All right. Well, we are going to go ahead and get started. Sorry again about the delay. We had a little bit of AV technical issues, but my name is Alex Lauder. I'll be helping moderate this session on recalcitrant cubital tunnel syndrome, and the overview of the session is really to start with the anatomy classification differential, and I'm tasked with kind of giving a quick 10-minute overview to start everyone thinking about this as we move on to diagnostic workup, surgical management, and then how to treat the advanced neuropathy from our expert panel. Starting with some background, so recalcitrant cubital tunnel syndrome is a clinical challenge. Understanding the anatomy and pathophysiology is critical when you're treating this, and conservative management can play a role, but surgical management in the form of revision neuroplasty, neural lysis, reconstruction, and really managing the perineural environment is pretty critical when addressing these cases. So cubital tunnel syndrome is the second most common compressive neuropathy and has been increasing in incidence over time. The failure rate is reported as high as 25 percent, and there's really no difference between in situ versus transposition based on the literature, but understanding what was done in the index procedure is critical when addressing the revision cubital tunnel release, which requires a thorough diagnostic workup, a review of the indications, and really understanding what's going on because revision neuroplasty has less predictable outcomes. So just a quick review of the ulnar nerve. In the neck, the nerve roots of the C7 through T1 forms the medial cord, and then in the axilla as the brachial plexus advances behind the pectoralis major, the ulnar nerve is formed. In the arm, it descends medial to the brachial artery, deep to the arcata struthers, and then in the elbow, it courses posterior to the medial intermuscular septum in the brachialis triceps interval, and then into the cubital tunnel between the medial epicondyle and the olecranon with the Osborn's ligament as the roof, the ulnar collateral ligament as the floor, and here it gives off typically an articular branch. In the forearm, it courses deep to the flexor pronator aponeurosis and then proceeds distally between the two heads of the FCU. There it meets with the ulnar artery and courses distally in the FCU-FDS interval to innervate the FCU and the ulnar half of FTP, and then in the wrist and hand, it gives off the dorsal sensory branch of the ulnar nerve proximal to the styloid, crosses within about a centimeter of the ulnar styloid tip, and innervates the dorsal aspect of the wrist and hand, but it's important to note that it does have a variable course, especially if you're approaching this aspect of the wrist with surgery. The ulnar nerve on the vulvar form becomes superficial and radial to FCU and then enters the distal ulnar tunnel as it traverses superficial to the transverse corporeal ligament, deep to the vulvar corporeal ligament, and then divides into the superficial and deep branches. The superficial branch provides sensation to the small finger, ulnar half of the ring finger, and the palmaris brevis, and the deep branch innervates the hypothenar interosseus, the ulnar-sided lumbricals, adductor pollicis, and the deep branch of FPV. It's important to know there's tons of anatomic variations and interconnections in the forearm and hand between the median and ulnar nerve, just when trying to understand physical exam findings. Pathophysiology of compressive neuropathy is typically divided into acute and traumatic, the acute or traumatic, and chronic, and chronic is what we're focusing on with compressive neuropathy, which is acquired, typically results from mechanical deformation and ischemia, and specific to the elbow, the cross-sectional area of the cubital tunnel decreases from extension and deflection with medial translation, flattening of the ulnar nerve, and this can cause pressure and ischemia. While ulnar nerve instability is common, the relationship to ulnar neuropathy is not completely clear. So here's just a description of the compressive neuropathy, which can cause compression, endoneural edema, loss of perineal resistance, reduction in venous return, causing stasis, extra neural edema, decreased axonal transport, increased endoneural pressure, decreased microcirculation, ischemia, and fibrosis, and this ultimately results in demyelination, axonal degradation and neurologic symptoms, and the picture on the right is a picture of the median nerve in the carpal tunnel, but the similar type of findings with the flattened ischemic portion and the more proximal bulbous edema can be seen in the ulnar nerve as well. So classification, in the literature it's been typically divided into persistent, recurrent, or new symptoms associated with the recalcitrant cubital