Peer Support for Chronic Pain in Online Health Communities: Quantitative Study on the Dynamics of Social Interactions in a Chronic Pain Forum.

BACKGROUND: Peer support for chronic pain is increasingly taking place on social media via social networking communities. Several theories on the development and maintenance of chronic pain highlight how rumination, catastrophizing, and negative social interactions can contribute to poor health outcomes. However, little is known regarding the role web-based health discussions play in the development of negative versus positive health attitudes relevant to chronic pain. OBJECTIVE: This study aims to investigate how participation in online peer-to-peer support communities influenced pain expressions by examining how the sentiment of user language evolved in response to peer interactions. METHODS: We collected the comment histories of 199 randomly sampled Reddit (Reddit, Inc) users who were active in a popular peer-to-peer chronic pain support community over 10 years. A total of 2 separate natural language processing methods were compared to calculate the sentiment of user comments on the forum (N=73,876). We then modeled the trajectories of users' language sentiment using mixed-effects growth curve modeling and measured the degree to which users affectively synchronized with their peers using bivariate wavelet analysis. RESULTS: In comparison to a shuffled baseline, we found evidence that users entrained their language sentiment to match the language of community members they interacted with (t198=4.02; P<.001; Cohen d=0.40). This synchrony was most apparent in low-frequency sentiment changes unfolding over hundreds of interactions as opposed to reactionary changes occurring from comment to comment (F2,198=17.70; P<.001). We also observed a significant trend in sentiment across all users (ß=-.02; P=.003), with users increasingly using more negative language as they continued to interact with the community. Notably, there was a significant interaction between affective synchrony and community tenure (ß=.02; P=.02), such that greater affective synchrony was associated with negative sentiment trajectories among short-term users and positive sentiment trajectories among long-term users. CONCLUSIONS: Our results are consistent with the social communication model of pain, which describes how social interactions can influence the expression of pain symptoms. The difference in long-term versus short-term affective synchrony observed between community members suggests a process of emotional coregulation and social learning. Participating in health discussions on Reddit appears to be associated with both negative and positive changes in sentiment depending on how individual users interacted with their peers. Thus, in addition to characterizing the sentiment dynamics existing within online chronic pain communities, our work provides insight into the potential benefits and drawbacks of relying on support communities organized on social media platforms.

Understanding Collective Human Behavior in Social Media Networks Via the Dynamical Hypothesis: Applications to Radicalization and Conspiratorial Beliefs.

The dynamical hypothesis has served to explore the ways in which cognitive agents can be understood dynamically and considered dynamical systems. Originally used to explain simple physical systems as a metaphor for cognition (i.e., the Watt governor) and eventually more complex animal systems (e.g., bird flocks), we argue that the dynamical hypothesis is among the most viable approaches to understanding pressing modern-day issues that arise from collective human behavior in online social networks. First, we discuss how the dynamical hypothesis is positioned to describe, predict, and explain the time-evolving nature of complex systems. Next, we adopt an interdisciplinary perspective to describe how online social networks are appropriately understood as dynamical systems. We introduce a dynamical modeling approach to reveal information about emergent properties in social media, where radicalized conspiratorial beliefs arise via coordination between user-level and community-level comments. Lastly, we contrast how the dynamical hypothesis differs from alternatives in explaining collective human behavior in social networks.

Pleasant Deep Pressure: Expanding the Social Touch Hypothesis.

Neuroscientific research on pleasant touch has focused on the C-tactile pathway for gentle stroking and has successfully explained how these sensory fibers transmit information about affective social touch to the brain and induce sensations of pleasantness. The C-tactile social/affective touch hypothesis even proposes that C-tactile fibers form a privileged pathway underlying social touch. However, deep pressure is a type of touch commonly considered pleasant and calming, occurring in hugs, cuddling, and massage. In this paper we introduce a paradigm for studying pleasant deep pressure and propose that it constitutes another important form of social touch. We describe development of the oscillating compression sleeve (OCS) as one approach to administering deep pressure and demonstrate that this touch is perceived as pleasant and calming. Further, we show that deep pressure can be imaged with functional magnetic resonance imaging (MRI) using the air-pressure-driven OCS and that deep pressure activates brain regions highly similar to those that respond to C-tactile stroking, as well as regions not activated by stroking. We propose that deep pressure constitutes another social touch pathway of evolutionary importance signaling the close proximity of conspecifics.

Innocuous pressure sensation requires A-type afferents but not functional ΡΙΕΖΟ2 channels in humans.

The sensation of pressure allows us to feel sustained compression and body strain. While our understanding of cutaneous touch has grown significantly in recent years, how deep tissue sensations are detected remains less clear. Here, we use quantitative sensory evaluations of patients with rare sensory disorders, as well as nerve blocks in typical individuals, to probe the neural and genetic mechanisms for detecting non-painful pressure. We show that the ability to perceive innocuous pressures is lost when myelinated fiber function is experimentally blocked in healthy volunteers and that two patients lacking Aß fibers are strikingly unable to feel innocuous pressures at all. We find that seven individuals with inherited mutations in the mechanoreceptor PIEZO2 gene, who have major deficits in touch and proprioception, are nearly as good at sensing pressure as healthy control subjects. Together, these data support a role for Aß afferents in pressure sensation and suggest the existence of an unknown molecular pathway for its detection.

PIEZO2 mediates injury-induced tactile pain in mice and humans.

Tissue injury and inflammation markedly alter touch perception, making normally innocuous sensations become intensely painful. Although this sensory distortion, known as tactile allodynia, is one of the most common types of pain, the mechanism by which gentle mechanical stimulation becomes unpleasant remains enigmatic. The stretch-gated ion channel PIEZO2 has been shown to mediate light touch, vibration detection, and proprioception. However, the role of this ion channel in nociception and pain has not been resolved. Here, we examined the importance of Piezo2 in the cellular representation of mechanosensation using in vivo imaging in mice. Piezo2-knockout neurons were completely insensitive to gentle dynamic touch but still responded robustly to noxious pinch. During inflammation and after injury, Piezo2 remained essential for detection of gentle mechanical stimuli. We hypothesized that loss of PIEZO2 might eliminate tactile allodynia in humans. Our results show that individuals with loss-of-function mutations in PIEZO2 completely failed to develop sensitization and painful reactions to touch after skin inflammation. These findings provide insight into the basis for tactile allodynia, identify the PIEZO2 mechanoreceptor as an essential mediator of touch under inflammatory conditions, and suggest that this ion channel might be targeted for treating tactile allodynia.