All right, I want to welcome everybody to AAP Virtual Diabetics today. My name is Sterling Herring, I'm a PGY3 at Vanderbilt. As always, I want to recognize and appreciate those of you who are on the front or who are or have been on the front lines of the COVID-19 pandemic, we recognize that this burden has not been shared equitably. So we appreciate those of you who have been more professionally or personally affected than the rest of us. And if there's anything that we as your colleagues can do to support you, please let us know. The goals of this online lecture series have been to augment didactic curricula that are ongoing at your home institutions, to offload overstretched faculty and provide learning opportunities for off-schedule residents, as we know there have been many logistical challenges associated with this pandemic, to develop more digital learning resources and to support physiatrists in general during the COVID-19 pandemic. We're going to keep everybody's video and audio muted except for our presenter. If you have any questions, you should be able to click on the participants list. And if you scroll up near the top, you should see my name, Sterling Herring, if you double click that, you'll be able to send me questions for our presenter, which I can then relay at appropriate times. Typically, that's at the end of the lecture, but also as invited. If you have any questions, suggestions or concerns, feel free to reach out to Candice Street there, her email is on the screen, or you can track us down via Twitter. Just a side note, today is our last round of these virtual didactic lectures. So we want to appreciate and recognize everybody who has participated up to this point, specifically I want to call out Candice at AAP and all of the members of the AAP Education Committee who have been incredibly supportive, done a lot of work, again, specifically Candice. So thank you, Candice, and all the AAP staff. So without further ado, we're excited to have Dr. Ensred here from the University of Oregon. Thank you for joining us today. Thanks for having me. It's great to be here. So you can click that green share screen button there and take over from me. Okay, great. Okay. Looks great. Okay, great. I'm going to, I'm just trying to minimize that there, great. I'm going to talk with you guys about a real interesting topic today, and it's something that has, as I'll show you some evidence for, has been really overlooked and is probably much more common than we realize. And I think by taking just a few of these key points to heart today, you will definitely be seeing patients with this condition and contributing significantly to their improved outcomes. So this talk is about what I like to call Bell's palsy of the brachial plexus. As I'll relate to you later, I can't claim the origin of that term, but I think it's a really good way to communicate with other providers and even with patients as well. So this is something, the eponym is Parsonage-Turner syndrome, and I'll talk about advances in understanding and treatment, of which there have been many. Okay. So the objectives of this talk are to describe the clinical syndrome of Parsonage-Turner, how to identify it in the acute stage, which muscles are most likely to be effective, and that's really a key point here. And if the most involved muscles aren't tested, this will likely be missed, and how to assess for their involvement, to describe some potential benefits of immunomodulation for Parsonage-Turner. And this is the type of immunomodulation that is well within the practice scope of physiatrists, and then be able to communicate and inform your patients in clear language about the expected outcomes of Parsonage-Turner syndrome. I'm going to start with a patient. This is a 37-year-old athletic nurse practitioner, and my chart message from September of 2017 was actually not to me, it was to her primary care physician. But it's interesting, because this is a communication from the very onset of Parsonage-Turner. She's writing because she injured her left shoulder in the morning, and she was playing with her kids. She heard a popping sound and had some mild tenderness, and then she went to work, and a few hours later, she began to have very significant pain, and couldn't raise her left arm, and had radiating pain that went down to her fingers. The next day, it felt a little bit better, but the pain was off and on. She's quite stoic, and decided to give it some time. But still after two weeks, she was experiencing pain with a number of motion positions. She had full range of motion, passive, but really prominent pain, daily since onset, and notably, it wakes her at night. And so she's asking, is there anything that I can do here? Should I just go to PT? So I'm going to take you back to the original article that described this syndrome. This is from 1948, and this really involved veterans that were soldiers in the Second World War. So this paper was published by Parsonage and Aldine Turner, and they talk about a syndrome of pain and flaccid paralysis of the muscles around the shoulder girl that occurred pretty often during the war