Inspired Pain

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Eifert, G. H., and Heffner, M. (2003). The effects of acceptance versus control contexts on avoidance of panic-related symptoms. J. Beh. Ther. Exp. Psychiatry 34, 293–312.

Pain Hustlers | TIME The True Story Behind Pain Hustlers | TIME

Menon, V., and Uddin, L. Q. (2010). Saliency, switching, attention and control: a network model of insula function. Brain Struct. Funct. 214, 655–667. Atlas, L. Y., Bolger, N., Lindquist, M. A., and Wager, T. D. (2010). Brain mediators of predictive cue effects on perceived pain. J. Neurosci. 30, 12964–12977. De Peuter, S., Van Diest, I., Vansteenwegen, D., Van den Bergh, O., and Vlaeyen, J. W. (2011). Understanding fear of pain in chronic pain: interoceptive fear conditioning as a novel approach. Eur. J. Pain 15, 889–894. For centuries, the perception of pain had been conceptualized as a linear read-out of incoming nociceptive information: the more nociceptive information enters the sensory system, the stronger the pain. However, over the recent years numerous studies have demonstrated that pain is substantially influenced by cognitive-affective processes, including motivational factors such as “fear of pain” or the prospect of pain relief. The following section will mainly focus on the influence of fear as one of the most basic motivations but will also highlight recent advances on the influence of social factors as a new, emerging field of research. For a discussion of other, more complex cognitive processes on pain, we refer the reader to two review articles ( Wiech et al., 2008; Wiech and Tracey, 2009). Fear and Anxiety Pain Hustlers began as a 2018 article for the New York Times Magazine by Evan Hughes, chronicling the travails of Insys, founded by billionaire John Kapoor. Insys produced Subsys, the spray described above, which thrived through a "speaker program," in which doctors were paid to spread the gospel of their product to colleagues, essentially giving them money for prescribing a potentially very dangerous drug. Ultimately, in 2020, Kapoor would be sentenced to 66 months in prison for bribing medical practitioners.

Avoiding ‘when, then’ syndrome

But Tower's script takes big dramatic license. For example, none of the characters on screen are strict one-to-one representations of Insys employees. "This isn't the Insys story in detail at all," Yates said. "It's inspired by that—the fringes of that industry and how they exploit one very marginal sector of the healthcare industry and make a fortune out of it." Zubieta, J.-K., and Stohler, C. S. (2009). Neurobiological mechanisms of placebo responses. Ann. N.Y. Acad. Sci. 1156, 198–210. So at first we might start talking about knives and stabbing but then we might start asking who is wielding the knife and after that, why is that person or God wielding the knife. A line of questioning that becomes absurd. Lissek, S. (2012). Toward an account of clinical anxiety predicated on basic, neurally mapped mechanisms of Pavlovian fear-learning: the case for conditioned overgeneralization. Depress. Anxiety 29, 257–264.

Pain and Machine Learning – The Spectator Pain and Machine Learning – The Spectator

Editors select a small number of articles recently published in the journal that they believe will be particularly Research on social influences on pain is still in its infancy but has already proven to add valuable insights into a more comprehensive view on pain [for an excellent overview on motivational and learning aspects of pain communication see Hadjistavropoulos et al. (2011)]. Future studies could aid in understanding the specific neurobiology underlying persistent pain states caused through interpersonal violence (e.g., from torture), which are known to be particularly resistant to treatment. Outlook Despite its long-standing history, research on associative learning and its relevance for chronic pain will remain a topic of interest with many facets. In addition to learning about interoceptive and proprioceptive cues discussed above, associated research lines have, for instance, begun to explore the generalization of fear responses to stimuli that resemble the CS ( Lissek, 2012) or aim at understanding extinction learning to improve therapeutic interventions targeting learned maladaptive responses ( Milad and Quirk, 2012). Pain and Avoidance Learning

Data Availability Statement

Lapate, R. C., Lee, H., Salomons, T. V., Van Reekum, C. M., Greischar, L. L., and Davidson, R. J. (2012). Amygdalar function reflects common individual differences in emotion and pain regulation success. J. Cogn. Neurosci. 24, 148–158.

Bio‐Inspired Multi‐Mode Pain‐Perceptual System (MMPPS (PDF) Bio‐Inspired Multi‐Mode Pain‐Perceptual System (MMPPS

Experimental studies approach avoidance learning by investigating responses to cues that predict the omission or absence of adverse outcome. Neuroimaging studies using this paradigm have shown that avoidance learning critically involves the amygdala ( Schlund and Cataldo, 2010; Prévost et al., 2011). The presentation of cues that signaled the possibility to avoid future money loss or escape from immediate escalating money loss both led to increased activation of this structure ( Schlund and Cataldo, 2010). Although additional brain regions such as the striatum and hippocampus have been implicated in avoidance learning ( Schlund et al., 2011), their role is considerably more controversial.

