Descending Modulation of Pain and the Endocannabinoid System: Sites, Mechanisms, and Therapeutic Potential

Susan Ingram, PhD; Mark Lumley, PhD; Karen Davis, PhD

Chronic pain affects approximately 30% of the US population but current treatments are ineffective in a significant proportion of patients. The lack of effective treatments for chronic pain and the opioid epidemic are significant public health issues. Emerging data indicate that cannabis and other drugs that target the endocannabinoid system are effective in animal models and in adult chronic pain patients but research on the basic science and clinical effectiveness of cannabinoids is limited to date. This symposium will address current research in endocannabinoid mechanisms in modulating the descending control of pain that integrates cortical and subcortical responses to pain. This system includes the periaqueductal gray (PAG) and rostral ventromedial medulla (RVM) that modulate peripheral nociceptive information in the spinal cord. Dr. David Finn will discuss the importance of the endocannabinoid system within key components of the descending modulatory system in reciprocal interactions between pain and negative effect. Dr. Susan Ingram will give evidence that persistent inflammatory pain alters the endocannabinoid system in the RVM and describe the cellular mechanisms involved. Dr. Mark Wallace will talk about the therapeutic potential of cannabinoid drugs and their clinical applications.

See media coverage from Medscape on this session. 

Exploiting Cellular and Molecular Mechanisms of Neuroinflammation for New Treatments of Chronic Pain

Jelena Janjic, PhD; Theodore Price, PhD; Edgar Alfonso Romero-Sandoval, MD PhD

Dr. Janjic and Dr. Pollack will discuss how neuroinflammation associated with chronic pain can be modulated with low dose drug delivery via nanoparticles. This treatment causes changes in protein and RNA expression in both the sciatic nerve and the dorsal root ganglia. Their work highlights potential of targeting specific intracellular pathways in macrophages, leading to changes in cellular behavior that produces changes in inflammation and consequently changes in pain behavior. Dr. Romero-Sandoval will discuss how the modulation of specific genes in macrophages could alter the development of chronic pain. He will focus on the strengths and limitations of targeting particular genes such as CD163. He will describe how this molecule could regulate macrophage function and restore a phenotype that is required for the resolution of inflammation following tissue damage or nerve injury. Dr. Price will discuss the growing area of AMPK targeting in chronic pain. He will focus on what we have learned from the diversification of pharmacological and genetic approaches to targeting AMPK. He will then relate this knowledge to the growing evidence that AMPK activation can lead to disease modification and/or the prevention of the development of chronic pain in a large number of preclinical pain models.

Mechanism-Based Approach to Clinical Trial Design in Chemotherapy-Induced Peripheral Neuropathy

Jennifer Gewandter, PhD; Patrick Dougherty, PhD; Roy Freeman, MD

Chemotherapy-induced peripheral neuropathy (CIPN) occurs in approximately 60% of patients who receive neurotoxic chemotherapies and becomes chronic in approximately 50% of those patients. CIPN symptoms include pain, tingling, cramping, numbness, and weakness. CIPN can cause chemotherapy dose-reductions and discontinuation, potentially increasing mortality. CIPN also adversely affects patient quality of life. No preventive treatments for CIPN are available. Advances in understanding of basic science and clinical mechanisms of CIPN are imperative to identifying novel preventive and symptomatic treatments. Furthermore, these mechanisms should be used to inform clinical trial design. Dr. Dougherty will present data from clinical studies that appear to validate findings from laboratory studies that highlight key risk factors for the development of CIPN. Dr. Freeman will discuss the mechanisms underlying the neurotoxicity of different chemotherapeutic agents; their varying clinical manifestations; and their clinical course. Dr. Gewandter will review clinical trial design considerations for clinical trials of preventive and disease modifying CIPN treatment developed at an expert consensus meeting. She will emphasize consideration of the mechanisms of the experimental treatment and CIPN when designing inclusion criteria, outcome measures, and biomarkers. These considerations will also serve as an example for RCTs of pain prevention in other areas.

