Podcasts about nociception

**Alert! The name of this podcast is changing on June 4th! Be sure to subscribe so you don't miss the announcement. Be sure to subscribe to the newsletter!**Pain is real. Ignore it at your own peril. Think of it as your check engine light. While pain is not a good parameter for how much damage has happened, it does play a role in helping you assess how dangerous the situation is.Boots Knighton and her physical therapist, Ann Alton, take you through a 40-minute lesson on pain, the brain's role in pain perception and recovery. They compare different types of pain, from broken legs to open-heart surgery, emphasizing the brain's influence and the importance of context. Ann shares her journey from chronic pain to becoming a pain neuroscience expert. They discuss the importance of clear medical explanations, the impact of emotional scars, and the brain's ability to rewire for healing. Ann highlights the need for patient-provider teamwork and in order to address healthcare biases.Ann also walks us through how pain involves the whole body and all systems. Nociception is the perception of pain. Areas of the brain used to determine pain are: sensory cortex, somatosensory cortex, anterior cingulate cortex, insular cortex, prefrontal, visual, thalamus, cerebellum, and premotor motor. Big thanks to Ann Alton for spending time with Boots today and in the clinic to help her navigate healing from a tib/fib spiral fracture!00:00 Experiencing chronic pain led to becoming a physical therapist, inspired by pain neuroscience.03:58 Pain is an alarm system, not a measure of damage.09:30 Pain perception is based on context and prior experience.11:36 Chronic body issues trigger brain's perceived danger, intervention options.13:52 Pain perception is subjective; varies based on individual experience and expectations.18:10 Extra nerve endings and inflammation signal danger to brain, causing concern and irritation.22:44 Bias in medical system affects care for diverse patients. Research based on white men overlooks differences in care needs.26:24 Practitioners struggle to keep up with new information and must learn independently.29:57 Our brain helps us evaluate and visualize situations for appropriate action and memory recall.34:01 Understanding and clarity bring relief.35:19 Seek help for understanding medical information, simplify explanations.How to connect with BootsThe Heart Chamber - A podcast for heart patients (theheartchamberpodcast.com)Email: Boots@theheartchamberpodcast.comInstagram: @theheartchamberpodcast or @boots.knightonLinkedIn: linkedin.com/in/boots-knightonIf you enjoyed this episode, take a minute and share it with someone you know who will find value in it as well. You can share directly from this platform or send them to:The Heart Chamber - A podcast for heart patients (theheartchamberpodcast.com)

Welcome to The Nonlinear Library, where we use Text-to-Speech software to convert the best writing from the Rationalist and EA communities into audio. This is: Research summary: The evolution of nociception in arthropods, published by abrahamrowe on April 17, 2024 on The Effective Altruism Forum. This post is a short summary of A long-read draft assembly of the Chinese mantis (Mantodea: Mantidae: Tenodera sinensis) genome reveals patterns of ion channel gain and loss across Arthropoda, a peer-reviewed, open-access publication in G3: Genes | Genomes | Genetics under a CC BY license. The paper and supplemental information can be accessed here. The original paper was written by Jay Goldberg, R. Keating Godfrey, and Meghan Barrett; the research conducted in the paper was funded by Rethink Priorities as part of our research agenda on understanding the welfare of insects on farms. This post was written by Abraham Rowe and reviewed for accuracy by Jay Goldberg and Meghan Barrett. All information is derived from the Goldberg et al. (2024) publication unless otherwise cited, and some text from the original publication is directly adapted for this summary. Introduction Mantids that engage in sexually cannibalistic behaviors (e.g., where the female eats the male during copulation) are often cited as a pinnacle example of insects' lack of pain sensation and, therefore, sentience. In their seminal paper on insect sentience, Eisemann et al.'s ( 1984) Do insects feel pain? - A biological view, the authors cite the fact that male mantids continue to mate while being cannibalized as a behavioral indicator of a lack of pain sensation in insects more broadly ( Eisemann et al. 1984). This behavior suggests that male mantids might not even be able to sense, and thus respond reflexively to, the noxious mechanical damage that occurs during the copulatory experience. One mechanism by which animals can sense mechanical damage is through nociceptive ion channels, proteins found in their peripheral sensory neurons. At the time of Eisemann et al.'s publication, insects were not known to have nociceptive ion channels (a fact they also discuss). It has now been determined that many arthropods (including insects) have nociceptors that perceive chemical, mechanical, and thermal injuries. Indeed, many of their nociceptive ion channels are homologous to mammalian channels (homologous, meaning that the genes for these channels were inherited from a common ancestor to both mammals and insects). However, whether mantids have these ion channels - thus presenting a challenge to the 'peripheral sensory perception' part of the Eisemann argument against insect pain as demonstrated by male mantid behavior - is not known. Genes can be gained and lost across species. Finding evidence of the presence or absence of these channels in the genome of a sexually cannibalistic mantid species would be an important first step to understanding the weaknesses or strengths of Eisemann et al.'s claims about how we might interpret their behavior. Further, by looking at the genes of arthropods across families, we can assess how nociception may have evolved in insects and possibly begin to understand why there is a variance in nociceptive ion channel expression across the arthropods. This understanding might help us identify what kinds of noxious stimuli are perceived negatively by different insect species in the future as, for instance, some other animals are known to lack certain categories of nociceptors (e.g., cold nociception is lacking in some fish species; Sneddon 2019). Additionally, gene copy number (how many copies of that gene the species has in its genome) can also play a role in the strength of their response to a noxious stimulus ( Jang et al., 2023; in Drosophila melanogaster). Determining gene copy number could eventually lead us to understand the high degree of variance in response to noxious stimuli among insects. Of course, in all cases, surveying genetic data is on...

1-2% of the world's population have red hair. So, we're giving the phenomenon its own episode! Today, we discuss the gene/protein that causes red hair, as well as its psychological and possible medical effects... Sources for this episode: Bryant, NIH Research Matters (2021), Study finds link between red hair and pain threshold (online) (Accessed 12/01/2024). Gradwohl, S. C., Aranake, A., Abdallah, A. B., McNair, P., Lin, N., Fritz, B. A., Villafranca, A., Glick, D., Jacobsohn, E., Mashour, G. A. and Avidan, M. S. (2015), Intraoperative awareness risk, anesthetic sensitivity, and anesthetic management for patients with natural red hair: a matched cohort study. Canadian Journal of Anesthesia 62: 345 355. Massachusetts General Hospital, Science Daily (2021), Research reveals why redheads have different pain thresholds (online) (Accessed 12/01/2024). Regan, K. O. (2014), “Red hair in popular culture and the relationship with anxiety and depression”. Thesis submitted for University College, Cork. Rees, J. L. (2000), The Melanocortin 1 Receptor (MC1R): More Than Just Red Hair. Pigment Cell Research 13: 135-140. Robinson, K. C., Kemény, L. V., Fell, G. L., Hermann, A. L., Allouche J., Ding, W., Yekkirala, A., Hsiao, J. J., Su, M. Y., Theodosakis, N., Kozak, G., Takeuchi, Y., Shen, S., Berenyi, A., Mao, J., Woolf, C. J. and Fisher, D. E. (2021), Reduced MC4R signalling alters nociceptive thresholds associated with red hair. Science Advances 7: eabd1310. Author unknown, Wikipedia (date unknown), Nociception (online) (Accessed 12/01/2024). Author unknown, Worldometer (date unknown), World Population Clock: 8.1 Billion People (LIVE, 2024) (online) (Accessed 11/01/2024).

A lot of things have changed since we started the Healing Pain Podcast five years ago. From our conversations with leading names in the pain management and related fields, we have gone down the rabbit hole of no return, exposing us to the wide, wonderful, and in many ways, untamed world of pain science. What exactly is pain science? There is a lot to unpack about this concept, and we're excited to announce that that is going to be the focus of this podcast moving forward. In this episode, Dr. Joe Tatta, PT, DPT, announces the rebrand from Healing Pain Podcast to Pain Science Education Podcast. He explains the rationale behind the move and the new direction this whole initiative is taking. Exciting things are on the horizon starting this year, and it all starts here. Tune in!   Love the show? Subscribe, rate, review, and share! Here's How »   Join the Healing Pain Podcast Community today: integrativepainscienceinstitute.com Healing Pain Podcast Facebook Healing Pain Podcast Twitter Healing Pain Podcast YouTube Healing Pain Podcast LinkedIn Healing Pain Podcast Instagram

Follow us-https://linktr.ee/metalmaniacsmi Follow The boys-https://linktr.ee/Nociception The Metal Maniacs Podcast: Episode 16 - Unleashing Michigan's Death Metal Titans, Nociception Are you ready to plunge headfirst into the world of unrelenting death metal? Welcome back to the Metal Maniacs Podcast, your go-to destination for all things heavy, brutal, and ear-shattering! I'm your host, Jay Ingersoll, alongside my metal connoisseur co-host, the one and only Nick Modd. Today, we have a treat that's bound to leave you headbanging for days - an exclusive interview with Jared and Dylan from the Michigan Death Metal giants, Nociception! In this electrifying sixteenth episode, we're diving deep into the dark and heavy world of Nociception. We'll share some laughs, discuss their upcoming record, unravel the mysteries behind the band's name, and get to know the men responsible for delivering a sonic assault on our eardrums. **Meet the Titans: Jared and Dylan from Nociception** Nociception, hailing from the metal-rich state of Michigan, is a band that's been relentlessly pushing the boundaries of death metal. With an uncompromising sound that's as heavy as it gets, Nociception is here to bring the pain. In our exclusive interview, we'll get up close and personal with Jared and Dylan, the masterminds behind this powerhouse of a band. They'll take us on a journey through their musical influences, their beginnings, and their unwavering commitment to delivering face-melting death metal. **Demystifying the Name: Nociception** First things first, we dive into the mystery of the band's name, Nociception. We'll learn how to correctly pronounce it and the meaning behind this enigmatic moniker. Nociception isn't just another word; it's a representation of the raw intensity and aggression that defines their music. We'll also discuss the band's evolution and how they've crafted their unique sound. Whether you're already a fan or just getting acquainted, you'll gain a deeper understanding of what makes Nociception's brand of death metal so spine-tingling. **Upcoming Record: A Symphony of Brutality** One of the most exciting parts of our conversation is the inside scoop on Nociception's upcoming record. Jared and Dylan give us a sneak peek into the creative process, the themes explored in the album, and what fans can expect from this brutal release. We'll dive into the recording process, the challenges they faced, and the collaboration that went into creating what promises to be a death metal masterpiece. Prepare to be enthralled by the passion and dedication that goes into crafting music that's as heavy as a ton of bricks. The bond of brotherhood and their shared love for the darkest corners of metal come to life as we explore their journey from humble beginnings to becoming a force to be reckoned with in the Michigan metal scene. Their story is one of passion, perseverance, and a relentless pursuit of sonic destruction. **Beyond the Studio: Shows and Live Performances** Nociception doesn't just exist in the recording studio; they come alive on stage. Jared and Dylan take us behind the scenes of their live performances, discussing the energy they bring to the stage and the sheer power of their live shows. We'll also get the lowdown on the shows they're booking and working on, giving you a glimpse into what's on the horizon for Nociception. Subscribe to the Metal Maniacs Podcast on your favorite podcast platform and follow us on social media to stay updated on all things metal. The world of Nociception and the Metal Maniacs community await you, so subscribe and follow now! It's time to unleash the darkness, it's time to get brutal, and it's time to dive headfirst into the world of Nociception with Jared and Dylan. Don't miss out on this epic metal experience - subscribe, follow, and join us in celebrating the raw power of death metal.

