|>||World Congress on Pain|
|>||15th World Congress on Pain|
|>||14th World Congress on Pain|
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Milano Convention Centre | August 27-31, 2012
An exciting line-up of internationally known speakers on the field of pain highlight IASP's 14th World Congress on Pain. The Congress will feature a wide array of topics and issues designed to keep both basic scientists and clinicians up to date on the latest scientific developments and how they will impact the management and treatment of pain. The program will include:
Tuesday, August 28, 2012
08:30 – Cancer Pain: From Mechanism to Therapy (PL 01)
Patrick Mantyh, PhD, JD, University of Arizona (USA)
In the past decade there has been a remarkable increase in our understanding of the mechanisms that drive different types of cancer pain. Importantly, many of these findings have been translated into new therapies to treat cancer pain as well as a host of therapies that are currently in clinical trials or in preclinical studies. This talk aims to be understandable by physicians, nurses and basic scientists alike and will focus on examples (anti-RANKL, C-FMS inhibitors, NGF/TrkA, anti-Sclerostin, and PAR2 antagonists) where rapid progress was made by close collaboration between clinicians and basic scientists. The talk will finish by emphasizing the need for continued collaboration between pain clinicians/scientists and cancer clinicians/scientists so that relief from cancer pain becomes an integral part of the treatment of cancer.
14:00 – Doctor-Patient Communication: The Key to Patient Care and Adherence (PL 02)
Phyllis Butow, PhD, University of Sydney (Australia)
In this presentation I will review the role of communication in the care of patients with chronic pain, focusing particularly on how communication can influence adherence to treatment recommendations. Many patients do not take their pain medication due to misconceptions (such as about addiction) and symbolic meanings they ascribe to pain relief. They do not admit non-adherence to health professionals to avoid offending or arguing with them or being judged. Patients sometimes feel options have not been adequately explained, or that their concerns have not been heard. Patient and family, and family and health professionals, also sometimes fail to communicate adequately about pain. Thus effective communication is vital to enable a trusting relationship to develop in which open discussion can occur, misconceptions can be addressed, barriers can be overcome and a shared decision regarding pain control can be reached. Specific communication strategies will be presented, along with the evidence to support their use.
14:30 – Endocannabinoids: A Unique Opportunity to Develop Multi-Target Analgesics (PL 03)
Vincenzo Di Marzo, PhD, Consiglio Nazionale delle Ricerche (Italy)
Endocannabinoids (eCBs) are endogenous agonists of cannabinoid CB1 and CB2 receptors, the G-protein-coupled receptors for Cannabis psychoactive ingredient, delta-9-tetrahydrocannabinol (THC). Anecdotal reports of Cannabis analgesic and anti-inflammatory effects date back 5000 years and led to studies on the anti-hyperalgesic actions of THC and synthetic CB1 and CB2 agonists. The discovery of eCBs and their inactivating enzymes, e.g. fatty acid amide hydrolase (FAAH) and monoglyceride lipase (MGL), and the finding in animal models of neuropathic/inflammatory pain of altered eCB levels only in tissues involved in nociception, suggest the use of FAAH and MGL inhibitors to elevate eCB levels and activate CB1 and CB2 "from inside" in a site-specific way, without the unwanted side effects of agonists. Yet, this approach is not without complications as these enzymes are not selective for eCBs, which in turn can be metabolized also by cyclooxygenase-2 (COX-2) and modulate pain also via molecular targets other than CB1 and CB2 receptors (e.g. TRPV1 channels). The use of drugs simultaneously targeting eCB inactivation and TRPV1 or COX-2 against pain and inflammation will be discussed.
Wednesday, August 29, 2012
08:30 – Opioid Receptors: Old and Novel Views (PL 04)
Brigitte Kieffer, PhD, Institute of Genetics and Molecular and Cellular Biology (France)
Opiates, such as morphine and heroin, produce their extraordinarily potent analgesic and addictive activities by activating opioid receptors in the brain. In vivo, opioid receptors interact with a family of endogenous peptides to regulate nociceptive processing, responses to stress, as well as mood and well being, and these receptors are primary therapeutic targets for pain control and addictive disorders. Opioid-controlled behaviors are multiple and complex, and genetic approaches have tremendously helped our understanding of opioid receptor properties, signaling, and function in vivo. Moving from the receptor as a concept, to the receptor as a visible molecule in the brain, the presentation will describe our current views of opioid receptors in physiology and disease of the nervous system.