Migraine and Sleep Deficiency in Adolescents: Understanding Shared Mechanisms from Bench to Bedside

Emily Law, PhD; Christopher King, PhD; Andrew Russo, PhD

Dr. Andrew Russo will present recent data from animal migraine models examining the impact of sleep deficiency on the development of peripheral and central sensitization associated with transition to chronic pain. Follow sleep deprivation, findings indicate cellular changes in the trigeminal ganglion and spinal trigeminal nucleus are temporarily correlated with nocifensive behaviors in episodic and chronic pain migraine pathology models. Novel therapeutic interventions that influence pain modulation pathways will be presented.
Dr. Christopher King will present recent imaging research examining neurobiological differences between adolescents with and without migraines, including alterations in resting cerebral blood flow and functional connectivity between limbic and frontal cortical regions related to migraine frequency and sleep assessments. Finding suggest sleep deficiency can impact structural and functional brain areas, which could be normalized with treatment.

Dr. Emily Law will present treatment mechanism data examining the impact of insomnia treatment on migraine frequency in adolescents. Results from a clinical trial of cognitive-behavioral therapy for adolescents with co-occurring chronic migraine and insomnia will be presented. Discussion will focus on designing novel studies to evaluate treatments for sleep deficiency while testing biobehavioral migraine mechanisms.

Through case examples and interactive discussion with audience members, current controversies and clinical implications will be discussed.

Muscle Pain Mechanisms: It’s Time to Dive Deep

Kathleen Sluka, PT PhD; Michael Jankowski, PhD; Cheryl Stucky, PhD

There is great need for preclinical and clinical studies that investigate the role of deep tissues in driving chronic pain. This symposium will focus on muscle tissue, with the hope that highlights of other deep tissues, including tendon and bone will follow in future symposia. Three experts in muscle pain mechanisms will present their preclinical and clinical findings in chronic pain conditions involving skeletal muscle. Kathleen Sluka, University of Iowa, will discuss the underlying problem and mechanisms of activity-induced pain in animal models of pain and human subjects with fibromyalgia. Michael Jankowski, Cincinnati Children’s Hospital Medical Center, will deepen our understanding of the complex interplay between muscle afferents and target derived signaling molecules in the development of ischemic myalgia. Cheryl Stucky, Medical College of Wisconsin, will highlight the role of muscle-driven pain in sickle cell disease pain, a devastating disorder of severe, cycling deep pain. Together they will help the audience take a deeper dive into understanding muscle afferents, sensitization, circuitry and CNS pathways, and the critical role of the under-appreciated deep tissues in so many chronic pain disorders that plague and decrease the daily quality of life for millions of individuals worldwide.

This symposium is dedicated to the memory of Edward R. Perl, MD, and William D. Willis, Jr., MD PhD, both of whom made seminal contributions to the fields of pain and neuroscience.

Novel Directions in Basic Research: Rita Allen Scholars

Katherine Hanlon, PhD; Arkady Khoutorsky, PhD DVM; Kyle Baumbauer, PhD

In collaboration with the Rita Allen Foundation, basic science researchers carrying out innovative investigations into pain are chosen yearly. Three projects will be discussed in this symposium:

Dr. Kyle Baumbauer: Spinal cord injury produces chronic pain that results from the recruitment of primary afferent nociceptors. Recent work from our laboratory suggests that Acid Sensing Ion Channel Subunit 3 (ASIC3) may recruit nociceptors following central injury.

Dr. Arkady Khoutorsky: In the presented project we investigated how nerve injury-induced remodeling of the extracellular matrix in the spinal cord contributes to the dysregulated processing of sensory information and the development of pain hypersensitivity.

Dr. Katherine Hanlon: Although macrophages mediate many aspects of inflammation, the idea of limited functionality restricted to immediate innate phase immune response persists. Recent data from our lab and others is changing this perception – we will discuss function of DRG macrophages and macrophage involvement in ascending pain pathways.