Are you ready to challenge everything you thought you knew about pain treatment with our special guest, Lars Avemarie. As a physiotherapist hailing from Denmark, Lars is walking the talk daily with patients in his clinical practice.Join us as we unravel Lars' unique journey, the complexities of pain, and the implications of traditional physiotherapy practices.You will hear Lars breaks down the intricate world of pain management, exposing the therapeutic illusion and the oversimplification of cause and effect in treatments. Together, we'll explore the detrimental impacts of these misconceptions and the power of a holistic approach.   Lars shares his perspectives on the interplay of biological, psychological, and social elements in pain treatment. Toward the end of our discussion,  we dive into the world of pain education and therapeutic alliances. You will want to listen close as Lars emphasizes the importance of a co-constructive approach and shares cutting-edge techniques like narrative-based approaches, motivational interviewing, and acceptance and commitment principles. Finally, learn about Lars' ongoing work and how you can keep a pulse on his groundbreaking research. Embark on this journey with us and let's redefine the narrative about pain together.***LINKS***Lars website Nociception necessary for pain? - Lars' blog Pain neuroscience education is dead.  Long live pain education - Lars' blogThe biggest error - Lars' blog*********************************************************************

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.31.551339v1?rss=1 Authors: Patel, A. A., Cardona, A., Cox, D. N. Abstract: Metazoans detect and differentiate between innocuous (non-painful) and/or noxious (harmful) environmental cues using primary sensory neurons, which serve as the first node in a neural network that computes stimulus specific behaviors to either navigate away from injury-causing conditions or to perform protective behaviors that mitigate extensive injury. The ability of an animal to detect and respond to various sensory stimuli depends upon molecular diversity in the primary sensors and the underlying neural circuitry responsible for the relevant behavioral action selection. Recent studies in Drosophila larvae have revealed that somatosensory class III multidendritic (CIII md) neurons function as multimodal sensors regulating distinct behavioral responses to innocuous mechanical and nociceptive thermal stimuli. Recent advances in circuit bases of behavior have identified and functionally validated Drosophila larval somatosensory circuitry involved in innocuous (mechanical) and noxious (heat and mechanical) cues. However, central processing of cold nociceptive cues remained unexplored. We implicate multisensory integrators (Basins), premotor (Down-and-Back) and projection (A09e and TePns) neurons as neural substrates required for cold-evoked behavioral and calcium responses. Neural silencing of cell types downstream of CIII md neurons led to significant reductions in cold-evoked behaviors and neural co-activation of CIII md neurons plus additional cell types facilitated larval contraction (CT) responses. We further demonstrate that optogenetic activation of CIII md neurons evokes calcium increases in these neurons. Collectively, we demonstrate how Drosophila larvae process cold stimuli through functionally diverse somatosensory circuitry responsible for generating stimulus specific behaviors. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

“I experience your wounds as if they were my own,” reads the last line of Clint Smith's poem “Nociception.” Directed to a child, it explains that just as a sea creature that loses an appendage feels discomfort across its entire body, so does a parent whose child is in pain. The poem is part of Smith's new collection “Above Ground,” which also celebrates the joy, wonder and even occasional absurdity of being a parent. We talk to Smith about his poetry and what he calls the “simultaneity the human experience:” our capacity to hold fear and anxiety alongside joy and awe. This segment originally aired April 11, 2023. Guests: Clint Smith, poet and staff writer, The Atlantic - his new collection of poetry is "Above Ground." His previous books include "How the Word is Passed."

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.14.536947v1?rss=1 Authors: Kollmansperger, S., Anders, M., Werner, J., Saller, A. M., Weiss, L., Suess, S. C., Reiser, J., Schusser, B., Baumgartner, C., Schneider, G., Fenzl, T. Abstract: Chicken culling is forbidden in Germany since 2022, male/female selection and male elimination must be brought to an embryonic status prior to the onset of nociception. The present study evaluated the ontogenetic point when noxious stimuli potentially could be perceived/processed in the brain in ovo. EEG-recordings from randomized hyperpallial brain sites were recorded in ovo and noxious stimuli were applied. Temporal and spectral analyses of the EEG were performed. The onset of physiological neuronal signals could be determined at developmental day 13. ERP/ERSP/ITC analysis did not reveal phase-locked nociceptive responses. Although no central nociceptive responses were documented, adequate EEG- responses to noxious stimuli from other brain areas cannot be excluded. The extreme stress impact on the embryo during the recording may overwrite the perception of noniceptive stimuli. The results suggest developmental day 13 as the earliest embryonal stage being able to receive and process nociceptive stimuli. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

“I experience your wounds as if they were my own,” reads the last line of Clint Smith's poem “Nociception.” Directed to a child, it explains that just as a sea creature that loses an appendage feels discomfort across its entire body, so does a parent whose child is in pain. The poem is part of Smith's new collection “Above Ground,” which also celebrates the joy, wonder and even occasional absurdity of being a parent. We talk to Smith about his poetry and what he calls the “simultaneity of the human experience:” our capacity to hold fear and anxiety alongside joy and awe. Guests: Clint Smith, poet and staff writer, The Atlantic - His new collection of poetry is "Above Ground." His previous books include "How the Word is Passed."

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.22.533230v1?rss=1 Authors: Smith, J., Ji, Y., Lorsung, R., Breault, M., Koening, J., Cramer, N. P., Masri, R., Keller, A. Abstract: The parabrachial nuclear complex is a nexus for aversion, and for the sensory and affective components of pain perception. We have previously shown that, during chronic pain, parabrachial neurons in anesthetized rodents have amplified activity. We report a method to record from parabrachial neurons of behaving, head-restrained mice, while applying reproducible noxious stimuli. We find that both spontaneous and evoked activity are considerably higher in awake animals. We show that these neurons can be rapidly conditioned to respond to innocuous stimuli, after pairing these with nociceptive stimuli. In both males and females with neuropathic or inflammatory pain, responses of parabrachial neurons remain amplified for at least 6 weeks, in parallel with increased pain metrics. Fiber photometry of calcium responses from CGRP-expressing parabrachial neurons in male mice demonstrate that they respond to nociceptive stimuli, and that their responses are amplified in inflammatory pain. In contrast, in females these neurons evoke smaller responses at baseline, and only small increases in neuropathic pain. This sex difference may relate to our finding that, in females, a small percentage of neurons expresses CGRP. Finally, we show that changes in parabrachial activity are correlated with changes in arousal, measured as changes in pupil diameter. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.18.533004v1?rss=1 Authors: Raut, N. G., Maile, L. A., Oswalt, L. M., Mitxelena, I., Adlakha, A., Sprague, K. L., Rupert, A. R., Bokros, L., Hofmann, M. C., Patritti-Cram, J., Rizvi, T. A., Queme, L. F., Choi, K., Ratner, N., Jankowski, M. P. Abstract: Pain of unknown etiology is frequent in individuals with the tumor predisposition syndrome Neurofibromatosis 1 (NF1), even when tumors are absent. Schwann cells (SC) were recently shown to play roles in nociceptive processing, and we find that chemogenetic activation of SCs is sufficient to induce afferent and behavioral mechanical hypersensitivity in mice. In mouse models, animals show afferent and behavioral hypersensitivity when SC, but not neurons, lack Nf1. Importantly, hypersensitivity corresponds with SC-specific upregulation of mRNA encoding glial cell line derived neurotrophic factor (GDNF), independent of the presence of tumors. Neuropathic pain-like behaviors in the NF1 mice were inhibited by either chemogenetic silencing of SC calcium or by systemic delivery of GDNF targeting antibodies. Together, these findings suggest that Nf1 loss in SCs causes mechanical pain by influencing adjacent neurons and, data may identify cell-specific treatment strategies to ameliorate pain in individuals with NF1. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.02.526866v1?rss=1 Authors: Bustin, K. A., Shishikura, K., Chen, I., Lin, Z., McNight, N., Chang, Y., Wang, X., Pei, L., Lin, J. J., Arellano, E., Morton, P. D., Gregus, A. M., Buczynski, M. W., Matthews, M. L. Abstract: Chemical platforms that facilitate both the identification and elucidation of new areas for therapeutic development are necessary but lacking. Activity-based protein profiling (ABPP) leverages active site-directed chemical probes as target discovery tools that resolve activity from expression and immediately marry the targets identified with lead compounds for drug design. However, this approach has traditionally focused on predictable and intrinsic enzyme functionality. Here, we applied our activity-based proteomics discovery platform to map non-encoded and post-translationally acquired enzyme functionalities (e.g. cofactors) in vivo using chemical probes that exploit the nucleophilic hydrazine pharmacophores found in a classic antidepressant drug (e.g. phenelzine, Nardil (R)). We show the probes are in vivo active and can map proteome-wide tissue-specific target engagement of the drug. In addition to engaging targets (flavoenzymes monoamine oxidase A/B) that are associated with the known therapeutic mechanism as well as several other members of the flavoenzyme family, the probes captured the previously discovered N-terminal glyoxylyl (Glox) group of Secernin-3 (SCRN3) in vivo through a divergent mechanism, indicating this functional feature has biochemical activity in the brain. SCRN3 protein is ubiquitously expressed in the brain, yet gene expression is regulated by inflammatory stimuli. In an inflammatory pain mouse model, behavioral assessment of nociception showed Scrn3 male knockout mice selectively exhibited impaired thermal nociceptive sensitivity. Our study provides a guided workflow to entangle molecular (off)targets and pharmacological mechanisms for therapeutic development. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

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How does language and logic impact the management and experience of chronic pain? Asaf Weisman, PT, Phd(c), joins Dr. Joe Tatta on the Healing Pain Podcast to discuss this topic. Asaf is a physical therapist, a PhD candidate, and a lab manager of the Spinal Research Laboratory at Tel Aviv University. He has 20 years of clinical experience as a full-time musculoskeletal physical therapist and studies musculoskeletal medicine, spinal health, as well as chronic pain. He discusses how language impacts pain, unpacks the positive and the negative aspects of cognitive approaches to chronic pain, and shares his thoughts around some of the more popular pain neuroscience analogies or metaphors and how they may not be so acceptable to people living with pain. Most crucially, he clearly defines pain as an experience and its relation to nociception. Tune in for more!

In session 101 Lorimer Moseley stated "Nociception is neither sufficient nor necessary for pain" There was a good deal of pushback on social media regarding this and Asaf Weisman has stepped up to discuss why that is. Jack and Asaf discuss nociception from an evolutionary stand point and why this is important, they then go on to discuss the brain centric nature of research. Its a complex evolving conversation and one thing everyone can agree on is definitions need to be agreed upon! Sponsored by rehabmypatient.com get 3 months free exercise prescription and virtual appointment software HERE

