Their Pain Score Was The Same — Their Nervous System Wasn't | #556

Hello and welcome to The Evidence-Based Chiropractor. I'm your host, Dr. Jeff Langmaid. This week we are back with more research all around dysregulated pain responses for chronic low back pain. Fantastic brand new study. We're going to dive into all the details, clinical pearls, how you can use this in conversation, and much more. Before we get started, Big shout out to Care Plan Pro. If you are somebody looking to basically sell more care plans, memberships, or concierge type plans, my opinion, there's no better software out there. Care Plan Pro helps you sell and it does the hard work so you don't have to feel like you're selling a timeshare presentation. Makes it super clean, super easy, and I am super proud of what we've come out with. You have not checked it out? I'll drop a link down below, or you can go to careplanpro.

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careplanpro.ai. Additionally, a big shout out to Leander Tables, $750 off their Series 950 using the code EBC2026 or connecting with their team. So if you're looking to upgrade that clinical equipment, Leander Tables is there for you. But today we're going to talk about autonomic responses to nonspecific chronic low back pain. Really, the question here is, what if a patient's chronic low back pain isn't only changing how they experience pain, but also changing how their nervous responds to it. And it's not the usual conversation around like tight muscles, restricted joints, sensitized tissues. We're talking about the automatic behind-the-scenes responses of the sympathetic nervous system. That subtle shift matters because many of our chronic low back pain patients tell a pretty similar version of the same story. My back just feels like it's always on high alert. They could describe it as easily aggravated. They might feel guarded. They might have trouble relaxing. Their symptoms flare up during stressful periods. even when they can't identify like a new physical trigger or a new injury. So none of those observations, as we know, prove that the autonomic nervous system is causing their pain. But this new study published in Pain Research and Management gives us a pretty interesting window into how pain processing and how autonomic activity may interact with people that have nonspecific chronic low back pain. Title of the study, I'll drop a link down below in the show notes, of course, is Dysregulated pain, autonomic responses in patients with nonspecific chronic low back pain. So what makes this paper pretty interesting is that the researchers didn't ask people just how much pain they felt. They also measured electrical activity related to the cortical pain processing and the sympathetic nervous system's response to that painful heat. So their central finding was that people with chronic low back pain did not necessarily report more experimental pain than their healthy controls, and that their cortical responses look largely similar, but the sympathetic nervous system took longer to respond. And that creates an interesting possibility. And that possibility is the pain signal coming in may be relatively normal, while the body's automatic response going out might be dysregulated. So today we're going to unpack what the researchers measured, what they found, what they did not find, and really kind of why this study matters as part— a part of a broader scope of literature in this arena. So nonspecific chronic low back pain, you're probably pretty aware of what that is, persistent low back pain without one clear identifiable pathoanatomical cause that fully explains the symptoms. So the authors in this study point out that 80% to 95%, which seems so exaggeratedly high to me, but 80% to 95% of chronic low back pain cases seen in primary care are often classified as nonspecific. Now, part of that, quite frankly, is the amount of due diligence and the amount of, or lack thereof, of movement assessments and really specific, let's say, evaluation tools that the primary care physicians are using, but it's a big percentage. So the overwhelming majority of chronic low back pain patients don't walk in with one clean, easily identifiable, structural diagnosis that explains everything. It does not mean, of course, that the pain is imaginary. It means that it's more complicated than just one damaged structure, probably what we see and what you're familiar with every single day in your practice. So researchers out there, as we've highlighted many of these studies on this podcast, increasingly study factors like nociceptive processing, sensitization, psychological state, cortical activity, all to better understand why pain persists. Brought to you by CarePlan Pro. Build care plans in seconds, present them with confidence, and grow your recurring revenue through memberships and concierge. See how at careplanpro.ai. So the research— this research team, I should say, focused on 3 areas. First, they measured contact heat-evoked potentials, usually shortened to CHEP. So CHEPs, CHEP, are electrical responses recorded from the brain after A brief painful heat stimulus. So researchers applied heat to the body and they measured how quickly and how strongly that signal was processed at the cortical level. Secondly, they measured sympathetic skin responses, SSRs. A sympathetic skin response reflects activity in the autonomic nervous system, specifically and particularly sympathetic pathways that influence sweat gland activity, of course. So this is kind of a one-way street measuring the body's— autonomic response to that threatening stimulus. And third, they measured or examined habituation. Habituation is what happens when a response decreases after repeated exposure. So like a habit, right? So the first time you hear a loud noise, you might jump. By the 10th time, your response is not as big because it's not a new threat. So the same general idea can be applied to painful stimulus. A person's reported pain and physiological responses can decrease across repeated stimuli, and that suggests— habit or habituation. So the researchers noted that CHEPS, sympathetic skin responses, and habituation had not previously actually been studied together in this specific population. So their goal was to compare these and see what the scoop was. So the final analysis included 56 patients with nonspecific chronic low back pain, 40 age and sex match healthy controls. So the patients had experienced low back pain for more than 3 months, chronic by definition, and had been evaluated to exclude things like fracture, malignancy, hyperspasticity, infection, systematic inflammatory diseases, et cetera. So this was not a group of people who had experienced kind of like a sore back for 2 weeks. The median duration was actually 60, 6-0, months, so 5 years. The range was pretty enormous, from 4 months, just on the verge of that chronicity, all the way to 670 months, which if you do the math on that, that's over 55 years. That's chronic low back pain. Their median current pain level was not extreme, but it was the present, 3 out of 10, and their average pain during the previous 4 weeks weeks was 4 out of 10. So kind of on the verge of moderate, mild moderate there. So it was a chronic pain group, but not severe pain, right? So the chronic low back pain group also had statistically higher scores for anxiety, depression, and pain catastrophizing than the healthy group. No surprise there. However, the average pain scores— excuse me, the average scores were not necessarily at extreme clinical levels. So Each participant received controlled heat stimulus at 2 locations, kind of how it worked. The first location was the lower back. So for each patient, the researchers identified the most painful area between, like, basically the lumbar spine, between T12 and S2. They matched healthy control, was then tested at the corresponding location. Second location was the back of the non-dominant hand, which served as kind of the pain-free control area. So at each location, The participants received 2 blocks of 15 heat stimuli. So 15 stimuli in the first block, short break, another 15 stimuli. And that process was completed at both the back and the hand. The temperature rapidly increased from baseline, usually from 42 degrees Celsius to 52 degrees, so like 125 degrees Fahrenheit. But the stimulus was brief and delivered with specialized equipment, so it wasn't like abject pain or something. So after every heat stimulus, the participants rated their pain from 0 to 10. While all this was happening, the researchers recorded the participants' brain responses using the chaps and their sympathetic skin responses using electrodes placed on the hand. So that's kind of how this worked. Now, the first finding might surprise you. The chronic low back pain patients did not rate the experimental heat as more painful than the healthy controls. A little surprising there for me. There was essentially no difference between the groups. At baseline, the average pain on the ham stimulus, 4.1 healthy controls, 4.0 chronic pain. For stimulus to the back, 5.2 in healthy controls, 5.4 in chronic low pain. So the chronic low back pain group did not demonstrate a generalized or dramatic hypersensitivity to the pain stimulus. Both groups did rate heat applied to the back as more painful, interestingly, than heat applied to the hand, and the difference was statistically strong. The back appears to be more sensitive to the heat stimulus than the hand.

Interesting.

The number 2 finding was the researchers also found no statistically significant group differences in the contact heat-evoked potentials. So there was no statistical significance between low back pain patients and healthy controls in N2 latency, P2 latency, or N2 to P2 amplitude. So there's no meaningful group differences as far as that's concerned. Now, number 3 was the headline result. The latency of the sympathetic The sympathetic skin response, as we touched on at the top, was significantly prolonged in the chronic pain group compared to the healthy controls. The statistical model produced an F-value of approximately 9.3 and a p-value of 0.003. So looking at the averages, after hand stimulation, the sympathetic response began 1.7 seconds later in the healthy controls, 1.9 in the chronic low back. In the back stimulation, 1.7 in healthy controls, 1.8 in the chronic low back. So the differences sound small, but we're talking about fractions of a second. So neurophysiological research often lives in milliseconds and fractions of a second. And that's important because the difference was consistent amongst both groups in both ways. And that was a major, major detail. Had the difference only occurred when the researcher stimulated the back, we could interpret that as a localized response.

Right.

But because it appeared in both the hand and the back, it actually represents a more interesting finding, which is a more generalized alteration to the pain-autonomic interaction. So the researchers interpreted this, I agree, as potential dysregulation in the efferent response to pain. So afferent, as you know, sensory information traveling toward the central nervous system, efferent traveling away from the central nervous system. So the CHEP results suggested That incoming nociceptive signal and cortical processing were just about the same, no big deal. But the delayed skin response suggested the autonomic outgoing response could and was ultimately altered. So that's an important component. And the response was delayed, but not bigger. So the timing differed between the groups, the size of the response did not. So the study did not show that chronic pain patients had a massively exaggerated flight or fight response.

Yeah.

fight or flight response. It did show that the response took longer. So that's where the dysregulation potential certainly comes from. So I thought that this was like super interesting because it just showcases these, like, in what I would consider to be very nuanced differences in how the body is responding, and especially across multiple points, back of the hand and the back. To see that it affected not only the response, the delay, or excuse me, the response time, I should say, in the back, but also the hand, is just really, really fascinating. Now, the researchers found a few correlations between the experimental results and clinical pain. The correlations were pretty modest, but they were also present. They ran many, many correlations, but there wasn't, there really wasn't enough to be extrapolated in terms of causation by any stretch of the imagination. So, I thought that this study was super fascinating because it highlights, again, a better understanding of pain. So my first takeaway is to avoid reducing low back pain to one tissue, one mechanism, one thing. This is really complex. The nervous system is not simply transmitting a damage signal. Pain involves an array of different things. There's sensory input, there's interpretation, there's attention, emotion, behavioral context, Autonomic physiological responses, all of it. And the second takeaway is that autonomic regulation is very likely part of the picture for some patients. Doesn't mean every chronic pain patient needs to be told that their autonomic system is broken by any stretch, but factors that you probably talk about, sleep, stress, perceived threat, emotional state, these alongside with your movement assessments, examinations, manual care, all of what you do, can really help understand what's going on with this patient and looking at the patient from a holistic point of view, because the effects of the chronic low back pain were being extended in this case, in terms of the delayed time, to the hand. So I always say, look at the next body region. Somebody comes in with low back pain, you should examine the pelvis and the thoracic spine. They come in with a thoracic spine issue, examine either the cervical spine, shoulder, and/or low back. I always recommend looking at the next region, but man, this showcases that central pain processing is exactly what it says. It's central pain processing. So it can affect things beyond not only that region, but also beyond the adjacent region. So this study doesn't give us any, aha, A plus B equals C, this happened, that happened, let's do this, but it just continues to showcase to us, man, The nervous system is really complex, and trying to have an understanding of it is exactly that, and that's okay. It's a trying. It's a— you're never going to know everything, but being able to piece together changes that people might be experiencing. And I think from a clinical perspective, like real-world, face-to-face, knee-to-knee, this is also about just understanding when people give you feedback. My low back's killing me, but this other thing, right? And that other thing, while it might seem, and while in some cases it might have nothing to do with their low back, Yeah. It might be their actual central nervous system that is affected and dysregulated and ultimately impacting, no surprise to us as chiropractors thinking holistically, but it can affect the whole organism. So it's an important reminder from my perspective not to continue to be super myopic in terms of how you interpret pain and in terms of how you communicate that with your patients, but really understanding that even if they have a quote-unquote nonspecific issue in one region, it can really impact them throughout all the different regions of their body. Not every patient every time, but some of the patients some of the time. And that is something we all should keep top of mind with every patient in our practice. As we wrap up, big shout out to Shockwave Centers of America, $500 off and a free cart by saying you're a listener. Big savings just by being a listener to this podcast. Thank you so much for tuning in.

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Thank you.

And I will talk to you soon.

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