Ask an Expert: Can Prolonged Suboxone Use Cause Pain Sensitivity?

By Jeffrey Junig 10/28/16

Endorphins are our own "pain treatment chemicals" that block or reduce pain in certain situations. Pain pills and heroin hijack endorphin pathways, activating receptors in place of endorphins.

A hand with bones and redness indicating pain.
Shouldn't this be helping?

Q: I've been on Suboxone for several years and I think that my pain tolerance has gone down. I've heard that there is a phenomenon where people who take opioids too long become more sensitive to pain, rather than less. Does this apply to people on Suboxone? And if so, would it go away if I were to go off? 

Dr. Jeffrey Junig: Pain is a complicated sensation that is difficult to study in humans. We know that the intensity of pain varies widely across a number of interventions. Chronic pain feels worse when patients are depressed, and pain is less severe when people are distracted, rather than focused, on the discomfort. People also have varying tolerance to pain. 

Pain can be divided into a sensation component and a "suffering" component, with the latter more related to mood and expectations, such as whether the pain will be short-term or will be present for a long time. If you are like most people, you can probably tolerate a higher amount of pain if you know it is temporary. On the other hand, endless, unstoppable pain is more likely to result in suffering.

My point is that in any one person, evaluating and treating pain requires an understanding of many aspects of the person’s life, as those things impact how the signal in pain fibers will be processed by the brain. The pain signal will be amplified or decreased according to many different things, including the effects of opioids, both natural (endogenous) and artificial (exogenous).

Opioids act as "mu receptors," which are proteins on neurons that are activated by endorphins. Endorphins are our own "pain treatment chemicals" that block or reduce pain in certain situations. Pain pills and heroin hijack endorphin pathways, activating receptors in place of endorphins. Over time, those receptors become less sensitive to pain pills and heroin, causing "tolerance" and withdrawal if those substitute chemicals are discontinued.

Research into opioid pathways suggests that people who take opioids for a long time experience worse pain than people who don’t use opioids for a given painful stimulus. This effect is called OIH, or Opioid-Induced Hyperalgesia. The concept of OIH has been around for a long time, and has been a topic of some controversy. Lately, OIH is getting more attention because of efforts to reduce the use of opioids. Support for OIH has been reported in both animal and clinical studies. But the effect is hard to quantify for any one patient, because of all of the other factors that impact the sensation of pain. You will find a broad review of OIH by clicking here.

Over the years I’ve had many patients who were on pain pills for back pain and other common conditions, who had almost complete relief of pain after changing from opioid agonists to buprenorphine medications. Patients often attribute the improvement to buprenorphine, but I’m reluctant to do the same, since people develop complete tolerance to the mu-receptor effects of buprenorphine. I assume their improvement instead comes from getting out of the cycle of opioid stimulation and withdrawal. Perhaps they benefit from having less OIH from buprenorphine than from opioid agonists, but I doubt that they can truly notice the relatively minor effect found in studies of OIH.

But you are reporting the opposite, i.e. an increase in pain on buprenorphine. I can’t say with any certainty whether your pain got worse from buprenorphine, or instead only feels worse because of one of the other factors I mentioned earlier. But research into OIH suggests that methadone and buprenorphine are less likely to cause hyperalgesia than other opioids, because of the effects of those two drugs on other brain chemicals. In short, OIH is thought to involve actions at glutamate receptors, and treatment of OIH includes use of glutamate antagonists such as dextromethorphan. Methadone has blocking actions at the glutamate receptor, and so is thought to create less risk of OIH. 

The effects of buprenorphine are much more complicated, but the conclusion is similar—that buprenorphine is less likely to cause OIH than other opioids. For the scientists reading this post, the link above reports that "Buprenorphine has been shown to be intermediate in its ability to induce pain sensitivity in patients maintained on methadone and control patients not taking opioids. Buprenorphine showed an enhanced ability to treat hyperalgesia experimentally induced in volunteers compared to fentanyl. And spinal dynorphin, a known kappa receptor agonist, increases during opioid administration, thus contributing to OIH. Buprenorphine is a kappa receptor antagonist. For these reasons, buprenorphine might be unique in its ability to treat chronic pain and possibly OIH."

In layperson’s terms, some opioids can make pain worse. But buprenorphine is thought to have less risk of OIH, and may protect against and even treat that effect. Research into OIH has a long way to go, and we are not at a point where reliable predictions can be made. If OIH is truly worsening your pain, opioid induced hyperalgesia is thought to gradually go away when opioids are discontinued.

Jeffrey T Junig, MD, PhD, received his PhD in Neuroscience from the Center for Brain Research and MD with Honor from the University of Rochester School of Medicine and Dentistry. Full Bio.

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