Putting the Spotlight on Social: An Innovative Multidisciplinary, Multi-Species Approach for Examining the Influence of Social Context in Pain

Kristen Jastrowski Mano, PhD: Loren Martin, PhD; Kai Karos

The proposed symposium will present multidisciplinary perspectives on the neural and psychological mechanisms underlying the social modulation of pain, as well as the overlap between chronic pain and affective disturbance. The first presenter will describe novel animal models for studying the influence of social context on pain, providing insight into the fundamental mechanisms that engage the neural circuits responsible for pain modulation via social context. Data reveal that familiarity between conspecifics is necessary for the social facilitation of pain behaviors and activation of glucocorticoid receptors within “affective” brain regions prevents this facilitation. The second presenter will discuss a series of ongoing experimental studies investigating the effects of a threatening social context on interpersonal processes and the perception and expression of pain in healthy adults. The third presenter will describe behavioral (eye movement and reaction time) data showing adolescent chronic pain patients’ responses to social threat and self-reported social anxiety symptoms. Drawing from a shared vulnerability model of chronic pain and anxiety, the link between attentional bias to social threat, fear-related avoidance and functional disability will be discussed. Speakers will facilitate a lively discussion of current controversies and future directions for mechanistic understanding, as well as allow sufficient time for Q&A.

Descending Modulation of Pain and the Endocannabinoid System: Sites, Mechanisms, and Therapeutic Potential

Susan Ingram, PhD; David Finn, PhD; Mark Wallace, MD

Chronic pain affects approximately 30% of the US population but current treatments are ineffective in a significant proportion of patients. The lack of effective treatments for chronic pain and the opioid epidemic are significant public health issues. Emerging data indicate that cannabis and other drugs that target the endocannabinoid system are effective in animal models and in adult chronic pain patients but research on the basic science and clinical effectiveness of cannabinoids is limited to date. This symposium will address current research in endocannabinoid mechanisms in modulating the descending control of pain that integrates cortical and subcortical responses to pain. This system includes the periaqueductal gray (PAG) and rostral ventromedial medulla (RVM) that modulate peripheral nociceptive information in the spinal cord. Dr. David Finn will discuss the importance of the endocannabinoid system within key components of the descending modulatory system in reciprocal interactions between pain and negative effect. Dr. Susan Ingram will give evidence that persistent inflammatory pain alters the endocannabinoid system in the RVM and describe the cellular mechanisms involved. Dr. Mark Wallace will talk about the therapeutic potential of cannabinoid drugs and their clinical applications.

Mechanism-Based Approach to Clinical Trial Design in Chemotherapy-Induced Peripheral Neuropathy

Jennifer Gewandter, PhD; Patrick Dougherty, PhD; Roy Freeman, MD

Chemotherapy-induced peripheral neuropathy (CIPN) occurs in approximately 60% of patients who receive neurotoxic chemotherapies and becomes chronic in approximately 50% of those patients. CIPN symptoms include pain, tingling, cramping, numbness, and weakness. CIPN can cause chemotherapy dose-reductions and discontinuation, potentially increasing mortality. CIPN also adversely affects patient quality of life. No preventive treatments for CIPN are available. Advances in understanding of basic science and clinical mechanisms of CIPN are imperative to identifying novel preventive and symptomatic treatments. Furthermore, these mechanisms should be used to inform clinical trial design. Dr. Dougherty will present data from clinical studies that appear to validate findings from laboratory studies that highlight key risk factors for the development of CIPN. Dr. Freeman will discuss the mechanisms underlying the neurotoxicity of different chemotherapeutic agents; their varying clinical manifestations; and their clinical course. Dr. Gewandter will review clinical trial design considerations for clinical trials of preventive and disease modifying CIPN treatment developed at an expert consensus meeting. She will emphasize consideration of the mechanisms of the experimental treatment and CIPN when designing inclusion criteria, outcome measures, and biomarkers. These considerations will also serve as an example for RCTs of pain prevention in other areas.

