So we'll go ahead and start with this afternoon. So our first lecture this afternoon is on CRPS case presentations given by our very own Dr. Mitch Friedman. Dr. Friedman is a staff physician at the prestigious Rothman Institute at the Sidney Kimmel Medical School at Thomas Jefferson University Hospital in Philadelphia. So he's a chief emeritus of rehabilitation medicine at the Rothman Institute, as well as a clinical professor at Thomas Jefferson University Hospital. And he is a fellow of the American Osteopathic College of Physical Medicine and Rehabilitation. Just a little plug on that, the fellowship in our college is not automatic like it is on the MD side. It's something that is earned. So if you're interested in being a fellow of AOC PMNR, please come and see me. I'd be happy to give you more information about that. But Dr. Friedman is one of our fellows. He is board certified in pain medicine and electromyography. He's authored multiple papers, chapters, and books on the topic of pain medicine, electromyography, and spinal cord injury. So please join me in welcoming Dr. Friedman. Thank you. Hopefully we'll be clapping in a few minutes. We'll see. So this is an audience participation lecture. It'll be mainly the people in the room. Jenny asked me to announce that it was my idea, really. If people are online, it's a little too unwieldy, I think, to go back and forth. So any questions with people that are virtual, we can save for after the lecture. So this is on CRPS. And this is kind of like the pebble I can't get out of my shoe. I started lecturing on what was then reflex sympathetic dystrophy when I was a resident, actually, because it was an area of interest after I saw a few of these folks, because they're very difficult patients, very tedious, and difficult, and emotionally grueling to take care of. Over the years, I've taken care of a fair amount of it, particularly when I ran a pain management program over at McGee, where we had a multidisciplinary team. In recent years, I haven't done as much. Interestingly, we'd written about it somewhat. So I got asked to lecture on this last year at the American Academy of Electrodiagnostic Medicine. So this gave birth to this lecture that you're going to see today. So this is audience participation. It makes it a lot more fun. So feel free to ask questions, contribute ideas. Nothing you're going to say is going to be good or bad. It's just a good way to get involved. So we're going to present four cases. First one will be kind of presenting to you more than anything with a few things. And then the other three cases will get you more involved. We'll review the diagnostic criteria. We'll present our approach to a diagnostic workup. And we'll go through treatment options. So this is the first case I ever took care of as an attending. So it was a long time ago. 35-year-old female struck by a car six weeks before I'd seen her. She now had severe pain, swelling, weakness in the right arm. She had a loss of consciousness. She was depressed, poor sleep patterns, married, not working. Her entire family was devastated. She was hit by a car turning a corner right in front of her family. So they all saw this go down. On her examination, she was guarding her right hand and arm. She had decreased motion in her intrinsics, decreased motion in the shoulder, elbow, or wrist. She had about a two-degree difference, with the right side being somewhat warmer. She had allodynia, hyperpathy, diminished sensation to the late pin on the right, and diffuse weakness. So this is a picture of her hand. You can see, it's interesting, because she certainly is artheminous. You can see the fusiform edema. You can see swelling up into the form. It has kind of a dystrophic look to it in the fingers. If you look at the contralateral hand, she's even a little bit worrisome there. It's a little mottled-looking. So any guesses on what we called it diagnostically? We called it diagnostically. I'll give you a hint. This is a lecture on CRPS, right? So she is CRPS. X-rays to that day were pretty much unremarkable. So we diagnosed her back then with reflex sympathetic dystrophy, is what we called it. So as we go, so I don't put you to sleep, I'll put up some different water pictures from all around the world where I've been. That was Long Island. So somewhere in the 1990s, the term from reflex sympathetic dystrophy went to complex regional pain syndrome. So complex because of very clinical phenomena seen in addition to the pain. Regional because it wasn't just in one small area in an extremity, but it was throughout the extremity classically. Could be in the disc limb, but often in the whole limb, rarely in the face or torso. Classically skips the knee or the elbow, but there are exceptions to all that. And pain is the cardinal symptom. So this really changed, really coming into the 90s where the term reflex sympathetic dystrophy began to go out of vogue. So why is that? Well, for one reason, some cases do have a sympathetic component, some do not. So sympathetically maintained pain, as you can see, there's a lot of syndromes that have sympathetic mediated pain that aren't CRPS. Conversely, a lot of CRPS patients do not have sympathetically mediated pain. So that was one of the reasons why that term began to fall out of the descriptor in this syndrome. So just like Dr. Creamer went over some of the terms, we'll review those very rapidly. So spontaneous pain, pain that just comes spontaneously without external cause. Evoked pain, so alidinia is pain that comes from a stimulus that is not normally noxious. So I touch the skin and they get a pain which is out of proportion to the stimulus that provoked it. Hyperalgesia, on the other hand, involves alidinia, but it's also pain that's disproportionate to a noxious stimulus. So a little bit different. So CRPS type one, the old reflex sympathetic