tunnel. Persistent symptoms are described as those symptoms that you have no relief after surgery, and typically a three-month postoperative course is what's been described. It accounts for approximately two-thirds of patients undergoing revision cubital tunnel release, and etiologies include incomplete decompression, other sites of compression, an inaccurate or incomplete initial diagnosis, or irreversible nerve pathology. So with incomplete release, this accounts anywhere from 40 to 90 percent. It's typically treated with a revision cubital tunnel, and sites of compression can be the fibrous arcatus struthers, the medullary muscular septum, Osborne ligaments, arcuate ligament, and fascial bands, which can extend up to 12 centimeters distal to the epicondyle. Secondary sites of compressions, also either treated with release or treating that pathology, and etiologies can include issues in the cervical spine, first rib, pancus, tumor, or vascular anomalies, ulnar humeral joint pathology, or don't forget about distal ulnar tunnel. And then secondary sites of compression can also be caused from the initial transposition, and the typical issue here is incomplete release of the medullary muscular septum, tethering at the proximal brachial fascia, or kinking as seen kind of in this picture with the ulnar nerve taking a 90-degree course. Persistent symptoms can also be due to this inaccurate or incomplete diagnosis, and the treatment is really to treat the diagnosis, and here's a myriad of potential etiologies, including thoracic outlet, brachial plexopathy, peripheral myopathy, multiple sclerosis, or mechanical symptoms such as snapping triceps. When there's irreversible nerve pathology or prolonged period of compression, it's important to review comorbidities with the patient, the age, duration of compression, and really discuss kind of expectations with how much they may recover. Recurrent symptoms are defined as symptoms that return after a period of initial relief, and this is typically considered, you know, about after six months of relief, accounts for about one-third of patients needing a revision surgery, and the typical ideology includes perineurofibrosis or adhesions, excessive scarring, or secondary sites of compression. Perineural adhesions are typically most accounted in revision surgery, or that's one of the most noted findings in publications, and it's treated with revision cubital tunnel release, and here's a clinical photograph of just the amount of scar that can be found in these procedures, and then new symptoms, which are defined as different from preoperative symptoms with etiologies including iatrogenic complications, incomplete decompressions with a new focal compressive site, or new ulnar nerve instability. With iatrogenic complications, it's typically treated with repair or reconstruction. Medial antebrachial cutaneous nerve neuromas are the highest reported, but the ulnar nerve can be injured as well. Vascular injuries have been reported, and instability resulting from the initial release has also been reported. So with that, I'm going to lead it to All right. Well, so thanks for having me. I want to talk about the diagnostic kind of workup. How do you determine it was a very nice review? Is it compressed in the same spot, different spot, wrong diagnosis, how do we figure that part out? These are my conflicts of interest. So as was brought up, there is a shockingly high risk of needing more surgery for this. I mean, how many procedures do we do where there's an 18 to 20% risk of having recurrent or precalcitrant surgery at five years? And after preparing for this talk, I feel like I have to tell my patients that now. And I wouldn't have said that three months ago. Now I'm like, oh my gosh, if we do this surgery, there's almost a one in five chance you might undergo more surgery in five years, which is scary as a surgeon. At least I know Andrew said that maybe there's no difference. This study found slightly higher risk if you did it in situ release as opposed to a transposition. So let's talk about different diagnostic workup. There's two main categories. I think nerve tests, which I think most of us feel pretty comfortable with, and then because I love ultrasound, I'm going to tell you about ultrasound and you'll probably hate me by the end. So the AANEM, American Association of Neuromuscular and Extradiagnostic Medicine, they define cubital tunnel syndrome as three different criteria. It can be one of the three. It can be all three. First, I think the easy one for all of us to recognize is a conduction velocity across a segment of less than 50 meters per second. So you get above elbow to elbow, it's 65. You get above elbow to below elbow, it's 40. And then below elbow to wrist, it's 60. You know, ding, ding, ding, we know it's compressed at the elbow. You can also have a change of 10 meters per second