This is a short session, and we have a bit of material to get through, so we'll try to kind of get started here, hopefully get you out of here on time. A few housekeeping items. We actually added a talk back in. It was taken off because the original speaker was sick, but Rob Wisocki came in on the 11th hour and kind of made us whole again, so we kind of thank him. We're happy to have him here and eager to kind of hear him speak. The other thing is that moderator Q&A function, so there's supposed to be a password up here that allows me to kind of moderate that. There is no password up here, so hopefully, again, this is a small enough session that you feel comfortable asking up at the mic if you have any questions. All right, so we'll get started. So we're actually part of members of the Hand Society's Evidence-Based Practice Committee. Our goals are to disseminate information based on the available literature. So many of you might ask, well, isn't that what everyone does and you'd be right, except that we try to select a topic that perhaps maybe we haven't done a deep enough dive into. You know, a big caveat here is obviously we didn't do a thorough systematic review, but we did try to kind of scour the literature to kind of present to you what we think are the best available evidence. And hopefully, we can all kind of take something away from this, maybe pick up a couple of references that we hadn't realized before, and hopefully learn. So without further ado, the first one's gonna be Aaron talking about suprascapular and axillary nerve compression. Thank you. Let's see if we can get this to load here. So we're gonna talk about an evidence-based approach to diagnosis management of suprascapular and axillary nerve entrapment. I don't have any disclosures relevant to this talk in particular. All right. So this is what we're gonna cover in this brief talk, talk a little bit about sort of review of anatomy and pathology. Diagnosis and management in operative versus non-operative treatment was sort of a bent towards the evidence. So talking about the suprascapular nerve, this is a branch of the C5 and C6 nerve roots, occasionally the C5 nerve root only, extending from Erb's point down to innervate the supraspinatus, traveling through the suprascapular notch, and then continuing on to innervate the infraspinatus through the spinal glenoid notch. It contains mostly motor fibers, but some sensory fibers coming from the joint. It travels through the suprascapular notch. We can take many different configurations from shallow to deep. There are V-type and U-types, as well as either a partial or ossified ligament, all of which can potentially contribute to the compression of that nerve as it travels through. It's a relatively unusual compression neuropathy, accounting for a one to 2% of chronic shoulder pain. And of course, it can be associated with trauma, such as scapular fractures. It can be iterogenic, associated with other surgeries, with scarring around the nerve, and lack of motion of that nerve. Particularly, it seems to be associated with overhead athletics, such as volleyball and baseball, and potentially accounting for up to 33% of elite-level volleyball players' chronic shoulder pain. Commonly, it can be compressed by, for instance, paralabral cysts or other masses, in particular in the spinal glenoid notch as it comes close to the labrum. And it can also be, compression can be caused by retraction associated with massive rotator cuff tears, and as that tendon retracts, the nerve can go with it, and it can sort of tent itself as it comes around those structures where it's relatively tethered. Let's talk about the axillary nerve here in the anatomy. So again, C5 and C6 nerve roots, a branch of the posterior core of the plexus. This also contains motor fibers, as well as sensory fibers, innervating the skin overlying the deltoid. It travels along the subscap muscle, inferior to the glenoid and the capsule, before coming through the quadrilateral space and branching into the anterior and posterior divisions, as well as innervating the anterior deltoid, the posterior deltoid, sending a branch to the teres minor, and then the overlying skin as well. Again, the axillary nerve, like the suprascapular nerve, can be associated with a compression associated with fractures or dislocations of the shoulder. In particular, it's the most common nerve associated with that. It can be surgical or iatrogenic, including surgical positioning, such as a lateral cubitus position, or with a tractor placement when performing total shoulder arthroplasty or other surgeries around the shoulder. It can be associated with direct contusion. So for instance, a helmet hitting the lateral shoulder, and again, cysts or mass. And then, while relatively uncommon, it can be associated with a syndrome called quadrilateral space syndrome, where the nerve and accompanying vessels are compressed as they come through the quadrilateral space. So what about diagnosis? So again, the suprascapular nerve, going back to that nerve, cause chronic pain, usually posterior or superior shoulder. Again, fairly nonspecific. It can cause atrophy of the supraspinatus or the infraspinatus, or both. Frequently, when just the infraspinatus is affected, the patient or that athlete may not be particularly symptomatic and can compensate pretty well and may not realize it for quite a long time. In terms of exam tests, one is the suprascapular nerve stretch test, where the neck is retracted opposite and the shoulder is retracted as well, which results in reproduction of that pain in the posterior and superior shoulder. X-rays and CTs, of course, to look for associated fractures. Really, the mainstay treatment is gonna be MRI, looking for a cyst, and looking for muscle atrophy or associated rotator cuff or labral pathology. And then EMG, which is really the gold standard at this point. I don't know if you can see, that's not really projecting very well, but with this example showing denervation at the supraspinatus and infraspinatus muscles. Here's an example of an MRI showing some fatty atrophy, and you can see the difference with the supraspinatus and infraspinatus relative to the other muscles surrounding the shoulder, suggestive of atrophy. The axillary nerve, in terms of diagnosis, again, weakness and atrophy may be presenting signs, can be the whole muscle or even just the posterior portion only. The sensor exam can help to some degree. There are other tests, such as the Sparrow test, where the arms are extended and the patient's asked to hold them in place. With a lack of ability to hold it in place, a positive test. X-ray or CT, once again, looking for fractures. And then again, it's gonna be the mainstay is MRI and then EMG nerve conduction study, looking for, again, labral pathology or masses. And there are reports of people using angiograms to look for compression of the vessels as they run along with the nerve through the quadrilateral space, but just keep in mind that those vessels can be compressed in asymptomatic individuals. So perhaps that's not a particularly