dystrophy, and a million other names for that matter, there's terms a whole page long, is a syndrome that develops after an initiating noxious event, although five to 10% of people do not have an initiating injury. You get spontaneous or evoked pain, not limited to the territory of a single nerve and disproportionate to the exciting event. And it's usually nociceptive, not neuropathic, but type one is nociceptive. Type two, on the other hand, the old causalgia is a syndrome that comes after a nerve injury with all the other criteria that go with CRPS. It can be very difficult to separate pure neuropathic pain from CRPS. So this is the Budapest criteria, which really changed CRPS dramatically and has been a huge addition to having some criteria for the diagnosis because this is a syndrome where there's no laboratory or x-ray or diagnostic imaging, which creates the diagnosis. So you're relying on your history and physical. So there are two components. So one is the symptoms and one is the signs. So classically, you're looking for one symptom in three out of four categories. So you're looking sensory, a history of hyperseizure, aldenia, and this is all reported by the patient, right? Vasomotor, temperature and or skin color changes in asymmetry. Pseudomotor, edema and or sweating changes. So sweating and swelling is how I remember pseudomotor. And then motor trophic, decreased range of motion and or motor dysfunction, weakness, tremors, dystonias, and along with trophic changes. I grew up in Philadelphia, which was the home of Robert Schwarzman, who was both famous and infamous on one statement. And he was really ahead of his time, I think in many things. Clinically, he was a bit shaky at times. I'd walk into rooms at Jefferson where there'd be at times he had 34 people, 30, 40 people in the hospital with CRPS. Husband and wife teams. And you didn't know if they were psychiatric or CRPS, but he was really big in this motor and trophic thing. And he was spot on on it. So he did a lot of really great things. He was a very controversial character. In terms of signs now, what you see on your exam, and I will caution you, and this is one of the challenges with CRPS. This may vary from episode to episode where you encounter the patient. You may not always see these signs. And that's one of the problems with making the diagnosis. And that's one of the reasons there's a beauty to having a symptom component and a sign component. Because you have to look for it in your subsequent evals if you don't see it the initial time. So this really mirrors the symptoms. So again, you're looking for a hyperalgesia to PEMPREC, or allodynic to light touch and temperature sensation. You're looking at vasomotor. You usually want more than one degree difference from side to side. Skin color changes or asymmetry. Pseudomotor edema, edema and or sweating changes. And then again, you have your motor and trophic. And some of these dystonias, you almost wonder if they're real. And they can be extremely dramatic. So you're doing a scorecard. So in our initial patient, if we kind of go backwards for a minute, in terms of what she complained of, she had a lot of hypersensitivity that she complained of to me. She did have a temperature asymmetry to the touch. She clearly had erythema into her hand. And she was complaining of these things as well. She had lots of swelling. And she was diffusively weak and had range deficit. So on the history side and the physical side, she had CRPS. The other criteria is no other diagnosis that better explains the signs or symptoms. So each one of the cases I'm gonna be presenting to you brings out a slightly different flavor in terms of the diagnosis and the treatment. Now, if you wanted to compare clinical versus research criteria, you get a little more stringent. So our clinical, we said three out of four symptoms and two out of four signs. So if you raise that to four out of four symptoms, now your sensitivity goes down, but your specificity goes up. So that's just something to be aware of when you read the articles on this. So the subtypes, we talked about type one and type two, but this is an article by Norman Hardin, who is the guy in CRPS in the world, has done a lot of wonderful work on it. At the time this came out, there were the whole slew of people with the diagnosis is CRPS. And now with the Budapest criteria, they didn't necessarily fit the criteria, which became a significant issue to them potentially in terms of disability and things like that. So they included the people that not otherwise specified, included the people with that diagnosis that might not meet the criteria, and also signs and symptoms, which could not be explained by another diagnosis. So that is the not otherwise specified limb of the diagnosis. This is Florida on the West Coast. So when I teach my residents how to treat pain, I always say there's five ways to treat pain. A lot of times when you see chronic pain, people have tried just about everything. So it's an organizational tool to me how to go in and look for a little bit of gold that may not have been tapped out, right? So the basic five ways to treat pain are surgeries, injections, therapies, medicines, and lifestyle. And that's how I work through it, particularly in the chronic patient. So I can see what they've had done and what's a gap in their treatment. This diagram is from a book that Lynn Kamen and I wrote along with George Young and Jim Garrett, All I Say Pass, called Challenging Pain Syndromes, came out right before the pandemic and about four people bought it. So if you wanna make five, you guys can buy a copy. So at the very base of it is the approach to the treatment. And then down low, I don't know how this is coming out on the slides, there's a treatment of the underlying condition, sympathetic blocks, medications, edema control, range of