Podcasts about nociceptive

Podcast Show Notes: Peripheral Vascular Disease in PainManagement Episode Highlights: - Host: Dr. David Rosenblum - Podcast: Pain Exam Podcast - Focus: Peripheral Arterial Disease (PAD) in Pain Management Download the App Key Topics Covered: 1. Peripheral Arterial Disease (PAD) Overview - Definition: Arterial sclerosis condition developing over long term - WHO Definition: Exercise-related pain or ankle-brachial index (ABI) < 0.9 - Prevalence:   * 3-4% in 60-65 year olds   * Increases to 15-20% in 85-90 year olds   * Up to 50% of patients may progress to symptomatic stages 2. Diagnostic Considerations Diagnostic Tests: - Ankle Brachial Index (ABI) - Ultrasound - CT Angiography - Physical examination - Pulse volume recordings - Transcutaneous oximetry ABI Interpretation: - 1.0-1.4: Normal - 0.9-1.0: Acceptable - 0.8-0.9: Some arterial disease - 0.5-0.8: Moderate arterial disease - < 0.5: Severe arterial disease 3. Pain Characteristics Types of Pain: - Intermittent claudication - Chronic limb ischemia - Nociceptive pain - Neuropathic pain - Mixed pain syndrome 4. Pain Management Strategies Pharmacological Approaches: - Mild Pain: Paracetamol, NSAIDs - Neuropathic Pain: Lidocaine patches, gabapentin, duloxetine - Severe Pain: Morphine, fentanyl, ketamine Non-Pharmacological Interventions: - Music therapy - Aromatherapy - Psychotherapy - Massage - Acupuncture - TENS - Intermittent pneumatic compression Upcoming Conferences Mentioned: - ASPN - ASIPP - Pain Week - Latin American Pain Society Additional Resources: - Pain Exam newsletter: painexam.com - Virtual pain fellowship at nrappain.org Disclaimer: Always consult with a healthcare professional for personalized medical advice. Reference Garba Rimamskep Shamaki, Favour Markson, Demilade Soji-Ayoade, Chibuike Charles Agwuegbo, Michael Olaseni Bamgbose, Bob-Manuel Tamunoinemi, Peripheral Artery Disease: A Comprehensive Updated Review, Current Problems in Cardiology, Volume 47, Issue 11, 2022,101082, Maier, J.A.; Andrés, V.; Castiglioni, S.; Giudici, A.; Lau, E.S.; Nemcsik, J.; Seta, F.; Zaninotto, P.; Catalano, M.; Hamburg, N.M. Aging and Vascular Disease: A Multidisciplinary Overview. J. Clin. Med. 2023, 12, 5512. https://doi.org/10.3390/jcm12175512 Maier, J.A.; Andrés, V.; Castiglioni, S.; Giudici, A.; Lau, E.S.; Nemcsik, J.; Seta, F.; Zaninotto, P.; Catalano, M.; Hamburg, N.M. Aging and Vascular Disease: A Multidisciplinary Overview. J. Clin. Med. 2023, 12, 5512. https://doi.org/10.3390/jcm12175512  

Podcast Show Notes: Peripheral Vascular Disease in PainManagement Episode Highlights: - Host: Dr. David Rosenblum - Podcast: Pain Exam Podcast - Focus: Peripheral Arterial Disease (PAD) in Pain Management Download the App Key Topics Covered: 1. Peripheral Arterial Disease (PAD) Overview - Definition: Arterial sclerosis condition developing over long term - WHO Definition: Exercise-related pain or ankle-brachial index (ABI) < 0.9 - Prevalence:   * 3-4% in 60-65 year olds   * Increases to 15-20% in 85-90 year olds   * Up to 50% of patients may progress to symptomatic stages 2. Diagnostic Considerations Diagnostic Tests: - Ankle Brachial Index (ABI) - Ultrasound - CT Angiography - Physical examination - Pulse volume recordings - Transcutaneous oximetry ABI Interpretation: - 1.0-1.4: Normal - 0.9-1.0: Acceptable - 0.8-0.9: Some arterial disease - 0.5-0.8: Moderate arterial disease - < 0.5: Severe arterial disease 3. Pain Characteristics Types of Pain: - Intermittent claudication - Chronic limb ischemia - Nociceptive pain - Neuropathic pain - Mixed pain syndrome 4. Pain Management Strategies Pharmacological Approaches: - Mild Pain: Paracetamol, NSAIDs - Neuropathic Pain: Lidocaine patches, gabapentin, duloxetine - Severe Pain: Morphine, fentanyl, ketamine Non-Pharmacological Interventions: - Music therapy - Aromatherapy - Psychotherapy - Massage - Acupuncture - TENS - Intermittent pneumatic compression Upcoming Conferences Mentioned: - ASPN - ASIPP - Pain Week - Latin American Pain Society Additional Resources: - Pain Exam newsletter: painexam.com - Virtual pain fellowship at nrappain.org Disclaimer: Always consult with a healthcare professional for personalized medical advice. Reference Garba Rimamskep Shamaki, Favour Markson, Demilade Soji-Ayoade, Chibuike Charles Agwuegbo, Michael Olaseni Bamgbose, Bob-Manuel Tamunoinemi, Peripheral Artery Disease: A Comprehensive Updated Review, Current Problems in Cardiology, Volume 47, Issue 11, 2022,101082, Maier, J.A.; Andrés, V.; Castiglioni, S.; Giudici, A.; Lau, E.S.; Nemcsik, J.; Seta, F.; Zaninotto, P.; Catalano, M.; Hamburg, N.M. Aging and Vascular Disease: A Multidisciplinary Overview. J. Clin. Med. 2023, 12, 5512. https://doi.org/10.3390/jcm12175512 Maier, J.A.; Andrés, V.; Castiglioni, S.; Giudici, A.; Lau, E.S.; Nemcsik, J.; Seta, F.; Zaninotto, P.; Catalano, M.; Hamburg, N.M. Aging and Vascular Disease: A Multidisciplinary Overview. J. Clin. Med. 2023, 12, 5512. https://doi.org/10.3390/jcm12175512  

Podcast Show Notes: Peripheral Vascular Disease in PainManagement Episode Highlights: - Host: Dr. David Rosenblum - Podcast: Pain Exam Podcast - Focus: Peripheral Arterial Disease (PAD) in Pain Management Download the App Key Topics Covered: 1. Peripheral Arterial Disease (PAD) Overview - Definition: Arterial sclerosis condition developing over long term - WHO Definition: Exercise-related pain or ankle-brachial index (ABI) < 0.9 - Prevalence:   * 3-4% in 60-65 year olds   * Increases to 15-20% in 85-90 year olds   * Up to 50% of patients may progress to symptomatic stages 2. Diagnostic Considerations Diagnostic Tests: - Ankle Brachial Index (ABI) - Ultrasound - CT Angiography - Physical examination - Pulse volume recordings - Transcutaneous oximetry ABI Interpretation: - 1.0-1.4: Normal - 0.9-1.0: Acceptable - 0.8-0.9: Some arterial disease - 0.5-0.8: Moderate arterial disease - < 0.5: Severe arterial disease 3. Pain Characteristics Types of Pain: - Intermittent claudication - Chronic limb ischemia - Nociceptive pain - Neuropathic pain - Mixed pain syndrome 4. Pain Management Strategies Pharmacological Approaches: - Mild Pain: Paracetamol, NSAIDs - Neuropathic Pain: Lidocaine patches, gabapentin, duloxetine - Severe Pain: Morphine, fentanyl, ketamine Non-Pharmacological Interventions: - Music therapy - Aromatherapy - Psychotherapy - Massage - Acupuncture - TENS - Intermittent pneumatic compression Upcoming Conferences Mentioned: - ASPN - ASIPP - Pain Week - Latin American Pain Society Additional Resources: - Pain Exam newsletter: painexam.com - Virtual pain fellowship at nrappain.org Disclaimer: Always consult with a healthcare professional for personalized medical advice. Reference Garba Rimamskep Shamaki, Favour Markson, Demilade Soji-Ayoade, Chibuike Charles Agwuegbo, Michael Olaseni Bamgbose, Bob-Manuel Tamunoinemi, Peripheral Artery Disease: A Comprehensive Updated Review, Current Problems in Cardiology, Volume 47, Issue 11, 2022,101082, Maier, J.A.; Andrés, V.; Castiglioni, S.; Giudici, A.; Lau, E.S.; Nemcsik, J.; Seta, F.; Zaninotto, P.; Catalano, M.; Hamburg, N.M. Aging and Vascular Disease: A Multidisciplinary Overview. J. Clin. Med. 2023, 12, 5512. https://doi.org/10.3390/jcm12175512 Maier, J.A.; Andrés, V.; Castiglioni, S.; Giudici, A.; Lau, E.S.; Nemcsik, J.; Seta, F.; Zaninotto, P.; Catalano, M.; Hamburg, N.M. Aging and Vascular Disease: A Multidisciplinary Overview. J. Clin. Med. 2023, 12, 5512. https://doi.org/10.3390/jcm12175512  