years of 1941 to 1945, although previously, they'd been rare. And this is a nice case series of 136 cases. They talk about a clinical picture that pain starts suddenly across the top of the shoulder blade and may radiate down the upper arm or up into the neck, and the pain lasts for a circumscribed duration. And then after the onset of pain, a flaccid paralysis is noted of some of the muscles of the shoulder girdle. When the paralysis appears, the pain usually stops, but a dolate can last considerably longer. So what did they find in this original article? That about half of the patients were in the hospital, military hospitals, with other conditions when the syndrome started, and others had recently recovered from illness. Almost 100 of the 136 patients, a precipitating factor could be identified. And you can see the precipitating cause that they identified in these patients are associated operations, trauma, infections, which is interesting to put operations and infections in the same group. We've got a couple of patients with poliomyelitis, even some procedures such as lumbar punctures or a procedure that was done in the past called an air encephalogram, where you put air into this cerebral ventricle system. And other notes, they mentioned rapid development of weakness, again, after a period of pain, and less than half of the patients had sensory changes that couldn't be found on exam. About a third of the patients were bilateral, and all but the most severe cases improved over months. Before I go to the next slide, I should probably just, in the interest of full disclosure, those older gentlemen underneath the article there are actually not Parsonage and Turner. I looked all over and couldn't find their pictures, and I figured what, you know, all old British guys pretty much look the same. So I thought I might be able to slip it by you, but I'm coming clean on that. So where is this occurring? So there's been a lot of thought that it's occurring in the brachial plexus. And there are a lot of attempts to localize peripheral weakness to the brachial plexus. We've got a couple of diagrams here, I'm sure you've seen multiple ones yourself. And it's something that residents will get questioned on, and certainly in your in-service exams and your board exams, you may be asked to localize more distal weakness to a certain area of the brachial plexus. And you're going to need to be able to do that, but I want you to realize that that's really old school thinking, and I'll show you some pretty strong evidence that may actually not be accurate. I love this diagram, at least when thinking about the brachial plexus. This is done by an anatomy professor at the University of Illinois in Chicago, and she very generously was sharing it with the public on the Wikipedia page. It may not be there, but if you Google brachial plexus diagram in Google, and then just do an image search, you will eventually find this, because it's been indexed on other pages. And it really helps look at the brachial plexus and see how nerve roots course through the brachial plexus being color-coded. And we'll talk about the anatomy of these nerve cells, but that's very important. So why is this so important? So as I often discuss with patients, including yesterday, these spinal nerves, each sensory neuron and each motor neuron is headed to a specific group of either muscle fibers, in the case of motor nerve cells, or a specific area of tissue, as soon as it's formed at the nuclei there, either in the anterior horn or the dorsal root ganglion. So if you affect something proximally, you may get a focal abnormality there. If you've ever done any wiring, attempted house wiring or anything like that, you know, I've got some wires there on the left, and if you cut, say, the red wire anywhere along the length, the distal outcome or at the electrical device will be the same. So we have to be kind of careful about localizing distal deficits to a specific location. So what's happening here? So these peripheral nerves, myelin is around them, very tightly wrapped lipid bilayers, and it has a real specialized protein pattern that is very susceptible to stress-induced autoimmune attack because it's a repeating sequence, and we've got just a sample antibody or immunoglobulin there on the bottom left, and this goes out seeking a certain pattern and looks for things that mimic or match this pattern, and you can see in this animation here, it's going to match up with this repeating sequence here. It's going to attack it and cause injury. And in fact, the slide, the histo slide on the left is inflammation and destruction of a blood vessel there in the center, and all those dark blue dots are inflammatory cells. So because of this myelin structure, nerve cells are very susceptible to autoimmune reactions like in the central nervous system, multiple sclerosis. So in terms of trying to describe this syndrome, I was on the inpatient service at Brigham and Women's in my previous position in Boston, and we had a patient on the service with Parsonage Turner, and I'd worked there for a number of years and knew most of the nursing staff pretty