Li, F.; Gao, S.; Lu, Y.; Asghar, W.; Cao, J.; Hu, C.; Li, R. Bio-Inspired Multi-Mode Pain-Perceptual System (MMPPS) with Noxious Stimuli Warning, Damage Localization, and Enhanced Damage Protection. Adv. Sci. 2021, 8, 2004208. [ Google Scholar] [ CrossRef] [ PubMed] de la Fuente-Fernández, R., Phillips, A. G., Zamburlini, M., Sossi, V., Calne, D. B., Ruth, T. J., et al. (2002). Dopamine release in human ventral striatum and expectation of reward. Behav. Brain Res. 136, 359–363.

Inspired Artificial Receptor Machines | Free Full-Text | Bio-Inspired Artificial Receptor

Craske, M. G., Street, L., and Barlow, D. H. (1989). Instructions to focus upon or distract from internal cues during exposure treatment of agoraphobic avoidance. Behav. Res. Ther. 27, 663–672.

Conflicts of Interest

Ploner, M., Lee, M. C., Wiech, K., Bingel, U., and Tracey, I. (2010). Prestimulus functional connectivity determines pain perception in humans. Proc. Natl. Acad. Sci. U.S.A. 107, 355–360. Although to date research on avoidance behavior has mainly focused on learning, related aspects could aid in understanding the motivational basis of this behavior and its common resistance to extinction. For instance, dispositional inter-individual differences in exploratory behavior that might be determined by personality or genotype could add a relevant piece to the puzzle of understanding and targeting excessive avoidance behavior. Furthermore, contemporary theories on action selection suggest that our behavior is governed by at least two systems, a goal-directed system and a habitual system (see Rangel et al., 2008 for review). Avoidance behavior might require different intervention strategies, depending on the system driving it. If the behavior is goal-directed (or “model-based,” see Daw and Shohamy, 2008 for details), it could be targeted by challenging its underlying beliefs—an approach that is, for instance, indicated when avoidance behavior is driven by exaggerated irrational beliefs. In contrast, if the behavior is habitual, it might subsist despite successful treatment of pain that caused the avoidance behavior. Goal Conflict in the Context of Pain Despite recent advances in this field, additional studies are needed to understand the complex interaction between fear/anxiety and pain processing in more detail. First, a growing number of observations on the role of the (para-)hippocampal formation in pain modulation has to be integrated into the vast body of literature on this structure in fear and anxiety in general. Furthermore, the significance of this structure for pain-related and fear-related disruption of cognitive operations as discussed in the section on the interruptive function of pain warrants further investigation. For instance, a recent study showed that the pain-related disruption of memory encoding was reflected in the hippocampus ( Forkmann et al., 2013), suggesting that this structure is not only a mediator of pain modulation but might also be a target. Although the hippocampus is often considered a single functional entity, there is cumulating evidence suggesting a functional segregation into a dorsal part related to cognitive functions and a ventral part that is involved in emotional processing and stress (for an overview see Fanselow and Dong, 2010) which also show differential functional connectivity patterns under threat ( Satpute et al., 2012). The investigation of the role of both sub-divisions in pain-related fear and anxiety could reveal a more detailed picture of the relevance of the hippocampus in the modulation of pain. Wiech, K., Seymour, B., Kalisch, R., Stephan, K. E., Koltzenburg, M., Driver, J., et al. (2005). Modulation of pain processing in hyperalgesia by cognitive demand. Neuroimage 27, 59–69. But what exactly is the link between the dopaminergic system and (endogenous) analgesia? There is evidence suggesting that dopamine itself might have analgesia properties and might affect nociceptive processing directly (for an overview see Jarcho et al., 2012). Another possibility, however, that has been proposed in the context of placebo analgesia as a form of endogenous pain modulation and that is of particular interest from a motivational perspective is the notion that dopaminergic NAc signal might be involved in the “encoding of the incentive value of the placebo, possibly acting as a gate or permissive system for the formation of placebo effects” ( Scott et al., 2007). The expectation of reward (e.g., pain relief) triggers the release of dopamine in the NAc as the key structure of the ventral striatum. Studies on placebo effects in patients with Parkinson disease have shown that this expectancy-related release of dopamine in the ventral striatum precedes the release of dopamine in the dorsal striatum which leads to the placebo effect in patients with Parkinson disease ( de la Fuente-Fernández et al., 2002). Analogously, NAc dopamine release could drive the release of endogenous opioids, as recently proposed by Fuente-Fernández ( de la Fuente-Fernández, 2009). Although experimental evidence for this pathway is still missing, placebo-induced dopaminergic NAc activity has been found to be positively correlated with the activation of the μ-opioid system in brain regions showing a placebo effect ( Scott et al., 2008). Given the correlative nature of this finding, it is, however, difficult to discern whether the release of dopamine preceded or followed the release of opioids.