motion, stress loading, progressive strengthening, aerobic conditioning, at the top, vocational counseling, rec therapy, more hierarchical treatments, spinal stem pumps, ketamine, peripheral blocks, psychological conditioning, coping skills, biofeedback, and then some of the hotter things in the last 20 years, mirror therapy, graded motor imagery, and desensitization. So we'll talk about all this. I used to write this up as a pyramid type approach, but I don't think of it like that at all anymore. I think it depends when you see them, how acutely, it depends on their individual needs and the individual problem. And you may interact at multiple points on this. So I drew it up as a circle as opposed to a pyramid. So what did we do for our case one? So we did range of motion, sure of pain, contrast baths, which I love for CRPS, desensitization, co-band wrap for the fingers, Futura Glove, we worked on strengthening, psych support, give her a little bit of hydrocodone, not too much. And she did pretty well, so we'll talk to her in a minute. So therapeutic options, going a bit more formally, so desensitization is really the core of things. Having that person get used to being touched, you can do that with silk towels, contrast baths. A guy named Carlson wrote about stress loading, having people gradually put some pressure on the areas that are affected. Edema control, Isotoner Gloves, Job's Garments, co-band wraps, centripetal massage, getting the patient starting to do that rapidly. Range of motion, not past tolerance. I think if you overwork these people, you will make them worse. So you kind of take what their body has to give them and proprioceptive neuromuscular retraining. As you progress, you can work to, if it's a lower extremity, traumatic exercises, strengthening aerobic activities, aquatic therapy, massage, myofascial therapies, ergonomics, body mechanics. Somebody who's got really, is really dysfunctional and we're not getting anywhere, I've worked with transferred abdominics in patients. And you're always working toward function. That was the middle of my diagram. Pain management is a part of improving function because classically, I don't think you make lots of gains in people with terrible pain syndromes unless you get some control in their pain. You won't make much headway in terms of function. So mirror visual feedback is something that goes way back. It was done for strokes, done for pham limb. In 2003, McCabe looked at it with eight patients working to establish analgesic effect and less stiffness in the acute intermediate patients and to establish pain-free relationship between the sensory feedback and the motor execution. And they had pretty good results. And then Mosley in 2005, I think really, really added something nice to that. They took 38 patients who had six months of pain, so they were chronic by definition at that time, with a type one. They worked on hand laterality, where they just recognized ID photos of right and left hands. The second piece of it, and that was done for two weeks. And during the waking hours, they were supposed to do this three times an hour. So pretty stringent. The second two weeks, they looked at imagined hand movements, looking at pictures of the affected hand, and imagining the movement. And again, three times an hour during the waking hours. And the last piece was a mirror movement where the affected hand was concealed, and the visualized hand was the good hand, while they were looking at a mirror, basically. So it turned out pretty well, and it turns out that you have to do this in this order. And the theory is, and it's not quite clear, that you're sequentially activating pre-motor and then motor networks. And there's pretty good literature on this now that this can have some positive effect. As in everything, the more chronic the problem is, the less this is gonna be successful, particularly with CRPS. Once CRPS is really dug in, I haven't found this to be terribly useful, but I always give it a try. And also, the other little carly, which I'll say is, type 1s do better than type 2s. I think the people that had the fractures and have the type 1 CRPS do better than the chronic neuropathic pain. And there is some of that in the literature as well. Psychological interventions. One of the reasons why I don't like treating CRPS as much as I used to is I had a whole pain team when I was at McGee Rehab. We had psychological support, PT, OT, vocational services. Some of the best literature in pain management is still the interdisciplinary pain management. The outcomes are stronger than most of interventions. And they're very expensive, and at least on the East Coast where I'm from, nobody wants to pay for it anymore. But having these psychologists involved is gigantic. Work on biofeedback and relaxation strategies, imagery, hypnosis, are all very nice strategies. Classics and meds, so this is another thing, yes? Why don't you wait a couple, wait a couple, and you'll have plenty of time to talk. That was Len Kamen for you people out there who has a lot of good things to say. So I'm gonna go through this quickly because I want to get to the rest of the cases, but tricyclics from the original pain medicines that are really nice medicines but a little dirty, and some of the anticonvulsants that we use now, nonsteroidals, I didn't add steroids in there, but there is some literature, particularly early in things, on using short courses as steroids. Vitamin C has been shown to help tons, but it's fairly benign. Some of the opioids, particularly with some of the NMDA, receptor antagonists, methadone, ketamine, aminadine, dextromorphorphine, tramadol, nucenta, that's what Len had brought up before. Clonidine has a sympathetic component. It can help block the sympathetics. Baclofen was one of Bob Schwarzman's favorite drugs, works on substance P centrally, might be one