well, and one came up to me and said, hey, you know, Eric, what is this Parsonage Turner stuff? I don't quite understand what's going on with this shoulder. And I described to Sean what the syndrome was, and he looked at me and he said, oh, so you mean it's like Bell's palsy of the brachial plexus, to which I said, Sean, you're wicked smart. And I think that's such a great way to describe it, and I'll talk about some similarities of this to Bell's palsy, because Bell's palsy is something that many people recognize, both medical providers and patients themselves. So Bell's palsy is very analogous. It's an autoimmune attack on the facial nerve, and you can see in this gentleman in the picture on the left, he's being asked to smile, and his right face is not activating because he's got a right facial nerve palsy from Bell's palsy. And there's been a lot of really well-done research on this, and because of the inflammation of the nerve and how that damages the axon within the myelin, there really is a much improved outcome of Bell's palsy with treatment with steroids. And you can see here that satisfactory recovery, a total number of patients and patients who didn't get steroids was about 69%, and then you have a nearly 20% increase in treated patients. So it's much, much really standard of care and very effective in what can actually be pretty debilitating for someone, a long-term severe Bell's palsy. If you ever have a chance, I hope you don't, but Bell's palsy can rarely occur bilateral, and that's actually very devastating for patients because they lose facial expression a significant amount, which you realize is a very important part of communication. And that MRI there is just showing the yellow area of the inflamed facial nerve on the right side there. So this is something that is an autoimmune monophasic attack on peripheral nerve that responds very well to steroids. So this is a great paper. It's the largest study of Parsonage-Turner, but a lot of the lessons from this paper haven't really gotten out into clinical practice, and in fact, not as much to the type of people who might see these patients. I'll mention sports medicine specialists in particular. And this is from 2006, so sometimes things are very slow to spread in kind of the medical consciousness. So this paper is a very well-done paper on almost 250 patients with Parsonage-Turner syndrome. Parsonage-Turner syndrome has so many different names. You'll have brachial neuritis, neurologic amyotrophy, which they use here. I just prefer to use the eponym because I think the referrers and the providers are more likely to have heard of that than many of the other terms. So this is a national referral center. All patients with Parsonage-Turner in the Netherlands, 95% were seen at the center, and nearly four out of five were prospective seen acutely. So they referred in, you know, it's a small country that's pretty dense, and it's really able to do these type of studies. All patients with an attack of acute painful patchy brachial or lumbosacral plexopathy that followed a monophasic course. And they included patients with paresis or weakness before pain, painless but otherwise typical attacks, and attacks with nerves outside of the brachial plexus. They did a visual analog scale, you know, very methodical, severity of paresis, distribution, pain relief meds, their subjective overall recovery, and very importantly for us as physiatrists, their functional outcome. And so let's take a look at this large group of patients. So the patient characteristics. It was about two-thirds male, which is atypical for autoimmune disease. About 87% or 7% were right-handed. And as a left-hander, I was reassured by this, that one needn't worry that right, left-handers are at increased risk. Interestingly, about a fifth of the patients had a family history of Parsonage-Turner syndrome. It's hitting people on a mean, it can occur at any age, but the mean age of onset is 41. So not boomers and not millennials right there in the middle. mean number of attacks, 1.5. Really importantly here, and why we need to improve our recognition of this, the mean time to diagnosis after onset of symptoms was 44 weeks, so nearly four months. And nearly two thirds of the patients initially received another diagnosis, and you'll see this very commonly, that patients with Parsonage-Turner will be diagnosed with a cervical radiculopathy because of cervical MRI with very nonspecific changes, but often it's a C5-6 or glenohumeral pathology of the shoulder joint. And so what are the characteristics of these attacks? 