Transcription
Hello, I'm Anthony Chan reporting for RheumNow here at ACR '26 in Orlando. And one of the areas that have been studied quite a lot in this meeting is the whole area of nociplastic pain, where the pain can be coming from conditions such as fibromyalgia, particularly in the area of axSpA. And today there was a nice abstract 1337 which was presented here, and I'm together with Mohammed Beta from Oregon who actually was presenting this today. So Mohammad, very nice welcome to RheumNow. Thank you so much for having me.
Tell us a little bit about this study which you presented today, where you assess nociplastic pain in axSpA. Definitely, thank you. So one of the biggest challenges in axial spondyloarthritis is how to phenotype pain. You know, we have different phenotypes — nociceptive, which is stemming from active inflammation, neuropathic, and nociplastic. Nociplastic tend to be the trickiest part because there's pain coming from altered CNS processing and we cannot identify active inflammation or a threat to the tissue. And this is of course the prototype of it — it is fibromyalgia — but this is very common in patients with axial spondyloarthritis; up to 50% in some studies end up having nociplastic pain features.
The answer is not to cycle biologics or further intensify the immune suppression. The answer is to try to quantify and objectify this nociplastic pain and to target that in order to modulate pain and to get patients to a better outcome. So what we did in this study: first we tried to phenotype pain. We got patients, we did questionnaires — fibromyalgia survey questionnaires — and we also tried to look at objective evidence of inflammation by doing sacroiliac joint MRIs and by doing CRP levels. And then these patients would undergo what we call quantitative sensory testing. As you know, now in the clinic we ask patients to rate on a scale from 0 to 10 their pain — this is very non-specific; I personally do not know how to answer this question.
What we're trying to do from this quantitative sensory testing is to try to get to an objective number that can maybe help differentiate between different pain phenotypes. So we did three different techniques. One is pressure thresholds — using an algometer, we apply pressure to specific points in the body, whether it's a joint or a non-joint area, and whenever patients start feeling pain it gives us a threshold, it's a number. And we are doing other types of techniques such as temporal summation, where we have a neuropen and we do repetitive pricks on the trapezius muscle, which is a non-articular site, also to see at the end of that test what the number would be. We think that this is much more objective than asking for a scale from 0 to 10.
And the very interesting finding that we have is that quantitative sensory testing — specifically the pressure thresholds — was able to differentiate between patients who have nociplastic pain features versus those who do not. And how we defined it: we defined it based on a cutoff on the fibromyalgia survey questionnaire. Because if you're starting with this patient population that we phenotyped nicely — they do not have active inflammation on MRIs or lab work — and then you're having a score that's giving them widespread pain symptoms, that correlated very nicely with pressure thresholds on the quantitative sensory testing. This reflects the pain phenotype that we're trying to study.
We are hoping that we can probably implement this in the future, if possible, to be able to measure pain in a more objective way. If we can prove in the future that by employing these types of quantitative sensory testing early on in the patient journey, maybe we might be able to predict who will develop what type of pain, and then we can target their pain based on that. Of course there's a lot more things to do, but we're starting with the first step, right?
No, thanks very much. That seems a very comprehensive study that you presented. Are there people who can have both? Can they be nociceptive and nociplastic at the same time? In other words, these tests can be positive, but the MRI can also be positive. Definitely, this is a very important question, and yes, we can have patients who have both phenotypes — nociplastic and nociceptive. Of course, at this point in time in 2026 it's not possible really to know which one is the predominant phenotype until we target the inflammation.
So our approach is: first we target the inflammatory component. After some period of time — usually up to 6 months — where we give the anti-inflammatory medication a good amount of time to work, at that point we reassess. If we are still seeing active inflammation, we cannot label it as nociplastic because we might still have nociceptive pain. But if the nociceptive component is gone, at that point we are more confident that we're dealing with nociplastic pain features.
