Pain
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The combination of pain and depression or anxiety is commonly seen in clinical practice. Little is known about the influence of pain on psychopathology over time, as previous studies have been mainly cross-sectional. The objectives of this study are to determine the impact of pain on the course of depressive and/or anxiety disorders, and investigate to what extent the association between pain and course of these mental disorders is mediated by psychiatric characteristics. ⋯ This study shows that patients with pain are more prone to a chronic course of depressive and anxiety disorders. More attention to pain seems to be necessary when diagnosing and treating these disorders. Future research should focus on treatment modalities for this co-occurrence, with joint pain in particular.
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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
Differential effects of experimental central sensitization on the time-course and magnitude of offset analgesia.
Pain perception is temporally altered during states of chronic pain and acute central sensitization; however, the mechanisms contributing to temporal processing of nociceptive information remain poorly understood. Offset analgesia is a phenomenon that reflects the presence of temporal contrast mechanisms for nociceptive information and can provide an end point to study temporal aspects of pain processing. In order to investigate whether offset analgesia is disrupted during sensitized states, 23 healthy volunteers provided real-time continuous visual analogue scale responses to noxious heat stimuli that evoke offset analgesia. ⋯ Increased latencies to maximal offset analgesia and prolonged aftersensations were observed only in the primary regions directly treated by capsaicin-heat or heat alone. However, contrary to the hypothesis that offset analgesia would be reduced following capsaicin-heat sensitization, the magnitude of offset analgesia remained remarkably intact after both capsaicin-heat and heat-only sensitization in zones of both primary and secondary mechanical allodynia. These data indicate that offset analgesia is a robust phenomenon and engages mechanisms that interact minimally with those supporting acute central sensitization.
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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.