90%, so not all, so this can be painless, but nine out of 10 started with typical pain. The onset is usually over a few hours, and contrast this with an acute disc herniation, having had one of those as a resident, drying off my hair and feeling a pop in my neck, and then the pain's shooting down into the middle finger on the right hand, and I'm like, oh crap, here's a C7. But you know, the time course is very different. This is usually a little slower. When absent initially, two thirds of those eventually develop pain, and notably about 61% started at night, almost two thirds, and nighttime pain tends to be very prominent in these patients. And in this series, around a quarter of the patients were bilateral. So nerves outside of the brachial plexus were quite common at about one out of five. It can also occur in the lumbosacral plexus. An important thing to note is that nearly one out of 10 had phrenic nerve involvement, and this, many people, Sam Weiner, the PM&R Chair at University of Nebraska just published a really good study on diaphragmatic paraparalysis in Parsonage-Turner, and it's very common and under-recognized, and when you see a patient who's got a hemidiaphragm, or sometimes even bilateral diaphragm herpes, this is something to really think about. It occasionally causes recurrent laryngeal nerve paralysis. So about a quarter of the patients had recurrent attacks at an average of about two years to the reoccurrence. So what is the pain like? So nearly all patients, again, experienced typical severe pain at some point during the duration. Continuous initial pain, it's very severe. Look at that, nine out of 10, or 89%, the pain was worse at night. It can be increased by movement or pressure on a limb. You can have a LeSiege sign of the arm or pain with elevation of the arm, and here's a real important point for us. I think we're spine-centric and probably overly spine-centric, so a neck bend to the contralateral side increases the pain because that stretches the brachial plexus as opposed to a radiculopathy, which a neck bend to the ipsilateral side would increase pain. The median severe pain duration was about three weeks, longer in males, and then about two-thirds have subsequent musculoskeletal-type pain. A significant portion developed adhesive capsulitis and subluxation, and the location of the pain, most likely radiating from the shoulder to the arm, about a third will tell you that it radiates from the cervical spine, about 20% from the scapular chest into the arm. And this is a very severe pain, and in this setting, the short-term use of narcotics can be very helpful with all the precautions that we are normally doing these days. So how about the weakness that's involved here? So the first sign of weakness, only about a third have weakness within a day of the pain onset, and it takes up to a couple of weeks to have the onset of pain. Usually it's up to about two days, or two weeks, the mean onset, and this is similar to when we think about an acute nerve injury and how long it takes abnormalities to show up on an EMG. So the distribution of weakness, it can occur in the middle or lower plexus, but the upper part of the plexus is most common, about three-fourths of the patients, and about half of the patients have long thoracic nerve involvement affecting the serratus anterior, and this is very commonly affected. So you can look at the muscles affected in that table on the right, table four, and look at the three muscles that are the most affected, the infraspinatus, the serratus anterior, and the supraspinatus. And I'll talk about how to evaluate these. The infraspinatus is actually a very difficult, if not possible, muscle to isolate. A lot of people will say, oh, it's the first 15 degrees of abduction, that's kind of a folklore. If you put your hand on your contralateral deltoid and abduct your elbow 15 degrees, you'll feel a lot of deltoid activation, and it's a much, much larger muscle, but we can effectively isolate the serratus anterior and the supraspinatus. So let's talk about infraspinatus force testing. Sometimes you'll see people doing it like the method on the left, on one side, and pushing, and this is really not very accurate. It's hindered because the patient's trunk will rotate when you're pushing against the wrist. So I really recommend this method on the right, where you have the patient, I have the patient externally rotate their forearms. I ask them to pinch their ribcage with their elbows, hold the elbows against the ribcage, and then you push, not in on the wrist, because that would induce an additional joint with range of motion, or excuse me, not on the fist, I didn't make fist, but you're pushing on the wrist, and you can get a very accurate side-to-side comparison, and you shouldn't be able to discern a dominant versus a non-dominant arm here, unless there's someone like a bow hunter, or someone who does a lot of physical work with just, it's very asymmetric. I could go on about what a great muscle, the infraspinatus is also much more sensitive than either the deltoid or the bicep for a C5 radiculopathy, if you don't believe that, try it out on some patients with known C5 radiculopathy, and it's also a muscle that's really affected in a hemiparesis, and you can help to discern a mild hemiparesis or a more severe hemiparesis with this. This, the weakness of the intraspinatus is why a hemiplegic patient has the arm internally rotated and holds the fist against the chest, because they can't externally rotate the arm. So in patients, if you're doing stroke rehab, check that on patients who have a hemiparesis, and you'll find that it's got a really high sensitivity. So for the take-home