of the reasons why it helps. And he used to use it heavily. Methamphetamine, calcium channel blockers. Calcitonin and biphosphonates, there's a fair amount of literature on that. None of these are prospective randomized, so the studies aren't great, but it might help with remodeling bone, which becomes an issue in chronic CRPS. Now, Trexone, topical treatments, are all some of the medications. And I'll go through all these things sequentially to see what the person's had, what they haven't had, and what their response was, and what dose they tried, because sometimes they just didn't get to a good enough dose. There's a whole spectrum of drugs. I'll go through all of them. A good enough dose. There's a whole slew of sympathetic interventions. Before I got asked to do this lecture last year, I had a file of CRPS like this big, and I'd thrown it out, because we moved, so I'm trying to get rid of all my junk. And then they asked me to do this lecture, so I had to build a new file. And there's everything I've listed here. These are really different things to try to get at blocking the sympathetics and adrenergic receptors. And they all work somewhat, but not great. And of course, when everything works somewhat, not great, it kind of falls out of vogue. In the old days, in Jefferson, when Schwartz was there, people used to come in for three to five days and have all different types of blocks. They'd get sympathetic blocks that went on going where they got therapy. Some had lidocaine in low dose that was given intravenously, and nothing really stuck, because you don't see that now. The role, types of approaches are uncertain, maybe best with a sympathetic mediated component in these sympathetic blockers. Everything's better when you use it earlier more than later. And the goal is allowing some range of motion and analgesia so that you can begin to get it to function and break the cycle of swelling and tightness and contractures. So what happened to our lady that we started with? So she did well. She got back to work, pain levels under control. The somewhat amusing epilogue is she showed up in my office about 15 years later with a significant other. She had gotten divorced from her husband from years ago, which is not uncommon in my experience. I think when people develop pain syndromes and they're married, it sets up a new dynamic that doesn't always last. I've seen that happen a fair amount of time with chronic pain and she was looking for new options in treatment. So although she was relatively successful, it did leave a significant mark and she was never the same as she was before that injury. All right, so now we're going to the cases. So this is a 38-year-old Brazilian drummer, fell and suffered a fracture of the left ulna. Status post, overreduction, internal flexation of the ulna about eight weeks before. Now he's complaining of burning and tingling from the left elbow to the ulna two fingers, swelling in the left hand, hypersensitivity to touch throughout the left-handed arm and he's got diffused weakness. So we have swelling, we have hypersensitivity, we have weakness, so we have at least three of the criteria here, right? He's not really describing temperature changes and color changes. So we have three there. On the physical, he's guarding the arm. He has decreased motion in the intrinsics. He's got diffused sweating, so he does have some pseudomotor stuff. His hand is red and warm, so he's got the vasomotor stuff. He's got alabdinia throughout the arm to the touch and he's got four out of five strengths. So he's four out of four, right? So what do you want to call him diagnostically? CRP asks, do you want to call him a type one or a type two? Type one? Why do you want to call him a type one? So I'm going to repeat all the questions so everybody can hear it. If not, Jenny's going to beat me up. Because he broke it, and it's happening after the fracture. So that's a reasonable thought pattern. He fractured it, but his real pain is in the ulna two fingers, right? I'm glad you asked that question. I'm glad I planted you in the audience. Good job. So do you want to order any studies? So yes, let's do that EMG. Now EMGs are not something I do casually in people with CRPS. Because they will hate your guts, right? Because it's unpleasant in anybody, but in somebody who's got hyperpathy, alabdinia, not to mention the swelling, which may screw up your study. It's not a fun study. But this case, I thought was important. Because I did think that the pain generator underneath this was probably ulnar, right? Lesion at the elbow, classic radiating pattern. So I think you have to do it. So our NCVs are 40 meters across the elbow. So 43 is the magic number looking less than, or a difference of 15 meters per second from above the elbow to below the elbow. Our motor amplitude at the wrist and below the elbow is 10K. But above the elbow is 4K. Our sensory amplitude at the wrist is 40 microvolts. And dissolatancy is 3.4 milliseconds. And we have plus two fibs. So this is an ulnar lesion with evidence of axonopathy. Is there anything else we want to say about this study? Is there something I left out? What's that? All the other nerves that broke? Well, they were okay. What's that? All the other nerves that broke? Well, they were okay. They were okay. But there's a myelin block, right? We have 4K above the elbow, 10K below the elbow. Our amplitudes dissolutely are good. 10K is great. So what do you think the prognosis on this just as an ulnar nerve lesion? Do you think it's good or bad? Good. Good, why Ed? Well, it's demyelinating, so necessarily it's got a drop off there, but you should do a remyelinate and improve. Yeah, I mean, the literature on the ulnar nerve is that the people that do best are the people where they have a dissolatancy in the motor, which is maintained, and they have a conduction block. That's