The International Association for the Study of Pain hosted the 16th World Congress on Pain in Yokohama, Japan from 26-30 September 2016.
Attracting over 4,400 participants, the meeting was a great success bringing together one of the largest international groups of clinical and research experts in acute and chronic pain. Although the congress covered the wide range of conditions associated with acute and chronic pain, there were numerous workshops, lectures, and posters that highlighted extremely relevant teaching points to clinicians and researchers dedicated to improving the lives of women with endometriosis and pelvic pain. Its difficult to select only a few items to highlight in this newsletter since the conference boasted approximately 20 refresher courses, 13 plenary lectures, 70 topical workshops, and over 1000 posters. Here are only a few highlights from selected presentations and posters from the meeting.
Plenary lectures and topical workshops emphasised the importance of multimodal therapy and individual differences in the pain experience
Dr Roger Fillingim, Distinguished Professor at The University of Florida, delivered an engaging plenary lecture on “understanding the mosaic that makes pain personal.” He presented compelling evidence that demonstrates the experience of pain is complex and shaped by dynamic interactions among multiple biological (eg age, genetic, anatomic) and psychosocial factors (eg socioeconomic, cognitive, behavioural), each of which interact and influence each other. These biopsychosocial factors produce profound inter-individual differences in pain perception and its response to treatment, reminding clinicians and scientists alike the importance of considering this complex mosaic when studying and treating patients with pain.
Dr Irene Tracey, University of Oxford, delivered a compelling lecture on how neuroimaging discovery science is beginning to translate directly into patient benefit. While many laboratories across the world have shaped our understanding of the underlying mechanisms of acute and chronic pain, much of this knowledge can now be utilised to directly benefit patient care. Examples include utilising neurobiological markers for pretreatment stratification and prediction of response to therapeutic interventions.
Dr Stephen McMahon, King’s College London Faculty of Life Sciences and Medicine, enthralled the audience with his lecture entitled “Why me? Neurobiological Mechanisms of Pain Vulnerability.” As many endometriosis experts already know, Dr McMahon reminded the audience that for many conditions that cause pain, there is little and sometimes no correlation between the degree of pathology and amount of pain reported by patients. He presented fascinating data to show that neurobiological mechanisms that drive pain resilience or vulnerability are being uncovered, and genetic and epigenetic factors are important contributors to these underlying mechanisms.
Cutting edge research
There were multiple posters that presented cutting edge research in the areas of endometriosis, dysmenorrhea, and chronic pelvic pain. In two different posters, Katy Vincent and colleagues demonstrated that while menstrual abnormalities were far more common in women with chronic pelvic pain versus pain-free controls, a systematic review of published studies in women with chronic pelvic pain showed that only a small proportion of studies adequately assess the impact of cyclicity and menstrual phase factors on pain symptoms.
Next, J Brawn and colleagues presented interesting findings from an ongoing prospective neuro-imaging study of women diagnosed with chronic pelvic pain awaiting their first laparoscopy for the evaluation of endometriosis. Using functional MRI techniques, they found that women with longer duration of pelvic pain symptoms prior to surgery had greater differences in connectivity between the periaqueductal gray and hippocampus, two regions of the brain known to play a significant role in modulation of pain and mood. Furthermore, these women also reported greater psychological distress and pain catastrophising. The authors were correct to point out that these findings support the need for prompt treatment of pelvic pain symptoms, before central changes become a dominant, independent mechanism of pain.
Additional brain imaging studies included that by L Lee and colleagues who showed that the overall integrity of functional brain architecture in young women with primary dysmenorrhea (mean age 23.1 years) was intact and similar to pain-free controls, suggesting young dysmenorrhea subjects may retain integrity of brain function that allows for normal cognitive and affective functioning in daily living. It may be that the cumulative effects of persistent pain, through chronification processes and genetic factors, lead to disruption of large-scale brain networks later in life in vulnerable dysmenorrhea patients. This again suggests an important opportunity for early prevention.
In two different studies, S Wei, W Li, and colleagues presented very interesting studies on the relationship between genetic polymorphisms and changes in the central nervous system pain modulatory system in women with primary dysmenorrhea, providing further evidence of genetically-influenced central mechanisms of pain in dysmenorrhea. Another study by C Tu and colleagues identified decreased levels of GABA, an important inhibitory neurotransmitter, in key pain regulatory regions within the brain, but no difference in glutamate, an important excitatory neurotransmitter. These findings suggest that central mechanisms of pain may be due to decreased central inhibitory mechanisms rather than increased excitatory mechanisms. Finally, F Tu and colleagues presented findings that suggest that when dysmenorrhea is associated with subclinical bladder hypersensitivity (ie. viscero-visceral convergence), sensory amplification of unpleasant visual stimuli is also present. This innovative study suggests that that frontal cortical networks associated with higher order processing may amplify sensory unpleasantness.