En episodios anteriores sobre los desórdenes de conciencia, hablábamos de la conciencia desde la filosofía y la neurociencia. También en otro episodio, introdujimos los diferentes desórdenes de conciencia, sus características y diferencias fundamentales. Sin lugar a dudas, la clave dentro de la valoración de estos desórdenes de conciencia está en la capacidad de dar un pronóstico de recuperación y, embebido en ello, la capacidad de detectar cambios de transición entre la vigilia sin respuesta y el estado de mínima conciencia. Es importante conocer ciertas escalas y pruebas que se realizan para valorar distintos aspectos que están relacionados con la conciencia y con la transición entre, por ejemplo, una vigilia sin respuesta a una mínima conciencia. Podemos distinguir dos tipos de valoraciones: las valoraciones clínicas, que se pueden realizar a pie de cama, que básicamente sistematizan las respuestas a distintos estímulos o respuestas espontáneas; y por otro lado las valoraciones neurofisiológicas que tratan de valorar el sustrato de la conciencia que permite comprender las respuestas comportamentales de los pacientes. Referencias del episodio: 1. Cuadernos FEDACE sobre daño cerebral adquirido: síndrome de vigilia sin respuesta y de mínima conciencia (2011) (https://fedace.org/files/MSCFEDACE/2016-10/17-19-28-40.admin.13_vigilia_conciencia.pdf). 2. Giacino JT, Kalmar K, Whyte J. The JFK Coma Recovery Scale-Revised: measurement characteristics and diagnostic utility. Arch Phys Med Rehabil. 2004 (https://pubmed.ncbi.nlm.nih.gov/15605342/). 3. Manual de la CRS-R (Coma Recovery Scale-Revised) (https://www.tbims.org/combi/crs/CRS%20Syllabus.pdf). 4. Noé E, Olaya J, Navarro MD, Noguera P, Colomer C, García-Panach J, Rivero S, Moliner B, Ferri J. Behavioral recovery in disorders of consciousness: a prospective study with the Spanish version of the Coma Recovery Scale-Revised. Arch Phys Med Rehabil. 2012 (https://pubmed.ncbi.nlm.nih.gov/22277244/). 5. Schnakers C, Vanhaudenhuyse A, Giacino J, Ventura M, Boly M, Majerus S, Moonen G, Laureys S. Diagnostic accuracy of the vegetative and minimally conscious state: clinical consensus versus standardized neurobehavioral assessment. BMC Neurol. 2009 (https://pubmed.ncbi.nlm.nih.gov/19622138/). 6. Shiel A, Horn SA, Wilson BA, Watson MJ, Campbell MJ, McLellan DL. The Wessex Head Injury Matrix (WHIM) main scale: a preliminary report on a scale to assess and monitor patient recovery after severe head injury. Clin Rehabil. 2000 (https://pubmed.ncbi.nlm.nih.gov/10945425/). 7. Turner-Stokes L, Bassett P, Rose H, Ashford S, Thu A. Serial measurement of Wessex Head Injury Matrix in the diagnosis of patients in vegetative and minimally conscious states: a cohort analysis. BMJ Open. 2015 (https://pubmed.ncbi.nlm.nih.gov/25900459/). 8. Zasler ND, Formisano R, Aloisi M. Pain in Persons with Disorders of Consciousness. Brain Sci. 2022 (https://pubmed.ncbi.nlm.nih.gov/35326257/). 9. Rossi Sebastiano D, Varotto G, Sattin D, Franceschetti S. EEG Assessment in Patients With Disorders of Consciousness: Aims, Advantages, Limits, and Pitfalls. Front Neurol. 2021 (https://pubmed.ncbi.nlm.nih.gov/33868153/). 10. Pruvost-Robieux E, Marchi A, Martinelli I, Bouchereau E, Gavaret M. Evoked and Event-Related Potentials as Biomarkers of Consciousness State and Recovery. J Clin Neurophysiol. 2022 (https://pubmed.ncbi.nlm.nih.gov/34474424/). 11. Kondziella D y cols. European Academy of Neurology guideline on the diagnosis of coma and other disorders of consciousness. Eur J Neurol. 2020 (https://pubmed.ncbi.nlm.nih.gov/32090418/). 12. Formisano R, Contrada M, Aloisi M, Ferri G, Schiattone S, Iosa M, Buzzi MG. Nociception Coma Scale with personalized painful stimulation versus standard stimulus in non-communicative patients with disorders of consciousness. Neuropsychol Rehabil. 2020 (https://pubmed.ncbi.nlm.nih.gov/31088203/). 13. Formisano R, Aloisi M, Iosa M, Contrada M, Rizza F, Sattin D, Leonardi M, D'Ippolito M. A new tool to assess responsiveness in disorders of consciousness (DoC): a preliminary study on the Brief Post-Coma Scale (BPCS). Neurol Sci. 2018 (https://pubmed.ncbi.nlm.nih.gov/29948469/). 14. Cortese MD, Arcuri F, Nemirovsky IE, Lucca LF, Tonin P, Soddu A, Riganello F. Nociceptive Response Is a Possible Marker of Evolution in the Level of Consciousness in Unresponsive Wakefulness Syndrome Patients. Front Neurosci. 2021 (https://pubmed.ncbi.nlm.nih.gov/34975378/). 15. Chatelle C, Thibaut A, Bruno MA, Boly M, Bernard C, Hustinx R, Schnakers C, Laureys S. Nociception coma scale-revised scores correlate with metabolism in the anterior cingulate cortex. Neurorehabil Neural Repair. 2014 (https://pubmed.ncbi.nlm.nih.gov/24065132/). 16. Chatelle C, Thibaut A, Whyte J, De Val MD, Laureys S, Schnakers C. Pain issues in disorders of consciousness. Brain Inj. 2014 (https://pubmed.ncbi.nlm.nih.gov/25099024/). 17. Lin K, Wroten M. Ranchos Los Amigos. 2021 (https://pubmed.ncbi.nlm.nih.gov/28846341/). 18. American Congress of Rehabilitation Medicine, Brain Injury-Interdisciplinary Special Interest Group, Disorders of Consciousness Task Force, Seel RT y cols. Assessment scales for disorders of consciousness: evidence-based recommendations for clinical practice and research. Arch Phys Med Rehabil. 2010 (https://pubmed.ncbi.nlm.nih.gov/21112421/). 19. Disorder of Consciousness & Cognitive Recovery Following TBI Levels 1-10 with Dr. Alan Weintraub (Craig Hospital) (https://www.youtube.com/watch?v=ZWJUfSWYppM&t=2516s&ab_channel=CraigHospital).

Asaf Weisman is a clinical physiotherapist currently doing a PhD in artificial intelligence and computer vision. He has a particular interest in nociception and pain theory. Evie and Asaf had this discussion following an interview with Lorimer Moseley by Jack Chew on The Physio Matters Podcast. You can watch that interview here https://youtu.be/xUBA7qQJ6vk Asaf responds to some points made by Lorimer in the TPMP interview, and we discuss more broadly the topics of nociception, pain science and the treatment of chronic pain by physiotherapists.

From the archives, audio from webinar on Pain is Really Strange on 30 Mar 2022. You can also view as a video podcastThere is an epidemic of pain - huge studies in Europe and USA consistently indicate 1 in 5 people regularly experience moderate to severe persistent pain. It often feels helpless and overwhelming living with pain. This podcast will introduce some models from the latest pain science that have helped many people shift their pain experience. Learning to explore your pain story and learning to find safety in movement and feeling are simple practical tools. The podcast discusses the complexity of pain and some myths around pain. 

References Dr Guerra's Neuroscience lecture notes --- Send in a voice message: https://anchor.fm/dr-daniel-j-guerra/message

Dr. Trites explains how most people don't know the cause of their pain or what continues to cause pain

Alaa Abd Elsayed, MD on Nociception and Physiology - The CME experience for this Podcast is powered by CMEfy - click here to reflect and unlock credits & more: https://earnc.me/1HrheI IPA Pain Management Board Review Course- Dr. Rosenblum presents his friend and colleague, co-founder of the International Pain Academy, Alaa Abd Elsayed, MD.  In this podcast, Dr. Elsayed Dallas 2022 Lecture on the anatomy and physiology of nociception, Dr. Elsayed covers high yield testable material, sample multiple choice questions and pain management board preparation strategies... Subscribe to the International Pain Academy's Newsletter http://eepurl.com/gcRCbz Upcoming Events... NRAP's Blocks and Brunch Ultrasound CME Workshop- NYC July 10th, 2022  Advanced Ultrasound Guided Injection Training Workshop! Lock in Your Spot Today! Register Now! ASPN's Annual Conference- July 14th-17th, 2022! American Society of Pain and Neuroscience Annual Conference is organized by ASPN and will be held from July 14th-17th, 2022 at the Loew's Hotel in Miami Beach, FL.   Get Your Tickets to ASPN's Annual Conference Today! Register Now! NYNJ-PS 2022 Annual Symposium- Nov. 3rd-6th, 2022! NYSIPP/ NJSIPP's Annual Pain Medicine Symposium Come and join us in New Jersey in November | NYNJ-PS 2022  Save the Date! Nov. 3rd-6th, 2022 Get Your Tickets Today! Register Now!   Clarius Discount! Click on the following link and you can enter your credit card info, billing and shipping and your code (DARO) for 20% off! https://store.clarius.com/collections/accessories/products/package-2-in-1-charging-station-hd Podcast Resources: -David Rosenblum, M.D. -Alaa Abd Elsayed, M.D., MPH, FASA New Updates- New 1 on 1 Training Service! New Hospital and Medical Network Group Training Program! Exclusive Dr/Medical Professional affiliate program! Leverage Your Social Network! PainExam "Complete" Complete CME Course now available! Subscribe to the PainExam mailing list * indicates required Email Address * Download the PainExam Official Apps for Android and IOS Devices! https://play.google.com/store/apps/details?id=com.painexam.android.painexam&hl=en_US https://apps.apple.com/us/app/the-pain-management-review/id997396714 Follow PainExam- https://painexam.com/blog/ https://www.facebook.com/PainExam/ https://twitter.com/painexams https://www.instagram.com/painexam/ https://www.linkedin.com/company/painexam https://www.pinterest.com/painexam https://www.youtube.com/user/DocRosenblum/videos

Alaa Abd Elsayed, MD on Nociception and Physiology - The CME experience for this Podcast is powered by CMEfy - click here to reflect and unlock credits & more: https://earnc.me/1HrheI IPA Pain Management Board Review Course- Dr. Rosenblum presents his friend and colleague, co-founder of the International Pain Academy, Alaa Abd Elsayed, MD.  In this podcast, Dr. Elsayed Dallas 2022 Lecture on the anatomy and physiology of nociception, Dr. Elsayed covers high yield testable material, sample multiple choice questions and pain management board preparation strategies... Subscribe to the International Pain Academy's Newsletter http://eepurl.com/gcRCbz Upcoming Events... NRAP's Blocks and Brunch Ultrasound CME Workshop- NYC July 10th, 2022  Advanced Ultrasound Guided Injection Training Workshop! Lock in Your Spot Today! Register Now! ASPN's Annual Conference- July 14th-17th, 2022! American Society of Pain and Neuroscience Annual Conference is organized by ASPN and will be held from July 14th-17th, 2022 at the Loew's Hotel in Miami Beach, FL.   Get Your Tickets to ASPN's Annual Conference Today! Register Now! NYNJ-PS 2022 Annual Symposium- Nov. 3rd-6th, 2022! NYSIPP/ NJSIPP's Annual Pain Medicine Symposium Come and join us in New Jersey in November | NYNJ-PS 2022  Save the Date! Nov. 3rd-6th, 2022 Get Your Tickets Today! Register Now!   Clarius Discount! Click on the following link and you can enter your credit card info, billing and shipping and your code (DARO) for 20% off! https://store.clarius.com/collections/accessories/products/package-2-in-1-charging-station-hd Podcast Resources: -David Rosenblum, M.D. -Alaa Abd Elsayed, M.D. New Updates- New 1 on 1 Training Service! New Hospital and Medical Network Group Training Program! Exclusive Dr/Medical Professional affiliate program! Leverage Your Social Network! PainExam "Complete" Complete CME Course now available! Subscribe to the AnesthesiaExam mailing list! * indicates required Email Address * Download the PainExam Official Apps for Android and IOS Devices! https://play.google.com/store/apps/details?id=com.painexam.android.painexam&hl=en_US https://apps.apple.com/us/app/the-pain-management-review/id997396714 Follow PainExam- https://painexam.com/blog/ https://www.facebook.com/PainExam/ https://twitter.com/painexams https://www.instagram.com/painexam/ https://www.linkedin.com/company/painexam https://www.pinterest.com/painexam https://www.youtube.com/user/DocRosenblum/videos

Alaa Abd Elsayed, MD on Nociception and Physiology - The CME experience for this Podcast is powered by CMEfy - click here to reflect and unlock credits & more: https://earnc.me/1HrheI   IPA Pain Management Board Review Course- Dr. Rosenblum presents his friend and colleague, co-founder of the International Pain Academy, Alaa Abd Elsayed, MD.  In this podcast, Dr. Elsayed Dallas 2022 Lecture on the anatomy and physiology of nociception, Dr. Elsayed covers high yield testable material, sample multiple choice questions and pain management board preparation strategies... Subscribe to the International Pain Academy's Newsletter http://eepurl.com/gcRCbz Upcoming Events... NRAP's Blocks and Brunch Ultrasound CME Workshop- NYC July 10th, 2022  Advanced Ultrasound Guided Injection Training Workshop! Lock in Your Spot Today! Register Now! ASPN's Annual Conference- July 14th-17th, 2022! American Society of Pain and Neuroscience Annual Conference is organized by ASPN and will be held from July 14th-17th, 2022 at the Loew's Hotel in Miami Beach, FL.   Get Your Tickets to ASPN's Annual Conference Today! Register Now! NYNJ-PS 2022 Annual Symposium- Nov. 3rd-6th, 2022! NYSIPP/ NJSIPP's Annual Pain Medicine Symposium Come and join us in New Jersey in November | NYNJ-PS 2022  Save the Date! Nov. 3rd-6th, 2022 Get Your Tickets Today! Register Now!   Clarius Discount! Click on the following link and you can enter your credit card info, billing and shipping and your code (DARO) for 20% off! https://store.clarius.com/collections/accessories/products/package-2-in-1-charging-station-hd Podcast Resources: -David Rosenblum, M.D. -Alaa Abd Elsayed, MD New Updates- New 1 on 1 Training Service! New Hospital and Medical Network Group Training Program! Exclusive Dr/Medical Professional affiliate program! Leverage Your Social Network! PainExam "Complete" Complete CME Course now available! Subscribe to the PMRExam mailing list for Free Board Prep Material & More! * indicates required Email Address * Email Format html text Download the PainExam Official Apps for Android and IOS Devices! https://play.google.com/store/apps/details?id=com.painexam.android.painexam&hl=en_US https://apps.apple.com/us/app/the-pain-management-review/id997396714 Follow PainExam- https://painexam.com/blog/ https://www.facebook.com/PainExam/ https://twitter.com/painexams https://www.instagram.com/painexam/ https://www.linkedin.com/company/painexam https://www.pinterest.com/painexam https://www.youtube.com/user/DocRosenblum/videos

From Theresa Mallick-Searle, MS, PMGT-BC, ANP-BC, this episode presents a discussion of the various nonpharmacologic approaches that are available for pain management. Listen as Ms Mallick-Searle provides an overview of the available nonpharmacologic approaches to pain management, including details on cognitive behavioral therapy, hypnosis, patient education, and physical therapy. In this concise podcast, practitioners can gain valuable clinical pearls on how to incorporate a multidisciplinary, nonpharmacologic approach for their patients with chronic pain.This activity is supported by an independent educational grant from the Opioid Analgesic REMS Program Companies. Please seehttps://bit.ly/3mgrfb9 for a listing of REMS Program Companies. This activity is intended to be fully compliant with the Opioid Analgesic REMS education requirements issued by the FDA.Provided by Clinical Care Options, LLC, and in partnership with the American Academy of Physical Medicine and Rehabilitation, Practicing Clinicians Exchange, and ProCE.Link to full program:https://bit.ly/3mcDHsi

"Precision anesthesia [...] where we can give patients the anesthetic and the doses that they require on a patient specific basis" This piece looks at nociception, the neural processes of encoding and processing "noxious" stimuli. By monitoring this anesthetic practitioners can deploy a level of precision not previously possible. Regular listeners may wish to refer back to previous podcasts on this subject: EBPOM LIVE from London | Pain monitoring - with Frank Overdyk, Professor of Anaesthesiology, Charleston, South Carolina: https://www.topmedtalk.com/11813-2/ TopMedTalks to … | Dan Longrois on nociception: https://www.topmedtalk.com/topmedtalks-to-dan-longrois-on-nociception/ Presented by Desiree Chappell and Monty Mythen with their guest Anil Hormis, Professor, Consultant in anesthesia and Critical Care Medicine, Rotherham NHS Foundation Trust.

