Pain
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Chronic central neuropathic pain after central nervous system injuries remains refractory to therapeutic interventions. A novel approach would be to target key intracellular signaling proteins that are known to contribute to continued activation by phosphorylation of kinases, transcription factors, and/or receptors that contribute to changes in membrane excitability. We demonstrate that one signaling kinase, calcium/calmodulin-dependent kinase II (CaMKII), is critical in maintaining aberrant dorsal horn neuron hyperexcitability in the neuropathic pain condition after spinal cord injury (SCI). ⋯ To demonstrate causality, treatment of SCI rats with KN-93, which prevents CaMKII activation, significantly attenuated at-level mechanical allodynia and aberrant wide dynamic range neuronal activity evoked by brush, pressure, and pinch stimuli and a graded series of von Frey stimuli, respectively. Persistent CaMKII activation contributes to chronic central neuropathic pain by mechanisms that involve maintained hyperexcitability of wide dynamic range dorsal horn neurons. Furthermore, targeting key signaling proteins is a novel, useful therapeutic strategy for treating chronic central neuropathic pain.
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Limited research has addressed processes underlying parents' empathic responses to their child's pain. The present study investigated the effects of parental catastrophizing, threatening information about the child's pain, and child pain expression upon parental emotional and behavioral responses to their child's pain. A total of 56 school children participated in a heat pain task consisting of 48 trials while being observed by 1 of their parents. ⋯ The same pattern was found for parental fear-potentiated startle reflex, particularly when the child's facial pain expression was high. In addition, parents who reported high levels of catastrophizing thought about their child's pain engaged, in comparison with low-catastrophizing parents, in more pain-attending talk when they received threatening information. The findings are discussed in the context of affective-motivational theories of pain.
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Patients with borderline personality disorder, mostly female, exhibit severe autoaggressive behavior, namely an intentionally performed, nonsuicidal self-injury and severe blunting of pain perception, the mechanism of which is hitherto not understood. Because the nociceptive system displays a high degree of plasticity, the aim of this study was to analyze the relationship of pain perception to self-injurious behavior. Pain perception of mechanical and chemical noxious stimuli was studied by quantitative sensory testing in 22 patients (15 female, 7 male) with borderline personality disorder (BPD) according to DSM-IV and 22 age- and gender-matched controls. ⋯ Blunting of pain sensation was significantly predicted by the recency of self-injurious behavior (multiple r=0.58). In line with recent data, we suggest an excess of endogenous antinociception in BPD patients resulting from self-inflicted multiple injuries. This exaggerated pain control is conceived to operate via an uncoupling of the evaluative or emotional-affective from the sensory-discriminative dimension of pain.
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A motor unit consists of a motoneurone and the multiple muscle fibres that it innervates, and forms the final neural pathway that influences movement. Discharge of motor units is altered (decreased discharge rate and/or cessation of firing; and increased discharge rate and/or recruitment of new units) during matched-force contractions with pain. This is thought to be mediated by nociceptive (pain) input on motoneurones, as demonstrated in animal studies. ⋯ Discharge rate of motor units decreased during pain (P<.001) and anticipation (P<.01) compared with control contractions. De-recruitment of 1 population of units and new recruitment of another population were observed during both anticipation and pain; some changes in motor unit recruitment persisted after pain ceased. This challenges the fundamental theory that pain-related changes in muscle activity result from direct nociceptor discharge, and provides a mechanism that may underlie long-term changes in movement/chronicity in some musculoskeletal conditions.
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To identify endogenous factors involved in herpetic pain, we performed genome-wide microarray analysis of the spinal cord of mice that suffered from herpetic allodynia induced by inoculation with herpes simplex virus type 1, which revealed marked induction of galectin-3, a β-galactoside-binding lectin. Therefore, we investigated the role of galectin-3 in herpetic allodynia. The expression levels of galectin-3 mRNA and protein were increased with a temporal pattern similar to that of herpetic allodynia. ⋯ Intrathecal injection of galectin-3 produced mechanical allodynia in naive mice, and intrathecal injections of anti-galectin-3 antibodies significantly reduced herpetic allodynia. The present results suggest that galectin-3 in infiltrating macrophages and/or resident microglia in the spinal dorsal horn contributes to herpetic allodynia. Galectin-3 may be a new therapeutic target for the treatment of herpes zoster-associated pain.