useful test at this point. So let's start looking at the management and the evidence here. So for the suprascapular nerve, of course, we can divide it up into non-operative and operative treatments. So we'll start with the non-operative. NSAIDs and physical therapy. And when we look at the evidence, there's very limited evidence here. So we're talking about a handful of case series. You can see, going back to 1991, 1997, they're listed here. And it's fairly conflicting and fairly low quality evidence, unfortunately. It goes from very good results with non-operative treatment all the way to everybody needed surgery. So it really doesn't help us. But what we're left with is essentially expert opinion, considering non-operative treatment for relatively recent problems, so less than six months symptom duration, in patients that maybe don't have a mass lesion or rotator cuff tear. But that's all we have for non-operative treatment. Operative treatment for a decompression of the suprascapular nerve can be either done open or more frequently now, and most of the evidence is looking at the arthroscopic treatment, but it can be done open through a relatively large approach, trapezial approach, posteriorly, or a deltoid split, if necessary, to get to the spinal glenoid notch. But more commonly, it can be treated arthroscopically, where the transvascular ligament can be cut arthroscopically as you follow it medial to the CC ligaments through the modified divisor portal, or at the spinal glenoid notch through the sub-coronal space, or just by treating the intra-articular pathology, for instance, decompressing the cyst, and then repairing the labrum to prevent that sort of valve effect. Here are some pictures here. You can see in this arthroscopic image, with the ligament, the nerve traveling under the ligament, and the vessels traveling over the ligament. So you have to be careful to avoid those vessels if you're treating it. These images, courtesy of one of my partners, you can see the transvascular ligament with the nerve going underneath it, and then with a biter, this is transected, and you can see the nerve able to be mobilized as well. So what about the evidence for operative treatment? So slightly better evidence, with several either meta-analyses or systematic reviews of the literature. But again, keep in mind the evidence that makes up these systematic analyses are relatively low quality, unfortunately. So these are all case series, no real randomized controlled trials. There's, I think, one prospective trial in one of these. But in general, according to every one of these reviews, for the most part, patients do pretty well with a good resolution of their symptoms on treatment, and even resolution of their findings on EMG. So most of these patients ended up returning to their level of play and their activity level. So last, let's look at the axillary nerve and some of the evidence in the management. So once again, this can be treated non-operatively, again, consisting of anti-inflammatories, physical therapy, consideration for diagnostic lidocaine injection if necessary, to sort of identify quadrilateral space syndrome. You can consider an EMG for baseline at three weeks to six weeks, and then recheck if necessary. And then just continue to follow them. Again, for non-operative treatment, when you look at the evidence, there's really not a whole lot. And so again, we're left with just expert opinion suggesting considering non-operative treatment for about six months or so, with consideration for operative treatment if they fail, particularly in the absence of a space-occupying lesion such as a cyst or a mass, and any other associate pathology if it's not there. So operatively, again, this is gonna be a rare compression neuropathy as compared to suprascapular nerve, but really depends on the overlying cause. So neuralysis, either through an anterior or posterior approach or a combined approach, particularly posteriorly to decompress it as it comes through the quadrilateral space. Of course, with trauma, either repair or nerve grafting, and then nerve transfer, of course, which is beyond the scope of this talk here. So looking at the evidence there, unfortunately, again, the evidence is relatively low quality, and there's really almost none out there in the literature as compared especially to suprascapular nerve. There are really just a handful of studies, and overall, they suggest that people do fairly well when it's decompressed, but as you can see with the numbers here, it's not particularly robust evidence supporting or refuting one way or the other the treatment of axillary nerve compression or quadrilateral space syndrome. And that's all I have. Thank you. Okay. Anyways, I'll try to get us back on time here. So proximal median nerve compression in the forearm, like I said, a slightly less obscure topic. The problem is the evidence is still pretty crappy. But at the end of the day, I think the issue is that we just have to find the best available evidence so that we can hang our hat on something. And so I'm going to present a couple of studies that I hang my hat on so that when you do see it in clinic, you have something to talk to the patient about, obviously, and then perform the surgeries and try to get the best possible outcome as possible. So my goals here are to briefly talk about the differential and really spend most of the time on pronator versus lacertus and then just kind of touch on AIN syndrome. When you look at the literature, very variable incidents, Jin Bo-Tang study were retrospective. Their reported incidence of proximal median nerve compression in the forearm was 1%. And then when you go to continental Europe, it's 30%. And that's a huge difference, I mean, 1 in 10 versus 1 in 3. I definitely don't think I see 1 in 3 proximal median nerve compressions in clinic. And so this really kind of makes studying something like this awfully difficult and even contributes to controversies. I think a couple years ago, the Journal of Hand Surgery published a review article where the authors actually talked about how some people don't actually even believe that proximal median nerve compression happens. And I remember early in fellowship, when I was too kind of scared to kind of argue with my attendings, I remember one attending actually mentioned briefly that he didn't really think that this was a real entity either. But maybe things have changed. I certainly think it's a real thing. So but what are the issues? I mean, as we will see in all these talks, I mean, most of these studies are all retrospective and they have all their inaccuracies and biases that I'm sure you're all aware of. Referral patterns might contribute to it. In Green's operative textbook, Scott Wolfe kind of meant, I forget who exactly the original person quoted this, but he mentioned about the I see what the mind knows. And I think this is really kind of relevant to something like this where if you're just not looking for it, it probably is there, just the old adage, it saw you, but we didn't see it. And then I think the other big problem