Migraine and Sleep Deficiency in Adolescents: Understanding Shared Mechanisms from Bench to Bedside

Emily Law, PhD; Christopher King, PhD; Andrew Russo, PhD

Dr. Andrew Russo will present recent data from animal migraine models examining the impact of sleep deficiency on the development of peripheral and central sensitization associated with transition to chronic pain. Follow sleep deprivation, findings indicate cellular changes in the trigeminal ganglion and spinal trigeminal nucleus are temporarily correlated with nocifensive behaviors in episodic and chronic pain migraine pathology models. Novel therapeutic interventions that influence pain modulation pathways will be presented.
Dr. Christopher King will present recent imaging research examining neurobiological differences between adolescents with and without migraines, including alterations in resting cerebral blood flow and functional connectivity between limbic and frontal cortical regions related to migraine frequency and sleep assessments. Finding suggest sleep deficiency can impact structural and functional brain areas, which could be normalized with treatment.

Dr. Emily Law will present treatment mechanism data examining the impact of insomnia treatment on migraine frequency in adolescents. Results from a clinical trial of cognitive-behavioral therapy for adolescents with co-occurring chronic migraine and insomnia will be presented. Discussion will focus on designing novel studies to evaluate treatments for sleep deficiency while testing biobehavioral migraine mechanisms.

Through case examples and interactive discussion with audience members, current controversies and clinical implications will be discussed.

Muscle Pain Mechanisms: It’s Time to Dive Deep

Kathleen Sluka, PT PhD; Michael Jankowski, PhD; Cheryl Stucky, PhD

There is great need for preclinical and clinical studies that investigate the role of deep tissues in driving chronic pain. This symposium will focus on muscle tissue, with the hope that highlights of other deep tissues, including tendon and bone will follow in future symposia. Three experts in muscle pain mechanisms will present their preclinical and clinical findings in chronic pain conditions involving skeletal muscle. Kathleen Sluka, University of Iowa, will discuss the underlying problem and mechanisms of activity-induced pain in animal models of pain and human subjects with fibromyalgia. Michael Jankowski, Cincinnati Children’s Hospital Medical Center, will deepen our understanding of the complex interplay between muscle afferents and target derived signaling molecules in the development of ischemic myalgia. Cheryl Stucky, Medical College of Wisconsin, will highlight the role of muscle-driven pain in sickle cell disease pain, a devastating disorder of severe, cycling deep pain. Together they will help the audience take a deeper dive into understanding muscle afferents, sensitization, circuitry and CNS pathways, and the critical role of the under-appreciated deep tissues in so many chronic pain disorders that plague and decrease the daily quality of life for millions of individuals worldwide.

This symposium is dedicated to the memory of Edward R. Perl, MD, and William D. Willis, Jr., MD PhD, both of whom made seminal contributions to the fields of pain and neuroscience.

Novel Mechanisms Underlying Risk for Acute and Chronic Post-Surgical Pain: Role of Peripheral Pain Processing, Central Sensitization, and Genomics

Vidya Chidambaran, MD; Jennifer Rabbitts, MD; Chad Brummett, MD

Inadequately controlled acute post-surgical pain contributes to morbidity in the immediate postoperative period and increases risk for persistence of post-surgical pain, associated with long-term disability and significant socioeconomic consequences. Understanding of the mechanisms underlying risk factors and the impact on patient’s recovery is critical to developing successful targeted interventions. Clinician scientists will present multiple directions based on their research. Dr. Rabbitts will present data from her longitudinal study characterizing the relationship between pain processing phenotypes (quantitative sensory testing) and psychosocial factors, and the persistence of postsurgical pain in children undergoing major surgery. Dr. Brummett will discuss the impact of central sensitization (including brain imaging data) on acute and chronic pain outcomes in adults undergoing joint arthroplasty and hysterectomy. Dr. Chidambaran will present findings from her studies in children undergoing major surgeries, regarding associations of genetic variants with functional roles in opioid-pain pathways and gene-environmental interactions (epigenetics), with acute and chronic pain phenotypes and opioid effects. Dr. Chidambaran will facilitate an interactive discussion with speakers and attendees using case-scenario simulations in a pro-con debate framework, focused on translational implications and future directions, for preventive and therapeutic individualized interventions, aimed at improving pain and functional outcomes in adults and children undergoing surgery.

Psychological Treatments for Chronic Pain: Who Benefits & Why?

Melissa Day, PhD; Beverly Thorn, PhD; Mark Jensen, PhD

Two trans-therapeutic models will be introduced by the first speaker, Dr. Day: (1) The Limit Activate and Enhance model for predicting who will benefit from which psychological pain treatment (moderation; Day et al., 2015), and (2) an organizational framework for predicting why people benefit (mediation; Day et al., 2014; Jensen, 2011). Drs. Thorn, Jensen, and Day will then present the findings from analyses testing specific hypotheses from these two models using data from three different completed chronic pain randomized clinical trials evaluating: (1) cognitive-behavioral therapy versus pain education (2 arms, Thorn), (2) mindfulness training versus cognitive therapy versus mindfulness-based cognitive therapy (3 arms, Day), and (3) cognitive therapy versus hypnosis versus hypnotic cognitive therapy versus pain education (4 arms, Jensen). The findings with respect to the moderators and mediators that are both shared and unique to each intervention across the three trials will be compared and contrasted, and discussed within the context of the theoretical models presented. Speakers will engage with the audience through interactive learning exercises, brief experiential demonstrations of the treatments evaluated in the trials, as well as via a Q&A period at the end of the symposia.

See media coverage from Medscape on this session. 

The Biology of Infant and Childhood Pain: It All Begins Here

Maria Fitzgerald, FMedSci, FRS

Infants respond to noxious stimulation from birth, but the neural pathways underlying pain behavior and pain perception change through infancy, childhood, and adolescence. Evidence from animal models and clinical studies have demonstrated important epochs in nociceptive information processing through development. Understanding how pain is processed at each stage has considerable impact upon the clinical assessment and treatment of pain in children. The development and plasticity of cortical pain networks underlying the perception and memory of pain is an important area of recent research, particularly as there is increasing evidence that pain and stress in childhood may alter brain development and impact upon future adult pain sensitivity.
Variability in the Pain Experience after Injury
James Eisenach, MD

Physical, metabolic, or chemical injury to tissues typically results in acute pain followed by resolution. Individuals vary considerably not only in the degree of resolution but also in the speed of this process. Recent work is exploring the day to day progress of resolution from pain after the physical injury of major surgery and probing biologic mechanisms responsible for this variability which might be manipulated to speed recovery in all and prevent or diminish the likelihood of long lasting severe pain in the few with this problem. This lecture will summarize these results and discuss current hypotheses on the psychosocial, genetic, and neurobiologic factors which underlie this variability as well as clinical trials testing how these can be manipulated to speed recovery.
Spinal Mechanisms of Spinal Cord Injury-Induced Neuropathic Pain: Implications for Novel Therapeutic Targets
Susan Dorsey, PhD RN FAAN

