Addiction to opioids often begins in the doctor’s office. These drugs are typically the only option to manage pain after an operation or in patients with serious injuries. They’re also frequently prescribed to patients with chronic pain, and it’s these patients who are most at risk for opioid addiction.
Ted Price is an associate professor of neuroscience at the University of Texas at Dallas. His work focuses on the molecular mechanisms that cause pain to persist even after the injury that triggered it has healed.
What he and his colleagues have discovered is that a buildup of a particular substance between neurons plays a major role in our experience of ongoing pain. That new understanding could help lead to a new treatment for chronic pain that leaves addictive drugs out of the equation altogether.
On KERA’s Think, he talks about the future of chronic pain research — and what it might mean for the U.S. opioid crisis, which claimed more than 50,000 American lives in 2016.
The signals behind chronic pain
Chronic pain is defined as pain that persists at least three to six months beyond the period of normal healing, according to NIH’s National Center for Complementary and Integrative Health.
It can go beyond acute feelings of pain. Chronic pain can result in a host of problems including cognitive disorders, clinical depression and hair loss. The NIH reports about 11 percent of American adults suffer from this condition.
“For many, it’s very disturbing. Even when they’re not doing anything, they’ll feel this stabbing or burning pain coming from the limb,” Price says. “Normally, pain is a danger signal to the brain that something’s wrong, but when they look, nothing looks wrong.”
When we feel pain, nerve cells called “nociceptors” are activating and sending that signal to the brain. When working normally, this process is helpful: It tells you that you’re hurt and you need to protect yourself. After a severe injury or a surgery, nociceptors fire frequently and are meant to stop once you’ve healed.
But in the roughly 30 percent of patients who develop chronic pain, nerve cells rewire themselves before healing, which can cause them to fire at random, months after the injury is gone.
Price’s research focuses on this “rewiring” process, called “neuroplasticity.” It’s the idea that the nervous system can “rewire” itself throughout our lives to help us adapt to our surroundings.
“We were originally looking at how brains learn. We had this idea that pain is a learning phenomenon, too. Synaptic plasticity, or the cellular process of learning, is common to things that are beneficial and things that aren’t.”
There are some really complex genetic factors at play,” Price says, “but it really is a plasticity disease.”
Opioids, tolerance and chronic pain
Chronic pain, like opioid abuse, is often stigmatized. Price argues it’s not as important to try and quantify pain as it is to treat it more effectively. Chronic pain often affects every aspect of people’s lives. In that sense, the chronic pain epidemic and the opioid crisis are one and the same.
“There’s no question that opioids are effective for acute pain,” Price says, “but the issue that we have right now is that the drugs that we have to treat chronic pain don’t work very well and the drugs that are efficacious are incredibly dangerous.”
While opioids are still often necessary after surgeries, Price says there’s evidence that they may actually increase the likelihood of chronic pain after surgery.
“We need to have better, non-addictive therapeutics that are not only going to treat acute pain but also prevent the development of chronic pain," he says. "When you take a drug more frequently over time, it requires a larger dose to achieve the same efficacy. This actually happens in almost everyone taking opioids."
Tolerance is most problematic when people begin taking opioids again after a period without, Price says. Many chronic pain patients experience pain after a long period following surgery. They may take what used to be their normal dose of opioids. In many cases, this dose is enough to induce an overdose, as they may have lost their tolerance, he says.
The leap from the lab to the pharmacy
There is no cure yet. But Price says that the science is very mature.
The leap from preliminary research to clinical trials is difficult to navigate for many scientists, especially those in an academic setting. So Price, and many researchers like him, are starting their own companies to try and bring their research into realization on their own.
“If … there is one thing I try to convey to [my colleagues] … there really isn’t anybody else who is going to be quite as passionate about [turning] your ideas into medications as you are. […] It’s a steep learning curve … but it’s very exciting and extraordinarily rewarding.”
I would argue [we’re] completely failing in trying to treat this,” Price says. “There are some interesting treatments [for migraines] which may be approved by the FDA this year, but we need to see successes like this across the board.”
Price stresses the need to conduct clinical trials as early as safely possible so researchers don’t waste time on disproved hypotheses and patients can get treatments sooner. Price points to McGill University, in Montreal, as a good example. He attributes the success to the Canadian university to its emphasis on collaboration between basic science researchers and clinical trial labs.
Treating chronic pain takes a multimodal approach, Price says. Treatments should go beyond painkillers and other medications; for example, exercise, whenever possible, can help dramatically. Managing pain, much like managing an epidemic, requires creativity and collaboration.
Megan Zerez is an intern at KERA.