with proximal median nerve compression is that when you're trying to look for something more objective, quote unquote, such as electrodiagnostics, they don't help you really. Oftentimes they're normal. The theory behind that is either it's dynamic compression or it's just not bad enough that it shows up on electrodiagnostics. I think the other issue is that if you do see some abnormalities, it may actually be still carpal tunnel, which is vastly more common than something like this. And so it adds to, quote unquote, the subjective diagnosis. If you need a reference for this, I'm happy to provide it. Just wanted to kind of throw it up there that, again, if we're looking for evidence, this is peer reviewed. It kind of has a pretty thorough differential that you can look at on your own time. Sites of compression, again, I threw this reference up there because I think it's a really, really good review article from Jennifer Wolf. But the sites of compression are pronator teres, which are pretty much just tendinous and fibrous bands, not necessarily the muscle. There are variations in how the median nerve passes by the pronator teres, the two heads of pronator teres, which add to a possible site of compression, Lassertus fibrosus, FDS arch, which I think anecdotally, you know, eminence-based medicine, I think this is where a lot of them do happen. But others think it's pronator teres versus Lassertus. In the Struthers, curious to know, at some point, how many of you get x-rays to look for that bony prominence, ganser muscles, and then, you know, much less common things like vascular arches, bony axostoses, et cetera. So pronator syndrome. So this is really kind of the best available evidence that I can find. And I use it in clinic. I follow the technique. This is out of Sue McKinnon's group. I think, even though it's retrospective, they're thorough. And as much as, you know, we know about all the limitations retrospective, this is pretty much, I think, the best that we have. But their diagnosis is that it's not just proximal, it's not just forearm pain. They have to have provocative signs such as pronator compression, resisted long finger flexion, resisted pronation supination, and then scratch collapse tests, which, again, you know, controversial. But it's more than just pain. But interestingly, when you look at their table, it doesn't have to be just one because even when you look at provocative tests, only about 89% of them were positive. So it's really a combination. But I think the moral story, and I think something that I use in practice is just that you need to find something more than just someone that's complaining of proximal forearm pain. The technique that McKinnon describes, again, something I used is described in the literature, their reported results. I'll show you in a second. But her steps are lengthen the pronator teres distally, release the lacertus, and then identify your median nerve. I'm not sure it really matters. She argues that it is because then it allows you to find the median nerve easier. It is a deep hole, as she describes it. Certainly, it very much is. So just kind of believe your anatomy, and it should be there. And then she goes on to a more distal release of the deep head of the pronator teres, which is where she thinks most of the compression happens. And then you go on even further distally to the FDS arch. So in her study, 27 patients. Only two didn't get any relief, but the majority had a statistically significant decrease in their pain. And again, like I said earlier, we just have to hang our hat on something, and this is what I use. Lacerta syndrome. So Dr. Haggard has been really kind of a big, big proponent of this. And again, she's published a couple of studies of this. And this is, again, what I use to hang my hat on. Her diagnosis is a triad, looking for weakness of FCR, FPL in the index FTP, tenderness or tonels under Lacerta's, and then a positive scratch collapse test. This is courtesy of her. So she does these wide awake. And this is prior to the release. Oops. Can I ask you to please flex your thumb? And keep it flexed. And resist, resist. And again. And resist. And flex your finger. And resist. And again, resist. So very clearly weak. And this is immediately after release. Not two weeks, not one week. This is immediately. And keep it flexed. And resist, resist. Oops. Sorry. And. And flex your fingers. And resist with your index finger. And flex your thumb again. And resist. And resist. Perfect. Well done. So pretty remarkable. I mean, and this is done under local wide awake, a two, three centimeter incision in the antecubital fossa, look for Lacerta's, and then divide it. And flex. In her study, 44 patients at six months, again, statistically significant decrease in numbness, pain, and overall satisfaction. This is, again, level five evidence, eminence, but this is a quote from her that, you know, she believes that majority of proximal median nerve compressions are actually Lacerta's. She's only really done five of these. And if you did have to look for something more objective, she believes that ultrasound is the way to go. And then just briefly, AIN syndrome, this is Scott Wolf's group. I'm not going to kind of go into it too much, but the moral of the story is that there's increasing evidence that AIN syndrome is not really a compression neuropathy. It is part of or a consequence of Parsonage-Turner, and what's really happening is these basically fascicular constrictions. And he recently published, I believe, a study a year ago talking about basically internal neural lysis of the nerve for these types of problems. So they mentioned these sort of five summary points, which I think really summarize it well. But yeah, I think, you know, this is just something to be on the lookout for. And that's pretty much it. I think, overall, when you look at the literature, most patients do okay, 76 to 93 percent, whether it's pronated syndrome or Lacerta syndrome. And so, you know, again, something to just kind of hang your hat on is really kind of the moral story here. So and that's it. Rob's going to talk about radial nerve compression. Thanks. And just a reminder, this is Cliff's talk, so he gets 99.9 percent credit here. I'm trying to double-click, which we learned from the last one, and I'm just turning blue. Did you do something different, Kevin? I did. I eventually just kind of kicked in or something. Maybe it's a triple-click. I need to do a triple-click. I mean, that means you'll have to do four to get yours to open. We go from one condition of debatable existence to another, although I do believe radial tunnel syndrome exists. I seem to see a lot of people who hurt there, but all right, so to get started, the anatomy of the radial nerve, remember, it comes off the posterior cord, C5 through T1, enters through the triangular space with the profunda brachii vessels, and then traverses from medial to lateral, posteriorly across the spiral groove, and then will travel and pierce the intramuscular septum. It's variable, but probably around 12 centimeters or so proximal to the