What is the relationship between nonsuicidal self-injury (NSSI) and pain? Are individuals who self-injure less sensitive to pain than those who don't self-injure? What are the ethics involved in conducting research on pain? In this episode, Dr. Julian Koenig describes the research on the experience of pain among those who self-harm. Learn more about Dr. Koenig and his research lab at www.koeniglab.de, and follow him on Twitter/X at @koeniglab.Below are links to some of the research referenced in this episode:Koenig, J., Thayer, J. F., & Kaess, M. (2016). A meta-analysis on pain sensitivity in self-injury. Psychological Medicine, 46(8), 1597-1612.Koenig, J., Klier, J., Parzer, P., Santangelo, P., Resch, F., Ebner-Priemer, U., & Kaess, M. (2021). High-frequency ecological momentary assessment of emotional and interpersonal states preceding and following self-injury in female adolescents. European Child & Adolescent Psychiatry, 30(8), 1299-1308.Kaess, M., Hooley, J. M., Klimes-Dougan, B., Koenig, J., Plener, P. L., Reichl, C., Robinson, K., Schmahl, C., Sicorello, M., Schreiner, M. W., & Cullen, K. R. (2021). Advancing a temporal framework for understanding the biology of nonsuicidal self-injury: An expert review. Neuroscience and Biobehavioral Reviews, 130, 228-239.Störkel, L. M., Karabatsiakis, A., Hepp, J., Kolassa, I.-T., Schmahl, C., & Niedtfeld, I. (2021). Salivary beta-endorphin in nonsuicidal self-injury: an ambulatory assessment study. Neuropsychopharmacology, 46(7), 1357-1363.Sigrist, C., Kaess, M., & Koenig, J. (2023). Autonomic nervous system function in nonsuicidal self-injury—A Research Domain Criteria perspective on the arousal/regulatory systems. In E. E. Lloyd-Richardson, I. Baetens, & J. Whitlock (Eds.), The Oxford handbook of nonsuicidal self-injury (pp. C18S1–C18S23). Oxford University Press.Naoum, J., Reitz, S., Krause-Utz, A., Kleindienst, N., Willis, F., Kuniss, S., Baumgärtner, U., Mancke, F., Treede, R.-D., & Schmahl, C. (2016). The role of seeing blood in non-suicidal self-injury in female patients with borderline personality disorder. Psychiatry Research, 246, 676-682.Follow Dr. Westers on Instagram and Twitter/X (@DocWesters). To join ISSS, visit itriples.org and follow ISSS on Facebook and TwitterX (@ITripleS).The Psychology of Self-Injury podcast has been rated #1 by Feedspot  in their list of "10 Best Self Harm Podcasts" and #5 in their "20 Best Clinical Psychology Podcasts." It has also been featured in Audible's "Best Mental Health Podcasts to Defy Stigma and Begin to Heal."If you or someone you know should be interviewed on the podcast, we want to know! Please fill out this form, and we will be in touch with more details if it's a good fit.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.27.550880v1?rss=1 Authors: McPherson, J. G., Bandres, M. F. Abstract: The purpose of this study is to determine whether intraspinal microstimulation (ISMS) intended to enhance voluntary motor output after spinal cord injury (SCI) modulates neural population-level spinal responsiveness to nociceptive sensory feedback. The study was conducted in vivo in three cohorts of rats: neurologically intact, chronic SCI without behavioral signs of neuropathic pain, and chronic SCI with SCI-related neuropathic pain (SCI-NP). Nociceptive sensory feedback was induced by application of graded mechanical pressure to the plantar surface of the hindpaw before, during, and after periods of sub-motor threshold ISMS delivered within the motor pools of the L5 spinal segment. Neural population-level responsiveness to nociceptive feedback was recorded throughout the dorso-ventral extent of the L5 spinal segment using dense multi-channel microelectrode arrays. Whereas motor-targeted ISMS reduced nociceptive transmission across electrodes in neurologically intact animals both during and following stimulation, it was not associated with altered nociceptive transmission in rats with SCI that lacked behavioral signs of neuropathic pain. Surprisingly, nociceptive transmission was reduced both during and following motor-targeted ISMS in rats with SCI-NP, and to an extent comparable to that of neurologically intact animals. The mechanisms underlying the differential anti-nociceptive effects of motor-targeted ISMS are unclear, although they may be related to differences in the intrinsic active membrane properties of spinal neurons across the cohorts. Nevertheless, the results of this study support the notion that it may be possible to purposefully engineer spinal stimulation-based therapies that afford multi-modal rehabilitation benefits, and specifically that it may be possible to do so for the individuals most in need - i.e., those with SCI-related movement impairments and SCI-NP. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

This week, we take a look at the practical management of pain and the advancement of science regarding it, with our guest Dr. Dan Clauw. Co-author of the paper: “Identifying and Managing Nociplastic Pain in Individuals With Rheumatic Diseases: A Narrative Review”, Dr. Clauw joins us today to discuss the work to introduce the three types of pain classified by “The International Association for the Study of Pain” and the mechanisms that underlie pain, as it relates to the field of rheumatology.  

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.14.549006v1?rss=1 Authors: Coll, M.-P., Walden, Z., Bourgoin, P.-A., Taylor, V., Rainville, P., Robert, M., Nguyen, D. K., Jolicoeur, P., Roy, M. Abstract: Pain perception and its modulation are fundamental to human learning and adaptive behavior. This study investigated the hypothesis that pain perception is tied to pain's learning function. Thirty-one participants performed a threat conditioning task where certain cues were associated with a possibility of receiving a painful electric shock. The cues that signaled potential pain or safety were regularly changed, requiring participants to continually establish new associations. Using computational models, we quantified participants' pain expectations and prediction errors throughout the task and assessed their relationship with pain perception and electrophysiological responses. Our findings revealed that subjective pain perception increases with prediction error, that is when pain was unexpected. Prediction errors were also related to physiological nociceptive responses, including the amplitude of the nociceptive flexion reflex and EEG markers of cortical nociceptive processing (N2-P2 and gamma-band ERS). Additionally, higher pain expectations were related to increased late event-related potential responses and alpha/beta decreases in amplitude during cue presentation. These results further strengthen the idea of a crucial link between pain and learning and suggest that understanding the influence of learning mechanisms in pain modulation could help us understand when and why pain perception is modulated in health and disease. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

