Chronic pain needs to be thought of as a disease in itself
Camilla Svensson is a researcher in long-term pain. Joint diseases, such as rheumatoid arthritis (RA), form the basis of the studies she and her research team are undertaking. The ultimate goal of the work is to identify new ways to relieve pain. They want to increase the understanding of the molecular neurochemical and immunological mechanisms that lead to long-term joint pain.
Who are you?
My name is Camilla Svensson and I am a professor of cellular and molecular pain research. I am passionate about studies with a very clear clinical foundation, which tries to answer a question that is relevant to people with chronic pain. Chronic pain lowers the quality of life for many and imposes many costs on society. Many of the available drugs either do not provide adequate pain relief, or have significant side effects.
I really like my job! I have to be a detective and I can direct our work in the lab towards what I think is important. As a researcher, I am the spider in the web, connecting with people with different expertise. I currently have a research team of 14 people from many different continents.
Why is pain research necessary?
Pain affects many people: between 10 and 30 percent of the adult population suffers from long-term pain which affects their quality of life. It is not only that the pain that is problematic, but that the pain itself can itself become like a disease. We know chronic pain affects many aspects of life; everything from reduced quality of sleep and physical activity to effecting the entire immune system, which all leads to major impacts on health.
We have an incomplete picture of what is known as pain physiology, i.e. how pain functions “normally”, and even less of its pathology, i.e. how an injury or illness affects the nervous system over the long term. For example, why can pain remain even after the inflammation heals? If we can solve that, maybe we can find tools to reduce the pain.
As pain researchers, we usually provoke the discussion by saying we should look at pain as a disease in itself. It is very important that we understand what it is that causes pain to become chronic. There are still so many basic questions we don't yet know the answers to.
During the eleven years I have been working in this field, a lot has changed in how we view pain. Pain gets so much more attention today, both in terms of research and treatment.
What are you working on now?
Today, we’re learning that antibodies relevant to autoimmune diseases can affect the nerve directly. There need not be inflammatory cells in between. We have long known that when antibodies activate immune cells the inflammatory cells can release substances that irritate pain nerves, but now we know that in addition to that, the antibodies themselves can act directly on the nerves.
Right now we are investigating why pain nerves can continue to be more irritable or activable, despite inflammation having healed. We look both at the nerve itself and at cells located around it. We’ve seen that changes in connection with the inflammation do not revert when the inflammation recedes. We are also examining the central nervous system and seeing that there are changes there as well.
What research do rheumatologists want?
I would say the difficult-to-treat pain that the anti-rheumatic drugs sometimes don’t reach. The patient might respond to the treatment in terms of inflammation, but their pain does not disappear completely.
Between 10 and 50 percent of patients get insufficient pain relief from anti-rheumatic therapy. Most pain-relieving drugs that produce very good results for acute pain work poorly over long-term use and can cause problems in the form of various side effects. This means that when the pain goes into a more chronic or prolonged phase, there are very few drugs we can add to a patient’s therapy We simply need more knowledge about the underlying changes in the nervous system that lead to long-term pain so that we can identify new routes of attack.
What do you see is the future for research into chronic pain?
In the future, I believe that we will find out which cells and factors affect pain signaling in the body and brain in a way that leads to long-term pain, and also exactly which nerves are involved in that process. It is important to understand where the problem arises. Is it at the nerve end of the joint or somewhere on the way to or in the brain and does this change over time?
I also imagine we strengthen the link between research and clinical activities even more. Pain doctors and rheumatologists who work clinically will collaborate with researchers. So what we do in the lab bench will be even more relevant, and we will have even more access to patient samples.
The challenge with today's animal studies and pain is that we can only look at the actual physical effect, a pain signal, but the experience of pain is something that is colored by so many aspects for us humans. That’s something that is much more difficult, if not impossible, to study in a mouse. It is a big gap that is difficult to bridge. We need to find smart ways of working to define the knowledge that is transferable between animals and people.
What do you think is especially important for someone with RA to know?
When I think about what my colleagues around the world are doing, the new lines of research in my own lab, and the increased collaboration between different specialties, for example between pain researchers and immunologists, I feel very hopeful about RA and pain. We are learning that factors we previously did not understand can regulate the activity of the nervous system. We still have much to learn about communication between the immune system and the nervous system and how it can cause consequences such as severe pain in certain conditions. There is a lot of interest in how things are going now, which makes being in research very exciting!
In the long run, I think we will understand that the immune system can affect the nervous system, even though we cannot see that the immune system is affecting the tissue. Although we cannot see classic signs of inflammation, the immune system can trigger activity in the nerve cells.
I think we will take a few big steps towards increasing our knowledge of what makes pain chronic, and then we will find new strategies. Research goes in waves and right now we’re in a phase of pain research.