exam on this, on weakness, check the intraspinatus force, and then you really need to take the shirt off and look for inferior angle scapular winging, because remember, the serratus anterior is the most commonly, you know, very affected nerve in these patients and muscle, and it's especially good to differentiate from the rotator cuff or a supraspinatus tendinitis. You can't really do this through the, through, you know, through a gown. You can pull the gown to the side. In female patients, if we usually have them, unfortunately, like a strong bra will fixate the scapula, leading to under-diagnosis of this in female patients, so it's often helpful to have them take off the bra and then just weave in tape with a couple pieces of tape, the gown, along the side of the thorax there. So I'm gonna show you where, this is something that's in publication in the publication process, but this is a patient who I saw who was a 30-year-old right-handed male who was involved in police academy training. He's currently a police officer. In the fall of 2018, and during the last session of defensive tactics class, it was, you know, quite vigorous, and he noted some shoulder, soreness of the shoulder that evening, and the next day, he was doing burpees and push-ups and noted right scapular instability, and then that initial mild pain got very severe in the left shoulder to where it woke him up in the middle of the night. Again, a typical nocturnal Parsonage-Turner pain, and he never really had significant pain in the right shoulder, and he was unsignificant or unaware of weakness in the left arm. So the interesting thing about this patient is that in one patient, you can see both types of scapular winging, and on the left side, he's got rhomboid, dorsal scapular, and trapezius, or spinal accessory nerve weakness, so there's the scapula goes out laterally, and on the right side, he's got serratus anterior weakness. So I'm gonna actually pull up here, we've got a video that we're gonna be part of the publication here, and I'm gonna show that to you here. This will be coming out later this year. See these, again, these are two, it's real helpful because you can see both mechanisms in one patient. So when you do shoulder flexion, you're looking for medial scapular winging. So watch, the green arrow is the normal, you're looking at the inferior angle, and see it going out laterally as the serratus anterior contracts, and see how the right side, you start getting some winging of the inferior angle, and it doesn't go out laterally, because on the right side, he has weakness of the serratus anterior, and this is what you check with shoulder flexion. Now we're gonna have him return to baseline, and we're gonna have him abduct the arms, you always want the elbows to be extended, so you get the full force of that fulcrum. And this is lateral scapular winging. So look at that left scapula on the left side of your screen. You can look at the right and see how that medial border comes in towards the midline, so the scapula on the left is actually winging laterally, because see the weakness, see that medial edge of the scapula is not being pulled in. Okay, let me get the PowerPoint up there, that's the best video that we have, the one that has been submitted. So let's talk about sensory symptoms, about a third of the patients don't report them, about three-fourths of patients or two-thirds do. On clinical exam, this series, they were able to find large number of patients with a mild sensory disturbance, hypesthesia, paresthesias, and they were most common over the deltoid or lateral arm, you can see on the table there on the right. And they also looked into predisposing factors or antecedent events, and in their series, about half reported an event, and those about, half of those occurred the week before the attack, and about 17% had occurred hours before. In my experience, that tends to be more common when it's associated with the stress of vigorous physical activity. And likely what's happening, what's the common denominator of these things like surgery, delivery, stress, trauma, exercise, you're stressing the body, which puts the immune system on a higher state of alert, and you're more likely to have a more vigorous response. I even found one paper that, this was kind of, I guess making a lemon out of lemonades, but a physician who, a patient developed Parsonage-Turner after Botox injections, and they published a paper on it. So lots of things can set off a heightened and inaccurate immune response. So lab tests, EMG, as I mentioned, you have to wait. It's not gonna be good in the very acute phase, so this is a clinical diagnosis. It's best at three weeks or more after symptom of onset. They did it, 87% of the patients, and almost all of those, it was abnormal. And we'll talk about, it's going to be missed if you just check for nerve roots, and you, if you don't carefully check the uncommon muscles on EMG, such as infraspinatus and supraspinatus and serratus anterior, and those aren't in most groups that are sampled for cervical radiculopathy. So imaging patients about, imaging studies, about a third of the