We don't all strive for elite physical performance, but we do all place demands on our bodies. Some of the internal signals that we receive as a result could be interpreted as pain, so how do we know when we should push through and when we should pull back? We have talked in previous episodes about the complex phenomenon of pain, and how deeply enmeshed our perception of pain is with our beliefs and previous experiences. Today that conversation continues with host Rachel and returning guest and Doctor of Physical Therapy Marnie Hartman. In this episode, Marnie and host Rachel explore what neuroscience can teach us about physical performance. Listen in as we discuss the importance of bringing curiosity and playfulness into our physical pursuits, choosing to question our assumptions, and learning to listen deeply – but with discernment – to our internal signals. Show Notes: Defining physical performance as how our bodies interact with the environment [4:56] Athletes' relationship to pain [7:38] Sensory science 101: perception, interoception, nociception [9:38] Nociceptive signals in physical performance [13:56] The magic of training: creating a gap between signal and response [17:49] Recognizing and reframing less desirable experiences in the past [22:59] A case study in context and the impact of stress [27:35] Learning to discern our internal signals [31:35] Choosing to bring that awareness into physical challenges [36:31] Having our assumptions reflected back to us [40:12] Playfulness unloads our stress cup [48:22] Exploring the role of yoga practice [49:55] How our “patterning” can become an obstacle to overcome [58:42] Final thoughts and resources [1:02:21] Links Mentioned: Watch this episode on YouTube Previous Yoga Medicine Podcast Episodes: Episode 15: Shifting Persistent Pain Episode 64: Impactful Pain Strategies Pain Science for Yoga Teachers Online Course Yoga Medicine® Online Resources: Pain vs Suffering: Where to Begin Neuroscience Enhanced Performance Connect with Marnie Hartman: Body IQ PT | LinkedIn | Email | Yoga Medicine® Online Guest Teacher You can learn more about this episode, and see the full show notes at YogaMedicine.com/podcast-78. And you can find out more about insider tips, online classes or information on our teacher trainings at YogaMedicine.com. To support our work, please leave us a 5 star review with your feedback on iTunes/Apple Podcasts.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.06.30.547270v1?rss=1 Authors: Kaya, B., Cioffi, I., Moayedi, M. Abstract: Orofacial pain is thought to be more unpleasant than pain elsewhere in the body due to the importance of the face in social, feeding, and exploratory behaviors. Nociceptive information from the orofacial region is carried to the brain via the trigeminal nerve (CNV) via the trigeminal brainstem sensory nuclear complex (VBSNC). Pre-clinical evidence revealed a monosynaptic circuit from CNV to the lateral parabrachial nucleus (latPB), which underlies the greater unpleasantness elicited by orofacial pain. The latPB further projects to the central amygdala (CeA), which contributes to the affective component of pain in rodents. However, this circuit has yet to be delineated in humans. Here, we aimed to resolve this circuit using 7T diffusion-weighted imaging from the Human Connectome Project (HCP). We performed probabilistic tractography in 80 participants to resolve the CNV-latPB-CeA circuit. The basolateral amygdala (BLAT) was used as a negative control, given that we did not anticipate CNV-latPB-BLAT connectivity. Connectivity strengths were compared using a repeated- measures ANOVA with factors 'hemisphere' (left; right), and 'target' (CeA; BLAT), with sex included in the model for both pilot and validation samples. Only the 'target' factor was significant in both samples (FPilot = 11.4804, p = 0.005; FValidation = 69.113, p less than .001). Post hoc tests showed that the CeA had significantly stronger connectivity strength than the BLAT (pTukey-Pilot = 0.005; pTukey-Validation less than 0.001). This study delineates the human CNV-latPB-CeA circuit for the first time in vivo. This circuit may provide a neuroanatomical substrate for the affective dimensions of orofacial pain. 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/2023.04.12.536477v1?rss=1 Authors: Bandres, M. F., Gomes, J. L., McPherson, J. G. Abstract: Electrical stimulation of spinal networks below a spinal cord injury (SCI) is a promising approach to restore functions compromised by inadequate excitatory neural drive. The most translationally successful examples are paradigms intended to increase neural transmission in weakened yet spared motor pathways and spinal motor networks rendered dormant after being severed from their inputs by lesion. Less well understood is whether spinal stimulation is also capable of reducing neural transmission in pathways made pathologically overactive by SCI. Debilitating spasms, spasticity, and neuropathic pain are all common manifestations of hyperexcitable spinal responses to sensory feedback. But whereas spasms and spasticity can often be managed pharmacologically, SCI-related neuropathic pain is notoriously medically refractory. Interestingly, however, spinal stimulation is a clinically available option for ameliorating neuropathic pain arising from etiologies other than SCI, and it has traditionally been assumed to modulate sensorimotor networks overlapping with those engaged by spinal stimulation for motor rehabilitation. Thus, we reasoned that spinal stimulation intended to increase transmission in motor pathways may simultaneously reduce transmission in spinal pain pathways. Using a well-validated pre-clinical model of SCI that results in severe bilateral motor impairments and SCI-related neuropathic pain, we show that the responsiveness of neurons integral to the development and persistence of the neuropathic pain state can be enduringly reduced by motor-targeted spinal stimulation while preserving spinal responses to non-painrelated sensory feedback. These results suggest that spinal stimulation paradigms could be intentionally designed to afford multi-modal therapeutic benefits, directly addressing the diverse, intersectional rehabilitation goals of people living with SCI. 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/2023.02.13.528015v1?rss=1 Authors: Dourson, A. J., Fadaka, A. O., Warshak, A. M., Paranjpe, A., Weinhaus, B., Queme, L. F., Hofmann, M. C., Evans, H. M., Donmez, O. A., Forney, C., Weirauch, M. T., Kottyan, L. T., Lucas, D., Deepe, G. S., Jankowski, M. P. Abstract: These systems are vulnerable to effects of early life injury which can influence outcomes related to nociception following subsequent injury later in life (i.e. neonatal nociceptive priming). The underpinnings of this phenomenon are largely unknown, although macrophages can be epigenetically trained by injury. We found that macrophages are both necessary and partially sufficient to drive neonatal nociceptive priming possibly due to a long-lasting epigenetic remodeling of peripheral macrophages. The p75 neurotrophic factor receptor (NTR) was observed to be an important effector in regulating neonatal nociceptive priming. p75NTR modulates the inflammatory profile and responses of rodent and human macrophages. This pain memory was able to be transferred to a naive host to alter sex-specific pain-related behaviors. This study reveals a novel mechanism by which acute post-surgical pain may transition to chronic pain in children. 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/2022.11.29.518364v1?rss=1 Authors: Thorell, O., Ydrefors, J., Svantesson, M., Gerdle, B., Olausson, H., Mahns, D., Nagi, S. S. Abstract: Introduction: The role of pain as a warning system necessitates a rapid transmission of information from the periphery for the execution of appropriate motor responses. The nociceptive withdrawal reflex (NWR) is a physiological response to protect the limb from a painful stimulus and is often considered an objective measure of spinal nociceptive excitability. The NWR is commonly defined by its latency in the presumed Adelta-fiber range consistent with the canonical view that fast pain is signaled by Adelta nociceptors. We recently demonstrated that human skin is equipped with ultrafast (A beta range) nociceptors. Here, we investigated the short-latency component of the reflex and explored the relationship between reflex latency and pain perception. Methods: We revisited our earlier work on NWR measurements in which, following convention, only those reflex responses were selected that were in the presumed Adelta range (taken to be latencies greater than or equal to 90 ms in that study). In our current analysis, we expanded the time window to search for shorter latency responses and compared those with pain ratings. Results: In both cohorts, we found an abundance of recordings with short-latency reflex responses. In nearly 90% of successful recordings, only single reflex responses (not dual) were seen which allowed us to compare pain ratings to reflex latencies. We found that shorter latency reflexes were just as painful as those in the conventional latency range. Discussion: We found a preponderance of short-latency painful reflex responses. Based on this finding, we suggest that short-latency responses must be considered in future studies. We predict these might be signaled by the ultrafast nociceptors, warranting further investigation. 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/2022.10.20.513010v1?rss=1 Authors: Li, K., Tsukasa, Y., Kurio, M., Maeta, K., Tsumadori, A., Baba, S., Nishimura, R., Murakami, A., Onodera, K., Morimoto, T., Uemura, T., Usui, T. Abstract: Appropriate modulation of escape behaviors in response to potentially damaging stimuli is essential for survival. Although nociceptive circuitry has been studied, it is poorly understood how genetic contexts affect the relevant escape responses. Using an unbiased genome-wide association analysis, we identified a Ly6/-neurotoxin family protein, Belly roll (Bero), which negatively regulates Drosophila nociceptive escape behavior. We show that Bero is expressed in abdominal leucokinin-producing neurons (ABLK neurons) and bero knockdown in ABLK neurons resulted in enhanced escape behavior. Furthermore, we demonstrated that ABLK neurons responded to the activation of nociceptors and initiated the behavior. Notably, bero knockdown reduced the persistent neuronal activity and increased the evoked nociceptive responses in ABLK neurons. Our findings reveal that Bero modulates an escape response by regulating distinct neuronal activities in ABLK neurons. 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/2022.10.07.511265v1?rss=1 Authors: Yoshino, J., Mali, S., Williams, C., Morita, T., Emerson, C., Arp, C., Sophie, M., Yin, C., The, L., Chikaya, H., Motoyoshi, M., Ishii, K., Emoto, K., Bautista, D. M., Parrish, J. Z. Abstract: Somatosensory neurons (SSNs) that detect and transduce mechanical, thermal, and chemical stimuli densely innervate an animal's skin. However, despite the fact that epidermal cells provide the first point of contact for sensory stimuli. our understanding of roles that epidermal cells play in SSN function, particularly nociception, remains limited. Here, we show that stimulating Drosophila epidermal cells elicits activation of SSNs including nociceptors and triggers a variety of behavior outputs, including avoidance and escape. Further, we find that epidermal cells are intrinsically mechanosensitive and that epidermal mechanically evoked calcium responses require the store-operated calcium channel Orai. Epidermal cell stimulation augments larval responses to acute nociceptive stimuli and promotes prolonged hypersensitivity to subsequent mechanical stimuli. Hence, epidermal cells are key determinants of nociceptive sensitivity and sensitization, acting as primary sensors of noxious stimuli that tune nociceptor output and drive protective behaviors. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.08.30.505953v1?rss=1 Authors: Liu, F., Su, S., Zhang, L., Fang, Y., Cui, H., Sun, J., Xie, Y., Ma, C. Abstract: Background: Neuropathic pain is difficult to treat in clinical practice, and the underlying mechanisms are insufficiently elucidated. Previous studies have demonstrated that Fc{gamma} receptor I (Fc{gamma}RI) is expressed in the neurons of the dorsal root ganglion (DRG) and may be involved in chronic pain. Methods: Chronic constriction injury (CCI) was used to induce neuropathic pain in rats. Primary neuron-specific Fcgr1 conditional knockout (CKO) rats were established by crossing rats carrying a Fcgr1loxP+/+ with the PirtCRE+ line. Behavioral and molecular studies were conducted to evaluate the differences between wild-type and CKO rats after CCI. Results: We first revealed that CCI activated neuronal Fc{gamma}RI-related signaling in the DRG. CCI-induced neuropathic pain was alleviated in CKO rats. C-reactive protein (CRP) was increased in the DRG after nerve injury. Intraganglionic injection or overexpression of the recombinant CRP protein in the DRG evoked pain accompanied and activated neuronal Fc{gamma}RI. CRP-evoked pain was significantly reduced in CKO rats. Furthermore, microinjection of native IgG into the DRG alleviated neuropathic pain and the activation of neuronal Fc{gamma}RI-related signaling. Conclusions: Our results indicate that the activation of neuronal CRP/Fc{gamma}RI-related signaling plays an important role in the development of pain in CCI. Our findings may provide novel insights into the neuroimmune responses after peripheral nerve injury and might suggest potential therapeutic targets for neuropathic pain. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer

Did you know there are different types of pain? In this episode of the Big Questions Podcast, we chat to Dr Lydia Coxon, a researcher in the Nuffield Department of Women's and Reproductive Health at Oxford. Lydia is looking at the mechanisms that cause pain in patients with endometriosis - a common gynaecological condition where tissue that normally grows inside the womb is found outside the womb. Through her research she hopes to better understand the type of pain that endometriosis causes, so that it can be treated more effectively.

Bone marrow stem cell transplants are some of the most important tools in treating diseases like leukemia and multiple myeloma. However, harvesting enough stem cells for transplantation is often a big issue for doctors. Finding new ways to elicit stem cell mobilization from the bone marrow to improve harvesting could go a long way in improving treatment. Today's episode of Beyond the Abstract features work by scientists who find a surprising role for pain nerves, known as nociceptive neurons, in promoting stem cell mobilization. Ellen and Derek discuss how they stumbled upon this finding and how there might be more to a chili pepper than meets the eye. Gao et al. Nociceptive nerves regulate haematopoietic stem cell mobilization. Nature, January 2021. DOI: https://doi.org/10.1038/s41586-020-03057-y (10.1038/s41586-020-03057-y) The information presented here is not medical advice. Consult your physician on any questions regarding your personal health.

From Theresa Mallick-Searle MS, PMGT-BC, ANP-BC, and the Opioid REMS Education Initiative, an introduction to nociceptive pain and expert insight on recognizing the signs, symptoms, and pathophysiology of somatic and visceral nociceptive pain. This episode also features an interview with a standardized patient who has been experiencing chronic severe back pain. Listen as the patient details the impact of pain on his life and as Ms. Mallick-Searle investigates his pain history and symptoms to elicit a diagnosis of somatic nociceptive pain.Presenter:Theresa Mallick-Searle, MS, PMGT-BC, ANP-BCDivision of Pain MedicineStanford University Medical CenterPalo Alto, CaliforniaAdult Nurse PractitionerDivision of Pain MedicineStanford Health CareRedwood City, CaliforniaThis 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 Link to full program:www.opioidremseducation.com

Nihkil Verma is a medical doctor who specializes in treating and managing spinal health, mobility, chronic pain, and athletic health among others. In this episode, we discuss chronic pain, the various ways chronic pain is managed, transhumanism, muscular tension, and the possible future interventions in managing chronic pain. You can find Nihkil on Twitter at VermaN21 and on Instagram at dr.nvsportandspine. Enjoy! (5:44) What is a notochord? (10:18) What portion of pain is subjective and what portion is objective? How much do we know about each of these components? Nociceptive vs Neuropathic pain. (14:40) What do we know about the memory component of subjective and chronic pain? And why is it so misunderstood? (18:02) Why opioids are terrible widespread methods for treating chronic pain. (19:54) How can we get better in touch with our endogenous opioids? (24:50) Is there such a thing as too much mobility? (26:44) Is there evidence that weightlifting helps manage chronic pain? (29:56) How does the brain create a unitary picture of experience? (33:10) Transhumanism, the ways people apply it to managing chronic back pain, and the problems with it. (41:45) Is there a relationship between muscular tension and chronic pain? Why are float tanks so effective? (48:55) What is the potential of stem cell regeneration for chronic pain? Do psychedelics or ketamines play any role in the future of treating chronic pain? (55:53) Will exoskeletons ever become mainstream? Are there any disadvantages to this?        

Migraines are no longer considered a vascular headache and now considered a neurologic disorder of dysfunctional nociceptive processing.  Diagnosis is completed clinically with no lab or imaging usually needed.  Treatment includes - Antidopaminergics (Metoclopramide & Prochlorperazine) - Triptans (Sumatriptan) - Nonsteroidals (Ketorolac).  Consider steroids to lessen the risk of recurrence.  Opioids should be avoided and are last line. Most patients don't need specialist referral.  To learn more, visit https://courses.ccme.org/course/em-prep

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.11.21.392548v1?rss=1 Authors: de Lima, C. K. F., Sisnande, T., da Silva, R. V., da Silva, V. D., do Amaral, J. J., Ochs, S. M., Roedel dos Santos, B. L., Miranda, A. L. P., Lima, L. M. T. d. R. Abstract: Zinc (Zn) is an essential micronutrient involved in a large diversity of cellular metabolism, included in the physiology of nervous system and pain modulation. There is little evidence for the role of Zn nutritional alternations to the onset and progression of neuropathic and inflammatory pain. We investigate the effects of a zinc restricted diet on the development of pain. Weaned mice were submitted to different diets: AIN-93 (38mg/kg of Zn) and Zn-deficient (AIN-93 with 11mg/kg of Zn), during four weeks. Mechanical allodynia was measured weekly using Von Frey hairs. Plantar assays for cold and heat allodynia, formalin-induced nociception and carrageenan-induced mechanical allodynia were performed at the 4th week. Plasma, DRG and livers samples were obtained for biochemical and metabolomics analysis. Zn deficient diet completely changed mice sensitivity pattern, inducing an intense allodynia evoked by mechanical, cold and heat stimulus since weaning and during four weeks. Showed also an increased sensitivity of neurogenic phase of formalin test but the inflammatory pain behavior was drastically reduced. Zn restriction increased the ATF-3 and SOD-1 levels at DRG and reduced that of GFAP, leading an increase of neuronal activation and oxidative stress, and reduced neuroimmune activity. Plasma TNF was also reduced and metabolomics analyses suggest a downregulation of lipid metabolism of arachidonic acid, reinforcing the impact of Zn restriction to the inflammatory response. Reduction of Zn intake interferes in pain circuits, reducing inflammatory pain, however enhancing nociceptive pain. Accordingly, Zn imbalance could be predisposing factor for NP development. Therefore, dietary zinc supplementation and its monitoring present clinical relevance. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.10.29.360222v1?rss=1 Authors: Zamorano, A. M., Kleber, B., Arguissain, F. G., Vuust, P., Flor, H., Graven-Nielsen, T. Abstract: Repetitive movements and multisensory integration promote use-dependent plasticity, which has been consistently demonstrated using musical training as a model. Prolonged and repeated execution of motor patterns is also a main risk factor for developing pain syndromes, yet the neural underpinnings that link repetitive movements and use-dependent plasticity to abnormal pain processing in humans are unknown. Employing nociceptive and non-nociceptive electrical stimulation to evoke brain responses, we demonstrate that healthy musicians compared to non-musicians show larger non-nociceptive N140 and nociceptive N200 responses, smaller non-nociceptive P200 responses, and faster reaction times (RTs) to both stimuli. Across participants, larger N140 and N200 amplitudes predicted the RTs, whereas the amount of daily practice in musicians predicted RTs, non-nociceptive P200, and nociceptive P300 components. These novel findings indicate that the mechanisms by which repetitive sensorimotor training and multimodal integration promote neural plasticity in multisensory neural structures may also increase stimulus-selectivity to nociceptive cues in healthy individuals. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.10.27.358267v1?rss=1 Authors: Ng, S. Y., Lee, A. T.-H., Ariffin, M. Z., Woon, P. J., Chng, T. S. H., Khanna, S. Abstract: The forebrain medial septum (MS), implicated in affective-motivational behaviours, is enriched in substance P (SP) sensitive neurokinin-1 receptors (NK1R) and somatostatin (SST) receptors (SSTR) that are located almost exclusively on cholinergic and GABAergic neurons, respectively. However, the physiological function of these receptors is poorly understood. This study characterized the actions of intraseptal SP on electrophysiological indices of septo-hippocampal activation, then utilised NK1 receptor antagonist, L-733,060, and SST to investigate the physiological role of endogenous neurotransmission at NK1R, and SST-sensitive mechanisms, in novel open field and formalin test of inflammatory pain. The findings showed that neurotransmission at NK1R mediates formalin-induced electrophysiological responses in the septo-hippocampus in anaesthetized and behaving animals. Furthermore, parallel NK1R- and SST-sensitive mechanisms affect different aspects of animal behaviours in both tests, collectively modulating attention and habituation in open field and driving formalin-induced nociception. This brings out a newer peptidergic dimension of septal physiology in nociception. Copy rights belong to original authors. Visit the link for more info