lateral epicondyle. It's going to divide into its two branches, motor and sensory, proximal to the supinator. It's by about three centimeters proximal to the supinator, and then the PIN will head distally. Remember, it becomes at risk again at the radial neck surgically, and then it'll go down the IOM and be on the floor of the fourth dorsal compartment all the way to the dorsal wrist, where you can still dissect it free from the capsule. There's really just two sites of compression we're going to be speaking about. The first is at the proximal forum, the area of the radial tunnel, and we're going to very briefly cover Wartenberg's at the end, but there's almost no literature, sadly, on Wartenberg, so if you're looking for something ripe to study, if you can find Wartenberg's patients and study them, that would be good. The anatomy of the radial tunnel specifically, it's typically about five to eight centimeters. It starts at the radiocapitular joint proximally, and then really goes the full length of the supinator. If you think of the walls of it, you're going to have your radial wrist extensors over on the lateral side, and almost all surgical approaches will go through them. On the medial side is going to be your brachialis, and then your biceps right after it. The roof, so to speak, will first be those superficial fibers of the supinator that is piercing, and then the brachioradialis almost comes across the top from lateral to anterior at the mobile wad, so that'll be part of your roof as well. The sites of compression listed here, the radiocapitular joint is one. This is almost always going to be either a space-occupying lesion like a ganglion cyst from the joint, or you can have a synovial pannus like in rheumatoids. Usually just in an average patient without a cyst, it's really hard for this to be the point of compression. The leash of Henry, you will see, those are branches from the radial recurrent, and if you do enough radial tunnel releases, you will sometimes see a vessel that you need to take down and cauterize that seems to be pinching it. They describe an ECRB, aponeurotic margin, although I don't think I've ever noticed it or been aware of it personally. The arcate of Roche is considered probably the structure that places it most at compressive risk, and that's a little aponeurotic band right as it enters the supinator between the superficial and deep fibers. The supinator muscle itself can be a compressive source, and occasionally you can identify another little aponeurotic band where the PIN is exiting from the supinator distally. So radial tunnel syndrome versus PIN compressive neuropathy. So two very different things, right? One can be very clearly diagnosed because someone has weakness, they're EMG positive. One is classically EMG negative and is only pain, and whenever we have patients who just have pain and no diagnostic test that can explain it, it always becomes debatable how real it is, right? So that's what you end up with, and one is just a dorsolateral forearm pain with no weakness, versus little to no pain and pure motor weakness. It's debatable as far as gender predilection, but it seems maybe more common in women than men. As far as the prevalence of it, you can see just compared to carpal tunnel syndrome, carpal tunnel is about three to ten times more common than radial tunnel syndrome, and about 30 or 100 times more common than dorsal sensory radial nerve involvement. The age range classically listed there is 30 to 50, definitely more on the dominant side and it's described as being more in manual laborers, but I have to say I feel like I see a lot of people in their 20s or 30 that work at a computer that come in with forearm pain and are very tender at the radial tunnel. So I almost feel like the demographic of the disease has shifted a little bit as far as I've seen. They may have a history of other compressive neuropathies or stenosynthetis and synovitis conditions, maybe something genetic about this. Physical exam findings, the hallmark is going to be tenderness to palpation about four to five centimeters distal to the lateral epicondyle, and it should really be along a line to Lister's. So if you were to mark along your forearm down to Lister's, the tenderness should be along that line. They may very well have pain with resisted wrist or long finger extension, and the key is to try to differentiate it from lateral epicondylitis. And another key is to get it separated from a biceps tendinopathy, because those can be easily confused. Lowe and colleagues described this rule of nine, where really they said one and two, the red circles you see, are where people should be tender with radial tunnel. I actually think it's more like two and three, personally. One is high, as far as I'm concerned, as far as radial tunnel. And they say those other blues on the left side of the screen would certainly not be relevant. But I think it's a nice little slide to see. To me, five and six are where the distal biceps tendinopathy people are going to be tender. And you can see it's really not far away from two and three. It's right next to it. So you always want to have in your mind looking for that, because it's a very different condition, potentially treated differently. So just be in mind that I think it's often one that's hidden. Differential diagnosis. If there are the motor findings, you could have brachial plexus injury or brachial neuritis. Very concomitant with lateral epicondylitis would be on the lookout, and we mentioned biceps tendinitis. The only other thing, even in that neighborhood, is a posterior plica. But that should be all the way down in the soft spot. It should just be a different anatomic area. The role for diagnostics. X-rays, if you're really thinking about radiocapitular joint, would really be the one reason for that to look for any signs of, let's say, rheumatoid disease that could have a PANUS affecting the PIN if there's motor findings or a space-occupying cyst. As far as MRI, this is a little bit akin to what Aaron was talking about, I think, with some of the reasons to get an MRI there. Basically to look for a cyst, and it could show muscle denervation, although that's probably going to be in more your PIN syndrome rather than radial tunnel, where motor disease is, by definition, absent. An EMG will always be positive for a PIN syndrome, and it'll almost never be positive in radial tunnel. So treatment. Non-surgical. You try to do this as long as you can. Three to six or even nine months of just kind of basic avoidance of provocative activities. NSAIDs, because we do believe there is inflammation of the radial nerve contributing. A wrist splint can help a lot. Therapy maybe is more hand-holding than anything, although maybe some modalities could help. And I'm always surprised how much cortisone shots help these people, because when I'm giving them, I kind of have no idea where I am anatomically. You know, it's this big form, and you're pushing, and you say, does it hurt a lot here? Does it hurt more here or more here? And I typically go down with the needle at the