the ideal person to do an ulnar nerve procedure to. So now there's plus two fibs, but the more important issue is maintenance of the amplitude. Yes, there's some axonal compromise, but most of the axons are good, right? When you put the lead over the ADM, you're looking at the whole ADM, not just a little spot where you have the needle. So this person should do well. So why do I make a big deal out of that? Well, this is CRPS. People are fearful doing anything to these folks because you can make them worse. So who here wants to operate? No surgery? Raise your hand who wants to operate. See, Ed was with me at Rothman, so we're in an orthopedic place, so if you have an arm, you get surgery. So the question is, how about injecting a little steroid to the ulnar nerve? I don't see that done frequently. I'm not a big fan of steroid injections for carpal tunnel or ulnar nerve, personally. And in this guy, I don't think he's wrong to do it. I wouldn't do it, but that doesn't make me right. But it's a good thought. So what do we do? So let's go back to our paradigm. There's surgery, injections, therapies, medicines, and lifestyle. So if we work through this, I mean, this guy's got lots of swelling, he's got range deficits, he's got to go right to therapy, right? But you better be careful but you better be careful. What do you guys think about nerve glides? Who likes nerve glides? I hate nerve glides. What am I doing? I'm flossing the nerve across that area. So to me, I mean, everything you do with anything, you always have to be asking the patient, is it making it better or worse? But nerve glides scare the heck out of me with things like ulnar nerve and things like that, because I think I'm just inflaming it. But he needs to work on wrapping those fingers. He needs to get back some motion. He needs to start moving things. Just be real careful at the elbow. You're not going to do a lot of stress loading here. You could work with sympathetic blocks. We'll go through that in a little bit. At the base of it, I put treatment of the underlying condition. Well, you have that opportunity here. You have an effective treatment for that underlying condition. That ulnar nerve transposition or release is a reasonable thought. And if you wait too long in this guy, you're going to lose that window. Because the longer they have pain, the more it goes cortical, the less chance you're going to have success. You could do mirror therapy. That's a 12-week program, really. Psychological counseling, that's fine. And then the hierarchical things, we're not at yet. So I did send him to surgery. And he did well. He did very well. He had contrast baths, range of motion, desensitization, Coban wraps, centripetal massage. We got him that Futura glove, strengthening. He had a relatively successful ending. The last time I saw him was, Lenny, you would know the name. What's the place near Penn where they have all the music venues? It's real famous in Philly. Obviously not that famous. But he was doing his Brazilian drumming and he was doing it. He got back to it. But he told me he was never the same. He didn't feel like he had the same ability to do what he'd always done. And I think I looked him up just for fun. His name's not out there anymore, so I don't think he's doing it anymore. But he did have a good success at it. But he did have a good success out of this. And I think this is one of the cases where it's a reasonable way to go with surgery. So let's go to case three. So this is a 40-year-old canine officer, two and a half years of left knee pain. He had a work injury requiring a medial meniscectomy, progressive pain since then. He's got circumferential pain from the groin to the ankle. It's severe. The left leg feels cold and swollen and weak. He's had multiple sympathetic blocks. They have all failed. Lyrica's no help, no PT. So in the old days, and even now, you do see a lot of people that get tons of sympathetic blocks. The first thing, all the orthopedic surgeons do it at the Rothman Institute where I work, if they think somebody's got CRPS, which half the time they're incorrect, but they wanna go straight to sympathetic blocks. And a lot of times people go through a lot of blocks and get nowhere. And if you get one or two blocks, you don't go over, why keep doing them? The definition of insanity is doing the same thing over and over again, expecting a different outcome. So I do less and less suggestions of sympathetic blocks. If they have a big sympathetic component, I'll try one or two perhaps. Beyond that, that's it. He tried a membrane stabilizer, no help, no PT. So his gait, antalgic on the left, diffused hyperpathy in the left leg. He's got three out of five strength in the left leg. Spotty color changes. Temperature's two degrees cooler. No sweating or swelling. And his knee only flexes 20 degrees. So let's go through at least the physical part on this now. So diffused hyperpathy, right? So he's got that criteria. He's got weakness. He's got that criteria. He's got color changes. So he has vasomotor. He has no pseudomotor. So does he meet the criteria? Yes. He meets the criteria, right? He's got CRPS. So is it a type one or type two? So do we have a peripheral nerve distribution? So, so egg's question is, egg's thought pattern could be femoral, and it could be femoral. The other thing I've seen a few nasty syndromes from are saphenous nerve. I've seen a few CRPSs from saphenous nerve, from people hitting dashboards and catching the medial branch going to the knee. But this is going beyond that now, but it may, there may be a neuropathic component, but in general it seems more type one. But I can't say for sure there's not. And this is one of the problems in separating out type one versus two. Sometimes it's very, very difficult. But I would call this more of a type one, but I had the same thought pattern. Could this