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Milano Convention Centre | August 27-31, 2012

Plenary Sessions

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.

Educational Objectives:

• Understand the extent and prevalence of cancer pain.
• Understand many of the mechanisms that drive cancer pain.
• Understand the need to develop novel mechanism based therapies to treat cancer pain.
• Understand novel mechanism-based therapies to treat cancer pain that are in clinical trials.
• Understand how analgesic therapies to treat cancer pain may also reduce disease progression.

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.

Educational Objectives:

• Be aware of the prevalence of non-adherence to pain medication.
• Understand the contribution of health-professional-patient-family communication to non-adherence many of the mechanisms that drive cancer pain.
• Be aware of specific strategies that can be used to improve communication to facilitate adherence.

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.

Educational Objectives:

• Understand the general strategy of action of the endocannabinoid system.
• Understand the role of endocannabinoids in pain control at peripheral, spinal and supraspinal levels.
• Understand the cross-talk between the endocannabnoid system and other signaling systems involved in pain control appreciate the possible use of endocannabinoid-TRPV1 interactions for the development of new analgesics.
• Appreciate the possible use of endocannabinoid-COX-2 interactions for the development of new analgesics.

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.

Educational Objectives:

• Acquire basic knowledge on G protein coupled receptors.
• Get a general view on opioid receptor function in vivo.
• Understand implications of mu and delta receptors in pain control.

09:00 – Opioids and Non-Cancer Pain (PL 05)

Scott Fishman, MD, University of California, Davis (USA)

Opioid use for chronic pain is increasingly controversial in light of evidence for efficacy and potential detrimental impact ranging from prescription drug abuse to altered hormonal and neurologic functioning. This presentation will provide an overview of the medical and social controversies associated with chronic opioid use for chronic pain and an assessment of research on clinical outcomes, neuroimaging data, and recent developments in prescription drug abuse associated with opioid prescribing and efforts to increase risk management.

Educational Objectives:

• Understand controversies associated with chronic opioid prescribing for chronic pain.
• Understand how research has viewed outcomes from chronic opioid therapies.
• Understand the known impact of chronic opioids on neurologica and hormonal processing.
• Understand how prescription drug abuse with opioids has escalated in some countries.
• Understand emerging approaches to risk management with chronic opioid prescribing.

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.

Educational Objectives:

• Have an improved understanding of the role of psychological factors on the impact of chronic pain in older people.
• Have an updated knowledge of the effectiveness of psychosocial interventions in older people with chronic pain.
• An updated knowledge of the clinical implications of this field.
• An improved understanding of important issues and directions for clinical applications of psychosocial interventions in this population.

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.

Educational Objectives:

• Upon completion of this session attendees will be knowledgeable in current concepts associated with etiological pathways associated with common persistent pain conditions.
• Upon completion of this session attendees will be knowledgeable in how to assess the biopsychosocial and molecular pathways that underlie heterogeneous common persistent pain conditions.
• Upon completion of this session attendees will be knowledgeable of the emerging concepts and technologies that may improve the diagnosis and treatment of patients with common 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.

Educational Objectives:

• To hear about neuropathic pain disorders and their classification.
• To see examples of biomarkers for neuropathic pain.
• To hear about the struggle for a mechanism-based understanding and management of neuropathic pains.

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.

Educational Objectives:

• To have a mechanistic definition of chronic pain.
• To understand molecular mechanisms in the transition from acute to chronic pain.
• To have a broader understanding of the biology of the pain sensory neuron.

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.

Educational Objectives:

• To acquire knowledge of the mutual interactions between sleep and pain cortical processes.
• To understand that deleterious sleep perturbation by pain may remain undetected unless instrumental procedures are applied.
• To understand that cortical pain processing persists during all sleep stages, but changes in quality, intensity and internal relationships within cortical networks.
• To understand that dissociation between operculo-insular and cingulate networks during paradoxical sleep underlies persistence of sensory analysis but absence of orienting / motor reactions to pain.
• To be introduced to models aiming to explain how pain stimuli can be incorporated into dreams without awakening the subject.

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.

Educational Objectives:

• To notify the importance of visceral pain.
• To recognize relation between visceral pain and negative emotion.
• To know the position of irritable bowel syndrome in visceral pain research.
• To catch candidate substances regulating stress and visceral pain.
• To obtain the future perspective of visceral pain as prevalent medical condition.

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.

Educational Objectives:

• Different types of glial cells, such as microglia, astrocytes, and satellite glia are activated following nerve injury, inflammation, or drug treatment.
• Glial cells exhibit different activation states after different injury and insult.
• Activated glia produce glial mediators such as proinflammatory cytokokines and chemokines and neurotrophin to enhance pain states.
• Glial mediators such as TNF-alpha, IL-1beta, and MCP-1 can powerfully regulate spinal cord synaptic transmission and central sensitization.
• Specific targeting of glial signaling pathways may provide 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.

Educational Objectives:

• To understand the unique relationship between visual aura and the delayed onset of migraine headache.
• To recognize signs of peripheral and central sensitization during migraine.
• To understand better the progression of disease and the impact of early treatment.
• To .understand how light can make the headache worse.
• To learn about thalamocortical pathways that modulate cortical activity relevant to migraine headache.

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 carers in making the best decision for them.

Educational Objectives:

• To understand what the current evidence is for common treatments of common acute and chronic pain conditions.
• To be introduced to current best practice in evidence synthesis and analysis.
• To gain a good understanding of bias in clinical trials and in systematic reviews.
• To .understand how light can make the headache worse.
• To understand how to present data on risks and benefits in a way that is clinically useful.

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.

Educational Objectives:

• To know the International Classification of Spinal Cord Injury Pain and understand the difficulties in the diagnosis of different pain types.
• To be familiar with the clinical characteristics, impact, and prognosis of neuropathic pain following spinal cord injury.
• To insight into the current knowledge of the mechanisms.
• Be updated on the current state of evidence-based treatment for spinal cord injury pain.

Note: Titles and topics are subject to change.