Overall, the cutting edge research presented at IASP further support the growing body of evidence that chronic pelvic pain and dysmenorrhea are associated with changes in the brain, which may explain why the degree of pelvic pathology does not consistently correlate with the severity of symptoms and why some women do not respond to medical or surgical therapy aimed at pelvic implants or disease. Furthermore, these pain conditions are likely comprised of heterogeneous populations with variable individual mechanisms of chronic pain, emphasising the importance of individualised therapies that include mechanism-based medical, surgical and behavioural treatments. However, much works remains to be done to optimise the care of women with these complex conditions.
Updating the classification of chronic pain conditions
The forthcoming ICD-11 classification of chronic pain was presented in several venues and received much attention. One goal of the new classification system is that it be equally useful in primary care settings, as well as those in specialised pain management. IASP has been actively involved in shaping the classification of chronic pain conditions and established a task force to address this issue. Comprised of pain experts from across the world, the task force has considered pain aetiology, pathophysiologic mechanisms and body site to create a multilayered classification system. The goal of the ICD-11 system is to allow coding of chronic pain syndromes in a comprehensive and straightforward manner, thereby improving the recognition and management of these chronic pain conditions. Chronic primary pain, chronic visceral pain and chronic post-surgical pain are among the new diagnoses within ICD-11. Chronic pelvic pain, primary and secondary dysmenorrhea are recognised conditions within the proposed classification system. Optional specifiers for each diagnosis will allow recording measures of pain severity, which can be graded based on pain intensity, pain-related distress, and functional impairment. In addition, evidence for the presence of psychosocial factors may be recorded.
Treede RD, Rief W, Barke A, Aziz Q, Bennett MI, Benoliel R, Cohen M, Evers S, Finnerup NB, First MB, Giamberardino MA, Kaasa S, Kosek E, Lavandʼhomme P, Nicholas M, Perrot S, Scholz J, Schug S, Smith BH, Svensson P, Vlaeyen JW, Wang SJ. A classification of chronic pain for ICD-11. Pain 2015 Jun;156(6):1003-7.
References for posters
Poster PW0252: S. Hodgson, J. Reavey, S. Kirtley, J. Moore, C. Becker, K. Vincent. Cyclicity is Rarely Assessed or Accounted for in Chronic Pelvic Pain Trials in Women
Poster PTH250: L. Buck, K. Vincent. Disruption of the menstrual cycle is common in women with chronic pain.
Poster PTH249: J. Brawn, J. Bijsterbosch, L. Buck, C. Becker, I. Tracey, K. Vincent. Delayed pain treatment impacts central networks in women with chronic pelvic pain
Poster PTH081: C. Tu, W. Li, D. Niddam, J. Hsieh, H. Chao. Primary Dysmenorrhea May Be Associated with Reduced GABA Concentration in Menstrual Pain-Related Brain Area: An MRS Study
Poster PF007: L. Lee, Y. Chen, C. Lin, W. Li, I. Low, C. Tu, C. Chou, C. Cheng, T. Yeh, H. Chao, L. Chen, J. Hsieh Unaltered Integrity of Functional Brain Architecture in Young Women with Primary Dysmenorrhea
Poster PW0093: W. Li, C. Tu, H. Chao, M. Lin, L. Chen, J. Hsieh Association of BDNF Val66Met Polymorphism with Hippocampal Volume Plasticity in Primary Dysmenorrhea
Poster PTH064: S. Wei, L. Chen, M. Lin, H. Chao, J. Hsieh. The OPRM1 A118G Polymorphism Modulates the Expressions of Functional Connectivity of the Pain Modulatory Systems in Women with Primary Dysmenorrhea.
Poster PTH470: F. Tu, R. Silton, K. Dillane, K. Polnaszek, S. Harte, K. Hellman. Cortical Mechanisms of Sensory Amplification in Visceral Pain Conditions
About the author
Dr Sawsan As-Sanie is an Assistant Professor and Director of the Minimally Invasive Gynecologic Surgery Program and Fellowship at the University of Michigan, Department of Obstetrics and Gynecology.
After receiving her medical degree from the Johns Hopkins University School of Medicine, she completed her residency in Obstetrics and Gynecology at the Case Western Reserve University School of Medicine. Dr As-Sanie then earned her Masters in Public Health in epidemiology from the University of North Carolina School and completed a Fellowship in Minimally Invasive Gynecologic Surgery and Chronic Pelvic Pain at the UNC Department of Obstetrics and Gynecology. Her research interests are aimed at defining the underlying mechanisms involved in the initiation and maintenance of chronic pelvic pain and post-surgical pain, with a focus on endometriosis-associated pelvic pain. Dr As-Sanie is on the editorial board of the Journal of Minimally Invasive Gynecology and is an active member of various professional societies, including the International Pelvic Pain Society (IPPS) and AAGL (American Association of Gynecologic Laparoscopy). She currently is Treasurer for the International Pelvic Pain Society, is the 2016 IPPS Scientific Program Director, the 2017 AAGL Scientific Program Chair, and serves on several committees for the AAGL, including the Fellowship Curriculum Standardization Committee. She won the 2011 Rodolphe Maheux Award for best clinical presentation at the 11th World Congress on Endometriosis.