point of max tenderness. I bump into the radius, and then from there on, I start to feel where the IOM is, where I plunge. I go back to that radius, and then just start to inject, and probably inject along almost a little spectrum heading immediately from there. But it really can get a lot of these patients out of your office and try to avoid a surgery that is only marginal. The surgical treatment, there's several ways to do it from the outside in, but really once you get to the deep interval, they're all going to be the same. So it's a matter of how posterior you want to be versus how anterior you want to be. Because the more posterior you are, you're going to see the more distal parts better, the supinator and the exit point. The more anterior you are, you're going to be able to see the radiocapitular joint better and the entry point. So as you can see this red line, the ECRB, the EDC Thompson approach is well known due to fracture work, is a bit of a middle of the road access point, versus if you look way up here, brachioradialis ECRL is going to be much more anterior, but make it hard to see the exit point. The one that I like the most is this ECRL, ECRB. It's a really nice interval because you have the red fibers of the ECRL above. You have the white of the EDC aponeurosis and the ECRB below. And it's a really nice interval to follow. And to me, it's the perfect balance of you can see just proximal enough to release a vascular leash if it's there, clearly the arcade approach, but a really safe visualization distally. And I think if you're going to go all the way to the end of the supinator, if you believe that's a potential problem, you've got to see it. Because if there's one thing you can do probably bad in this operation, it's undue tension on the recurrent little motor branches that head to the EDC and these patients can get a finger drop and that'll really bother them. So I think the spot you need to see really safely is if you're looking distally. Another example of an anterior approach is the transmuscular. So a volar approach, which would be all the way around between brachialis and brachioradialis, is really just going to give you proximal visualization. But if you have a radiocapitular cyst, that's probably the best approach to use. There's just a couple images showing that dorsal approach. So this one is going between brachioradialis and ECRL. So it's all red. Right? So you have two red muscles that you're working between. There you can see the obliquely entering PIN. Proximal is on the right, distal is on the left. This is a surgeon now using a tenotomy scissor to release the supinator. Almost imagine like you're going down the supinator in that schematic on the left until it's fully released. And this image shows those risky little recurrent motor branches that are headed up towards the muscle in this image. So what you don't want to do is put a retractor going up towards the top left where there's those little nerve branches you can see traversing up because those will go to sleep on you. Outcomes a little bit all over the board. So a success rate 67 to 92% is pretty broad. But I would kind of agree with that. Like the way I counsel patients on this is that I think the vast majority of patients you do the surgery on feel like you made them better. They're happy they had it done. If they had the option, they would do it again. But to me, that's not a home run operation. Like I'll mention that maybe almost like lateral epicondylitis, maybe around one-third of patients will still have some degree of ongoing pain, especially with heavier activities. So it's also hard because there's a fair amount of secondary gain in this population. A lot of them will be workers' compensation patients, and we know that that affects outcomes. Patient satisfaction rate, again, all over the board. Wardenburg syndrome, this last couple slides. Remember the anatomy of the superficial radial nerve. Up high, it's going to be lateral to the radial artery, and then it's going to run on the undersurface of the BR, heading all the way distally to where it will then lie on top of the flexors, and then pierce the fascia to become subcutaneous about six to seven centimeters proximal to the radiocarpal joint. And that's where the point of compression is believed to be. I know this slide is a little small. Hopefully you can still read it. The patients might endorse a history of handcuffs or tight jewelry as far as maybe some reason why this started. Main things you want to try to differentiate from would either be decrevains or intersection syndrome. That should be more musculoskeletal pain rather than neurologic. Really not any value to any diagnostics here, I don't think, even for anything that you're trying to differentiate it from. And then treatment will be pretty much the same conservatives I mentioned for radial tunnel. And then surgery for refractory, which will be just finding that pierce point through the fascia and cutting anything that looks tight. You know, if you need to recess some of the muscle of the outcroppers, but definitely generously releasing any of the fascia where it's becoming superficial. Thanks. So I'm going to be talking about evidence-based approach and diagnosis management of distal ulnar nerve compression at the wrist. Nothing to disclose. So the Ulnar Tunnel Syndrome is the second most common compression of the ulnar nerve behind the elbow. Traditionally thought to be a diagnosis based on history and exam. So anatomy is key. Briefly, refresher of the ulnar nerve before it enters the ulnar tunnel. It's the terminal branch of the medial cord which contains contributions from spinal root C8 to T1. Travels through the axilla and posterior to the medial epicondyle as it enters the forearm to give innervation to the FCU. And the FTPs of the ring and small finger. And about six to eight centimeters proximal to the pisiform, the ulnar nerve gives rise to the dorsal cutaneous branch. So muscle testing of the intrinsic innervated muscles of the ulnar nerve and sensation on the dorsal ulnar hand can help distinguish compression at the elbow versus the wrist. Now the ulnar tunnel originates at the proximal edge of the transverse or volocarpal ligament and extends distally to the fibrous arch of the hypothenar muscles at the level of the hook of the hamate. The boundaries of the tunnel vary along its course. Within the tunnel, the ulnar artery travels radial to the nerve and the nerve bifurcates into the superficial and deep motor branches. Approximately six millimeters distal to the distal pole of the pisiform. In 1969, Shea and McLean reported clinical descriptions of three different types of ulnar nerve compression syndromes based on its anatomical course. And in 1985, Gross and Gelberman published a cadaveric study to help understand the relationship between these symptoms and three different anatomic zones of compression of the nerve at the wrist. Type one or zone one is compression before the bifurcation of the nerve. So this manifests with weakness of all the ulnar innervated muscles and sensory deficits over the hypothenar eminence and sensory deficits of the small finger and the ulnar half of the ring finger. Zone two, compression affects exclusively the motor branch distal to the bifurcation of the nerve. In type three, compression of the superficial branch results in pure sensory loss within the small finger and the ulnar half of the ring finger. Now more recently, two more types based on location of the lesion or compression have been described. Type four is a pure motor deficit but occurs after the branch to the hypothenar muscles. In type five, pure motor but limited to the firstosoneurasi and adductor muscle. And that seems pretty straightforward. You know the anatomy, so based on the physical exam, one should be able to understand the type or zone of the lesion. But pathology doesn't always follow our attempts to divide lesions into types or zones or classifications. You can have pure sensory symptoms caused by a lesion that compresses only the radial palmar aspect of the nerve in zone one, and that's secondary to the topography of the ulnar nerve at the wrist. And cases of this have been reported. Now ganglia are the most reported, are reported by numerous studies to be the most common cause of ulnar tunnel syndrome. And they've been reported in all the zones of the ulnar tunnel. Anomalous anatomy or muscles have been reported to be responsible for 16% of cases. Trauma, whether it be repetitive such as cyclist palsy, or occupational from use of impact or vibratory tools can result in hypothenar syndrome. Or acute, such as hook of hamate fractures or other fractures or fracture dislocations secondary to swelling and traction. Some studies have reported that 1 5th to 1 3rd of patients with carpal tunnel have concurrent ulnar tunnel syndrome. And majority get relief of their symptoms with a carpal tunnel release. So presentation is gonna be variable based on history, anatomy, compression site, comorbidities and coexisting pathology. A thorough sensory, motor and or vascular exam needs to be performed. But again, not all patients present like the textbooks. They can present with vague complaints, associated complaints of parasitias in the median nerve distribution and possibly trace weakness. So if you tap hard enough on the ulnar nerve at the elbow, you can always obtain a positive to NELS. Therefore, the diagnosis can be challenging. So if the presentation is atypical for cubital tunnel, don't forget about ulnar tunnel. Use of nerve studies, EMGs, imaging can help confirm the diagnosis and provide useful information for preoperative planning. So evidence based recommendations. Unfortunately, there are no high level studies to make recommendations on the diagnosis of ulnar tunnel syndrome. But our understanding of the anatomy and improved diagnostic tools have improved our ability to more accurately localize the lesions of which again, mass lesions are the most common cause. Non-operative versus operative management really depends on the etiology, duration and severity of the presenting symptoms. Although conservative management can be successful in some cases such as cyclist palsy, the mainstay of treatment is surgical. Again, evidence based recommendations. Again, no randomized controlled studies or even large case series to make recommendations, but case reports have generally reported good to excellent results with surgical intervention, particularly for mass lesions. So in conclusion, ulnar tunnel syndrome is rare, but it is well described. The incidence or true incidence in propellants is difficult to accurately estimate as most published studies or case reports or review of case reports. One study reported ulnar tunnel syndrome occurring at about 1 20th the frequency of compression at the elbow. So as a consequence of the aforementioned, it's difficult to offer evidence based diagnosis and management recommendations. I think that again, most individuals with mass lesions get good results, be on the lookout along with the theme of the other studies. This is rare, rare, but you may, it'll see you if you don't recognize it. Thank you. Good morning, everybody. Thanks for attending this session. I'll be talking today about Neurogenic Thoracic Outlet Syndrome. So we'll talk a little bit about the diagnosis, treatment, and what's the evidence to guide different treatment strategies for management of neurogenic TOS. So Thoracic Outlet Syndrome is a group of disorders that occurs when arteries, veins, or nerves in the space between the clavicle and first rib are compressed. The vast majority of these are neurogenic in nature, probably about 90%, and 10% of cases have a vascular component. And really, there are several locations of compression, the interscalene triangle, as you can see on the image in the center, most cephalically, the costoclavicular space, and the coracopectoral triangle, more caudally. And symptoms endowed by extremity can include pain, numbness, as well as weakness. So the diagnosis is really an issue of some controversy. So what I find most useful in my practice is a physical examination. The Edson's test is one maneuver that has been described, as you see on the image on the top over here, where the patient is asked to turn the head to the same side, extend and abduct the shoulder, and take a deep breath. Personally, I don't find this maneuver that useful in my practice. I find the Roux's test and the upper limb tension test a lot more useful. So the Roux's test is when the patient bends the elbow at 90 degrees, abducts the shoulder at 90, and repeatedly opens and closes the fingers. And then the presence of a positive sign, there's rapid fatigue or reproduction of symptoms, such as numbness and pain in the upper extremity. The upper limb tension test, as you see here on the right side, is a graded maneuver, where first the arm is abducted, and then the wrist is extended, and the head is then turned to the opposite side. So with each gradation of the maneuver, the patient, if positive for neurogenic TOS, will have a worsening of the symptoms. EMG and MRI has been used as well, but again, personally, in my practice, I don't find it very useful for diagnosis of neurogenic TOS, because in most cases, these investigations will be normal. Sometimes on an X-ray, a cervical rib can be seen, and some people use scalene muscle blocks or Botox injections to treat cases of neurogenic TOS, and these have been shown to be effective. So treatment, in the first instance, relies on non-surgical and physical therapy, and if this does not work, then the next options for treatment are surgical, and this may include a supraclavicular incision with a scalenectomy with or without a first rib resection, infraclavicular incision, which normally would include a pec minor tenotomy, and other approaches that have been described include transexillary first rib resection as well as transthoracic robotic first rib resection, which in general are not performed by hand surgeons. So this is an example of a neurogenic TOS. One of my patients, on the left side, you can see before it's decompressed, you can see the phrenic