be a saphenous? Of course, the saphenous comes off the femoral at Hunter's Canal, right? So I had the same thought pattern. So what do you want to do? Let's go back. Do you ever check any vascular studies? So the question is, do I ever check vascular studies? I do sometimes. So the other paradigm I create in my brain when I'm creating a differential that I want to look at, because sometimes this is tricky and we're always looking for that thing that we can treat at the base of it, right? Treat the underlying problem. So I always think of what stuff radiates into an extremity. So we have mechanical. So if you're talking mechanical things, disc, SI, facet, muscle, right? Disc can radiate down, muscle, you can get some radiation. Then the next step along the mechanical is hip joint, pelvic fractures, insufficiency fractures, femoral fractures. And then I think neuropathic, root, plexus, peripheral nerve, peripheral neuropathy, upper motor neuron, and then I think vascular. And when somebody comes into me and they don't have a firm diagnosis why, my exam is going to mirror that. I'm going to look at all that. I'm going to look in the entire chain to look for something like that. So this guy had good pulses. So I did not think that that was the case, but that is the way to think. You want to think through this very sequentially in a very holistic manner. And it's kind of fun because sometimes you'll pick up something that nobody else has picked up. So I did not think it was vascular though. So what do you want to do? So do we want to do surgery on this guy? Nothing to operate, right? He's already had knee surgery. It didn't really help. So we want to fall into our rehab hats, right? So he's never had mirror imagery or greater motor imagery. So that could be one of your options. Again, we're trying to optimize function. This guy is not working. He's barely walking. He didn't have much in the way of edema control to do. He did need work on range, but you better be careful. This guy is well into this now. We're two and a half years into this. So if you crank on that knee too much, you're just going to make it angry. Psychological counseling, absolutely. He needed it. The problem is he was workers comp. Forget it in our area. You know, everybody across the country wants to talk about good, solid things to do, and psychological counseling is one of them. The problem is nobody wants to pay for it, which is a big, big issue. Big issue. They'll pay for all the procedures in the world if it's going to be a fix it, but they don't want to pay for a lot of the rehab issues, which is a major issue in this population. Antibiotic blocks, he's had it, medications, managed pain. So we can look at that. We'll look at that. So treatment, we tried him on physical therapy, desensitization, greater motor imagery. It didn't help. Gained some psychological support. Didn't really help. Different types of membrane stabilizers, Baclofen again. Some people, a nice neuropathic agent is like a third line. I like the membrane stabilizers most, then the tricyclics, and then Baclofen for lancinating pain where spasticity component, sometimes it can be very effective, nortriptyline, minimal relief. The other options we're getting him are spinal cord stimulation, so we'll talk about that in a minute, peripheral nerve stimulation, TENS, deep brain stimulation. I had one patient years ago who did receive electroconvulsive therapy, and he had terrible CRPS, and he would get a few days of relief. And it wasn't very effective. It was done multiple times without success. It stuck. But it's done. So his spinal stimuli, there's a number of articles out there. Kemler is one of the nicer ones. At five years, pain levels were similar in both groups. Diminishing pain relief was seen particularly in the first two to three years. At two years, complication rate was about 38%. Seventy-two percent of complications were in the first two years. Despite diminishing pain relief over the five years, 19 out of 20 people would have repeated the procedure. There's at least two other articles out there. One goes out 11 or 12 years. One goes out seven or eight years that both say that a fair number of their patients got sustained relief with CRPS even at the close of those studies. But all the studies say it becomes less effective over time. I've had several patients who got spinal cord stimulators who then developed pain at the site of the stimulator, and it didn't work. Ultimately, they had to take it out. It's interesting. A lot of times, you're chasing your tail on these patients. You do one thing, and something else pops up. There is a fair amount of literature on drosary root ganglion stimulators, some positive, but like everything you see here, PSLVIC's kind of, yeah, it's pretty good, but it doesn't last. I think in terms of the block, I don't know if they would have done a femoral nerve block for a scope. I don't think they would for a scope, but you see a fair amount of them, and I do see a lot of damage from them. The literature, I've seen a lot of plexopathies for shoulder ones, to the point where my wife fell and broke her shoulder last year, and I said, you can get the block for your surgery. I wouldn't let her touch me, and she got away with it. I see alignment foot and ankle, a lot of bad... Yeah. Yeah, I mean, unfortunately, we're victims of what we see to a degree, nobody's going to give me a block. There's no way, but you're right, I mean, that is one of the modes that you can get this with. So I think literature is good on simulators. It's one of the better options for these folks, but it may not last forever. Best early in the clinical course, there's literature on that, and again, best with CRPS type 1. You said something, when you say early, how early is early? If somebody has a really full-blown CRPS, I think starting to look at it at three to six months would be reasonable. So the question is, what does early mean? So it is a moving target, it's a relative thing. I would say, if somebody has really bad CRPS that you're not doing anything with at the base of it, or particularly if it's a type 2, I think looking at a simulator at three to six months is reasonable, I think it's reasonable. So he got no relief. He did get a simulator placed, ultimately had it taken out, and that could sometimes be an issue because the insurance companies say, well, there's no reason to take it out because we're not taking it out, it's a cosmetic, but he had his taken out, and he's on a low dose of baclofen and fairly dysfunctional, and his main calls to me are he wants the insurance company to pay for a new house for him that's accessible, which of course is not going to happen. So he did not do well. Are there any other options? This is Cape Horn in Patagonia. Any other options for this guy? You could, so the comment, it was, well, so the question was, would a geniculate nerve block, could that have been employed in this scenario? So we are actually, we actually try to get a study going on that at Rothman, and some people do get good relief. It would have been an option. I mean, my gut feeling to him was nothing was going to help, but it certainly would be a reasonable option with low downside, which is always a good thing. So the other option, which I'm just not really, which I did offer him here, is ketamine. Ketamine is one of the hot things on the block. Ketamine mechanism of action inhibits glutamine activation of NMDA receptors, enhances inhibitory neurotransmitter GABA, inhibits pro-inflammatory cytokines that are involved in central and peripheral sensitization. NMDA is activated and is upregulated in the dorsal horn when there is no susceptive barrage, so inhibiting that is a good thing. Results in enhanced transmission of the cortex and thalamus via central projecting neurons, and again, one of the things that when these things get more chronic, it begins to go central is one of the theories. You get a spread of cutaneous receptor fields of central and projecting neurons, changes in your spinal cord and cortex, and you end up with spontaneous pain. So this is from 2021, where they did a systematic review of ketamine, and what they came up with, there's no high-quality evidence available to support the efficacy. Manuscripts are all moderate to low quality, only weak evidence. What the conclusion was, yet, there's clear rationale for definitive study. And that is what echoes here. Zal, who's from Jefferson, did a systematic review as well, and he came to the conclusion that it can help for up to three months, but more studies are needed. And then Zhu et al. tried to look at the different protocols, inpatient, outpatient, duration of ketamine, what doses should be used, things like that, and it's all over the map. So this is clearly something which shows some promise, but we're not there yet. They used to put people into ketamine comas. Schwarzman was one of the original guys doing that, and they would go to Germany because it wasn't approved in the country, and they put them in comas for sometimes two or three weeks. So conclusion's uncertain. We need prospective blinded studies. It's expensive. Significant potential for complications. Anxiety, nightmares, sleep disturbances, dysphoria, potential infections. This particular patient, I did offer this to him. He wanted no parts of it. So what Len brought up is now Traxone, which is an option. There is literature on that in CRPS. Like everything in CRPS, it's unclear. But certainly, these difficult pain syndromes, there's the literature and what's accepted and what's evidence-based. And there's the individual in front of you, which is 100% of the people in the room you're interested in. So it's always about looking for the gaps and looking at the risk and the benefit. That's what it all comes down to. And they're doing it in a reasonable manner and being objective about whether or not you're helping them and aborting if you're giving them more side effects than benefit. How about like an intrathecal pre-op or opioid treatment? Opioids in CRPS, the literature is not great on. Intrathecal things, there's all kinds of things in the literature. Certainly a reasonable way to go for that angst-age patient. Do they do well? At the angst-age, I don't think any of them do that well. But making it better than worse. Amputations, the other thing I wanted to bring up, very controversial area in the literature. I would not amputate this guy. Let me make that clear. This is from 1995, 28 patients with 34 amputations and 31 limbs. Indications for pain, limb obstructive function. I had several patients in my career. I had one patient that had a contracture of her hip like this. She was injured at Disneyland. And I had another person who had a 45-degree ankle flexion contracture that ended up with amputations. In this study, recurrent RSD in 28 cases, two developed RSD in another extremity, two had pain not caused by RSD. Conclusion was no functional benefit. Only two wear a prosthesis, but 24 of the people were satisfied. There's another study. It's from 2019, where they had 66% of, this was a systemic review, 66% had improved quality of life, 12% deteriorated, 37% could use a prosthesis. Phenomenal in pain was seen in 65%, recurrent CRPS, 45%, stunt pain 30%, use only resisting CRPS. Better outcome with an interdisciplinary program, which I agree 100%, and make it clear what the goals are. It's gigantic. I think there is a role for some of these people for function, but not necessarily for pain. My experience in these people, they didn't get great pain relief. It's like a guacamole. It pops up somewhere else. So controversial, FAST was a guy in 1995 who wrote a whole editorial, and they said, what are you