09:00 – Opioid Therapy for Chronic Non-Cancer Pain: Promise and Peril (PL 05)
Mark D. Sullivan, MD, PhD, University of Washington (USA)
Opioid therapy for chronic pain has become widespread in the US and other developed countries based on the promise of sustained pain relief and low risk for addiction. Recent epidemiological studies and clinical experience have shed doubt on these promises. Opioid overdose and abuse are escalating rapidly. Opioid therapy does not appear to promote functional restoration and long-term helpfulness is difficult to distinguish from opioid dependence. Risks of opioid therapy arise from both the patients treated and the medications used. Contrary to treatment guidelines, patients with substance abuse and mental health disorders are the most likely to receive long-term opioid therapy in clinical practice. They also receive higher doses for longer durations accompanied by sedative-hypnotics. We have termed this combination of high-risk patients with high-risk regimens 'adverse selection.' Multiple risks of long-term opioid therapy have been shown to be related to both prescribed dose and patient characteristics. Policies to reduce opioid risks have been initiated at Federal, state and local levels.
14:00 – John D. Loeser Distinguished Lecture – Psychosocial Interventions for Managing Pain in Older Adults: Outcomes and Implications for Clinical Practice (DL 01)
Francis Keefe, PhD, Duke University School of Medicine (USA)
This presentation highlights recent clinical and research efforts focused on psychosocial approaches to managing pain in older adults. The presentation is divided into three parts. In part 1, a conceptual background for work in this area will be presented. In part 2, empirical studies examining the efficacy of psychosocial interventions for older adults will be presented and discussed. Intervention approaches to be highlighted include cognitive behavioral therapy, emotional disclosure, partner-assisted treatments, and couples based approaches. In part 3, important issues and future directions will be described. These include treating older adults who have pain and comorbid conditions (e.g obesity, depression), new technologies for enhancing the dissemination of psychosocial interventions (web-based and telephone interactive voice response methods), and ways to integrate psychosocial interventions into the health care system in which most persons with persistent pain are treated.
14:30 – Unraveling Complex Persistent Pain Conditions with Genetic and Phenotypic Biomarkers (PL 06)
William Maixner, DDS, PhD, University of North Carolina, Chapel Hill (USA)
Common persistent pain conditions (CPPCs) are composed of aggregates of phenotypes (signs and symptoms) associated with peripheral and central nervous system dynamics, stress responsiveness and inflammatory states. Complex molecular networks underlie these heterogeneous phenotypes and these networks are shaped by intrinsic polygenetic factors and environmental events such as physical injury and psychological stressors. Dr. Maixner will discuss emerging concepts and knowledge of the contribution of genetic variants, including recent discoveries that emphasize a genetic contribution to human pain perception CPPCs. He will present findings from recently completed and ongoing (see www.oppera.org) cross-sectional and prospective studies that examine the biopsychosocial and genetic factors contributing to the onset and maintenance of CPPCS. Finally, he will discuss emerging bioinformatic technologies that are proving useful in unraveling molecular networks that contribute to the clinical phenotypes observed in subpopulations of patients with persistent pain conditions.
Thursday, August 30, 2012
08:30 – John J. Bonica Distinguished Lecture – Neuropathic Pain: Is it an Entity? (DL 02)
Troels Jensen, MD, DMSc, Aarhus University Hospital (Denmark)
Differences in how somatosensory information is processed in experimental nerve injury and in inflamed tissue has had a major impact on how clinicians group their pain patients. Clinical pains are often classified into neuropathic and inflammatory types of pain and those pains that do not have these features are called idiopathic ones. Without a gold standard for what is neuropathic pain and what is not raises the question if such jump from basic science to the clinic is justified. The risk of classifying subjective phenomena such as pain is that we may force patients into a spin of academic terms which neither reflect the underlying pain generating mechanisms nor guide the management of patients' pain. John J. Bonica – as the eminent clinician he was – insisted on always listening to the patient and study his or her pain before making any assumptions about underlying mechanisms. The current interest to associate subjective symptoms and soft neurological signs in painful and non-painful nervous system diseases and disorders with structural, molecular, genetic and functional biomarkers may represent a new way to understand how pain is generated. It is to be hoped that each.
09:00 – Priming of Cutataneous Nociceptors: Toward a Cell Biology of Pain (PL 07)
Jon Levine, MD, PhD, University of California, San Francisco (USA)
The electrophysiological properties of sensory neurons activated by noxious stimuli (nociceptors) have been investigated intensively for half a century, and our knowledge of the molecular basis of transduction in nociceptors have increased greatly in the past decade. In contrast, our understanding of intracellular signaling mechanisms regulating nociceptor sensitization is still nascent. Signaling cascades, their role in nociceptor plasticity, and the importance of subcellular compartmentalization will be discussed. In addition, recent information regarding functional interactions with the extracellular matrix, cytoskeleton, intracellular organelles (e.g., mitochondria), and sex hormones will be introduced. This burgeoning literature argues that additional focus should be placed on understanding the cell biology of chronic pain.
14:00 – Ronald Melzack Lecture: Functional Brain Images in Neuropathic Pain (PL 08)
Luis Garcia-Larrea, MD, PhD, INSERM – University of Lyon (France)
Medicine is fascinated by images. Anatomical images do not give much insight on mechanisms underlying neuropathic pain (NP), while functional (electrophysiological & metabolic) imaging provides relevant information. Experimental noxious stimuli give rise to a coordinated network activation («Pain Matrix»), comprising the thalamus, somatosensory and insular cortices, mid- and anterior cingulate, and with more variability the posterior parietal and prefrontal regions, brainstem and cerebellum. While activity in these areas increases with the intensity of experimental pain, NP is associated with activity decrease in some of them, in particular the thalamus and anterior/perigenual cingulate, which may be reversed by pain-relieving procedures. Such seemingly paradoxical results parallel electrophysiological changes documented by intracranial recordings. NP and allodynia do not merely represent excessive firing up of physiological pain systems, but rather the result of complex interactions within the PM, including changes in hemispheric balance. Studies have been so far limited to the investigation of location and magnitude of brain activities. Understanding their functional relationship, including their timing of activation, appears now mandatory to apprehend the brain substrate of the neuropathic pain experience.
14:30 – Stress and Visceral Pain (PL 09)
Shin Fukudo, MD, PhD, Tohoku University Graduate School of Medicine (Japan)
Recent advances in brain science have shown how brain function encoding emotion depends upon interoceptive signals like visceral pain. Visceral pain arose early in our evolutionary history. Bottom-up processing from gut-to-brain and top-down autonomic/neuroendocrine mechanisms in brain-to-gut signaling constitute a circuit. Brain imaging technique enables us to depict visceral pain pathway as well as relating emotional circuit. Irritable bowel syndrome (IBS) is defined by chronic recurrent abdominal pain or abdominal discomfort associated with bowel dysfunction. IBS is also presumed to be a disorder of the brain-gut link associated with exaggerated response to stress. There are some candidate substances which have salient roles in pathophysiology of IBS. Corticotropin-releasing hormone (CRH) is a major mediator of stress response in the brain-gut axis. Administration of CRH antagonists likely alleviate IBS pathophysiology. Serotonin (5-HT) is another candidate in association to brain-gut function in IBS. This notion is supported by effects of agents modifying 5-HT neurotransmission in IBS patients. Further studies on visceral pain neuropathways are warranted.
Friday, August 31, 2012
08:30 – Glia and Pain (PL 10)
Ru-Rong Ji, PhD, Duke University Medical Center (USA)
Glia activation is emerging as an important concept in the pain research field. Increasing evidence indicates that glial cells such as microglia and astrocytes in the spinal cord and brain as well as satellite glia in the dorsal root ganglions are activated after nerve injury, inflammation, or drug treatment (e.g., opioid and chemotherapy). Glial cells display different activation states: they are not only activated in severe conditions (e.g., nerve injury) with morphological changes (gliosis) but also activated in mild conditions (e.g., acute inflammation and single opioid treatment) without obvious morphological changes. The most important link between glia and pain is the production of glial mediators, such as proinflammatory cytokines (e.g., TNF-a, IL-1b), chemokines (e.g., MCP-1), and growth factors (e.g., BDNF). In the spinal cord, these glial mediators have been shown to powerfully regulate synaptic transmission, central sensitization, and pain behaviors. Activation of MAP kinases in microglia and astrocytes is known to increase the synthesis and release of these glial mediators. Thus, specific targeting of glial signaling may offer new therapies to treat chronic pain.
09:00 – The Pathophysiology of Migraine Headache and its Modulation by Light (PL 11)
Rami Burstein, PhD, Beth Israel Deaconess Med Center, Harvard Medical School (USA)
Migraine is a recurring, episodic, often unilateral headache. It can be preceded by abnormal visual, sensory, motor and/or speech functions (migraine with aura), perceived as throbbing, and be associated with nausea and vomiting, hypersensitivity to light (photophobia), noise (phonophobia) and smell (osmophobia), as well as muscle tenderness and cephalic and extracephalic cutaneous allodynia. This lecture will summarize current understanding of (a) the mechanism by which aura activates peripheral nociceptors in the cranial meninges, (b) the mechanisms by which repeated activation of meningeal nociceptors produces central sensitization and renders migraineurs allodynic, (c) the mechanisms by which light exacerbates the headache, and (d) the mechanisms by which thalamo-cortico-thalamic circuits produce many of the migraine-specific associated symptoms.
14:00 – What Works for Whom? Determining the Efficacy and Harm of Treatments for Pain (PL 12)
Andrew Moore, DSc, University of Oxford (UK)
Evidence. Clinicians and researchers have to consider evidence: what works, for whom, in what setting, and at what cost. It is time to re-evaluate evidence-based pain in the light of major changes in how we understand and interpret clinical trials, looking for clinical practice effectiveness rather than clinical trial efficacy. We now have a better understanding of how to control bias in individual trials, and how to control bias in systematic review; several new sources of bias have been discovered, effecting chronic pain trials especially. Another major change is in outcomes, where the move is from average results in populations to patient defined outcomes of adequate treatment. Patients want high levels of pain relief and consider anything less than mild pain as a failure, and individual patient analyses give that much greater weight. We are now in a position to present data on interventions for the most common pain complaints, including acute pain, headache, migraine, post-operative pain, neuropathic pain. Equally important is addressing benefits versus risks of treatment, to empower patients and their careers in making the best decision for them.
14:30 – Pain in Patients with Spinal Cord Injury (PL 13)
Nanna Finnerup, MD, Aarhus University (Denmark)
A spinal cord injury causes a lesion of the somatosensory pathways in almost all patients, and as a result about 50% develop chronic neuropathic pain. A new International Spinal Cord Injury Classification has recently been proposed and offers a mechanism-based approach for the diagnosis of different pain types, which is a prerequisite for adequate treatment. The classification organizes pain hierarchically into three tiers, the first including nociceptive pain, neuropathic pain, other pain, and unknown pain. Subclassification of neuropathic pain based on different clinical phenotypes may offer an even more detailed approach for a mechanism-based classification. Changes within the dorsal horn, the spinothalamic tract pathways, and the thalamus have been identified as important for the development of pain. Treating spinal cord injury pain is challenging and often requires a multidisciplinary approach. This presentation will cover the classification, diagnosis, assessment, and treatment of pain following spinal cord injury with particular focus on neuropathic pain, and will briefly touch upon recent advances in the understanding of the underlying pathophysiology.
Note: Titles and topics are subject to change.