nerve running over a very thick scalene anterior muscle, and on the right side, you can see the plexus very clearly over here once it's been decompressed, and this is pretty typical for supraclavicular approaches to neurogenic TOS. Here, another example where you can see, on the left side, you see this white fibrous bands, and these are pretty typical as well in compressing the trunks of the brachial plexus, and over here on the right side, you can see the phrenic nerve very well demonstrated as well as the upper, middle, and lower trunks of the brachial plexus after decompression. Sometimes there's more unusual pathology. This is an example where you can see the phrenic nerve running over the scalene, and then once everything is decompressed, you can see the subclavian artery as well as the trunks of the brachial plexus that have been retracted and the cervical rib in the center that is also encircled by a vessel loop, and then the cervical rib is resected, and there's good decompression of the brachial plexus. In the infraclavicular forecell, sometimes the pec minor is very prominent, as in this case, and you can see that after the pec minor is divided, the plexus is well visualized underneath. I want to spend some time talking about evidence-based practice as well, and really, this has several components. Firstly, is surgery effective? And secondly, is there a difference between the supraclavicular and transaxillary approach? And thirdly, and probably the most important thing that we consider in neurogenic TOS, is there a necessity for first rib resection? So I think the literature overwhelmingly supports that surgery is successful. No matter what you do, in good indications for the right patients, patients do get better. But really, I think the most important question in neurogenic TOS is should the first rib be removed? So first rib resection has the pros of simultaneous decompression of the thoracic outlet, and by definition, when you remove the first rib, all the function of the anterior and middle scalene muscles is eliminated, so you're gonna have a good decompression. But the cons are that when the first rib is resected, there's a higher risk of complications, such as hemorrhage, pneumothorax, brachial plexus injury from the retraction, chylothorax, as well as recurrence following incomplete first rib resection. So we did perform a systematic review and method analysis to just look at some of the published literature on this subject. We just did some of this research recently and came out with 23 final studies. Exclusion criteria are pretty standard, non-standard surgical approaches to the plexus, as well as non-English studies. So 23 studies meeting the inclusion criteria, 820 patients with a supraclavicular first rib resection, 485 with transexillary first rib resection, and 720 with supraclavicular rib-sparing scalenectomy. So the demographics-wise, the cohorts were pretty similar, and we found in terms of the preoperative dash score, there was no significant difference between the groups. This was pretty similarly bad among all the groups before surgery. After surgery, the dash score was lower in the rib-sparing scalenectomy group compared to the supraclavicular and transexillary first rib resection group, but this was not statistically significant. And we also looked at the cervical brachial symptom questionnaire. Again, no significant difference between the supraclavicular and transexillary approaches for first rib resection, and not enough data to look at this outcome measure for rib-sparing scalenectomy. And then we look at the visual analog scale, and again, no significant difference for supraclavicular and transexillary approaches for first rib resection and insufficient data for rib-sparing scalenectomy. What was significant, though, was when we look at the DER-CASH score of outcome measures, so this grades outcomes on excellent, good, fair, and poor, and we found that there was a statistically significant difference in the DER-CASH score between rib-sparing scalenectomy, which was better than supraclavicular first rib resection and better than transexillary first rib resection. So rib-sparing scalenectomy really seems to be the way to go. And then when you look at the complications, the rate of complications for transexillary first rib resection and supraclavicular first rib resection was also significantly higher than for rib-sparing scalenectomy. So again, as mentioned, there was a statistically significant higher complication rate for rib-sparing scalenectomy compared to supraclavicular first rib resection, and this was, again, more than transexillary first rib resection. So this is just a summary of the findings. Postoperative DER-CASH scores were less for the rib-sparing scalenectomy, but not statistically significant, and postoperative DER-CASH scores were significantly better for rib-sparing scalenectomy compared to transexillary first rib resection, which was the worst, and supraclavicular first rib resection was not so bad and kind of in between. So I think the data really, in terms of the evidence-based approach, it shows that the rib-sparing scalenectomy is equivalent to supraclavicular first rib resection and transexillary first rib resection in terms of outcomes, and I think in light of the significantly higher complication rate, the literature at this point suggests that the first-line treatment should be scalenectomy without first rib resection. Thank you very much for your attention. Thank you. Awesome. Any questions? I didn't see any in the Q&A function. Yeah. Thoughts? I think one initial thought I have actually is maybe thinking about sending it to neurology to work out for any genetic causes like, you know, liability to compression neuropathies. Not that that helps you surgically, but just something to think about as to why this particular person has three peripheral nerve compressions that responded initially to decompression and then recurred within a year. So this is a patient who got better and then had recurrent disease? Yeah, and it's a good question, because I think it then begs, what's the decision-making to find out if true recurrent disease is there? You know, is there something you can do? And like I think... I don't know if I undertreated recurrence, but unless there's a mechanical thing, like you did an in situ at the elbow and maybe they're subluxating, or you did an in situ and it turns out they're just someone who have, you know, Gelberman's traction phenomenon at the nerve. So I think there's a low threshold to convert, let's say, an in situ to a transposition maybe. Or if they're subluxating, something kind of obvious. But for me, I personally like to have an EMG that shows true worsening. So if they have a preoperative study, I know you get one four months after your release and it's worse than pre-op, I think that person probably would deserve a reoperation. Or if you didn't have a pre-op EMG and then you have two sequential studies, like at four months and nine months post-op, that show worsening function of whichever given nerve, then I would