At the 14th World Congress on Pain in Milan, Italy, 27-31 August 2012, the International Association for the Study of Pain (IASP) presented its annual awards to honor the achievements of young investigators. The PRF wanted to hear from these up-and-coming pain researchers, who responded to written questions we submitted to them.
The Ronald Dubner Research Prize, which honors “the best clinical or basic science research paper, series of papers, or doctoral thesis in the field of pain, published or in press while in training as a student, intern, resident, predoctoral fellow, postdoctoral fellow, or equivalent,” was awarded to David Seminowicz, PhD, University of Maryland School of Dentistry, Baltimore, Maryland, US. Seminowicz uses MRI to study the effects of acute and persistent pain on brain function and structure in humans and in animal pain models.
Giandomenico Iannetti, MD, PhD, University College London, UK, received the Patrick D. Wall Young Investigator Award for Basic Science, which “honors individuals who have achieved a level of independence as a scholar in the field of pain.” Iannetti studies the functional significance of the brain responses triggered by sudden and intense sensory stimuli in humans.
The Ulf Lindblom Young Investigator Award for Clinical Science, which “honors an individual who has achieved a level of independence as a scholar in the field of pain (in clinical science),” went to Steven George, PT, PhD, University of Florida, Gainesville, US. George focuses on biopsychosocial models to improve prevention and treatment of chronic musculoskeletal pain.
PRF posted five questions to each winner, asking about how he became interested in pain, his current research, and future directions. Seminowicz’s responses appear below. See also: Q&As with Steven George and Giandomenico Iannetti.
David Seminowicz, PhD, is an assistant professor in the Department of Neural and Pain Sciences at the University of Maryland School of Dentistry, Baltimore, US. He received his PhD at the University of Toronto under the mentorship of Karen Davis, and then completed postdoctoral studies at McGill University in the lab of M. Catherine Bushnell.
Seminowicz’s work has focused on the cognitive aspects of pain, individual differences in the response to pain, and the consequence of chronic pain on brain structure and function. His studies have clarified how pain- and cognitive-related brain activity interact, and how passive and active pain coping strategies affect these types of activity. His work further suggested a brain mechanism through which chronic pain might affect cognitive ability, and he tested this hypothesis in a longitudinal study in people with chronic pain. At McGill, he turned to rodent MRI to ask a question that could not be easily addressed in humans: how the brain changes over time from before the onset of an injury that leads to chronic pain to the time when the disease affects cognitive and affective behaviors. Ongoing studies in Seminowicz’s lab employ longitudinal designs to assess how various treatments affect brain function, in human disease and rodent models of chronic pain.
PRF: How did you first become interested in pain research?
DS: I was first interested in everything to do with the brain. During my undergrad years, I got involved in studies on dorsal premotor cortex function in cognition; a sexually dimorphic hypothalamic nucleus in pigs; the heritability of human corpus callosum morphometry; and the function of human dopamine receptors. I eventually ended up working on brain imaging in major depressive disorder, and shortly after that I discovered brain imaging in pain. One thing that attracted me to pain research was that it crossed several fields of neuroscience, involving peripheral, central, and autonomic nervous systems, immunology, psychology, and cognitive neuroscience. As I got more involved in pain organizations, like the Canadian Pain Society, the American Pain Society, and the IASP, I learned what a destructive and intrusive disease chronic pain is, and that has been my motivation for continuing in the field.
What is the overall aim of your research?
To develop better treatments for chronic pain by targeting specific brain networks. In order to do this, we first need to understand the brain systems involved in creating the experience of pain, and we’re using neuroimaging as one tool to achieve this. We can directly target brain regions and systems in several different ways, for example by using transcranial or deep-brain stimulation, or by training an individual to modulate specific brain areas with real-time fMRI. We can also target the systems less directly by using cognitive therapy, teaching mindfulness, and strengthening the existing cognitive networks to allow patients to keep pain out of mind. An approach we are currently using in the lab is to examine brain structural and functional networks in people with chronic pain before and after treatment. This allows us to see which brain networks are functioning abnormally, how treatment restores normal function, and how this recovery relates to clinical outcomes. It also allows us to examine differences in the brain responses between people who respond to treatment and those who don’t.
What is the most exciting or intriguing result you’ve gotten so far?
A few weeks ago I would have said the study I was involved in at McGill University, in which we reported that treatment in people with chronic low back pain led to structural and functional normalization of the left dorsolateral prefrontal cortex. But I’ve recently been drawn back to an intriguing finding from almost 10 years ago during my PhD studies with Karen Davis, when we reported that cognitive modulation of pain-related brain activity depended on the behavioral strategies that healthy subjects would naturally choose. In particular, one group of subjects we called the A group, in whom attention dominates, focused harder on a task when pain was present than when there was no painful stimulus, and these individuals would also decrease pain-related activity in several brain regions. Subjects in the P group (pain dominates), on the other hand, had poorer task performance when pain was present, and they did not modulate pain-related activity. A similar finding was recently reported by another group using a different paradigm and imaging technique, and recently the study has been replicated in Davis’ lab with a large sample of subjects. I find this area of individual differences in pain response intriguing because it enforces what pain clinicians have been telling us: Each patient needs to be considered individually, and treatment must be personalized. If we can figure out the biology behind some of these individual differences, we might be able to improve personalized treatment approaches.
What are you working on most intensely right now?
There are three main areas. The first is treatment responses in the brain. We need to figure out how treatment changes the brain, which changes are essential to good clinical outcomes, and whether we can predict clinical outcomes with pre-treatment brain scan data. The second area is ongoing pain, which is commonly described in neuropathic and some other chronic pain conditions. We need to understand how ongoing background pain affects brain networks involved in sensory and pain processing, as well as cognitive and emotional processes. The third area is the development of brain changes in chronic pain, for which we use high-field MRI in rodent models. This line of work is essential for understanding how pain changes the brain and addresses questions that cannot be easily addressed with human participants.
In your field, what do you hope we will know in five or 10 years that we don’t know now?
Two things: one specific to pain, the other to brain imaging more generally. The field of pain neuroimaging is rapidly accumulating data, and we need to translate the findings into real solutions for people who suffer from chronic pain. I expect that within the next 10 years we will have real guidelines for pain self-care that will include cognitive training and other activities that shape the brain in ways that are proven to relieve pain. That is the gap right now: the proof. Once there is sufficient evidence for a treatment, it can begin to be applied on a large scale.
One other specific area in which we expect to see huge growth is in the understanding of functional brain networks: how they are disrupted by various psychiatric and neurologic diseases, the similarities and differences in those disruptions across diseases, etc. Data sharing is allowing us to finally make these comparisons, and some very large-scale sharing initiatives are now underway. I hope that in the next 10 years, neuroimaging research advances our understanding of pain and other disorders beyond what I could imagine now.