squared over segments. So say that it was still 50, but it was 65 above the elbow. So that'd be a 15 meters per square difference, and that would also count. And then I think it was Holly earlier today talked about CMAP being a really nice predictor of severity. And so that's the other one. If there's a greater than 20% drop over that segment, that'd also be diagnostic for cubital tunnel syndrome. But it does get a little bit tricky in the post-op setting, as we all know. So very busy slide. I hid it. The only things that I kind of thought were important here. But if you look at pre-op, so in their series of patients, 91 cubital tunnel releases, about 10% had normal studies, 75% had delayed studies, and the rest were kind of non-detectable, very severe. If you look at two years post-op, there's still 50% of those patients still had delayed conduction velocity across the elbow. So that makes it really confusing. And I think we've all been there. If you don't have any pre-op nerve studies, and you get post-op nerve studies, and they're abnormal, are they better? That's usually what I look at. Did the velocity get better? So if someone had a conduction velocity of 30, and I did the surgery, and they're still telling me they have symptoms, but now their velocity's 45, I mean, that's still below 50 meters per second, but I think they're getting better. And I'd probably tell them I can't help them in that scenario. Another study looking at 15 patients, their pre-op motor conduction velocity was not recordable. Pre-op motor was 35 meters per second and was recordable in all patients, and the sensory was 43 and recordable in 12 patients. And so really what we're looking at here is, it does improve, it doesn't return to normal. And sorry if that was confusing. So that's the nerve studies, and I think that's pretty obvious kind of what to do. Ultrasound, you know, I love this. So if the nerve is compressed, it swells, we can measure that. We look at cross-sectional area. You can also look for different points of narrowing. So to be honest, the thing I've found the most useful is to scan across the length of the nerve, and even if the cross-sectional area isn't changing, you know, over some value, you can actually see narrowing. And I see this a lot when I've done transpositions. So I used to do a lot of either subcutaneous or subfascial transpositions, and the nerve would be of normal course above that, and then I could see it really shrink down right where the transposition was, and then get bigger afterwards. And I think that was that perineural fibrosis that you showed so nicely. So I think it's very helpful for that. In general, if you're just looking at cutoff values, it works just as well. So some of this is just kind of setting up the background. I know I talked about it in some of my other talks this weekend, but 22 patients, cubital tunnel, at the inlet of the cubital tunnel, the mean was 38 millimeter squares. These are huge nerves. Normal is less than 10, and so people that have very bad compression, you see a lot of that. And then that correlates pretty nicely with conduction velocity. So it's not a one-to-one. Like, I wish it was just a completely kind of straight line. Like, as your conduction velocity got less, your cross-sectional area got bigger. It does to a point, and I think Andrew very nicely talked about how you start to get perineural fibrosis towards the end. So when we see, like, the very bad nerves, like the dead nerves where it's not coming back, those actually start to shrink back down and sometimes look normal, which is really confusing when you have somebody that just has crazy symptoms. They're completely no sensation, they have no muscle, and then their nerve measure is 9. And that's kind of that WTF moment, what's going on with this nerve? I think I showed pictures like this earlier, but this is how you do the exam. There's kind of two different ways. If I have a younger patient, they can kind of lay down. It's nice if they just kind of do one of these. Some of the older patients, I'll have them kind of put their arm like this, then I can scan them from behind. I presented this study earlier, so I'm just going to skip over it. But in healthy controls, mean cross-sectional area is 6. In the ones with cubital tunnel, it's 19 millimeters squared. And again, this isn't really talking as much about the recalcitrant or the recurrent versions, but just kind of in general, we can measure these nerves pretty nicely. And it ends up being very obvious. Hopefully, if any of you get to take any of the ultrasound pre-courses, we do. Five minutes. Give me five minutes of your time. You'll be able to find these two nerves. You'll be able to measure them. And I think you'll actually be pleasantly surprised how easy it is. Again, correlation between cross-sectional area and nerve conduction velocity is near