Opiate-Induced Hyperalgesia (OIH)

And really, you can think of it as neuronal hyperexcitability. And diffuse paint with distribution beyond the site of pain. Think about this. This is really, really an important topic. Now I’m going to introduce them different places where this issue can come up. Okay. For many, many years, I was a professor of emergency medicine.

And I worked in county facilities for the most part. And I used to see a lot of people coming that you don’t have track marks and were obvious opiate addicts. And when residents or nurses would approach this folks, whether, and you know, they might be complaining of abdominal pain, left upper quadrant abdominal pain.

Okay. And so you’d approach. And these are young folks and the minute you touch their skin to start an Ivy, they would jump and withdraw or. You attended, just touch their skin and see where the pain is on the left upper quadrant of the abdomen. They would just really withdraw. And the general response from the clinical team was always, he’s faking it.

She’s faking it. They’re drug seeking. Okay. More than likely the person was suffering from opiate induced hyperalgesia. Okay. Extremely sensitive even to touch. Now let’s try to formalize this and see how much more difficult this is. Are we talking about an acute situation? Let’s say you’re going in for surgery and you’re getting a whole bunch of morphine.

And does that cost opiate induced hyperalgesia? Is it for chronic pain patients where it induces opiate induced hyperalgesia? Is it, the somebody who’s addicted to opiates, whether they’re using heroin, fentanyl, morphine, taking pills, where they have general opiate induced hyperalgesia, see how all of that makes a difference.

And the answer to that part of it is well for the most part. We’ve seen it in all areas. This is really important. We’ve seen it in all areas, but we don’t really have solid, formalized, retrospective data that we can work. It’s not retrospective data, but data that we can look at and formalize this captured and discuss it.

That’s number one, keep that in mind. Number two, what is the mechanism? I don’t know. Who knows? Kind of kidding, kind of not, we do know that it has to do with glutamate. What is glutamate? Many of, you know, it as MSG monologue sodium glutamate, right? It’s a, it’s actually an amino acid and it just happens to be the primary.

Excitatory neurotransmitter in the central and, I believe peripheral nervous system glutamate. It also has to do with N M D a receptors, N as in Nancy, M as in Mary, D as in dog, a and MDA receptors. Those are one type of center of receptors used in this glutaminergic system throughout the body. That’s different than the drug.

M D M a, which many of, you know, as Molly and ecstasy and so forth. We’re talking about an MDA receptors. Now, since we’re talking about Molly, here’s something else. That’s interesting. Antagonist ligands, which is things that go and bond into a receptor and sort of law. Can be used misused or abused as a recreational drug that hits that N N D a receptor.

One of those, one of those ketamine, which is the same family as PCP that is used in animal anesthesia procedures often. And it’s also a substance of abuse. And I know there’s so much more to talk about those, but here’s the thing I’m getting it right. What we do know about the mechanism and process of opiate induced hyperalgesia.

I think the best data to date is that it has to do something with the glutamate system in the central nervous system and, and MDA receptors. All right. So we know that we’ve asked the question, which area. Does it affect that acute giving someone of opiates and a surgical procedure, the drug addict, is it all over the body or just sites of pain for chronic pain patients?

And the answer is all of those have appeared in the literature and many of us have seen it clinically important to note. Here’s another reason why it’s so. Oh, I H opiate induced hyperalgesia. All right. Um, which is, you know, you increase the dose of the opiate and pain is getting worse. Well, this mimics think about it.

It mimics opiate tolerance, which is a real. Opiate withdraw. Right. Pain is worse. Okay. That’s a real thing. And it’s really, the effects are the same, that physiological road where someone gets there is extremely different. Okay. So, again, it comes down to the clinician being aware of this issue and addressing it.

Why is this important? And I’m going to bring in my favorite drug buprenorphine, Suboxone. I do. Although I see substance abuse patients over the years, I’ve, gathered a group of chronic patients. Yes, the question does Suboxone. Okay. Does Suboxone or buprenorphine and use opiate induced hyperalgesia?

It doesn’t seem like it does at least not to the same extent as straight agonist, opiate stoop. This is critical and huge. So wouldn’t have been better if we were using all these years, buprenorphine type of medication for chronic pain patients. And in fact, um, if you look at the history of the discovery of buprenorphine and led the sixties and whatnot, you know, what it was meant for.

It really shed some light on this question. Let me 0.1 other thing out for those of you that are the naysayers out there. Know that Suboxone buprenorphine, a lot of people don’t know that, but there’s a patch of the exact same drug called BW trends and it’s FDA approved for. But not for substance abuse.

And if you’re using the under the tongue, a soluble version of any of these medications for pain, you’re doing that off label. It’s the same drug as the past. And then that it’s really fascinating, right? How these things have evolved. And what I have seen over the years is a few things., and I don’t like to use, I do have a group of pain patients that I turned on.

Buprenorphine and medications has, has solved a lot of issues. I tell people right off the bat, once you switch your,  that pain that you had 10 years ago, that back pain, whatever it was from an injury or so forth, you know, you’re going to notice that over time, it’s not really as bad as it happened getting to in the last several years.

And as we taper off your opiate medication and some cases they don’t want to get on buprenorphine, you’re going to notice that your pain is not as bad as you thought that it was okay. And, increasing the dose of opiates comes with a lot of. Consequences, right. The substance abuse, the addiction, the mentation goes down the toilet.

Right? Number one, you can avoid all of that will be pornography, but this is one of the consequences of opiate induced hyper out Jesus. Okay. So diagnosis is based on clinical recognition. It is a real thing. You see it with chronic pain. And in acute situations, you see it declare itself in many, many different ways, but increasing your opiate dose has many dire consequences.

One of which is addiction, but just being dope doubt throughout the day is a big deal. And I have seen over and over and over again with my pain patients, the small group that I have, that, I tell all of them, whether we’re getting on buprenorphine or we’re going on really reducing opiates that they’re on, they all sudden realize that they have clarity or mentation as much.

And her pain is not what it was.