people doing? You should not be touching, it's inhuman. This is just wrong. You shouldn't be doing amputations for CRPS. So I think talk to your patients. It's a rare thing. Try to avoid it. But once in a while, with something that is really obstructing their function, it may be reasonable. Yeah. Does he have a contracture? Yeah, but it's more, it's like a pain-limited... So he's avoiding it. Yes, he's starting to develop that. Like his knees are starting to flex. How far into it is he? Over a year. So the question is, Ed has a gentleman who's got heel pain after a fracture. He's a year into it, and he can't weight bear. So should you do, would an amputation be an option? I had a case like that. You think he has CRPS? So he's got a CRPS. So I think this is a person, you could talk to him about it, talk to him about the goods in the bags. He may not be able to wear a prosthesis, because it may come up, he may end up with phantom pain. But if it's a functional issue where he can't clear in part, because either restricted range or he can't, that would be the goal. So I'd just be very clear on the goals, and I'd be very clear about the potential downsides. And I'd get him psychological counseling. I'd work him through everything, because there's no going back. All right, we're going to talk about this one minute because I'm getting booted here. Jenny's a terror. And so I have to wrap up this last page. I'll do this real quick because it's an important point. And then if you guys have questions, I'm happy to answer. So this is a 52-year-old right-handed male, five months of right arm pain after a stretch. Police officer, eight out of 10 with pain from the right shoulder to the three fingers, numbness in the arm and three fingers. Pain is clammy, no color temperature changes, diffuse weakness. So maybe he's got some pseudomotor, he's got some weakness, he's got pain, although not really allodynia or hyperpathy. So it's kind of like two to three historically. He's at therapy, but no graded imagery, no relief of the ancegs or tonil, no desensitization. He's decreased motion in the right shoulder. So he's got some motor issues. Intrinsic motion is fine. So a little atypical for a CRPS. No allodynia, hyperpathy. He's one degree coarser. He's got some vascular component. Again, he's got four out of five strength. Sensations altered. So he's kind of got like a two to three kind of borderline in the criteria for CRPS. This is Ushuaia, which is the southernmost city in the world. So I won't go through that again. I like to repeat these slides, because this is the basis of your diagnosis. That's Atlantic City. So other tests. So these were things that were ordered. So EMG, and EMG is subjective, right? So they came up with a C6 radic, and I don't trust that EMG-er. So I kind of think it's bologna. MRI shoulder is normal. Well, you come up with a few polys that you can say, I think he's got it. What does that mean, right? MRI cervical spine, non-compressive bulge at C5-6, he's got numbness in his only three fingers. He's got C5-C6, period. So I ended up, and I hate calling CRPS. He was well into this, but I didn't think he was crazy. I thought he had a real problem, and I thought he had elements. I called it elements of the CRPS. So to be not otherwise specified. You could fight me on that, and you wouldn't be wrong, but you wouldn't necessarily be right either. It's that kind of case. What I think that you have to be careful of is when they start chasing stuff like that, because they were sending him to a surgeon to get it operated on for non-compressive bulge at C5-C6 for numbness in these three fingers. That would definitely be wrong. So how do you want to treat him? This is in Israel. So I mean, you look for the goals. You look for the gaps, right? So what I ended up doing was we tried the greater motor imagery. It didn't change. Tried a sympathetic block. Didn't change. Tried membrane stabilizers, angst eggs, baclofen. Nothing really helped. At the end of it, in Pennsylvania, you're at maximal medical improvement when there's no changes being made. So that's where I put him, but I didn't want him to get surgery. I thought that would have been a real miscarriage. So conclusion, don't diagnose CRPS unless you're reasonably certain, which goes the opposite of what my last case was, of course, but we really worked that through. It may take more than one visit to make the diagnosis. Team approach is always best, and that's what's great. PM&R, we may not help every pain problem, but we can try to help people have better lives, which is one of the great things about our specialty. Address pain function, psychiatric needs. Sympathetic block's useful early in the course, maybe, if they have a similar component. Spinal cord stimulation, I think, earlier, more later, CRPS type 1, better than 2. But it can be useful, although it's not a panacea. And Ketamine, I think, does have something to offer. I think that's going to come out more over the years. Thanks. There was just one question from the audience, real quick. When the SES becomes less effective, do you take it out, or do you have them reprogram? Well, I think the insurance companies call it cosmetic and won't remove it a lot of time. Won't pay for it to be removed. I think the newer stimulators now are MRI compatible, so there's not the, you know. I think when you couldn't do MRIs because of spinal cord stimulators, I think there was a really good reason to take them out. Even now, I think you can make an argument to take them out. But a lot of times, they just stay in, because it's still another procedure, another chance for complications. Great. Thank you so much, Dr. Friedman.

Complex Regional Pain Syndrome

CRPS

treatment strategies

case studies

early diagnosis

sympathetic nerve blocks

spinal cord stimulators

interdisciplinary care

psychological support