Le début d'une petite série sur la douleur

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.30.228015v1?rss=1 Authors: Barkai, O., Lev, S., Butterman, R., Katz, B., Binshtok, A. M. Abstract: The output from the peripheral terminals of primary nociceptive neurons, which detect and encode the information regarding noxious stimuli, is crucial in determining pain sensation. The nociceptive terminal endings are morphologically complex structures assembled from multiple branches of different geometry, which converge in a variety of forms to create the terminal tree. The output of a single terminal is defined by the properties of the transducer channels producing the generation potentials and voltage-gated channels, translating the generation potentials into action potential firing. However, in the majority of cases, noxious stimuli activate multiple terminals; thus, the output of the nociceptive neuron is defined by the integration and computation of the inputs of the individual terminals. Here we used a computational model of nociceptive terminal tree to study how the architecture of the terminal tree affects input-output relation of the primary nociceptive neurons. We show that the input-output properties of the nociceptive neurons depend on the length, the axial resistance, and location of individual terminals. Moreover, we show that activation of multiple terminals by capsaicin-like current allows summation of the responses from individual terminals, thus leading to increased nociceptive output. Stimulation of terminals in simulated models of inflammatory or nociceptive hyperexcitability led to a change in the temporal pattern of action potential firing, emphasizing the role of temporal code in conveying key information about changes in nociceptive output in pathological conditions, leading to pain hypersensitivity. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.06.18.160077v1?rss=1 Authors: Wairkar, Y. P., Tang, S.-J., Bush, K., Barber, K., Martinez, J. Abstract: The success of antiretroviral therapy (ART) has improved the survival of HIV-infected patients significantly. However, significant numbers of patients on ART whose HIV disease is well controlled show peripheral sensory neuropathy (PSN), suggesting that ART may cause PSN. Although the nucleoside reverse transcriptase inhibitors (NRTIs), one of the vital components of ART, are thought to contribute to PSN, the mechanisms underlying the PSN induced by NRTIs are unclear. In this study, we developed a Drosophila model of NRTI-induced PSN that recapitulates the salient features observed in patients undergoing ART: PSN and nociceptive hypersensitivity. Furthermore, our data demonstrate that pathways known to suppress PSN induced by chemotherapeutic drugs are ineffective in suppressing the PSN or nociception induced by NRTIs. Instead, we found that increased dynamics of a peripheral sensory neuron may underlie NRTI-induced PSN and nociception. Our model provides a solid platform in which to investigate further mechanisms of ART-induced PSN and nociceptive hypersensitivity. Copy rights belong to original authors. Visit the link for more info