perfect. And that's one of the big things when I talk to surgeons. We're all pretty comfortable with nerve studies. I think sometimes we're guilty of not being able to interpret them all that well. But we're comfortable with them. And so we want something that's going to correlate well with that. And again, ultrasound is actually a pretty nice way to do that. We see it usually in the sulcus. So, you know, kind of right in the medial epicondyle. They're just below it. But again, I see it a lot with the transpositions. And this is kind of a long axis view. You can see some narrowing right in the middle of the screen right there. All right. So we talked about nerve studies and how after surgery, a lot of times they improve, but don't go back to normal. I think we see this in carpal tunnel syndrome, too. We all know if someone has a distance of 10 and you get a nerve study a year later, it's not going to be below 4. It's going to be something like 6. And so we see similar findings for cubital tunnel. So you can see pre-op, the mean cross-sectional area at the elbow was 13.8 millimeters squared. And then post-surgery at one year, well, 46 months, it was 12.9 millimeters squared. So that's not a huge difference. It gets better, but not a huge difference. And then the other crazy part is despite most of these patients getting better, only 36 of 48 showed a reduction in cross-sectional area. Again, it goes back to that nerve study that showed that, you know, still 50% of people had abnormal nerve studies. This is a large study out of Europe. And we actually see this a little bit for carpal tunnel, too. I know this is a cubital tunnel talk, but endoscopic release. So I do almost all endoscopic. My two partners do almost all open. And what we see is the people that get endoscopic, their nerve shrinks down quicker and kind of more reliably than the open surgery. And so I think that just shows maybe less soft tissue damage, maybe better blood supply, less scar tissue, hard to say. But this study found the same thing, that in the open release, it started at 10 millimeters squared, and then went down to 8.5 at 12 months. And the cross-sectional area went from 9 to 7. So this was a prospective study. The other one was a retrospective study. So maybe this gives us a little bit of hope that ultrasound is actually going to do the trick. Pulled this study, again, out of one of the plastic surgery journals. Thirty-seven nerves in 35 patients, 73% with persistent compression and ultrasound, and 71% with ulnar nerve swelling. And the nerve studies were only positive in 40%. So I talked in a different ICL this weekend about how we've all had patients where they come in with primary cubital tunnel, they're young, they're healthy, you get a nerve test, and their nerve studies are stone cold normal. And then when you do ultrasound in those, you'll find the ultrasound will be positive in 30 or 40% of them. I think this study kind of very nicely shows that as well. What about when you transpose? And we know that transposition does cause a trauma to the nerve. I think Holly talked very nicely earlier about how that's not a completely benign procedure when you transpose. So in the failed cubital tunnel group, so these people had recalcitrant symptoms. Their nerve was 17 millimeters squared. In the group that had a successful transposition, it was 13.5. So maybe it's not necessarily the transposition itself. Maybe it's actually decompressing the nerve and making the symptoms get better. So in summary, I would say that both nerve studies and ultrasound don't return to normal after surgery. So don't expect that. I think they can be very helpful if you have a baseline test. And patients, I would tell you, are much more likely to want to have an ultrasound post-op than to get shocked and stabbed again over and over again when they're having pain. And the thing I like about it is ultrasound can identify very specific points of compression. Now, the nerve study people have started doing these inching techniques, which should be very helpful. But I would tell you in the presence of a transposed nerve, a lot of times they have trouble finding it. I don't know if any of you have seen some of the nerve reports. If there's a transposition, they'll say, well, we can't really find the point of compression, but the nerve was transposed, so we can't tell. And I think a lot of our good neurophysiologists actually have started using ultrasound. Of course, this is, we all have our favorite niches and for some reason, when you were, at least when I was an orthopedic resident, when a back pain patient came in, you sort of wanted to hide. And when a ulnar nerve, recalcitrant ulnar nerve came in, these, for some reason, I somehow like these. And so my charge is to really discuss the surgical management and outcomes. And I think, hopefully, some of the slides you'll