Okay, very nice. So I think the message is that it's possible to have one or both in these patients, and these tools will help us to classify them a bit better. Definitely, that's correct. So thank you very much for that very nice abstract today. I'm Anthony Chan presenting here for RheumNow in Orlando at ACR 2026. Thank you.
Tell us a little bit about this study which you presented today, where you assess nociplastic pain in axSpA. Definitely, thank you. So one of the biggest challenges in axial spondyloarthritis is how to phenotype pain. You know, we have different phenotypes — nociceptive, which is stemming from active inflammation, neuropathic, and nociplastic. Nociplastic tend to be the trickiest part because there's pain coming from altered CNS processing and we cannot identify active inflammation or a threat to the tissue. And this is of course the prototype of it — it is fibromyalgia — but this is very common in patients with axial spondyloarthritis; up to 50% in some studies end up having nociplastic pain features.
The answer is not to cycle biologics or further intensify the immune suppression. The answer is to try to quantify and objectify this nociplastic pain and to target that in order to modulate pain and to get patients to a better outcome. So what we did in this study: first we tried to phenotype pain. We got patients, we did questionnaires — fibromyalgia survey questionnaires — and we also tried to look at objective evidence of inflammation by doing sacroiliac joint MRIs and by doing CRP levels. And then these patients would undergo what we call quantitative sensory testing. As you know, now in the clinic we ask patients to rate on a scale from 0 to 10 their pain — this is very non-specific; I personally do not know how to answer this question.
What we're trying to do from this quantitative sensory testing is to try to get to an objective number that can maybe help differentiate between different pain phenotypes. So we did three different techniques. One is pressure thresholds — using an algometer, we apply pressure to specific points in the body, whether it's a joint or a non-joint area, and whenever patients start feeling pain it gives us a threshold, it's a number. And we are doing other types of techniques such as temporal summation, where we have a neuropen and we do repetitive pricks on the trapezius muscle, which is a non-articular site, also to see at the end of that test what the number would be. We think that this is much more objective than asking for a scale from 0 to 10.
And the very interesting finding that we have is that quantitative sensory testing — specifically the pressure thresholds — was able to differentiate between patients who have nociplastic pain features versus those who do not. And how we defined it: we defined it based on a cutoff on the fibromyalgia survey questionnaire. Because if you're starting with this patient population that we phenotyped nicely — they do not have active inflammation on MRIs or lab work — and then you're having a score that's giving them widespread pain symptoms, that correlated very nicely with pressure thresholds on the quantitative sensory testing. This reflects the pain phenotype that we're trying to study.
We are hoping that we can probably implement this in the future, if possible, to be able to measure pain in a more objective way. If we can prove in the future that by employing these types of quantitative sensory testing early on in the patient journey, maybe we might be able to predict who will develop what type of pain, and then we can target their pain based on that. Of course there's a lot more things to do, but we're starting with the first step, right?
No, thanks very much. That seems a very comprehensive study that you presented. Are there people who can have both? Can they be nociceptive and nociplastic at the same time? In other words, these tests can be positive, but the MRI can also be positive. Definitely, this is a very important question, and yes, we can have patients who have both phenotypes — nociplastic and nociceptive. Of course, at this point in time in 2026 it's not possible really to know which one is the predominant phenotype until we target the inflammation.
So our approach is: first we target the inflammatory component. After some period of time — usually up to 6 months — where we give the anti-inflammatory medication a good amount of time to work, at that point we reassess. If we are still seeing active inflammation, we cannot label it as nociplastic because we might still have nociceptive pain. But if the nociceptive component is gone, at that point we are more confident that we're dealing with nociplastic pain features.
Okay, very nice. So I think the message is that it's possible to have one or both in these patients, and these tools will help us to classify them a bit better. Definitely, that's correct. So thank you very much for that very nice abstract today. I'm Anthony Chan presenting here for RheumNow in Orlando at ACR 2026. Thank you.
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