¡Gracias por escuchar! En este episodio hablaré del papel que juega la inflamación en la generación de dolor en pacientes con osteoartritis. La OA tiene una morbilidad asociada sustancial y constituye un creciente problema de salud pública derivado en gran medida del envejecimiento poblacional. Los síntomas de la OA pueden ser funcionales pero se manifiestan principalmente como dolor y el manejo de la enfermedad se centra principalmente en su control.Agradezco que escuchen este podcast y les recuerdo que se encuentra disponible en el catálogo de iTunes, en Google Play (siendo accesible a través del gestor de podcasts de su dispositivo móvil), así como en Spotify. Agradezco también su retroalimentación en estas plataformas y les pido amablemente que califiquen el podcast ya que esto es importante para su continuado desarrollo.A continuación se enlistan las referencias mencionadas en este episodio: Grace, P. M., Hutchinson, M. R., Maier, S. F. & Watkins, L. R. 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N.B.: This month's show notes are a departure from the usual summary.  Below is a reprint (with permission) of a soon-to-be released chapter, Horeczko T. "Acute Pain in Children". In Management of Pain and Procedural Sedation in Acute Care. Strayer R, Motov S, Nelson L (eds). 2017.  Rather than the customary blog post summary, the full chapter (with links) is provided as a virtual reference. INTRODUCTION Pain is multifactorial: it is comprised of physical, psychological, emotional, cultural, and contextual features.  In children often the predominant feature may not be initially apparent.  Although clinicians may focus on the physical component of pain, much time, energy, and suffering can be saved through a holistic approach.  What is the age and developmental stage of the child?  How is the child reacting to his condition?  What are the circumstances?  What is the family or caregiver dynamic? We rely much on how patients and families interact with us to gauge pain.  Assessing and managing children’s pain can be challenging, because they may not exhibit typically recognized signs and symptoms (Srouji 2010).  Further, children participate in and absorb their family’s culture and specific personality from a very young age (Finley 2009).  Knowing the context of the episode may help.  For example, a very anxious caregiver can easily transmit his or her anxiety to the child, which may either inhibit or amplify presentation of symptoms (Bearden 2012). The guiding principles in pediatric pain assessment and management are: know the child; know the family; and know the physiology.  Children have long suffered from an under-treatment of their pain, due both to our incomplete acknowledgement of their pain and our fear of treatment (Howard 2003).  As the pendulum on pain management swings one way or the other, do not let your pediatric patient get knocked by the wayside.  Take a thoughtful approach: know the signs and symptoms, and aggressively treat and reassess. ASSESSMENT Each stage of development offers a unique framework to the child’s signs and symptoms of pain.  In pre-verbal children, use your observational skills in addition to the parent’s report of behavior.  Verbal children can self-report; younger children require pictorial descriptions, while older children and adolescents may use standard adult scales.  In all ages, ask open-ended questions and allow the child to report and speak for himself whenever possible. Neonates Neonates are a unique group in pain assessment.  The neonate (birth to one month of age) has not yet acquired social expression of pain, and his nascent nervous system is only now learning to process it.  Do not expect typical pain behaviors in neonates.  Facial grimacing is a weak indicator of pain in neonates (Liebelt 2000).  When this behavior is present, look for a furrowed brow, eyes squeezed shut, and a vertically open mouth.  Tachycardia, tachypnea, and a change in behavior can be indicators not only to the presence of pain, but possibly to its etiology as well. Neonatal observational scales have been validated in the intensive care and post-operative settings; ED-specific quantitative scales are lacking.  CRIES is a 10-point scale, using a physiologic basis similar to APGAR: Crying; Requires increased oxygen administration (distress and breath-holding); Increased vital signs; Expression; and Sleeplessness (Krechel 1995).  CRIES (Table 1) was validated for post-operative patients; to adapt its use for the ED, the most conservative approach is to substitute “preoperative baseline” with normal range for age.  Although the numerical values of CRIES have not been validated to date in the ED, the clinician may find the domains included in CRIES to be a useful cognitive construct in assessing neonatal pain. Neonatal pain pathways are particularly plastic; prompt assessment of and increased alertness to neonatal pain may help to mitigate long-lived pain sensitivity and hyperalgesia (Taddio 2002).  In other words, treat the neonate’s pain seriously, as you may save him long-term pain sequelae in the future. Infants and Toddlers This group will begin to exhibit more reproducible, reliable signs and symptoms of pain. For infants of less than one year of age, the Neonatal Infant Pain Scale (NIPS) uses observational and physiologic parameters to detect pain (Table 2).  A score of 0-2 indicates no pain present.  A score of 3-4 indicates mild to moderate pain; non-pharmacologic techniques may be tried first.  A score of 5 or greater indicates severe pain; some pharmacologic intervention is indicated (Lawrence 1993). For children greater than one year who are preverbal, a well performing scale is the FLACC score: Face, Legs, Activity, Cry, Consolability (Table 3). Contextual and caregiver features predominate in this group.  Frequent reassessments are helpful, as the initial trepidation and fright in triage may not accurately reflect the child’s overall pain status. Preschool and School-age children Increasing language development offers the hope of more information to the clinician, but be careful not to ask leading questions.  Do not jump directly to “does this hurt?”.  Preschoolers will say ‘yes’ to anything, in an attempt to please you.  School-age children may passively affirm your “statement”, if only to validate their human need for care or attention.  Start with some ice-breaking banter, lay down the foundations for rapport, and then ask open-ended questions.  Be careful not to allow the caregiver to “instruct” the child to tell you where it hurts, how much, how often, etc.  Rather, engage the parents by asking them what behavior they have noticed.  Eliciting history from both the child and the parent will go a long way in constructing a richer picture of the etiology and severity of the pain, and will help to build rapport and trust. The Baker-Wong FACES Pain Rating scale (Figure 1) was developed with feedback from children and has been validated for use in those 3 years of age and older (Keck 1996, Tomlinson 2010). Adolescents Adolescents vary in their development, maturity, and coping mechanisms.  You may see a mixture of childhood and adult behaviors in the same patient; e.g. he may be initially stoic or evades questioning, then later exhibits pseudo-inconsolability.  Do what you can to see the visit from the adolescent’s perspective, and actively transmit your concern and intention to help – many will respond to a warm, open, non-judgemental, and helpful attitude.  The overly “tough” adolescent is likely secretly fearful, and the “dramatic” adolescent may simply be very anxious.  Take a moment to gauge the background behind the presentation. You may use the typical adult scale of 0 (no pain) to 10 (worst pain), or the Faces Pain Scale–Revised (FPS-R).  The FPS-R uses more neutral and realistic faces and, unlike the Wong Baker scale, does not use smiling or crying faces to anchor the extremes of pain (Tsze 2013). PAIN PHYSIOLOGY Pain includes two major components: generation and perception.  Generation of pain involves the actual propagation of painful stimuli, either through nociceptive pain or neuropathic pain.  Nociceptive pain arises from free nerve endings responding to tissue damage or inflammation. Nociceptive pain follows a specific sequence: transduction (an action potential triggered by chemical mediators in the tissue, such as prostaglandins, histamine, bradykinin, and substance P); transmission (the movement of the action potential signal along the nerve fibers to the spinal cord); perception (the impulse travels up the spinothalamic tract to the thalamus and midbrain, where input is splayed out to the limbic system, somatosensory cortex, and parietal and frontal lobes); and modulation (the midbrain enlists endorphins, enkephalins, dynorphin, and serotonin to mitigate pain) (Pasero 2011).  As clinicians we can target specific “stations” along the pain route to target the signal more effectively. Simple actions such as ice, elevation, local anesthetics, or splinting help in pain transduction.  Various standard oral, intranasal, or IV analgesics may help with pain’s transmission. Non-pharmacologic techniques such as distraction, re-framing, and others can help with pain perception.  The sum of these efforts encourage pain modulation. A phenomenon separate from nociceptive pain is neuropathic pain, the abnormal processing of pain stimuli.  It is a dysregulated, chaotic process that is difficult to manage in any setting.  Separating nociceptive from neuropathic symptoms may help to select specific pain treatments and to clarify treatment goals and expectations. Neonates Neonates are exquisitely sensitive to many analgesics.  Hepatic enzymes are immature and exhibit decreased clearance and prolonged circulating levels of the drug administered.  Once the pain is controlled, less frequent administration of medications, with frequent reassessments, are indicated. The neonate’s vital organs (brain, heart, viscera) make up a larger proportion of his body mass than do muscle and fat.  That is to say, the volume of distribution is unique in a neonate.  Water-soluble drugs (e.g. morphine) reach these highly perfused vital organs quickly; relatively small overdosing will have rapid and exaggerated central nervous system and cardiac effects.  The neonate’s small fat stores and muscle mass limit the volume of distribution of lipophilic medications (e.g. fentanyl, meperidine), also making them more available to the central nervous system, and therefore more potent.  Other factors that predispose neonates to accidental analgesic overdose are their decreased concentrations of albumin and other plasma proteins, causing a higher proportion of unbound drug.  Renal clearance is also decreased in the first few months of life. Clinical note: in the ED, neonates often require analgesia for procedures more than for injury.  Non-pharmacologic techniques predominate (see below).  Make liberal use of local anesthetics such as eutectic mixture of local anesthetics (EMLA; for intact skin, e.g. IV access, lumbar puncture) and lidocaine-epinephrine-tetracaine gel (LET; for superficial open skin and soft tissue application).  Oral sucrose (30%) solutions (administered either with a small-volume syringe or pacifier frequently dipped in solution) are effective for minor procedures (Harrison 2010, Stevens 2013) via the release of dopamine and through distraction by mechanical means.  Neonates with severe pain may be managed with parenteral analgesics, on a monitor, and with caution. Infants and Toddlers With increasing body mass comprised of fat stores in conjunction with an increase in metabolism, this group will require a different approach than the neonate.  For many medications, these children will have a greater weight-normalized clearance than adults (Berde 2002).  They will often require more frequent dosing.  Infants and toddlers have a larger functioning liver mass per kilogram of body weight, with implications for medications cleared by cytochrome p-450. Clinical note: some drugs, such as benzodiazepines, will have both a per-kilogram dosing as well as an age-specific modification.  When giving analgesics or anxiolytics to young children, always consult a reference for proper dosing and frequency. School-age children and Adolescents This group retains some hyper-metabolic features of younger children, but the dose-effect relationship is more linear and transparent.  Physiologic clearance is improved, and from a physical standpoint, these are typically lower-risk children.  From a psychological standpoint, this group may need more non-pharmacologic consideration and support to modulate pain optimally. NON-PHARMACOLOGIC TREATMENT The first line of treatment in all pain management is non-pharmacopeia (Horeczko 2016).  Not only is this the safest of all techniques, but often the most effective.  Some are simple comfort measures such as splinting (fracture or sprain), applying cold (acute soft tissue injury) or heat (non-traumatic, non-specific pain), or other targeted non-pharmacology. Many a pain control regimen is sabotaged without consideration of non-pharmacologic techniques, which may augment, or at times replace, analgesics.  Think of non-pharmacopoeia as your “base coat” or “primer” before applying additional coats of analgesic treatment.  With the right base coat foundation, you have a better chance of painting a patient’s symptoms a more tolerable and long-lasting new color. A tailored approach based on age will allow the practitioner to employ a child’s developmental strengths and avoid the frustration that results in asking the child to do what he is not capable of doing.  A brief review of Piaget’s stages of development will help to meet the child at his developmental stage for best effect (Piaget 1928, Sheppard 1977) during acute painful presentations and minor procedures. Sensorimotor stage (from birth to age 2): Children use the five senses and movement to explore the world.  They are egocentric: they cannot see the world from another’s viewpoint.   At 6 to 9 months, object permanence is established: understanding that objects (or people) exist even without seeing them. Preoperational stage (from ages 2 to 7):  Children learn to use language.  Magical thinking predominates. They do not understand rational or logical thinking. Concrete operational stage (from age 7 to early adolescence): Children can use logic, but in a very straightforward, concrete manner (they do well with simple examples).  By this stage, they move from egocentrism to understanding another point of view.  N.B. Some children (and adults) never completely clear this stage. Formal operational stage (early adolescence to adult): children are capable of abstract thinking, rationalizing, and logical thinking. It is important to assess the child’s general level of development when preparing and guiding him through the minor procedure or distracting him until his pain is controlled.  It is not uncommon for acutely ill or injured to regress temporarily in their behavior (not their development) as a coping mechanism. Neonate and Infant (0-12 months) Involve the parent, and have the parent visible to the child at all times if possible.  Make advances slowly, in a non-threatening manner; limit the number of staff in the room.  Use soothing sensory measures: speak softly, offer a pacifier, and stroke the skin softly.  Swaddle the infant and encourage the parent to comfort him during and after the procedure.  Engage their developing sensorimotor skills to distract them. Toddler to Preschooler (1-5 years) Use the same techniques as for the infant, and add descriptions of what he will see, hear, and feel; you can use a doll or toy to demonstrate the procedure.  Use simple, direct language, and give calm, firm directions, one at a time.  Explain what you are doing just before doing it (do not allow too much time for fear or anxiety to take root).  Offer choices when appropriate; ignore temper tantrums.  Distraction techniques include storytelling, bright and flashy toys, blowing bubbles, pinwheels, or having another staff member play peek-a-boo across the room.  The ubiquitous smart phone with videos or games can be mesmerizing at this age. School age (6-12 years) Explain procedures using simple language and (briefly) the reason (understanding of bodily functions is vague in this age group).  Allow the child to ask questions, and involve him when possible or appropriate.  Distraction techniques may include electronic games, videos, guided imagery, and participation in the minor procedure as appropriate. Adolescent (13 and up) Use the same techniques for the school age child, but can add detail.  Encourage questioning.  Impose as few restrictions as possible – be flexible.  Expect more regression to childish coping mechanisms in this age group.  Distraction techniques include electronic games, video, guided imagery, muscle relaxation-meditation, and music (especially the adolescent’s own music, if available). APPLIED PHARMACOLOGY No amount of knowledge of the above physiology, pharmacology, or developmental theory will help your little patient in pain without a well constructed and enacted plan.  Aggressively search out and treat your pediatric patient’s presence and source of pain.  Frequent reassessments are important to ensure that breakthrough pain treatment is achieved, when re-administration is indicated, or when a change of plan is necessary.  This is the time to involve the parents or caregivers to let them know what the next steps are, and what to expect. Start with the least invasive modality and progress as needed.  After non-pharmacologic treatments such as splinting, ice, elevation, distraction, and guided imagery, have an escalation of care in mind (Figure 2). From a pharmacologic perspective, various options are available.  Your pain management plan will differ depending on whether a painful procedure is performed in the ED (Table 4).  Once pain is addressed, create a plan to keep it managed.  Consider the trajectory of illness and the expected time frame of the painful episode.  Include practicalities such as how well the pain may be controlled as an outpatient.  Poorly controlled pediatric pain is more often managed as an inpatient than the same condition in an adult.  Speak frankly with the parents about what drug is indicated for what type of pain and that treatment goals typically do not include absence of all pain, but function in face of the pain, in anticipation for clinical improvement. A special note on codeine: Tylenol with codeine (“T3”) has never been a very effective pain medication, as up to 10% of patients lack enzymatic activity to metabolize it into morphine, its active form (Crews 2014).  New evidence is emerging on the erratic and unpredictable individual metabolism of codeine.  Some children are ultra-rapid-metabolizers of codeine to morphine, causing a rapid “bolus” of the available drug, with respiratory depression and death in some cases (Ciszkowski 2009, Racoosin 2013).  Author’s advice: take codeine off your formulary. COMMON SCENARIOS Head and neck pain Most common non-traumatic head and neck complaints can be managed non-pharmacologically (e.g. headache: improved hydration, sleep, stress, nutrition) or with PO medications, such as NSAIDs.  The anti-inflammatory nature of ibuprofen (10 mg/kg PO q 4-6 h prn, up to adult dose) for example, will treat the cause as well as the symptoms of ear pain, sore throat, and muscular pain.  Ibuprofen may be more effective than acetaminophen (paracetamol) for odontogenic pain (Bailey 2013).  For most applications, acetaminophen may be as effective; however, the combination of both NSAIDs is not likely to be more effective than either agent individually (Merry 2013). True migraine headache may be treated with all of the above, and rescue therapy may include prochlorperamide (0.15 mg/kg IV, up to 10 mg ) (Brousseau 2004), often given with diphenhydramine (1 mg/kg PO or IV, up to 50 mg) and IV fluids.  Ketoralac (0.5 mg/kg IV, up to 10 mg) may be substituted for ibuprofen (Paniyot 2016).  Other specific therapies may be considered, although evidence for them varies. Chest pain After ruling out important pulmonary (e.g. the under-recognized spontaneous pneumothorax) and cardiac (e.g. pericarditis, myocarditis) etiologies, many chest complaints are amenable to NSAIDs.  There is often a large component of anxiety in the child and/or parents in chest pain; no amount of medication will assuage them without addressing their concerns as well. Abdominal pain Abdominal pain in children is challenging, as it is common, often benign, but may be disastrous if the etiology is missed.  For mild pain, consider acetaminophen as indicated (15 mg/kg/dose q 4-6 h prn, up to 650 mg).  The oral route is preferred, but intravenous acetaminophen is an option for patients unable to tolerate PO, or for those in whom the per rectum (PR) route is contraindicated (e.g. neutropenia) (Babl 2011, Dokko 2014).  For children with moderate to severe abdominal pain in whom a nil per os (NPO) status is ideal, consider rehydration/volume repletion, and small, frequent aliquots of a narcotic agent.  Surgical pain is not “erased” by opioids (Thomas 2003, Poonai 2014); treating pain improves specificity to certain surgical emergencies with retained diagnostic accuracy (Manterola 2007).  If there is inter-departmental concern about prolonged effects, sedation, limitation in the physical exam, or there is a need to “see if the pain will come back”, you may opt to use fentanyl initially for its shorter half-life.  More frequent re-assessments may help the surgical team in its deliberations.  Transition quickly to a longer-acting opioid as soon as possible. Long-bone injuries Fracture pain should be addressed immediately with splinting and analgesia.  Oral, intranasal, and intravenous routes are all acceptable, depending on the severity of the injury and symptoms. Intranasal (IN) medications offer the advantage of a fast onset for moderate-to-severe pain (Graudins 2015), either as monotherapy or as a bridge to parenteral treatment (Table 4).  The ideal volume of IN medication is 0.25 mL/naris, with a maximum of 1 mL/naris.  Common concentrations of fentanyl limit its mg/kg use to the school-aged child; intranasal ketamine may be used for pain (i.e. sub-dissociative dose) up to adult weight. Long-bone injuries are a good opportunity to employ a speedy modality that requires little technical skill in administration: nebulized fentanyl.  Clinically significant improvement in pain scales are achieved with 3 mcg/kg/dose of fentanyl administered via standard nebulizer in children 3 years of age or older (Miner 2007, Furyk 2009).  Nebulized fentanyl is a rapid, non-invasive alternative to the IN route for older children, adolescents, or adults, in whom the volume of IN medication would exceed the recommended per naris volume (Deaton 2015). Consider an aggressive, multi-modal approach to control symptom up front.  For example, for a simple forearm fracture, you may opt to give an oral opioid, perform a hematoma block, and offer inhaled nitrous oxide for reduction, rather than a formal intravenous procedural sedation (Luhmann 2006). Ultrasound-guided peripheral nerve blocks are a good pain control adjunct, after initial treatment, and in communication with referring consultants (Ganesh 2009, Suresh 2014). Skin and Soft tissue Skin and soft tissue injuries or abscesses often require solid non-pharmacopoeia in addition to local anesthetics.  For IV cannulation, consider EMLA if the patient is stable and a minor delay is acceptable. Topical ethyl chloride vapo-coolant offers transient pain relief due to rapid cooling and may be used just prior to an IV start (Farion 2008).  Try this: engage your young child’s imagination to distract him and say, “have you ever held a snow ball? You are in luck – it’s just like that – here, do you feel it?”. Vibratory adjuncts such as the “BUZZY” bee can be placed near the IV cannulation site to provide mechanical and cognitive distraction (Moadad 2016). Needleless lidocaine injectors may facilitate IV placement without obscuring the target vein (Spanos 2008, Lunoe 2015).  The medication is propelled into the dermis by a CO2 cartridge that makes a loud popping sound; try this to alleviate anxiety, just before using it: “your skin looks thirsty – it needs a drink – there you are!”. As with any minor procedure, when you tell the child what you are doing, be sure to do it right away.  Do not delay or build suspense. Lidocaine-epinephrine-tetracaine gel (LET) is used for open or mucosal wounds.  Apply as soon as possible in the visit.  The goal of LET is to pretreat the wound to allow for a painless administration of injectable anesthetic.  A common practice to apply LET two or three times at 15-minute intervals for deeper anesthesia, in an attempt to avoid injection altogether.  Researchers are currently working to offer an evidence base to this anecdotal practice. Pediatric burns should be assessed carefully and treated aggressively.  Submersion of the affected extremity in room-temperature water (if possible) or applying room-temperature saline-soaked gauze will both thwart ongoing thermal damage, soothe the wound, and provide foundational first-aid.  Minor burns can be treated topically and with oral medications.  Major burns require IN, IM, or IV analgesics with morphine.  Treatment may escalate to ketamine (Gandhi 2010), in analgesic or dissociative dosing, depending on the context.  Post-traumatic disorders are common in burns; effective pain management is ever-more important in these cases. SPECIFIC SCENARIOS The child with chronic medical problems Children with acute exacerbations of their chronic pain or episodic painful crises require special attention.  Some examples of children with recurring pain are those suffering from sickle cell disease, juvenile idiopathic arthritis, complex regional pain syndrome, and cancer.  Find out whether these symptoms and circumstances are typical for them, and what regimen has helped in the past.  Previous unpleasant experiences may prime these children with amplified anxiety and perception of pain (Cornelissen 2014).  Target the disease process and do your best to show the patient and his family you understand his condition and needs. An equally challenging scenario is the child with chronic pain.  Treat the entire patient with a multimodal approach.  Limit opioids as possible.  As an opioid-sparing strategy or as rescue therapy, consider sub-dissociative ketamine, especially for conditions such as sickle cell crisis, complex regional pain syndrome, autoimmune disorders, or chronic pain due to sub-acute trauma (Sheehy 2015). Intranasal ketamine may be used for sub-dissociative pain control at 0.5 – 1 mg/kg (Andolfatto 2013, Yeaman 2013).  Intravenous infusions of ketamine at 0.1 – 0.3 mg/kg/h may be initiated in the ED and continued 4 – 8 h/d, up to a maximum of 16 h total in 3 consecutive days (Sheehy 2015).  In vaso-occlusive episodes, dexmedetomidine has been shown to be an effective adjunct for severe pain poorly responsive to opioids and/or ketamine (Sheehy 2015b). The child with cognitive impairment Children with cognitive impairment such as those with various genetic or metabolic syndromes, or primary neurologic conditions such as some with cerebral palsy are a challenge to assess and treat properly.  These children not only cannot explain their symptoms, but they also have atypical expressions of pain.  Pain responses in severely intellectually disabled children include a full-blown smile (which may or may not accompany inappropriate laughter), stiffening, and non-cooperation (Hadden 2002).  Other observed behaviors include the freezing phenomenon, in which the child acutely feels the pain, and he abruptly pauses without moving his face for several seconds.  Look also for episodes of unexplained pallor, diaphoresis, breath-holding, and shrill vocalizations. The FLACC has been revised (r-FLACC) for children with cognitive impairment and appears to be reliable for acute care (Malviya 2006). The most distressing and perplexing presentation is the parent who brings his or her child with cognitive impairment for “fussiness”, “irritability”, or “I think he’s in pain”.  Often, this is after significant investigations have been performed, sometimes repeatedly.  Poorly controlled spasticity is an often under-appreciated cause of unexplained pain; treat not with opioids, but with GABA-receptor agonists, such as baclofen or benzodiazepines. Take special precautions in the administration of opioids or benzodiazepines in children with metabolic disorders (e.g. mitochondrial disease) or various syndromes (e.g. Trisomy 21).  They may have a disproportionate reaction to the medication.  Start with a low dose in these children and reassess frequently, titrating in small aliquots as needed. After careful, meticulous investigation in the ED to rule out occult infection, trauma, electrolyte imbalance, or surgical causes, the child with cognitive impairment who continues to be symptomatic despite ED treatment may be admitted for observation.  However, in some cases, the addition of gabapentin to the typical regimen has been shown to manage unexplained irritability in these children (Hauer 2007) by treating visceral hyperalgesia. Multi-trauma The child with multi-trauma is in need of meticulous critical care.  Frequent assessments of pain analgesic response (typically via the intravenous route) are necessary to gauge the child’s trajectory.  Unexplained tachycardia may be the early signs of shock.  Without controlling the child’s pain, it is difficult to distinguish the extreme tachycardia from pain or from blood loss.  If intubated, control the pain first with a fentanyl drip, then use a sedative in addition as needed to keep him comfortable. The child under palliative care Children undergoing palliative care require a multidisciplinary approach.  This includes engaging the patient’s car team as well as “treating” members of the patient’s family.  Examples include the natural course of devastating chromosomal, neurologic, and other congenital conditions; terminal cancer; and trauma, among others (Michelson 2007).  Family dynamics and family members’ needs are often overlooked; the family as a whole must be considered.  Focus on the productive and beneficial treatments that can be offered.  Treat pain promptly, but speak with the parents about end-of-life goals as early as possible, as any analgesic or sedative may have an untoward effect.  You do not want to be caught in the position of potentially precipitously providing cardiopulmonary resuscitation in a child undergoing palliative care, because of a lack of understanding of how increasingly large doses of pain medications can affect breathing and circulation (AAP 2000). Children with ongoing opioid requirements may present not so much with an exacerbation of their chronic pain, but a complication of its treatment.  Identify, assess and aggressively treat constipation, nausea and vomiting, pruritus, and urinary retention (Friedrichsdorf 2007); treating side-effects of pain management may be just as important for quality of life as treating the pain itself. PEARLS AND PITFALLS IN PEDIATRIC PAIN Allow the child to speak for himself whenever possible.  After acknowledging the parent’s input, perhaps try “I want to make sure I understand how the pain is for you.  Tell me more.” Engage parents and communicate the plan to them.  Elicit their expectations, and give them of preview of what to expect in the ED. Opioids are meant for pain caused by acute tissue injury, for the briefest period of time feasible.  Older school-aged children and adolescents are increasingly at risk for opioid dependence and addiction. Premature infants present a challenge in pain control.  Their pain is under-recognized, as they often display atypical responses to painful stimuli.  Treatment is equally difficult, as they are particularly sensitive to analgesia-sedation.  This is important, as this group is even more likely to undergo painful procedures due to their higher-risk status. Give detailed advice on how to manage pain at home.  Set expectations.  Let them know you understand and will help them through your good advice that will carry them through this difficult time.  Patients and families often just need a plan.  Map it out clearly. SUMMARY In pediatric acute pain, know the child; know the family; and know the physiology. Use your observational skills enhanced with collateral information to assess and reassess for pain in children. Treat pediatric pain well and often. Failure to address the child’s pain has long-lasting consequences. Non-pharmacologic treatments for all, pharmacologic treatments for many. 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Pediatr Emerg Care. 2008 Aug;24(8):511-5. Srouji R, Ratnapalan S, Schneeweiss S. Pain in children: assessment and nonpharmacological management. Int J Pediatr. 2010;2010. Stevens B, Yamada J, Lee GY, Ohlsson A. Sucrose for analgesia in newborn infants undergoing painful procedures. Cochrane Database of Systematic Reviews 2013, Issue 1. Art. No.: CD001069. Suresh S, Sawardekar A, Shah R. Ultrasound for regional anesthesia in children. Anesthesiol Clin. 2014 Mar;32(1):263-79. Taddio A, Shah V, Gilbert-MacLeod C, Katz J. Conditioning and hyperalgesia in newborns exposed to repeated heel lances. JAMA. 2002;288(7):857. Thomas SH, Silen W. Effect on diagnostic efficiency of analgesia for undifferentiated abdominal pain. Br J Surg. 2003 Jan;90(1):5-9. Tomlinson D, von Baeyer CL, Stinson JN, Sung L. A systematic review of faces scales for the self-report of pain intensity in children. Pediatrics. 2010 Nov;126(5):e1168-98. Tsze DS, von Baeyer CL, Bulloch B, Dayan PS. Validation of Self-Report Pain Scales in Children. Pediatrics. 2013 Oct; 132(4): e971–e979. Voepel-Lewis T, Merkel S, Tait AR, Trzcinka A, Malviya S. The reliability and validity of the Face, Legs, Activity, Cry, Consolability observational tool as a measure of pain in children with cognitive impairment. Anesth Analg. 2002 Nov;95(5):1224-9. Yeaman F, Oakley E, Meek R, Graudins A. Sub-dissociative dose intranasal ketamine for limb injury pain in children in the emergency department: a pilot study. Emerg Med Australas. 2013 Apr;25(2):161-7   This post and podcast are dedicated to Sergey M. Motov, MD, FAAEM, for his integrity, hard-won expertise, humility, and innovation.  Thank you for making us better doctors, Sergey, and for getting us ever closer to a pain-free ED. Pediatric Pain Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP

Question: A patient has come to the healthcare clinic complaining of pain in his left arm after an injury. Which describes the characteristics of nociceptive pain? Select all that apply. Answer: A.  Nociceptive pain may be localized to the area of injury C.  Nociceptive pain is categorized as being either somatic or visceral pain E. […] The post QOD 68: Nociceptive Pain (Musculoskeletal/Basic Care and Comfort) appeared first on NURSING.com.

Question: A patient has come to the healthcare clinic complaining of pain in his left arm after an injury. Which describes the characteristics of nociceptive pain? Select all that apply. Answer: A.  Nociceptive pain may be localized to the area… The post QOD 68: Nociceptive Pain (Musculoskeletal/Basic Care and Comfort) appeared first on NURSING.com.

Transcript -- A doctor at the Royal Free Hospital's Pain Clinic performs a procedure and explains how medication can help alleviate pain.

A doctor at the Royal Free Hospital's Pain Clinic performs a procedure and explains how medication can help alleviate pain.

Transcript -- A doctor at the Royal Free Hospital's Pain Clinic performs a procedure and explains how medication can help alleviate pain.

A doctor at the Royal Free Hospital's Pain Clinic performs a procedure and explains how medication can help alleviate pain.

Enhanced Video PodcastAired date: 4/30/2007 12:00:00 PM Eastern Time

Enhanced Audio PodcastAired date: 4/30/2007 12:00:00 PM Eastern Time