"Precision anesthesia [...] where we can give patients the anesthetic and the doses that they require on a patient specific basis" This piece looks at nociception, the neural processes of encoding and processing "noxious" stimuli. By monitoring this anesthetic practitioners can deploy a level of precision not previously possible. Regular listeners may wish to refer back to previous podcasts on this subject: EBPOM LIVE from London | Pain monitoring - with Frank Overdyk, Professor of Anaesthesiology, Charleston, South Carolina: https://www.topmedtalk.com/11813-2/ TopMedTalks to … | Dan Longrois on nociception: https://www.topmedtalk.com/topmedtalks-to-dan-longrois-on-nociception/ Presented by Desiree Chappell and Monty Mythen with their guest Anil Hormis, Professor, Consultant in anesthesia and Critical Care Medicine, Rotherham NHS Foundation Trust.

Treatment of pain is challenging to say the least. For one it is difficult to understand the complexity of the pain experience. This episode explains the components of nociception and the pain experience.  It also examines the targets for pain control and thus provides comprehensive framework for choosing the right analgesic treatments!   Takeaways in This Episode Components of Nociception How a noxious injury becomes a pain impulse The pain perception pathways Interpretation of pain Modulation of pain Peripheral and central targets for pain control How various pain treatments work and at what levels 3 Unique features of pain - Wind-Up Phenomenon, Hyperesthesia, Central Sensitization Links Other Helpful Episodes: Episode 80. Stop Treating Pain Like a Symptom Episode 79. Pain Amongst Neonates, Infants and Young Children with Dr. Kanwaljeet "Sunny" Anand Proactive Pain Solutions Physicians Academy Clinicians Pain Evaluation Toolkit      

Updates in pain management by Gavin Pattullo Opioids are often a mainstay of therapy in trauma pain, though they are in turn the cause of much trauma. For every 4000 Australians prescribed an opioid there will be one death in the community as a result. In-patients similarly have greater risk of harm when their analgesia is opioid based. This presentation will focus on some of the valuable lessons learnt in pain management resulting from the opioid crisis. These include: Our need to differentiate clinically between pain and nociception. Pain - the affective unpleasant experience - is assessed by clinicians enquiring with the use of the words: coping, bothersomeness and troubling. While nociception is focussed on asking about physical feelings and sensations. Profound levels of nociception and the potential to lead to reports of significant pain, a major feature of trauma patients, requires firstly a focus on the two most effective anti-nociceptive strategies of neural blockade and NSAIDs/COX-2 inhibitors before introducing less effective strategies. Pain, the affective distressing unpleasant experience, when present with or without the use of anti-nociceptive strategies has historically been managed solely with biological strategies of opioids and adjuvant agents.  An increasing focus in clinical practice on non-pharmacological strategies to manage pain, including placebo enhancing communication strategies and message framing. Avoidance of over-reliance on pain scores. Clinicians are too often misled and poor decisions are made when the robustness of pain scores is over-relied upon. Pain scores can be useful provided there is clear understanding in both the enquirer and the patient of whether the question is relating to the level of nociception or pain being experienced. Ensuring optimal effectiveness of the opioid avoiding strategy of neural blockade. Four clinical assessment endpoints indicate effectiveness of neural blockade: presence of Dynamic pain relief, Analgesia, Sensory anaesthesia and Opioid sparing/elimination (DASO). For more head to: codachange.org/podcasts/

 Why should I care about my pelvic floor?- Because it's health leads you to greater pleasure.My pelvic floor is wrecked after having kids including the "sneeze dribble”, is there anything I can do? - You can strengthen and heal your pelvic floor with simple techniquesKegel's are for women only, aren't they? - Nope! Men have a pelvic floor too and a healthy one leads to so much more vitality and pleasureDid you know you can stimulate your Vagus nerve to promote pleasure and safety in your body?-Listen in today to learn 3 simple techniques to do soThis week the brilliant Dagmar Khan, a global leader and women's pelvic health expert, and founder of Flourish Institute, joins us today to dive deep in to our pelvic floor and all it's wonder.  In her work, Dagmar has helped thousands of women from all around the globe to deeply activate the healing codes inside of their body, escape surgeon's knives, and become the inner authorities of their healing. Listen in and learn:-  What the Vagus Nerve is and why it is so damn important for healing and pleasure-  How a healthier pelvic floor will make you a better lover (and better orgasms too!)-  3 simple techniques to improve your pelvic floor healthTo connect with Dagmar and her incredible work in this space, visit her at www.flourishinstitute.org or on IG/FB @dagmarkhanFor additional tips and guidance, download our complimentary e-book “Sacred Sexuality 101” hereOr want daily sexiness inspiration? Follow us on IG and FB @lovedeeplabPlease subscribe, rate, and review!Thank you for being brave in opening your hearts to LOVE DEEP!!See you next week…. And until then stay sexy… Because you already are!!

On connait tous les 5 sens de l'être humain ? Mais as tu ce fameux sixième sens ? Voire même plus...

Armed with a background in biomedical engineering, doubled with an EMBA in Finance, our guest has spent the past 20 years within the medical device industry. In 2010 he was instrumental in setting up MDoloris Medical Systems, with the mission to provide technologies that allow clinicians a reliable, continuous and non-invasive evaluation of autonomic nervous system (ANS) activity. Based on 23 years of academic research, performed by a French research lab, the technology allows anaesthetists and intensivists to effectively tailor analgesia; more so for patients who are unable to communicate. The technology is available for adults, paediatrics, neonates as well as animals (specifically horses, cats and dogs), in both standalone and more recently modular format. Presented by Desiree Chappell and Monty Mythen with their guest Fabian Pagniez, CEO and founder of MDoloris Medical Systems. For more details on EBPOM please visit www.ebpom.org Also, if you enjoyed this piece we cover nociception in more detail here: https://www.topmedtalk.com/topmedtalks-to-dan-longrois-on-nociception/

Armed with a background in biomedical engineering, doubled with an EMBA in Finance, our guest has spent the past 20 years within the medical device industry. In 2010 he was instrumental in setting up MDoloris Medical Systems, with the mission to provide technologies that allow clinicians a reliable, continuous and non-invasive evaluation of autonomic nervous system (ANS) activity. Based on 23 years of academic research, performed by a French research lab, the technology allows anaesthetists and intensivists to effectively tailor analgesia; more so for patients who are unable to communicate. The technology is available for adults, paediatrics, neonates as well as animals (specifically horses, cats and dogs), in both standalone and more recently modular format. Presented by Desiree Chappell and Monty Mythen with their guest Fabian Pagniez, CEO and founder of MDoloris Medical Systems. For more details on EBPOM Las Vegas please visit www.ebpom.org Also, if you enjoyed this piece we cover nociception in more detail here: https://www.topmedtalk.com/topmedtalks-to-dan-longrois-on-nociception/

Contributor: Don Stader, MD Educational Pearls: Pain is ubiquitous in the emergency department but it is not the enemy - suffering is Nociception is the ability to feel noxious stimuli which usually causes a reaction, like pulling a limb away when you feel something painful. Nociception is really a brainstem reflex. Pain is nociception plus cognition, meaning we process the noxious stimuli in our frontal cortex but it is not necessarily suffering.  Pain can be associated with euphoria, such as with distance running Suffering, unlike pain, is associated with emotional distress Nociception is a brainstem reflex, pain involves the brainstem and the frontal cortex, while suffering involves the brainstem, frontal cortex, and the limbic system attaching an emotional response Providers should educate patients’ expectations on pain as a part of the physiologic process and emphasize the focus on alleviating suffering References Sneddon LU. Comparative Physiology of Nociception and Pain. Physiology (Bethesda). 2018 Jan 1;33(1):63-73. doi: 10.1152/physiol.00022.2017. PMID: 2921289 Summarized by Jackson Roos, MS4 | Edited by Erik Verzemnieks, MD

Dans ce nouvel épisode, j'ai l'immense plaisir de recevoir Brigitte Gothière la cofondatrice de L214, En 1993, avec Sébastien Arscac, son mari, ils ont cofondés l'association L214 afin d'œuvrer pour une pleine reconnaissance de la sensibilité des animaux et l'abolition de pratiques (élevages, abattoirs...) qui leur sont nocives. Ils se font fait connaître du grand public par leurs videos choc dans lesquelles ils dénoncent les conditions, souvent déplorables, de certains abattoirs.Dans notre conversation de 2 heures que j'ai trouvé passionnante, Brigitte nous détaille son parcours et nous discutons plus particulièrement :   de son enfance, de sa rencontre avec Sébastien, et le moment clé qui a déclenché leur envie de s'investir pleinement dans la cause animale, des débuts de leur militantisme en 2003, en fondant à Stop Gavage, un collectif qui dénonce les pratiques de gavage des oies et canards, des débuts de L214 en 2008, des coulisses des premiers reportages chocs,  des actions contre les industriels et tout récemment la parodie de la pub Lidl « Allo Patron », nous faisons un tour d'horizon de la souffrance animale et abordons d'autres sujets comme le véganisme, la politique, l'avenir…, nous terminons par quelques questions personnelles, comme à l'accoutumé. Bonne écoute