see and some of the pearls and surgical pictures, you'll not only apply to the recalcitrant case but also your primary case. Because I think sometimes a lot of these may have some relative technical issues with them. And these are my disclosures. I don't think anything particularly pertinent to this talk specifically. But these are actually my other disclosures related to recalcitrant. One is that I haven't met the same case of cubital tunnel, recalcitrant cubital tunnel twice, meaning they all present with some different presentation, subjective history, diagnostic workup, and surgical findings. It's also important to realize that when we talk up here at the podium that a lot of this is personal experience, but also it's rare for us to publish poor outcomes. So when we say that it's got a 20 percent failure rate, it's probably higher than that. Because nobody stands up and gives talks about their poor outcomes. And remember that despite the consideration and the jump that your patient wants you to do something when you have a case of recalcitrant cubital tunnel syndrome, not all patients really will benefit from that surgery. So you have to really be careful about your surgical indications for these patients. I'm going to start with a case example that we've all probably seen in our office. A 27-year-old, initial improvement in symptoms after an in-site ulnar nerve decompression at the elbow, but then starts having dysesthesias in the ulnar nerve distribution three months after in-site ulnar nerve decompression. And really there's focal tenderness, and you can almost get a sense that there's an unstable nerve at the elbow. And it's really increased with maximal elbow flexion. And this is obviously the case that you're worried about, where this is a revision ulnar nerve, and if you watch carefully right about here, you'll see this patient with a very subtle instability of the nerve. And what happens when that occurs, and you can see why the patient's symptomatic, is every time the nerve does that, it fires off the FCU, obviously painful. And so this is the typical finding. This is a different patient. But here you can see the medial epicondyle, and the nerve is sort of perched. And probably they get better initially, but then they're tethered distally. And so the technical side here is the nerve is still tethered somewhere, and now it's mobile, and now you're introducing this relative traction neuritis across the ulnar nerve. So from this perspective, how do you go about managing this patient and managing the perineural environment? Slightly different case, 48-year-old, left ulnar nerve decompression and subcutaneous transposition at the elbow. This patient really got better, but complains of worsening symptoms beginning six months post-operatively after the initial improvement. So initial improvement, we learned probably the nerve was decompressed adequately, but now there's something else going on. And really for me, this is as much a clinical exam where you can really find a focal area of local... be very helpful. And this is just an example of somebody who's had a subcutaneous transposition at the elbow. This is what you find at the time of the revision. There is a very focal area of compression because you have a very narrow fascial sling. And after you've decompressed this, I think you can appreciate the relative fibrosis and tethering of the nerve really locally here. And if you just, this nerve isn't gliding anywhere. There's no independent tissue gliding as you're flexing and extending the elbow. And so this nerve is really just prone as you flex and extend the elbow to some form of kinking and tethering of the nerve. So hence, the worsening of their symptoms. So this is really, you put your detective hat on for many of these and you can almost explain by just looking at the surgical incision. And again, some people try, this is like minimally invasive surgery, or patients really are attracted to that notion. But sometimes with the nerve, with a transposition, that may not be the best solution. And really, we have to be very careful with our patients. This is a patient with immediate worsening of their condition. Here's the surgical incision following an anterior transposition. And I think you can all appreciate what you'll see intraoperatively. Here's the ulnar nerve. This is the medial epicondyle that you can see right here. My arrow's not showing. But intraoperatively, you can see here the intermuscular septum is still intact. The more healthy-looking nerve, more proximally, has suddenly got this bulbous appearance as it's going through this sort of zone of transition through this pseudo-transposition at the level of the medial elbow. And so this is really, this is the clue. You've got a patient that's immediately gotten worse, so you have to think of nerve injury. Is the nerve in a worse position than it