According to the 2011 Institute of Medicine (IOM) report on Relieving Pain in America, chronic pain is a public health epidemic costing more than $600 billion for utilization of healthcare services and lost work wages. Not only is chronic pain resistant to conventional treatments at doses that do not reduce quality of life or increase risk for opioid misuse and addiction, but in many cases, chronic pain with a neuropathic component worsens over time. The most common definition of neuropathic pain is pain that is caused by a disease of, or damage to, the somatosensory nervous system. Hallmarks include episodic or continuous pain arising from normally non-painful stimuli (allodynia) and/or unpleasant, abnormal sensations termed dysesthesias. Our research has focused on spinal cord injury (SCI)-induced neuropathic pain. The majority of SCI patients report long lasting neuropathic pain at or below the level of the lesion and rate the intensity as moderate to severe. Unfortunately, there is limited information regarding the mechanisms underlying spinal cord injury-induced chronic neuropathic pain and most pharmacological and non-pharmacological therapies provide inadequate pain relief. Given this, the identification of novel therapeutic targets that might be exploited to reduce or eliminate chronic SCI-induced pain are critically needed. Early after SCI, reactive astrocytes undergo morphological changes and demonstrate enhanced proliferation, migration and synthesis of glial fibrillary acidic protein (GFAP), leading to the formation of the glial scar. While the glial scar can be protective, it can also limit axonal regeneration. In addition, changes in glial cells post-SCI can also contribute to neuropathic pain through production of chemokines, pro-nociceptive growth factors and cytokines. We have been focused on the potential role of the truncated Brain-derived neurotrophic factor (BDNF) receptor, tropomyosin-related kinase B T1 (trkB.T1), in SCI-induced neuropathic pain. While BDNF has been shown to be a potent modulator of pain signaling by binding of mature BDNF to its catalytically-active full-length receptor, trkB.FL, much less is known about the function of the truncated trkB.T1 receptor and its possible role in pain signaling. However, we and others have shown that trkB.T1 receptor expression is up-regulated at early and late timepoints following SCI in rodent models, coincident with the development of nocifensive responses and locomotor dysfunction. Since astrocytes, which are the main component of the glial scar, express only the truncated isoform of the BDNF receptor trkB, we reasoned that trkB.T1 signaling in astrocytes could be contributing to the formation of the glial scar and in turn, neuropathic pain and locomotor dysfunction. Our data to date demonstrate that genetic deletion of trkB.T1 globally or specifically in astrocyte only, demonstrate less mechanical and thermal hypersensitivity, reduced mechanical hyperesthesia and better locomotor recovery following injury. We conducted differential gene expression analyses in cultured astrocytes derived from neonatal trkB.T1 knockout mice to examine transcriptional differences associated with the loss of trkB.T1, and found that genes related to proliferation and migration were significantly reduced relative to wildtype controls. These findings were confirmed in functional assays, in which we found that the lack of trkB.T1 significantly decreased both proliferation and migration in response to serum and exogenous BDNF application. In vivo in the spinal cord, we also found reduced astrocyte proliferation and gliopathy following SCI. These results provide mechanistic insight into post-SCI neuropathic pain provide insight into the contribution of trkB.T1 signaling in astrocytes.

See media coverage from Pain Medicine News on this session. 

Assessment and Management of Neuropathic Pain: Advances, Challenges, and Opportunities

Srinivasa Raja, MD

The Neuropathic Pain Special Interest Group (NeuPSIG) of the International Association for the Study of Pain suggested in 2008 that neuropathic pain (NP) be redefined as “pain arising as a direct consequence of a lesion or disease affecting the somatosensory system.” Considering the clinical presentations and possible confirmatory diagnostic tests, a revised grading system was published to better reflect clinical practice and allow appropriate treatment decisions to be made, despite diagnostic uncertainty. Extensive research in the last two decades have contributed substantially to our understanding of the pathophysiologic mechanisms of NP. However, the clinical management of NP continues to be challenging with only a minority of patients achieving a satisfactory response from drug therapy. A number of evidence-based clinical practice guidelines for the pharmacologic and interventional management of NP have been published in recent years with stepwise recommendations. These guidelines highlight factors that contribute to therapeutic challenges, such as modest efficacy of the active drugs, high placebo response in trials, the heterogeneity of NP patients and an inadequate classification of patients included in clinical trials. Recent reports emphasize the heterogeneity of the etiology, mechanisms, and clinical presentations of patients with NP and suggest algorithms for stratifying patients, based on their sensory profiles. This research direction offers the opportunity for developing a personalized, multimodal approach to the management.

Taking Aim is Easier When you Know the Target: Moving Toward Mechanism-Based Pain Assessment

Roger Fillingim, PhD

Existing treatments for chronic pain produce meaningful therapeutic benefit for only a minority of patients, and we have limited ability to predict which patients will benefit from which treatments. Current approaches to pain assessment and diagnosis provide little information regarding the mechanisms underlying patients’ pain. Because pain treatments target underlying mechanisms, this represents a major barrier to improving clinical outcomes. Thus, mechanism-based approaches to pain assessment have the potential to enhance treatment outcomes by better matching patients to the appropriate treatments. This session will explore the topic of mechanism-based pain assessment. First, the multiple categories of pain mechanisms will be described. Then, several examples of strategies available for mechanism-based pain assessment will be provided, including systematic measurement of pain characteristics, symptom-based clustering of patients, and quantitative sensory testing. Emerging evidence will be reviewed suggesting that these methods may enhance patient phenotyping leading to improved prediction of treatment outcomes. The session will conclude with clinical recommendations and some possible directions for future research.

See media coverage from Pain Medicine News on this session. 

See media coverage from Practical Pain Management on this session. 

In Pursuit of More Powerful Non-Pharmacologic Treatments for Musculoskeletal Pain with Centralized Features

Susmita Kashikar-Zuck, PhD

Safe and effective non-pharmacologic treatments that have strong and sustained effects are urgently needed for the proper management of widespread chronic pain with strong centralized components. The speaker will discuss how a novel approach to exercise – neuromuscular training, derived from injury prevention research and focusing on improving body biomechanics and movement competence can be used in combination with coping skills training to reduce pain and disability in JFM. The Fibromyalgia Integrative Training for Teens (FIT Teens) program potentially has stronger effects on pain and disability in JFM than previously studied non-pharmacologic treatments. Results show strong improvements in self-reported pain and disability after treatment. Moreover, objectively measured improvements are seen in physical ability using technologically advanced methods including 3-dimensional motion capture of movement biomechanics. The potential for incorporation of technological advancements such as motion capture and virtual reality into behavioral treatments for centralized musculoskeletal pain will be discussed. Finally, treatment studies of this type can be used to probe the underlying brain mechanisms of centralized pain and its treatment and point the way for exciting new research directions in pain management.

Fordyce Lecture: Simplifying Evidence-Based Pain Self-Management Therapies for Chronic Pain: Rationale, Efficacy, and Implementation

Beverly Thorn, PhD

Chronic pain is a major public health problem in the US, unequally borne by those with income and ethnic minorities. Treatment, when available, is biomedical, expensive, and fraught with undesirable side effects. Pain self-management treatments show promise as adjuncts or alternatives, but are usually unavailable to individuals with low socioeconomic status, and have not been adapted to their education or literacy levels. This lecture presents the rationale for adapting and simplifying pain self-management treatments for individuals with chronic pain and chronic illness, explains the process of making such adaptations, examines the efficacy of these simplified treatments, and discusses the opportunities and challenges of implementing such programs in low-resourced settings.

See media coverage from Practical Pain Management on this session. 

Kerr Lecture: Distributed Processing of Pain: From the Spinal Cord to the Brain

Robert Coghill, PhD

Historically, our knowledge of the neurophysiology of pain has been driven, in large part, by the study of single neurons. While such approaches have been valuable, they have been unable to provide adequate explanations for many aspects of clinical pain – such as spread of pain to unaffected body regions and the ability of pain to persist through a myriad of treatments. However, these aspects of pain can be better understood if one considers how populations of these neurons work together to encode nociceptive information. Over the course of nearly three decades, we have used functional imaging techniques to assess the responses of populations of neurons in the rat spinal cord and human brain. From these studies, we have identified a neural infrastructure that holds the potential to support these clinically challenging aspects of pain. Nociceptive processing is widely distributed at all levels of the central nervous system, and progressively larger populations of neurons are recruited with progressive increases in nociceptive stimulus intensity. This distributed processing mechanism creates a system that is highly resilient to disruption, while progressive recruitment of neurons within this general system provides a substrate that can allow pain to spread widely.