probably reoperate on that patient. But I don't know what the other panelists think. Other than that, I don't think I would do that. Yeah, I don't think I would do that. I mean, I think it's interesting that this is somebody that had so many nerve compression in the same limb in the first place, but, you know, I've occasionally seen it and there do seem to be certain people that it does recur and whether they tend to just scar more and, you know, in those handful of people when I've gone back, you do end up finding some scar around the nerve and sort of have to re-release, neuralyze, it almost looks worse than it did the first time. But, you know, in a patient that presented with so many nerve compressions in the first place, you know, I would, again, want some sort of evidence before I would want to reoperate on that person, whether that's diagnostic injections or EMG evidence. I will tend to use diagnostic injections for those patients, obviously it depends on which nerve we're talking about, sometimes it's just not feasible. But at least something that I can kind of hang my hat on before I would want to rush back because you just, you know, if you get there and you don't find anything and there end up being exactly the same, then you're sort of stuck. So I have a somewhat of a different thinking approach to these patients because fortunately or unfortunately I do see a lot of patients with atypical compression neuropathies because I treat neurogenic TOS and it just comes with the whole thing. And I think that it's a group of patients who are really scar formers, these are not that common. The majority of people you do surgery on, you know, anybody who does nerve surgery can tell you that the majority of them get better. But this population of patients, a small proportion keeps coming back. And I don't know if it's because they're scar formers or whatever, but somehow they just keep coming back with symptoms and people have operated on again and again. The problem with EMG postoperatively is that I found it's not reliable. And then MRI as well, very often for compression neuropathies does not show anything significant unless it's a really bad compression. So for me at least, I follow a different approach, I tend to go by clinical symptoms, but I try and do something different. So for example, obviously if I'm on a neuropathy, the first time we decompress it, the second time I would transpose it. And then if I did, for example, like a more proximal neuralysis or something like that, or I have a case of like radial tunnel, the first time I decompress it, the second time I try to put a nerve wrap around it, and then I have a case of very bad recurrent compression neuropathy of the median nerve, like in the medial arm after nerve grafting. The third time I took the patient back, I did a free flap to cover the nerve with good vascularized tissue. So after that, the patient's symptoms... And you think it's a cubital tunnel, yeah Yeah, I think Maybe the panel can correct me, but I'm I think there was actually a study at a wash you to that if in that population the the cubital tunnel release and transposition Actually do better than an in situ release so I think if if you had exhausted non-operative treatment and That person was miserable and you don't see any other reason why like Structurally with with with the elbow Then then if you are gonna do something with the ulnar nerve, I think I would transpose even though it's not unstable Yeah There's certainly a subset of young throwers that'll that'll have ulnar neuropathy I don't typically inject the cubital tunnel, but I And a 14-year-old kid is going to be a straight shooter. You know, if he gets better with a shot, then you could totally believe it. Do you think you'd inject someone? I don't inject ulnar nerves at the cubital tunnel. I think potentially with ultrasound, you could do that safely, but it just, I would worry about doing that safely. But I think, I mean, there's a little bit young, but, you know, there's a fairly high percentage of patients that come in, and, you know, exam-wise, they really seem like they have cubital tunnel, but there's, you know, they don't sublux, and they don't have any other evidence, and they seem to do okay with decompression and transposition. It's a fairly high percentage. So I think if the exam is fairly consistent with it, that's probably what it is. And certainly, you know, in the throwers that have, you know, underlying ligament pathology that end up needing to be reconstructed, I mean, those, at least in our practice, really all of those end up getting transposed, because they, one, from a safety standpoint, and that's somewhat controversial, but also a large percentage of those patients end up having ulnar neuropathy in addition to their ligament pathology, and they seem to do okay, even in that sort of age group. I similarly did not inject steroid in the cubital tunnel as well, but I've treated people with symptomatic subluxation and not much other symptoms with submuscular transposition, and I think it works well. So I guess, in your case, I would discuss with the patient, you know, what they want to do, and probably, if they want to have surgery, probably decompression and transposition. Thanks. There was a question about how do you determine whether you release only Listertis versus Pronator. I think I would go with your exam, like, if you have median, proximal median nerve weakness, or FPL, FTP, plus tenderness under Listertis, I would do that, but if it's more, you know, that plus, you know, Pronator, proximal form, then I think I would do a more thorough release. Any thoughts from you guys? I actually have seen intraoperatively both just Listertis compression alone, as well as more distal compression over the Pronator, hits of the Pronator and FDS arch. So I think it's really important to probably just expose the whole area, and make sure you decompress all points. Preoperatively, do you have any way to tell if you're going to do a much more limited release than, you know, the whole thing? I do not. I think it's hard to, because the diagnosis of Pronators in... Yeah, so I think that sometimes they can have compression neuropathies more distally as well. They can have spinal cord disease, cervical spine disease. So it's really important to examine the whole upper extremity. And sometimes I found this may occur delayed in a double-crush fashion. So you may actually decompress the thoracic outlet, and then they come back a few months later with a cubital tunnel or something like that as the nerve regenerates. So in that case, then I'll examine them again and make sure I haven't missed anything. The other thing, as you know, obviously, it's most important to make sure that if you don't do a first rib resection, do a complete scalenectomy, anterior and middle scalenectomy. Otherwise, the risk of the scalenes reforming is... Awesome, thanks guys.

thoracic outlet syndrome

compression

neurogenic TOS

physical examination

surgical interventions

first rib resection

rib-sparing scalenectomy

complications

research

efficacy