really started? As you start your surgical procedure, you have to now be aware of these things. And if you just find one of those two, you have to be aware that both could occur, obviously. You could have a nerve injury, and you can have a nerve that's in a worse position leading to other symptoms. And then this is the next case with the perineural adhesions, the left ulnar nerve, revision ulnar nerve decompression, and submuscular transposition at the elbow. When I was in training, submuscular was your bailout. So here you've got a bailout procedure that now needs some bailout. So no improvement immediately following symptoms, but now they're having worsening symptoms following their surgery. And here, just, if you follow the ultrasound of my, I don't think the arrow's pointing, but you'll see right there that is the ulnar nerve turning over itself as the elbow is flexed and extended. So this isn't looking for cross-sectional area. It's looking for the nerve right there, kinking. And if you see this is the same patient, you can see the ulnar nerve is certainly not gliding deep to the submuscular transposition. And this is the patient that you'll see in your office with very focal, very local pain with reproduction of symptoms distally and clearly not very happy. So you also have to be aware of other things. So it's not just the clinical exam, but sometimes we can get clues from other diagnostic imaging. This is the case where the nerve has been placed into not such a great a sub or an anterior position, you've moved it too far anteriorly and so you've developed this serpentine change to the nerve. So as Susan McKinnon and others have pointed out, the reasons for failure are multiple. It can be just poor tissue, in other words, perineural fibrosis, scarring. It can be we've introduced now a change in the position in the course of the nerve that's added tension across the nerve itself, so putting it into a new position. And so really as you think about how you go about treating these, we've talked about confirming the correct diagnosis. My focus here is really about the current state of the local nerve environment. And so obviously you have to take your time and decompress the nerve. This is not a small incision. You have to be able to directly visualize the nerve and follow it throughout its course. It'll often be tethered no matter what the cause of the recurrence. And then you want to do something for the nerve that's obviously going to prevent recurrence. If you have a 20 percent failure rate, as has been promoted here, revising your surgery doesn't always have the... So from a surgical strategy standpoint, this again, you have to expose the ulnar nerve to normal tissue, both proximally and distally, and then you start your expedition following the tissue planes. You really wanna be careful of the medial anabrachial cutaneous nerve. It may be a source of persisting pain from a neuroma, but at the same time, you wanna protect it so you don't now create a new problem for the patient. Remember that the medial anabrachial cutaneous nerve lies immediately anterior to the intermuscular septum for an in situ decompression that still may have an intermuscular septum intact, and it is not always distal to the medial epicondyle, so that's important to recognize. And if you do have an ankineus epitrochlearis, I've come across one patient who still had an intact ankineus epitrochlearis muscle intact after an in situ decompression, so I'm not quite sure what happened there. And then you have to be careful because an internal neuralysis is not always the go-to procedure. Even having microsurgical instruments available and a microscope very rarely may be something that's important. You're going to maybe come across a nerve that looks like this. And your focus may be right here, because that's the obvious place of your nerve compression and tethering. But if all you do is release the nerve, you may forget about distally and potentially another point of compression. So you really have to think of now the nerve as a whole unit. And really looking distally, it's not uncommon for the deep aponeurosis of your FCU to still be intact, particularly in cases of that in situ decompression that you saw as the first case, where now you may have some instability. And that now may be your tethering point for your ulnar nerve. And then as you go distally, you really want to end up having a really free and clear nerve, critically assessed with elbow flexion and extension, so you don't have any points of tethering. This is not an uncommon finding, again, is the intact aponeurosis. And you can see here just how swollen the ulnar nerve is as it's starting to descend between the two heads of the FCU. And you can see the relative almost 90 degree corner here for the ulnar nerve that's being compressed and tethered. And then you want to look at the epineurium and evaluate its integrity. There are times when a previous surgery, and maybe your own surgery, has introduced some form of epineurial injury. And then obviously your perineural environment will be critical. Chris D. published a nice article just sort of reviewing what's the ideal barrier to trying to prevent perineural adhesion formation, addressing these potential links to try to minimize ischemic change around the nerve and to promote nerve gliding at the end of surgery. And there can be some barriers to adhesions. There's local soft tissue flaps that we'll discuss, autologous vein wraps, as Dean Citerionis and others have described, and biologic wraps. And I have no typical use for biologic wraps unless there's a concern for an epineural injury, which you may be then using it to reconstruct your epineurium. So neuroplasty plus what? What's your step after you do your recurrent nerve decompression? Dean Citerionis has described a deepening of the ulnar groove, as some people may use after an in situ decompression. I haven't used this tremendously or a fair amount. But if you are in the situation of a previous neuroplasty and submuscular transposition is your bailout, again, you have to go back and say, well, what happens if the bailout needs a bailout? And I think that sometimes we worry about what do we do as a next step, because we don't want to create an ischemic nerve. We don't want to end up having a worse nerve, CRPS, and other issues. So this is actually, and Mel is standing in the back of the room, so I started doing an adipofacial flap reconstruction. It happened to be we were teaching in a course, you may remember this, with Jeff Greenberg. We went to the back and Mel said, hey, come and look at this. We dissected out a cadaver. One of the great things about being involved in courses, and even as a teacher, you learn a lot. And so Mel was the one who showed me. My technique slightly modified, because I couldn't understand his New York accent, perhaps. But this has really been very helpful in my practice. And part of the reason is that it's an anterior adipofacial flap. It's oftentimes never been involved in the original 1, 2, 3, 4 previous surgeries. And so it's a fairly native tissue. It's a medial approach. You, again, isolate the nerve proximal and distal to the zone of injury and identify your MABCN. This is a cadaver, but here's identifying your MABCN. And then you take down your intermuscular septum, if it's still intact. And you've lifted this full thickness flap off of your flexor pronator origin. And you should see this membranous basement layer of your subcutaneous flap. You also will see that your medial anterobaric cutaneous nerve sits immediately superficial to that basement layer that sits in the basement of your subcutaneous tissue layer. And so those are key. And that's really critical. deep layer of the subcutaneous tissue, separated by a beautiful membrane that you can preserve. Deep to it are the venous structures and your medial antebrae cutaneous nerve. And now you've got, you're separating this out into two layers. And this isn't a cadaveric specimen, but the nice thing for the nerve. And then as you've laid your nerve now anterior into that interval between the superficial and deep layers, then you can bring the deep layer back up and just like a hot dog or a burrito or whatever your favorite food is, you can then suture that into place as a barrier for subluxation of your nerve. Sometimes you can have proximal branching of your MABCM, which is sort of a challenge sometimes, but you can still bring the flap much more proximal and you can even develop a flap distal to your MABCM if you needed to increase your length. And then the other is what about thin people? And I've done this on some very thin individuals, but you can still find this layer. It's present. Never say never, never say always, but it's always there. And this is the thin layer. Even if you were to. So, just in terms of outcomes, very briefly, because I'm probably going over my time, this in terms of Mel's outcomes, several have pointed out the relative benefit of this flap without any significant worsening changes compared to an anterior fascial flap. At my previous institution at Duke, we had a follow-up. This is not published, but this was pulled up by one of our fellows, and the take-home message was that after multiple procedures in some patients, we had a significant reduction in VAS scores, which was really the patient's desire, and then had gradual improvement. And then this is a nice meta-analysis looking at outcomes for refractory cubital tunnel. Again, very similar in terms of identifying where the problems lay and just be aware of these as you do your own cases primarily, but then also be aware of these findings when you're going back on somebody for a follow-up case. And then, obviously, reconstructive