patients had a chest x-ray, and of those patients, about 4% had elevated one or both diaphragms due to phrenic nerve involvement. So again, not the usual and not common, but very, you know, always think of Parsonage-Turner in a patient with diaphragm weakness. So you might want to, for example, do a shoulder exam with their posterior shoulder exposed and look for scapular winging with flexion and abduction. So 44% of the patients had an MRI of the cervical spine, and to no surprise, half of those scans showed degenerative changes. And that's really a problem with musculoskeletal imaging, particularly MRI, is that there's a very poor specificity. And about 20% had brachial plexus MRI, and only three were abnormal. I'll talk about this later, but if you're gonna do MRI imaging of the brachial plexus to find something, you really need very specialized imaging. So let's talk about doing these uncommon muscles on needle EMG. So when you do needle EMG of the infraspinatus, it's really helpful to divide the edge of the medial border of the scapula to the edge of the scapula at the humeral head into thirds. And the infraspinatus, for example, is thick and dense more medially, and then very rapidly tapers. So you want to divide that distance into thirds, feel the medial edge of the scapula, and then go down vertically. So for the infraspinatus, you want to come from superior to inferior, so you're going straight down into that groove between the scapular spine and the scapula. And then the black arrow there is you go again about a third of the way in from the medial border, and you go perpendicular to the skin to check the infraspinatus. I may have been, so the top is the supraspinatus, and the bottom is the infraspinatus. The infraspinatus, you want to go perpendicular to the skin, and you want to go down to the bone and tell the patient, this is going to tap off the bone, and you'll feel a sharp tap to ensure that you're not recording from the trapezius. And the bone there will keep you from going in to the thorax and causing neuromuscular. So the serratus anterior, sometimes there's a lot of hesitancy to do this, and I like this Mayo version, comes from a Mayo publication, about how you have the patient's side line, and the mid or anterior axillary line, you isolate one rib by placing your two fingers in the adjacent inner spaces. So you've blocked off the inner spaces, and you've got just the rib between the fingers, and then you put the needle in there, and again, you tell the patient it's going to tap off the bone, which is going to feel sharp, okay? And that way, you're preventing yourself from causing a pneumothorax by going into the rib. So you go directly between the fingers that are straddling tightly the rib. And this actually is not a particularly difficult muscle to sample. Of course, you know, if there's a lot of subcutaneous tissue, it's harder. Oh, sorry, I have a strong Hoffman reflex. So functional recovery, this is really important for us. What were these functional recovery rates? So full recovery, according to the patients here, and inability to work in this Dutch study were really, really high. And we can look at persistent pain at three years or more, still about 60% have musculoskeletal pain, and close to 20% have neuropathic pain. Residual weakness. Nearly all patients, if the most commonly effective muscles were checked, had some mild weakness, you know, MRC score of four to five. The majority of patients did it three years out. So you will find some older publications that say, oh, well, patients are, you know, it's nearly 100% recovery and so on. That's not really accurate, and if you look at those publications in detail, you'll see that almost without exception, they didn't look at the infraspinatus and the serratus anterior. So the subjective overall recovery. So this was, you know, surprising to me, and still is kind of discordant with what I see in the United States. But the subjective overall recovery, only about a third or so of the patients, between 30 and 40%, had an 80 to 100% recovery, and about, oh, around 20, 20 to 30% had less than 50% recovery. And I actually have seen outcomes much better than this, and it got me to wonder, why are these outcomes so poor? And I'm just gonna point out this little story here that before I went to medical school, I lived and studied and worked in Shanghai. That's me on the bottom left with the little hedgehog there and a couple of friends. And this is when they had the Tiananmen demonstrations, and the university shut down. And there weren't a lot of foreigners living in Shanghai at the time. It's a much different place now if you've been there recently. But every once in a while, I'd see these kind of scruffy backpackers. There were very few foreigners, so I would say, hey, what are you up to? What are you doing? And there seemed to be a string of these Dutch backpackers, and they'd tell me, oh, I'm traveling the world. For how long? A year. And I'm like, well, how can you afford that? Or two years, sometimes three years, and go, oh, well, I'm on the Dole or disability payments from the Dutch government. And I