This is a repost from 2018, an article caled Wired Into Pain: a history of the science of pain. I hope you enjoy it. I’ve also recorded an audio version to go with it!I am a Physiotherapist. Almost every person I see in clinic is in pain, and most already have an idea about what has caused their pain. If they are old enough, they might say ‘overuse’, or ‘wear and tear’; if they are younger, they might say ‘bad posture’ or ‘tight muscles’; if they have had a scan, they might say a ‘slipped disc’ or a ‘bone spur’. We accept these explanations prima facie. We consider pain to be a readout on the state of the body’s tissues. Or, as one doctor wrote in 1917, it is “the unerring medical compass that serves as a guide to the pathological lesion”.But it is only very recently that we have come to understand our aches and pains in this way. Since medieval times, until surprisingly recently, people commonly understood their pains in terms of their relationship to God, often as punishment for sin. Physical and emotional pain were entangled, along with mind, body and soul. This was the grim logic of medieval torture and self-flagellation: the truth of the soul could be accessed through the pain of the body.But, as historian Joanna Bourke records in her book The Story of Pain, this mixture of mind, body, soul and God also allowed people to feel pain as comforting: a “vigilant sentinel […] stationed in the frail body by Providence”, as one writer put it in 1832. For others, pain was redemptive: take, for example, the early nineteenth-century labourer Joseph Townend, who resolved himself to God after undergoing surgery without anaesthetic, and reflected at the end of his life on his “sincere thanks to the Almighty God” for his agonising conversion.Pre-modern physicians had a different perspective. Most understood pain according to humoural theory. Hippocrates and his disciple Galen considered all illness to be caused by an imbalance of the body’s humours — phlegm, yellow bile, black bile and blood — which ebb and flow in response changes in the body or its environment. This notion endured for many centuries. To one 18th century writer, pain was a consequence of “viscid blood [stopping] at every narrow passage in its progress”; to another, it was a “Nature throw[ing] a Mischief” about his body. Humoural theory is pre-scientific and seems quaint to us now. But, as Bourke points out, it accounts for an abundance of influences, from our personal temperament and our relationships to the alignment of the planets above our heads, on the pain that we feel.Over the coming centuries, at great cost to people suffering from pain, this insight was lost. This is the story of that loss; of how we arrived at the strange, wrong idea that pain is a straightforward “guide to the pathological lesion”; and of how an emerging re-understanding of pain shows us that it is more complex and more astonishing than we have thought for centuries.Descartes, dualism and the labelled line“The ghost in the machine” — Gilbert RyleIt is in the sixteenth century that we find the beginnings of the dominant modern understanding of the body and its pains. The rise of Protestantism and, amongst secular thinkers, of humanism, contributed to an increased focus on the individual and an understanding of the body as a natural, rather than a supernatural entity. Medicine became more interested in anatomy and the physical laws of nature. Vesalius published his On the Fabric of the Human Body, a compendium of illustrations of dissected cadavers based on the author’s strict, first-hand observations at a time when doctors were not accustomed to performing their own dissections. Later, physicians like William Harvey took principles from physics and astronomy to show that in many ways, our bodies can be understood as machines: pumps, pulleys and levers. Slowly, the body became less sacred and more scientific.It was in this spirit that, in 1641, the French polymath Renes Descartes published his Meditations on First Philosophy. This work contains a drawing that became the seminal image of pain for the next three hundred years. The picture shows a kneeling boy with one foot perilously close to a small campfire. The heat of the flame sends a signal (an “animal spirit”) up a channel to the boy’s pituitary gland, which Descartes reckoned was the seat of consciousness. There, the signal elicits pain, “just as pulling one end of a cord rings the bell at the other end”.This picture makes sense to us, it seems intuitively correct. But this is because in matters of pain we are most of us now, in the Western world at least, the children of Descartes. For pain scientists on the other hand, who have fought in recent decades to emancipate themselves from Descartes, this picture has has come to represent the original sin, the first big lie of the Western world’s understanding of pain.It’s crimes are twofold. First, it is the essence of an idea called dualism, which holds that mind and body are separate. The body feels pain, and passes this information on to the mind. For Cartesian dualists, the body is a machine and we are a kind of ghost in the machine, receiving information about its status.Second, the picture represents pain as being felt by a specific detector in the body, and passed up a specific pathway, the long hollow tube, to a specific location in the boy’s brain. Pain detectors, at the end of a pain pathway, that leads to a pain centre. This idea is called specificity theory, but in this post I’m going to use the term labelled line theory because although it is less common, I think it is more descriptive — a labelled line for pain.As it happens, Descartes’ idea was more subtle than the picture and its subsequent interpretations made out. In his defence, the historians Jan Frans van Dijkhuizen and Karl A.E. Enenkel point out that Descartes knew that pain is not merely perceived, like a mariner perceives his ship, but felt, as if the mind and body are “nighly conjoin’d […] so that I and it make up one thing”. Descartes knew that we don’t just have a body; we are a body. But this subtlety was lost: the picture of the little boy with his foot in the fire has a memetic power that has carried it, along with dualism and the labelled line, through the centuries.The nineteenth century“Nothing less than the social transformation of Western medicine” — Daniel GoldbergThis change came gradually. It was not until the nineteenth century, two hundred years after Descartes’ Meditations, that dualism and the labelled line for pain finally established their authority in medicine.They set in as part of a wider change in the history of medicine following the French Revolution that is sometimes now called the ‘Paris School’. The physicians of the Paris School transformed large teaching hospitals in the city to dedicate them, for the first time, to furthering scientific knowledge through rigorous observation of patients and cadavers, and the classification of disease. They explicitly rejected humoural theory, which held that illnesses are processes that are distributed around the body through the movement of viscous humours. Rather, physicians of the Paris School considered diseases to be the result of lesions localised to a single, solid organ.Influenced by the Paris School, Victorian physicians across the Western world began to search their suffering patients’ bodies for a local, solid lesion to blame for their pain. As one New York physician wrote in 1880, “we fully agree that there can be no morbid manifestations without a change in the material structure of the organs involved”. For the first time, doctors began to think like detectives on the hunt for the smoking gun, following clues provided by the body and its sensations (it is no coincidence that Arthur Conan Doyle was a doctor before he wrote the Sherlock Holmes stories, or that he made his character Watson one, too).This approach has tremendous diagnostic power. But, as we will see, even modern researchers find that our pain, particularly our chronic pain, resists reduction by detective work. How did Victorian physicians respond when their investigations failed to turn up a local lesion to explain pain? According to historian and medical ethicist Daniel Goldberg, many doubled down, hunting for anything they could find. As one surgeon put it, “any lesion anywhere in the body will do to account for an otherwise inexplicable pain”. And that meant any lesion: the surgeon Joseph Swann, or example, baffled by a woman’s 11-year history of pain in an apparently healthy knee, eventually attributed it to an imperfection he found, after much searching, in a nerve in her hand.Those that could not find a lesion anywhere explained unexplained pain as one inevitably must if one subscribes to the logic of dualism: if it’s not in the body, it must be in the mind. Goldberg tells the story of the surgeon Josiah Nott who, in 1872, took on the care of an American soldier whose leg was crushed in a railway accident. The leg had already been amputated by another surgeon at a point about halfway up the calf, but the soldier had developed phantom limb pains. The original surgeon, assuming there must be a local lesion at the end of a labelled line, had then amputated the stump, but to no avail. Nott, making the same assumption, took still more from the stump the next year, and still the patient felt no relief. Later that year, Dr. Nott operated again, removing tissues from three major nerves in the shank. This pattern continued until Nott had removed the poor soldier’s leg up to four inches above the knee, and his sciatic nerve up to the pelvis. When the patient’s pain returned after this final operation, Dr. Nott reasoned that he must have acquired an addiction to opioids which was inciting him to malinger (to exaggerate or feign his disease). Nott had, horribly literally, followed the assumed cause of the disease up a labelled line through the body and, not catching it, decided it must therefore be in the mind.This logic played out on a broad scale in physicians’ understanding of the now-forgotten condition “railway spine”, the widespread and mysterious back pain felt by the victims of train accidents. Initially, physicians thought that the trauma of a crash caused compression of nerve filaments that in turn caused pain. But as time wore on and their investigations repeatedly failed to find a tissue lesion to explain railway spine, even in cadavers, their suspicion grew that railway spine was not a ‘real’ condition at all. After all, weren’t most victims also seeking compensation from railway companies? By the beginning of the twentieth century, railway spine was known instead as “hysterical spine […] merely a psychical condition”. Dualism dictated once more that if we can’t find it in the body, it must be in the mind.1900 to 1965Anomalies, non-anomalies, and opening the gateAnomalies“[Pain] reveals only a minute proportion of illnesses and often, when it is one of their accompaniments, is misleading. On the other hand, in certain chronic cases it seems to be the entire disorder which, without it, would not exist.” — Rene Leriche, 1937The break from Cartesianism began at the end of the nineteenth century, when the great neuroscientist Santiago Ramon y Cajal showed that our nerves, spinal cord and brain are not one thing but composed of many smaller things (which came to be called neurons) linked by gap junctions (which came to be called synapses). Decades earlier, the English neuroscientist Charles Bell had suggested that the function of the nervous system is less straightforward than the labelled line in Descartes’s picture, and Cajal’s work was proof.As we can see by his extraordinary drawings, Cajal meticulously mapped the peripheral neurons in our arms and legs, running to the spinal cord, and the neurons running up the cord, and many of those in our brain. But, according to pain scientist and writer Fernando Cervero, the terminus for incoming peripheral neurons, the foremost part of the spinal cord that we now call the dorsal horn, was so dense and chaotic that it resisted even Cajal’s fastidious eye. He called the dorsal horn a maremagnum, a Spanish word that means ‘confused and disorganised crowd’, as in the bustle of a busy railway station. Cajal’s vision of a network of individual cells, with nodes of incomprehensible complexity, opened up the possibility that signals aren’t simply passed upwards in a linear fashion as Descartes had assumed, but are modulated along the way.The idea that inputs to the nervous system are modulated before they ‘become’ our sensations hints at an explanation for the odd persistent pains for which Victorian physicians could find no lesion. It also begins to explain the opposite phenomenon, lesions that cause no pain, which became unignorable during the brutal first decades of the twentieth century. Doctors like Rene Leriche, on the front line in the Great War, found that soldiers with dreadful wounds often felt no pain and could undergo surgery without anaesthetic. Leriche knew this was not willpower but “certain movements of the hormones, or of the blood”, a presciently non-Cartesian thought.During the Second World War, the American anaesthesiologist Henry Beecher built on Leriche’s observations by conducting a more methodical study at his post in Italy. He found that as many as three quarters of wounded soldiers felt little pain at the time of their injury. As one doctor put it, it was as if wounds and diseases “carry for the most part — most mercifully — their own anaesthetics with them”.One might think that such cases would have alerted the scientific community to the fact that our nervous systems are doing something more than passively relaying pain into our brains, as labelled line theory implied. But for scientists and doctors at large, anomalies that defied labelled line went on hiding in plain sight, “discovered” periodically and then easily forgotten as they had been in the Victorian era. Phantom limb pain, for example, was unignorable during the American Civil War, and then slipped once more from popular consciousness. The doctor and writer Oliver Sacks called these periods of forgetting scotoma, dark gaps in the scientific awareness in which the prevailing theory cannot explain common phenomena and instead shoves them in the attic to think about another day. The progress of science, wrote Sacks, is faltering and haphazard, “very far from a majestic unfolding”.Non-anomalies“Pain is the physiological adjunct of a protective reflex” — Charles Sherrington, writing in 1900“Pain remains a biological enigma — so much of it is useless, a mere curse” — Charles Sherrington, writing forty years later.(Quoted in Understanding Pain by Fernando Cervero)Rather than explaining anomalies, scientists studying pain at the beginning of the twentieth century focused on a series of discoveries that appeared, at first, to confirm labelled line theory. The British neuroscientist Charles Sherrington had coined the term “nociceptor” for the neurons that convey danger messages (elicited by things like heat, intense mechanical pressure or an incision to the skin) to the brain, and in the following decades researchers slowly but successfully identified and isolated these cells.Starting in 1912, American scientists performed the first anterolateral cordotomy, slicing through the part of the spinal cord that was theorized to carry danger messages to the brain and appearing to stop pain in its tracks. Later, the success of such operations would prove to be temporary, but the procedure did show that this part of the spinal cord houses Sherrington’s nociceptors. In 1927, the Americans Herbert Gasser and Joseph Erlanger established that different nerve fibers conduct signals at different velocities, and classified them according to their diameter as A, B and C fibers. A fibers were widest and conducted signals the quickest; C fibers were the most narrow and slow. They found that one sub-type of A fibers, A-delta fibers, conducted the relatively quick sensation of dull pain we feel when we stub our toe; and that C fibers conduct the slower, stinging pain that arrives later. Again, this neat distinction would later prove to be more complicated, but the discovery was further evidence for a labelled line of pain. Gasser and Erlanger were only able to look at conduction signals from a whole bundle of nerves and so it was not until 1958 that Ainsley Iggo was first to record individual A-delta and C fibers and isolate Sherrington’s nociceptors for the first time.Opening the gate“It may seem easy, but it was not” — Ronald MelzackDespite this series of discoveries in favour of labelled line, some researchers could not shake from their minds those confounding anomalies: pain without lesion, and lesion without pain. And so, at last, the science of pain began to wake from its scotoma. Some scientists began to propose a theory to compete with labelled line called pattern theory, which held that it is not the stimulation of specific nerves that causes the sensation of pain, but that the way in which nerves are stimulated, spatially and temporally. Pattern theory was vague, and had nowhere near the amount of evidence that supported labelled line theory, but it did hint at an answer to some of the anomalies that had been documented in the recent scientific literature, such as the way pain spreads beyond the site of an injury and the way rubbing a pain can make it temporarily feel better. Pattern theory was taken up in Oxford in the 1940s and 50s, where the brilliant British neuroscientist Pat Wall was beginning to develop ideas he would turn into gate control theory, a whole new model of pain.In 1959, Wall moved from Oxford to the Massachusetts Institute of Technology where he met Ronald Melzack. Melzack, a Canadian, had just arrived at M.I.T. to take up a post as assistant professor of Psychology, and found to his annoyance that he could not perform research on animals in the university’s Psychology building. So, Melzack decamped to Wall’s lab. The two quickly took up a discussion on the inadequacy of Cartesianism and decided to come up with a new theory to “entice spinal-cord physiologists away from [labelled line]”.From his previous research, Melzack knew the brain sends messages down the spinal cord to inhibit the messages coming up it, exerting a kind of ‘top-down’ control on incoming information. From his own experiments, inspired by pattern theory, Wall knew that different inputs into the nervous system are weighed against each other somehow in the spinal cord, competing to be ‘sent up’ to the brain. Despite their discussions, Melzack and Wall’s ideas remained inchoate until, in 1962, Melzack stumbled on the Dutchman Willem Noordenbos’s pattern-theory hypothesis that large A-fibers carrying touch signals might somehow inhibit small C-fibers carrying danger signals.Melzack calls this moment a “flash of insight”. Noordenbos had theorized that this modulation happened in the substantia gelatinosa, which is part of the terminus for incoming information at the spinal cord. Wall knew that large fibers and small fibers entered the substantia gelatinosa at opposite ends, and theorised that it was this setup that allowed the one to inhibit the other, like closing a figurative ‘gate’. The weight of signals from large and small fibers would determine what kind of message was allowed up to the brain.In 1963, Melzack moved to McGill University in Canada, but travelled South over the border when he could to visit Wall’s home in Boston where, over large amounts of duty free whiskey, the two put the finishing, definitive touches to their work. Their theory differed critically from Noordenbos’ because they proposed that the brain itself plays a role in processing at the substantia gelatinosa, by sending signals down the spinal cord to make the ‘gate’ more likely to open or close to danger signals. This was gate control theory.For the first time, science had a model that began to explain pain anomalies. According to gate control theory, for example, the brain of a soldier who has sustained an injury can send messages down the spinal cord to close the gate to incoming danger signals. Over fifty years have passed, and gate control theory has turned out to be wrong in lots of little ways, but right in one big way: it is modulation in the spinal cord and the brain, or the central nervous system, that explains why pain is so rarely the reliable sign of tissue status that Victorian scientists assumed it was.Neuromatrix theory“We need to go… to the brain” — Ronald Melzack“When you feel a pain in the leg that has been amputated, where is the pain? If you say it is in your head, would it be in your head if your leg had not been amputated? If you say yes, then what reason have you for ever thinking you have a leg?” — Bertrand RussellGate control theory was a great advance but Melzack and Wall knew their theory was incomplete. According to Oliver Sacks, it is by studying anomalies — phenomena not explained by the prevailing theory — that researchers wake from scotoma and begin revolutions in scientific understanding. So it was that Melzack’s interest in the anomaly of phantom limb pain led to neuromatrix theory, the next great boost that finally allowed pain science to escape to orbit of CartesianismIf people without limbs have phantom pain, Melzack reasoned, it follows that the origins of the pattern of pain lie not in the limb but in the brain. And not only pain, but the sensation of having a body in its entirety — its place in the world, its shape, its movements — is housed, in what Melzack came to understand as a series of loops and patterns of neurons, inside our brains. This brain architecture is the neuromatrix.Incoming information, then, is not what holds the essence of our sensations; it merely triggers the neuromatrix, already inscribed in the brain, to ‘produce’ the sensations we feel. If a boy puts his foot in a fire, the nerves do not tell a passive brain “here is pain”; the nerves simply say “here is an intense input”, and the neuromatrix does the rest.How do we get a neuromatrix? Melzack says it is inborn, but then shaped by experiences. So, your neuromatrix develops your own personal signatures for familiar pains, like the pain you might feel in your back when you bend. Crucially, the neuromatrix uses our thoughts and emotions to generate our sensations, as well as sensory information. This makes sense: think of a stroke on the leg from your partner and one from an unappealing stranger. The same sensory input feels different.So, if you believe the cause of your back pain is something threatening, like a suspected spinal cancer or a ‘slipped’ disc, it willfeelworse than if you believe it is something benign, like a muscle strain. If a conscripted soldier sustains a battlefield injury that means he will likely have to leave the trenches to convalesce behind the front lines, that wound may not feel as bad as it would for a factory worker, for whom it could mean a loss of livelihood. If you have just been made redundant, or become divorced, than the incoming danger signals from an incipiently arthritic hip might suddenly start triggering your neuromatrix to produce a deep aching pain in your joints.Pain is intimately integrated with meaning, and informed by the broader context of our lives. And there is no labelled line: pain is the output of a widely-distributed neural process that takes input from countless biological, psychological and social factors.The sensitive nervous system“Not under conditions of my choosing / Wired into pain / Rider on the slow train” — Adrienne RichResearchers have used the neuromatrix as a foundation to develop our understanding of pain. For example, towards the end of the 1970s, scientists began to establish that the endings of our danger messenger neurons, the ones Sherrington christened nociceptors, become more sensitive the more they are used, a process called peripheral sensitization. But perhaps the most remarkable development since Melzack proposed the neuromatrix was Clifford Woolf’s discovery of central sensitization.On completing his medical training in South Africa in the early 1980s, Clifford Woolf joined Pat Wall’s laboratory in London. He was not content with measuring the readouts from individual chains of neurons, and instead began to monitor broader bursts of activity which he thought would give him more insight into the pain system as a whole. He started to measure the output of the neurons that cause muscles to flex away from a dangerous stimulus (think of touching a hot stove and retracting your hand before you are even conscious of pain). Investigating on rats, he found that most of these cells responded to dangerous stimuli, such as heat and pinch, in a fairly narrow field — say, one toe. But, some cells had a very wide receptive field and would respond to even light, non-dangerous touch. Why would rats have neurons designed to elicit a withdrawal response to light touch?It took Woolf some months to realise that he was only finding these neurons at the end of the workday, when his rats had already been subjected to hours of pain-inducing stimuli. He calls this his “eureka moment”. He had not discovered that rats have certain neurons that are super sensitive across a wide receptive field: he had discovered that a rat’s nervous system becomes super sensitive across a wide receptive field when it has been exposed to prolonged danger. Woolf had discovered an ‘amplifier’ mechanism in the spinal cord. This phenomenon is central sensitization.Woolf was the first person to show that the nervous system is not hard-wired for pain but plastic. Prolonged nociception can change the behaviour and the architecture of the nervous system so that non-dangerous inputs (like light touch) are felt as painful, and dangerous inputs (like a pinprick) produce more pain than they otherwise would have done. To top it off, this whole pain experience also spreads beyond the original site of injury. The great physiotherapist Louis Gifford described central sensitization as like tapping X on your computer keyboard three times, and 10 X’s of different sizes and colours popping up on the screen.A mild and benign form of central sensitization is common and almost immediate after most injuries — after you burn your hand or sprain your ankle, it is your body’s way of protecting itself. But central sensitization can wear on and, in many cases, persist and get worse long after any injury has healed. If you or someone you know has widespread back pain that flares up with the slightest movement, or has osteoarthritis in their hip that seems to spread all the way down their leg, they might have central sensitization.Central sensitization can affect many different functions, not just pain. People with ongoing, maladaptive central sensitization can be tense and forgetful, and sensitive to bright lights, loud noises and chemicals. It is also a feature of irritable bowel syndrome, migraine and chronic fatigue syndrome, and often goes hand in hand with anxiety and depression.So long, labelled line: Grappling with complexity“Pain cannot easily be divided from the emotions surrounding it. Apprehension sharpens it, hopelessness intensifies it, loneliness protracts it by making hours seem like days. The worst pain is unexplained pain” — Hilary Mantel“The basic idea of pain modulation implies that the output can be different to the input at every stage in the transmission of pain signals throughout the brain” — Fernando CerveroCentral sensitization is just one discovery that has enhanced our understanding of pain. There are many more examples. Descending modulation is the ongoing process by which the brain sends signals down the spinal cord to simultaneously inhibit and facilitate incoming danger signals, a mechanism Leriche anticipated when he observed that battlefield wounds “carry […] their own anaesthetics with them”. In people with persistent pain, descending modulation may be set for a net facilitation of incoming danger messages. Researchers have also expanded our understanding to include the immune system, which aids and abets the nervous system as it produces pain. They have found out that nociceptors, far from lying waiting for an intense stimulus as Sherrington imagined, are actually firing regularly throughout the day, every time we use a pair of scissors, ride a bike or go on a long walk, without (if we are lucky) our neuromatrix producing the experience of pain. Conversely, clever experiments have shown that nociception is not even necessary for pain, giving credence to the stories of people who narrowly escape injury but, believing they have been hurt, writhe in agony. And, we know that stress, even the stress of early life events, plays a vital role in ongoing pain, and that our stress system and pain production system are intimately linked.The contrast between the byzantine, distributed complexity of the mechanisms of pain and the singular experience of pain — I feel it here — is remarkable. Scientists have made various attempts to simplify the mechanisms into something more understandable and more useful to lay people. The neuroscientist VS Ramachandran has said that “pain is an opinion on the organism’s state of health rather than a mere reflective response to an injury”, a stark contrast to the old-fashioned idea of pain as “the unerring medical compass that serves as a guide to the pathological lesion”.The scientists and physiotherapists Dave Butler and Lorimer Moseley put it elegantly:“We will experience pain when our credible evidence of danger related to our body is greater than our credible evidence of safety related to our body. Equally we won’t have pain when our credible evidence of safety is greater than our credible evidence of danger.”In other words, pain is not measuring damage, it is a protective strategy, just one of many (along with local and systemic inflammation, changes in movement like tensing or bracing, the feeling of stiffness, and so on) that the body enacts in response to credible evidence of danger.This evidence of danger often includes nociception (signals from tissue damage), but the neuromatrix uses many other sources, too. For example, if someone has back pain and a doctor tells you your x-ray shows “wear and tear” or “degeneration” in your spine, they have received a clear message of danger related to your body that is likely to make their pain worse. Indeed, people with back pain who get an MRI actually reduce their chances of recovery. On the other hand, if that person’s doctor (or physiotherapist!) tells them that the findings on their scan are normal age-related changes (or, better yet, doesn’t order a scan at all), that is a clear safety message. Safety messages can come from anywhere. Exercise can send safety messages to your neuromatrix, and so can a supportive workplace or having a friend around to talk to.ReflectionsSlow progress, hopes for the future and a note of cautionSlow progress“I am still not happy with what has been accepted” — Pat Wall, 1999Danger sharpens pain; safety soothes it. Why, then, do health professionals continue to give people with persistent pain credible evidence of danger? Apart from the obvious — that there is money in telling people their spines are crumbling and their pelvises are out of line, that they have muscle knots that need releasing and cores that need stabilizing — it is because, just as Descartes’ model of pain took almost three centuries to reach its zenith in Western culture, the neuromatrix, still only forty years old, has been accepted only falteringly even in medical circles, and hardly at all in the wider culture.Indeed, in many ways the twentieth century has doubled down on labelled line. Take, for example, the dominance of the orthopaedic understanding of low back pain, which the late Scottish doctor and historian Gordon Waddell called “the dynasty of the disc”. Waddell traces the tenuous association of the lumbar disc with low back pain to a fateful cluster of papers published at the beginning of the century by orthopods searching, like Victorian physicians had done before them, for a pot of gold at the (wrong) end of the labelled line. Even today, routine orthopaedic surgeries like lumbar fusion, knee arthroscopy and shoulder decompression are amongst the most low-value, least evidence-based treatments in healthcare, still performed largely because of inertia and unexamined Cartesianism.Many physiotherapists practice with the same habits. Like Joseph Swann, we might conduct a questionable root-cause analysis up or down a kinetic chain to find an ‘issue in the tissues’, settling on a pronated foot, a slumped posture or a valgus (in-falling) knee. Like Josiah Nott, when a patient has failed a course of ‘corrective’ exercise to ‘fix’ their body we might decide their problem is primarily ‘psycho-social’, a euphemism for in-their-mind. This is understandable, it takes great effort to shift from Cartesianism to the neuromatrix; I have been trying for years and I am still astonished when a new study is published showing, for example, that there are no major physical risk factors for a first episode of neck pain, but multiple psychological ones, like depression, and social ones, like role conflict. Still, it is imperative that medical professionals of all stripes challenge their colleagues who promote themselves as experts but who practice with unreconstructed Cartesianism.Hopes for the Future“While pain sufferers do not have the luxury of denying the reality of their pain, they can and do deny its legitimacy, thereby internalising the stigma so frequently directed at people in pain.” — Daniel GoldbergThe neuromatrix model has the potential to be immensely liberating for patients. For people with everyday predicaments of life like the back or shoulder pain we all get from time to time, there is the reassuring message that pain is not an indicator of damage and they are safe to move. In fact, movement, as opposed to protecting the painful joint, is the way to go in the long run. For people with more profound, widespread and recalcitrant pain, understanding why their pain is the way it is can help with the process of acceptance, and knowing pain is multifactorial can open up new therapeutic options to help calm down a sensitive nervous system.The neuromatrix could also militate against the way Cartesian thinking drives stigmatization of people with chronic pain. Cartesian dualism casts pain as a two-step sequence of events: the body senses pain, then the mind reacts. As recently as the 1980s, words like “hysterical” or “psychogenic” were used to describe people who appeared to be ‘over-reacting’ to their pain. It is this thinking that allows us to sort people into those who are responding appropriately to their pain, and those who are ‘being dramatic’. The saddest effect of this stigma is when patients internalise it, believing that they are not ‘coping’ properly with ‘a bit of back pain’.So patients and health professionals need to know that dualism is bogus: as Pat Wall himself put it, “the separation of sensation from perception was quite artificial… sensory and cognitive mechanisms operate as a whole”. Or, in the words of neuroscientist Fernando Cervero, “emotional, sensory and cognitive elements aren’t organised in a hierarchical way, but in a cooperative way […] interacting to generate the final pain experience”.A note of caution“Nineteenth century physicians drain[ed] pain of any intrinsic meaning altogether, making it little more than a sign or symptom of something else” — Joanna Burke“[The challenge is] to allow a rapprochement between the world of the clinician and the world of the person in pain” — Quinter et. al (2008).The neuromatrix and all its attendant discoveries have revolutionised how medical and health professionals should approach people in pain. It is a rare true paradigm shift. But there is danger in complacency. “Now is not a time for professional hubris or the proclamation of truth by a few”, warn the rheumatologists John Quintner and Milton Cohen. The battle to understand pain is only half won. It is all too easy to be drawn back into the orbit of dualism, not only between the mind and body, but between the clinician and the patient, or the researcher and the sufferer. Centuries-old habits die hard, and we have long made the person-in-pain an object of enquiry. But this can only take us so far; as Quinter and Cohen assert, “the pain of another person is irreducible to its neuronal correlates”. We can only really know pain through dialogue.It is difficult to talk properly about pain. Being in deep pain can be a harrowing, abject, solitary experience. And apart from anything else, often we just don’t have the words: Virginia Woolf, no stranger to pain, lamented that English has a rich vocabulary for love, but a meagre one for pain. The poet Emily Dickinson said that pain “has an element of blank”.But it can be done. Joletta Belton, a blogger with persistent pain, recently tweeted about the two clinicians who had helped her the most. “It wasn’t just their words” she wrote, “it was that they listened first. And understood. Listening matters […] I wasn’t interrupted or lectured, they didn’t try to ‘educate’ me or alter my narrative to suit their own […] I felt what I said was of value. I felt human, of worth. That’s invaluable.”It may seem strange to end a post about science with a note on the importance of listening, but in the context of the neuromatrix it makes perfect sense. Listening to people in pain is what’s needed to undo the damage that has been done, and take the progress that’s been made to the next level.Belton’s experience echoes a vignette reported by Joanna Bourke in The Story of Pain.During a medical consultation in 1730, an embarrassed patient found himself apologising to his physician for boring him with “so tedious a Tale”. The patient’s physician protested: “Your Story is so diverting, that I take abundance of delight in it, and your Ingenious way of telling it, gives me a greater insight into your distemper, than you imagine. Wherefore, let me beg of you to go on, Sir: I am all attention, and shall not interrupt you.”Selected bibliographyJournal ArticlesAllan, D. and Waddell, G. (1989). An historical perspective on low back pain and disability. Acta Orthopaedica Scandinavica, 60(sup234), pp.1–23.Arnaudo, E. (2017). Pain and dualism: Which dualism?. Journal of Evaluation in Clinical Practice, 23(5), pp.1081–1086.Baliki, M. and Apkarian, A. (2015). Nociception, pain, negative moods, and behavior selection. Neuron, 87(3), pp.474–491.Bourke, J. (2014). Pain sensitivity: an unnatural history from 1800 to 1965. Journal of Medical Humanities, 35(3), pp.301–319.Brodal, P. (2017). A neurobiologist’s attempt to understand persistent pain. Scandinavian Journal of Pain, 15(1).Cohen, M., Quintner, J., Buchanan, D., Nielsen, M. and Guy, L. (2011). Stigmatization of Patients with Chronic Pain: The Extinction of Empathy. Pain Medicine, 12(11), pp.1637–1643.Chapman, C., Tuckett, R. and Song, C. (2008). Pain and stress in a systems perspective: reciprocal neural, endocrine, and immune interactions. The Journal of Pain, 9(2), pp.122–145.Eriksen, T., Kerry, R., Mumford, S., Lie, S. and Anjum, R. (2013). At the borders of medical reasoning: aetiological and ontological challenges of medically unexplained symptoms. Philosophy, Ethics, and Humanities in Medicine, 8(1), p.11.Goldberg, D. (2012). Pain without lesion: debate among American neurologists, 1850–1900. 19: Interdisciplinary Studies in the Long Nineteenth Century, 0(15).Goldberg, D. (2017). Pain, objectivity and history: understanding pain stigma. Medical Humanities, 43(4), pp.238–243.Iannetti, G. and Mouraux, A. (2010). From the neuromatrix to the pain matrix (and back). Experimental Brain Research, 205(1), pp.1–12.Kerry, R., Maddocks, M. and Mumford, S. (2008). Philosophy of science and physiotherapy: An insight into practice. Physiotherapy Theory and Practice, 24(6), pp.397–407.Latremoliere, A. and Woolf, C. (2009). Central sensitization: A generator of pain hypersensitivity by central neural plasticity. The Journal of Pain, 10(9), pp.895–926.Melzack, R. (1999). From the gate to the neuromatrix. Pain, 82, pp.S121-S126.Melzack, R. (2005). Evolution of the neuromatrix theory of Pain. The Prithvi Raj Lecture: Presented at the Third World Congress of World Institute of Pain, Barcelona 2004. Pain Practice, 5(2), pp.85–94.Melzack, R. and Katz, J. (2012). Pain. Wiley Interdisciplinary Reviews: Cognitive Science, 4(1), pp.1–15.Mendell, L. (2014). Constructing and deconstructing the gate theory of pain. Pain, 155(2), pp.210–216.Moayedi, M. and Davis, K. (2013). Theories of pain: from specificity to gate control. Journal of Neurophysiology, 109(1), pp.5–12.Moseley, G. and Butler, D. (2015). Fifteen years of explaining pain: the past, present, and future. The Journal of Pain, 16(9), pp.807–813.Moseley, G. (2007). Reconceptualising pain according to modern pain science. Physical Therapy Reviews, 12(3), pp.169–178.Neilson, S. (2015). Pain as metaphor: metaphor and medicine. Medical Humanities, 42(1), pp.3–10.O’Sullivan, P., Caneiro, J., O’Keeffe, M. and O’Sullivan, K. (2016). Unraveling the complexity of low back pain. Journal of Orthopaedic & Sports Physical Therapy, 46(11), pp.932–937.Perl, E. (2007). Ideas about pain, a historical view. Nature Reviews Neuroscience, 8(1), pp.71–80.Quintner, J., Cohen, M., Buchanan, D., Katz, J. and Williamson, O. (2008). Pain Medicine and Its Models: Helping or Hindering?. Pain Medicine, 9(7), pp.824–834.Thacker, M. and Moseley, G. (2012). First-person neuroscience and the understanding of pain. The Medical Journal of Australia, 196(6), pp.410–411.Wiech, K. (2016). Deconstructing the sensation of pain: The influence of cognitive processes on pain perception. Science, 354(6312), pp.584–587.Woolf, C. (2007). Central sensitization. Anesthesiology, 106(4), pp.864–867.BooksCervero, F. (2014). Understanding pain. Boston: Mit Press.Butler, D. and Moseley, G. (2015). Explain pain. Adelaide: Noigroup Publications.Bourke, J. (2014). The story of pain. Oxford: Oxford Univ. Press.Moseley, G. and Butler, D. (2017). Explain pain supercharged. Adelaide: Noigroup Publications.Blog postsPain is weird by Paul IngrahamPain really is in the mind, but not in the way you think by Lorimer MoseleyCentral sensitization in chronic pain by Paul IngrahamMy own chronic pain story by Paul IngrahamEasing musculoskeletal pain Information leafletTell me your story by Joletta BeltonPodcasts and lecturesThe Pain Revolution by Lorimer MoseleyPain: past, present and future with Mick ThackerUnderstanding Pain in 2025 by Mick Thacker Subscribe at tomjesson.substack.com