options, whether they're tendon transfers, nerve transfers, may be a part of your armamentarian, but again, out of the scope of this talk. So thank you very much for your attention, and hopefully this gives you a little bit of a perspective, but things to watch for in the perineural environment for when you're doing a recalcitrant cubital tunnel syndrome. Thank you. And that's whether it's a primary. But I want to talk about how we classify disease severity, because I think that that's really important when we start talking about how to optimize function distally. So we're all familiar with these common classifications that I have listed on the screen. We tend to focus on the clinical signs and symptoms. There are a couple of classifications that talk about nerve conduction study, but they only talk about conduction velocity. And we know that current classifications don't actually correlate well with clinical outcomes after surgery. So I think this paper that we did, we looked at 83 patients with cubital tunnel syndrome, and we showed that reduced CMAP... We kind of tried to put this all together and we modified the commonly used Dellen and McGowan classifications and we wanted to add so that surgeons would look at the electrodiagnostic studies and specifically the CMAP amplitude and EMG findings. And this, like I said, becomes really important when you're talking about adjunctive procedures. So the first one I'll talk about And this has actually a large in so patients that have a diagnosis need to be receptive to reinnervation. So that means. So we can now, with this knowledge, target that central aspect of the motor fascicle with our nerve transfer to optimize that. So this would be an example. And that brings me to my next point. So this nerve transfer, I think the results are really dependent on doing good post-op rehab. So as surgeons, we get the nerve to the muscle, but the And then a step further. Dr. McKinnon looked at her outcomes, 42 patients, severe cubital tunnel syndrome who had ulnar nerve transposition and the nerve transfer, 79% at 12-month follow-up had at least anti-gravity intrinsic strength, 7% had no improvement, so it's not perfect, and interestingly there was no CMAP amplitude below which the nerve transfer did not work. The main controversy, I guess, with these studies is that there's no comparison group, so you can't really say for certain how much of this improvement came from the elbow, how much of it came from the nerve transfer, which is why this recent randomized control trial is a really great addition to the literature. So this group looked at 93 patients. And this study, which is actually hot off the press, or in press I should say, is a Western Canadian multi-centre study. And the goal of this study was to try and figure out. And I was very surprised to see the results of this. They looked at McGowan 3 cubital tunnel syndrome. They had a group that had just decompression, a group that had the end-to-side nerve transfer, and then they had a comparison group of end-to-end transfers and that was specifically where they applied this novel nerve conduction study technique that allowed them to determine if there was any crossover. When they looked at reverse end-to-side, they found no crossover from the AIN into the ulnar nerve. Compared to, as you might expect with end-to-end transfer, there was crossover from the AIN to the ulnar, meaning axonal crossover. But they did find that the patients that had the end-to-side nerve transfer statistically significant better functional recovery than decompression alone. So with the results of the randomized control trial and this study, I think that it gives evidence to show that it offers it. So sensory recovery in inset nerve grafts. the collateral sprouting from the median nerve across. Again, no comparison group, so very difficult to, or not possible to say whether the recovery came from the elbow versus the nerve transfer. If the patient finds that they have weak ring and small finger DIP flexion, you can consider performing a profundus side-to-side tenodesis. This will improve their range of motion, but not Putting it all together, so Dr. McKinnon reviewed 136 of her patients with severe cubital tunnel syndrome. 49 had adjunctive procedures beyond the elbow and 87 had ulnar nerve transposition only. And she published this nice little algorithm that you can refer back to on when to use each of the procedures. But the bottom line is that they had better improvement in DASH score with the procedures beyond the elbow than the ulnar nerve transposition alone. And so, in summary, I would implore you to try and accurately, preoperatively classify your patients. Really focus.

recalcitrant cubital tunnel syndrome

ulnar nerve

elbow

surgical management

revision neuroplasty

diagnosis

nerve studies

ultrasound

individualized treatment