Pain
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The facial expression of pain plays a crucial role in pain communication and pain diagnostics. Despite its importance, it has remained unknown which dimensions of pain (sensory and/or affective) are encoded in the face. To answer this question, we used a well-established cognitive strategy (suggestions) to differentially modulate the sensory and affective dimensions of pain and investigate the effect of this manipulation on facial responses to experimental pain. ⋯ Furthermore, suggestions for either increased pain affect or pain sensation produced selective modulations in facial response patterns, with facial movements around the eyes mostly encoding sensory aspects, whereas movements of the eyebrows and of the upper lip were closely associated with the affective pain dimension. The facial expression of pain is a multidimensional response system that differentially encodes affective and sensory pain qualities. This differential encoding might have evolved to guarantee that the specific characteristics of one's pain experience are facially communicated, thereby ensuring adequate help and support from others.
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Comparative Study
Sex similarities and differences in pain-related periaqueductal gray connectivity.
This study investigated sex similarities and differences in pain-related functional connectivity in 60 healthy subjects. We used functional magnetic resonance imaging and psychophysiological interaction analysis to investigate how exposure to low vs high experimental pain modulates the functional connectivity of the periaqueductal gray (PAG). ⋯ In an extensive literature search, we found that female animals have been largely overlooked when the connections between the PAG and the amygdala have been described, and that women are systematically understudied with regard to endogenous pain inhibition. Our results emphasize the importance of including both male and female subjects when studying basic mechanisms of pain processing, and point toward a possible sex difference in endogenous pain inhibition.
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Menthol is a natural compound of plant origin known to produce cool sensation via the activation of the TRPM8 channel. It is also frequently part of topical analgesic drugs available in a pharmacy, although its mechanism of action is still unknown. Compelling evidence indicates that voltage-gated Na(+) channels are critical for experiencing pain sensation. ⋯ In current clamp recordings, menthol inhibited firing at high-frequency stimulation with minimal effects on normal neuronal activity. We found that low concentrations of menthol cause analgesia in mice, relieving pain produced by a Na(+) channel-targeting toxin. We conclude that menthol is a state-selective blocker of Nav1.8, Nav1.9, and TTX-sensitive Na(+) channels, indicating a role for Na(+) channel blockade in the efficacy of menthol as topical analgesic compound.
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Multiple firing of C nociceptors upon a single electrical stimulus has been suggested to be a possible mechanism contributing to neuropathic pain. Because this phenomenon maybe based on a unidirectional conduction block, it might also be related to neuropathic changes without a direct link to pain. We investigated painful neuropathy patients using microneurography and analysed nociceptors for the occurrence of multiple spiking and spontaneous activity. ⋯ Multiple spiking of nociceptors coincides with spontaneous activity in nociceptors of painful neuropathy patients. We therefore conclude that rather than being a generic sign of neuropathy, multiple spiking is linked to axonal hyperexcitability and spontaneous activity of nociceptors. It is still unclear whether it also is mechanistically related to the clinical pain level.
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Parental responses to children with chronic pain have been shown to influence the extent of the child's functional disability, but these associations have not been well studied in relation to children's pain-related school functioning. The current study tests the hypothesis that parental pain catastrophizing and parental protective responses to child pain influence the extent of school impairment in children with chronic pain. A mediational model was tested to determine whether parental protective behaviors serve a mediating role between parental pain catastrophizing and child school impairment. ⋯ Results show that, controlling for the known influences of pain intensity and child depressive symptoms, parental pain catastrophizing and parental protective responses to child pain each independently predict child school attendance rates and reports of overall school impairment. Parental protectiveness was found to mediate the association between parental cognitions (i.e., parent pain catastrophizing) and child school functioning outcomes. These findings underscore the importance of intervening with parents to foster parental responses to child pain that help children engage and succeed in the school environment despite pain.