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.08.11.245738v1?rss=1 Authors: Jeong, I., Yun, S., Shahapal, A., Cho, E. B., Hwang, S. W., Seong, J. Y., Park, H.-C. Abstract: Family with sequence similarity 19 (chemokine (C-C motif)-like), member A5 (FAM19A5) is a chemokine-like secretory protein recently identified to be involved in the regulation of osteoclast formation, post-injury neointima formation, and depression. Here, we identified FAM19A5l, an orthologous zebrafish gene that originated from a common ancestral FAM19A5 gene. FAM19A5l was expressed in trigeminal and dorsal root ganglion neurons as well as distinct neuronal subsets of the central nervous system of zebrafish. Interestingly, FAM19A5l+ trigeminal neurons were nociceptors that co-localized with TRPA1b and TRPV1, and responded to mustard-oil treatment. Behavioral analysis revealed that the nociceptive response to mustard oil decreased in FAM19A5l-knockout zebrafish larvae. In addition, TRPA1b and NGFa mRNA levels were down- and up-regulated in FAM19A5l-knockout and -overexpressing transgenic zebrafish, respectively. Together, our data suggested that FAM19A5l played a role in nociceptive responses to mustard oil by regulating TRPA1b and NGFa expression in zebrafish. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.16.206904v1?rss=1 Authors: Dourson, A. J., Ford, Z. K., Green, K. J., McCrossan, C. E., Hofmann, M. C., Hudgins, R. C., Jankowski, M. P. Abstract: A number of cellular systems work in concert to modulate nociceptive processing in the periphery, but the mechanisms that regulate neonatal nociception may be distinct compared to adults. Our previous work indicated a relationship between neonatal hypersensitivity and growth hormone (GH) signaling. Here, we explored the peripheral mechanisms by which GH modulated neonatal nociception under normal and injury conditions (incision). We found that GH receptor signaling in primary afferents maintains a tonic inhibition of peripheral hypersensitivity. After injury, a macrophage dependent displacement of injury-site GH was found to modulate neuronal transcription at least in part via serum response factor regulation. A single GH injection into the injured hindpaw muscle effectively restored available GH signaling to neurons and prevented acute pain-like behaviors, primary afferent sensitization, neuronal gene expression changes, and the long-term somatosensory changes observed after repeated peripheral insult. These results may indicate a novel mechanism of neonatal nociception. Copy rights belong to original authors. Visit the link for more info

Does pain get you down?  Do you feel it dictates your life?  Would you like to reduce your pain?  Within this episode you will learn the neurophysiology of pain and how it links to your emotional and mental health.  You will find out how pain can change from a sensation to a disease and what you can do to change this action.TO LEARN MORE, VISIT:www.TotalSomatics.comwww.HeidiHadley.comSupport the show (http://paypal.me/TotalSomatics)

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.08.194373v1?rss=1 Authors: Juliet Mwirigi, Moeno Kume, Shayne N Hassler, Ayesha Ahmad, Pradipta R. Ray, Changyu Jiang, Alexander Chamessian, Nakleh Mseeh, Breya P Ludwig, Benjamin D. Rivera, Marvin T Nieman, Thomas Van de Ven, Ru-Rong Ji, Gregory Dussor, Scott Boitano, Josef Vagner, Theodore J Price Abstract: ABSTRACTThe protease activated receptor (PAR) family is a group of G-protein coupled receptors (GPCRs) activated by proteolytic cleavage of the extracellular domain. PARs are expressed in a variety of cell types with crucial roles in hemostasis, immune responses, inflammation, and pain. PAR3 is the least researched of the four PARs, with little known about its expression and function. We sought to better understand its potential function in the peripheral sensory nervous system. Mouse single-cell RNA sequencing data demonstrates that PAR3 is widely expressed in dorsal root ganglion (DRG) neurons. Co-expression of PAR3 mRNA with other PARs was identified in various DRG neuron subpopulations, consistent with its proposed role as a coreceptor of other PARs. We developed a lipid tethered PAR3 agonist, C660, that selectively activates PAR3 by eliciting a Ca2+ response in DRG and trigeminal (TG) neurons. In vivo, C660 induces mechanical hypersensitivity and facial grimacing in WT but not PAR3-/- mice. We characterized other nociceptive phenotypes in PAR3-/- mice and found a loss of hyperalgesic priming in response to IL-6, carrageenan, and a PAR2 agonist, suggesting that PAR3 contributes to long-lasting nociceptor plasticity in some contexts. To examine a potential role of PAR3 in regulating activity of other PARs in sensory neurons, we administered PAR1, PAR2, and PAR4 agonists and assessed mechanical and affective pain behaviors in WT and PAR3-/- mice. We observed that the nociceptive effects of PAR1 agonists were potentiated in the absence of PAR3. Our findings suggest a complex role of PAR3 in the physiology and plasticity of nociceptors.Competing Interest StatementThe authors have declared no competing interest.View Full Text Copy rights belong to original authors. Visit the link for more info

This piece is a fascinating discussion regarding research and safety in anaesthesia management; "in the past five or six years there's been a shift from high risk patients to all types of patients". How are we improving methods, evaluation and monitoring? What are some of the more essential elements of the process? Where is the latest research? What is a sensible policy when it comes to opioids? Presented by Desiree Chappell and Monty Mythen with their guest Dan Longrois, Professor of Anaesthesia and Intensive Care Medicine, Department of Anaesthesia and Intensive care, Bichat Hospital. -- EBPOM 2020 - Live from London - is on! For those who have listened to Desiree's special announcement go now to: https://ebpom.org/EBPOM2020

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.05.24.112052v1?rss=1 Authors: olde Heuvel, F., Ouali-Alami, N., Wilhelm, H., Deshpande, D., Khatamsaz, E., Catanese, A., Woelfle, S., Schoen, M., Jain, S., Grabrucker, S., Ludolph, A. C., Verpelli, C., Michaelis, J., Boeckers, T., Roselli, F. Abstract: Patients suffering from Autism Spectrum Disorders (ASD) experience disturbed nociception in form of either hyposensitivity to pain or hypersensitivity and allodynia. We have determined that Shank2-KO mice, which recapitulate the genetic and behavioural disturbances of ASD, display increased sensitivity to formalin pain and thermal, but not mechanical allodynia. We demonstrate that high levels of Shank2 expression identifies a subpopulation of neurons in murine and human dorsal spinal cord, composed mainly by glycinergic interneurons and that loss of Shank2 causes the decrease in NMDAR in excitatory synapses on these inhibitory interneurons. In fact, in the subacute phase of the formalin test, glycinergic interneurons are strongly activated in WT mice but not in Shank2-KO mice. As consequence, nociception projection neurons in lamina I are activated in larger numbers in Shank2-KO mice. Our findings prove that Shank2 expression identifies a new subset of inhibitory interneurons involved in reducing the transmission of nociceptive stimuli and whose unchecked activation is associated with pain hypersensitivity. Thus, we provide evidence that dysfunction of spinal cord pain processing circuits may underlie the nociceptive phenotypes in ASD patients and mouse models. Copy rights belong to original authors. Visit the link for more info

Salt: the mineral so nice that much of early human civilization was based on its procurement! Now we put big chunks of it on tasty pretzels at the mall! If some ancient Greek person saw a big salty pretzel, I bet he'd be very excited and proud of us. Actually, they might have had pretzels back then, let me look. Nope doesn't look like they did, so I stand by my statement.    Follow us on Twitter @SciShowTangents, where we’ll tweet out topics for upcoming episodes and you can ask the science couch questions!    While you're at it, check out the Tangents crew on Twitter: Stefan: @itsmestefanchin Ceri: @ceriley Sam: @slamschultz Hank: @hankgreen   If you want to learn more about any of our main topics, check out these links:   [Truth or Fail] Salt Hotels https://www.lunasaladahotel.com.bo/ https://en.wikipedia.org/wiki/Palacio_de_Sal   Lake Peigneur https://gizmodo.com/thirty-years-ago-a-louisiana-lake-turned-into-a-swirli-5695711 https://news.google.com/newspapers?nid=2209&dat=19801121&id=mKUrAAAAIBAJ&sjid=0vwFAAAAIBAJ&pg=7170,4208269&hl=en   Underwater Icicles https://science.howstuffworks.com/environmental/earth/oceanography/underwater-brinicles.htm [Fact Off]   Coconut water IV http://www.mdpi.com/1420-3049/14/12/5144 https://podcasts.ufhealth.org/can-coconut-water-mimic-human-plasma/  https://www.sciencedirect.com/science/article/pii/S0735675700900627 https://www.npr.org/sections/health-shots/2011/08/15/139638930/saved-by-the-coconut-water-parsing-coconut-waters-medical-claims  https://www.ncbi.nlm.nih.gov/books/NBK154437/    Salt flats for satellite calibration https://www.semanticscholar.org/paper/Characterization-of-the-Salar-de-Uyuni-for-in-orbit-Lamparelli-Ponzoni/6b6a5037f838a2342d5681b642944fd68c775551 https://academic.oup.com/gji/article/172/1/31/2081107 https://www.nature.com/news/2007/071130/full/news.2007.315.html [Ask the Science Couch]   Salt in a wound history https://books.google.com/books?id=29gV_kCmZrIC&pg=PA141 https://www.abc.net.au/life/will-sea-water-help-heal-open-sores/11279036 http://utc.iath.virginia.edu/abolitn/abestwa8t.html   Saline solution https://www.npr.org/sections/health-shots/2018/03/31/597666140/why-did-sterile-salt-water-become-the-iv-fluid-of-choice https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4794509/   Nociception https://nba.uth.tmc.edu/neuroscience/m/s2/chapter06.html https://www.ncbi.nlm.nih.gov/books/NBK32659/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2903433/ [Butt One More Thing]   Rectal salt glands https://www.jstor.org/stable/1541076?seq=1 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5216465/ https://www.tandfonline.com/doi/abs/10.1080/00364827.1963.10410275?journalCode=ssar20

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.04.25.060939v1?rss=1 Authors: Mikhailov, N., Koroleva, K., Abdollahzadeh, A., Giniatullina, R., Gafurov, O., Malm, T., Sierra Lopez, A., Tohka, J., Noe, F. M., Giniatullin, R. Abstract: Background: A system of lymphatic vessels has been recently characterized in the meninges, with a postulated role in cleaning of the brain via cerebro-spinal fluid drainage. As meninges are an important tissue involved in the origin of migraine pain, we hypothesized that malfunctioning of a cleaning lymphatic system should affect the functional properties of meningeal nociception. To test this hypothesis, we studied migraine-related nociceptive and inflammatory mechanisms in the meninges, in a mouse model of primary lymphedema (K14-VEGFR3-Ig mice) characterized by the lack of functional meningeal lymphatic system. Methods: To study the migraine-related nociceptive and inflammatory mechanisms we recorded spiking activity from meningeal fibers of the trigeminal nerve, estimated the local mast cells infiltration, calcitonin gene-related peptide (CGRP) and cytokine levels (basal and under stimulating conditions), as well as the dura mater innervation in freshly-isolated hemiskull preparations from K14-VEGFR3-Ig (K14) or wild type C57BL/6 mice (WT). Results: We found that the level of CGRP and the production of TNF , which both are implicated in migraine, were reduced in meninges of K14 mice. There was a trend of having a larger number of dural mast cells, consistent with the increased level of the mast cell activator MCP-1 found in these animals. In addition, we found an increased spontaneous and ATP-induced nociceptive firing in the meningeal afferents of mice lacking meningeal lymphatic system. However, the patterns of trigeminal innervation in meninges remained unchanged. Conclusions: In summary, the lack of meningeal lymphatic system leads to a new balance between pro- and anti-inflammatory mechanisms implicated in peripheral nociception, affecting key cellular and humoral factors implicated in migraine. Copy rights belong to original authors. Visit the link for more info

This is Judy Gaman, author of the award winning book Age to Perfection: How to Thrive to 100, Happy, Healthy, and Wise and this is your Stay Young Medical Minute. Each day I bring you one new tip that will help you stay young and vibrant.  We all know the five senses. Sight, smell, taste, hearing, and touch—but did you know that those are just the beginning of our sensing capabilities? Our bodies have many other senses too. Balance, temperature, and time, as well as proprioception the body awareness that helps us not walk into things all the time and nociception, our sense of pain. Doctors suggest that these powerful abilities our bodies regulate are more important for our functioning that the well-known others, but they largely go unnoticed. We want to empower you with as much health information as possible. Visit Stayyoungamerica.com for free pod casts of the Staying Young Radio Show with over a hundred different health topics or you can follow us on Twitter @StayYoungMedia. Follow Us on Facebook! Tweet us on Twitter! Download the show on iTunes! Visit our website! Call us at 844-well100  Thank you for listening to the Stay Young Medical Minute! With all the mixed messages on health, you need information that you can use and that you can trust. Listen in as the experts discuss all topics health related. It's time to STAY YOUNG and stay healthy! Each week we tackle a topic and often with leading scientists, best-selling authors, and even your favorite celebrities! As a listener of our show, your input is important to us. Please take a moment to fill out this quick survey so we can serve you better - https://survey.libsyn.com/stayingyoung2 For more information on The Staying Young Show, please visit our website at www.StayYoungAmerica.com, and subscribe to the show in iTunes, Stitcher, or your favorite podcast app. You can also reach out to our host, Judy Gaman on www.judygaman.com for book purchasing, and speaking opportunities in your area!

The September 2018 #RehabCast from the Archives of Physical Medicine & Rehabilitation takes a look at the Nociception Coma Scale-Revised, one of the tools available to help clinicians assess potential pain responsiveness in their DoC patients, as well as the news headlines coming out of the University of Louisville on epidural stimulation for spinal cord injury. #RehabCast is the PM&R podcast for all of rehabilitation medicine: physiatry, occupational therapy, physical therapy, speech language pathology, neuropsychology, rehabilitation nursing and more.

Pain goes beyond what we physically feel in our bodies. It reaches back into other aspects—from the mental to emotional. Take a deeper dive and explore the neuroscience of nociception and the perception of a painful stimulus with Dr. Tor Wager, director of the Cognitive and Affective Control Laboratory and Professor of Psychology and Neuroscience at the University of Colorado, Boulder. He talks about the factors that influence pain as well as the facts or myths about pain as a learned experience. Also learn where the experience of pain comes from and the functions it serves while tracing the relationship between emotion and pain. Find out why exposure to pain may be the fastest way to overcome and alleviate it. Sign up for the latest episode at www.drjoetatta.com/podcasts.   Love the show? Subscribe, rate, review, and share! Here’s How » Join the Healing Pain Podcast Community today: drjoetatta.com Healing Pain Podcast Facebook Healing Pain Podcast Twitter Healing Pain Podcast YouTube Healing Pain Podcast LinkedIn

Connor Wander talked to Waylin Yu about his research in the overlap of pain, negative emotion, and addiction.  Waylin studies the fundamental roles of neurons in different areas of the brain, such as the amygdala, that may be responsible for these reactions, both independently and in relation to each other.  This includes chronic pain, anxiety, and alcohol and drug dependence, looking at activity in dopamine pathways, which play a role in reward-motivated behavior, and GABA, an important inhibitory neurotransmitter.  Hyperalgesia is an increased sensitivity to pain that can be caused by damage to neurons.  Nociception is the response of the nervous system to pain and harmful stimuli. About Waylin Originally hailing from Northern California, Waylin ventured eastward into salmon shorts and Sperry country for his undergraduate studies, where he graduated from Colby College with a BA in Psychology and Neuroscience.  There, he investigated the neuroprotective properties of choline in rodent models of depression and schizophrenia with Dr. Melissa J. Glenn.  Currently pursuing a PhD in Pharmacology at UNC Chapel Hill, Waylin is researching the neural circuitry of pain, aversion, and addiction by applying cutting-edge techniques like optogenetics, in vivo calcium imaging, and electrophysiology towards circuit-specific manipulations. Connect with Waylin on Twitter Learn more Find more information, publications, and Waylin's email address on the UNC Kash Lab website. Read accessible psychology and neuroscience articles on the PsychNeuro Blog. New project Neurator Blog to be announced! Reference papers Mu opioid receptor modulation of dopamine neurons in the periaqueductal gray/dorsal raphe: a role in regulation of pain. Alcohol dependence as a chronic pain disorder. Dorsal raphe dopamine neurons modulate arousal and promote wakefulness by salient stimuli. Contribution of dopamine receptors to periaqueductal gray-mediated antinociception.   Any other questions?  Let us know!  We appreciate your feedback. You can now support the podcast at https://www.patreon.com/sfspodcast.  Many thanks to our past and present supporters!  Thanks to Plant Warrior for their support.  Use discount code SFS10 at checkout for 10% off your purchase of plant-based protein.

The last few slides of this lecture are important and shouldn't be ignored - here is an audio recording to help understand them.

Fri, 18 Nov 2011 17

Professor Irene Tracey talks about her research into pain through using brain imaging technology to see exactly how the brain is affected by pain while discussing its implications to how we understand pain in society.

Professor Irene Tracey, director of the Oxford Centre for Functional Magnetic Resonance Imaging of the Brain, explains how MRI works and then talks about her research into people's perception of pain.

Some anesthetics activate TRPA1 channels to trigger pain and nerve-mediated inflammation.