remember one dentist in particular who was getting 75% of his salary. And he looked physically very good to me. Of course, I hadn't done residency training, but he was carrying a huge backpack and looked fine. So I got to wonder, is there, and this has come, for the AAPM&R, I recently was on an outcome study of orthopedic trauma with a big group of other physicians. And there's some physiatrists, I think Heidi Prather comes to mind, who's done research on PROMIS scores. And you really cannot estimate non-physiologic factors in patient outcomes. So in the Netherlands, the disability payments are that there's no legal maximum for levels of benefits. And some schemes result in, as I heard from that dentist, 70 to 80% of former salary and pay, but apparently some people can get even 100%. So you are actually paid really well for not getting better. And that can have a real significant impact on outcomes. I'm not sure we talk about that enough. I certainly encounter it in practice a lot. So back to Bell's palsy. So we've got this autoimmune attack on the facial nerve, and patients get so much better with steroids. And we talked about this autoimmune attack. And this being, you can tamper this or quell this down with steroids. So this is a great paper by the same group, and again, something that hasn't gotten into a widespread clinical practice as well as it would be very good for outcomes to do. And this is on an evaluation of prednisolone treatment in the acute phase of Parsonage-Turner. And it was an observational study. Retrospective, they looked at 50 patients, and they looked at patients treated within one month of symptom onset with a real simple regime of 60 milligrams a day for seven days, and then you taper over the next six days, first by 10 milligrams a day, and when you get to 10, then you go to five. So we're talking about a 13-day course. And I looked into prednisolone. It's a medication we don't use really in the United States. And prednisone is much cheaper. And the only difference is that prednisolone is usually seen as being better when patients with significant liver disease, but really they're equivalent. So this paper, you can do this same treatment scheme with prednisone. So look at this median time to pain relief. In untreated patients, about 21 days versus 13 days, really significant difference in the patients who got the very short 13-day course of steroids. Recovery of strength within one month tripled in patients who got steroids, nearly a fifth versus only 6% in the patients who didn't get it. Full functional recovery from the first year in the patients who didn't get steroids, 1%. In the patients who got steroids, 12 times as high. 12% had full, complete recovery. And this is even in that setting in Holland, which I said there are some powerful factors that may hinder reaching full recovery. So unfortunately, a double-blind study, the people who did this study, the results were so strong that they were unable to get a double-blind study approved, but it's become their clinical practice. And I use it commonly when I see the patients within 30 days and have seen also a string of much better than expected outcomes. So this is the type of finger picture that you may see on, again, an in-service exam or a board exam. And you'll want to recognize that this is an anterior interosseous neuropathy because there's weakness of the flexor digitorum profundus, that distal digit of the index finger, and the flexor pollicis longus, the distal digit of the thumb, both supplied by the AIN or the anterior interosseous nerve. And talking about nerve localization, so we can see the anterior interosseous nerve, the legend is on the bottom right there. And when patients have this, oftentimes hand surgeons will think, well, it must be at the branch point and we should go in and dig that out and release it. Because it's in the anterior interosseous nerve, and the other median nerve muscles aren't affected, it must be right there at the branch point. And this is this kind of mislocalization I've kind of been alluding to earlier in the talk. So this is a great study. This is from 2014 on anterior interosseous nerve syndrome. And they did very specialized nerve imaging, neurography. And you can see, these are the 20 patients. And you can see in cross section of the upper arm, not in the forearm, the nerve, the medial nerve fascicles are always the ones that are affected in these patients. And that's where the AIN fibers are in the median nerve in the upper arm. So actually, the injury is localized to the upper arm, not at the branch point, just along the wires. And you can see this single subject on the left there, the group avalanche in the middle. And then again, the nerve fibers are going to a specific point as soon as they leave. And often, as you might see in the spinal cord, there's some organization and the anterior interosseous fibers are posterior and medial. And so what they also found in these areas that there could be some narrowing of the nerve there, like sclerosis of the epineurium. And they were able to release this surgically. So there is a surgical indication here. