conditioned place avoidance (F-CPA) rat behavioral model that directly reflects the affective component of pain, the present study examined formalin nociceptive conditioning-induced changes in the expressions of NMDA receptor subunits NR1, NR2A, and NR2B in the rostral ACC (rACC) and its possible functional significance. ⋯ Selectively blocking either NR2A or NR2B subunit in the rACC abolished the acquisition of F-CPA and formalin nociceptive conditioning-induced Fos expression, but it did not affect formalin acute nociceptive behaviors and non-nociceptive fear stimulus-induced CPA. These results suggest that both NMDA receptor subunits NR2A and NR2B in the rACC are critically involved in pain-related aversion. Thus, a new strategy targeted at NMDA NR2A or NR2B subunit might be raised for the prevention of pain-related emotional disturbance.
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Using the chronic constriction injury (CCI) model of neuropathic pain, we profiled gene expression in the rat spinal cord, and identified SIP30 as a gene whose expression was elevated after CCI. SIP30 was previously shown to interact with SNAP25, but whose function was otherwise unknown. We now show that in the spinal cord, SIP30 was present in the dorsal horn laminae where the peripheral nociceptive inputs first synapse, co-localizing with nociception-related neuropeptides CGRP and substance P. ⋯ This neuropathic pain-reducing effect was observed both during neuropathic pain onset following CCI, and after neuropathic pain was fully established, implicating SIP30 involvement in the development and maintenance phases of neuropathic pain. Using a secretion assay in PC12 cells, anti-SIP30 siRNA decreased the total pool of synaptic vesicles available for exocytosis, pointing to a potential function for SIP30. These results suggest a role of SIP30 in the development and maintenance of peripheral nerve injury-induced neuropathic pain.
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Investigated was the relationship between pain catastrophizing and pain intensity in adolescents suffering from chronic pain (n = 38) and the extent to which they expressed communicative pain and pain-related protective behaviours. Adolescents were observed on video performing a 2-Min Walk Test (2MWT). Behaviours were coded on videotape. ⋯ Pain-related protective behaviours did not vary with the adolescents' level of pain catastrophizing, but varied with pain intensity. The findings corroborate the functional distinctiveness of different types of pain behaviours. The results are discussed in terms of the processes linking (1) catastrophizing to communicative pain behaviours and (2) pain to pain-related protective behaviours.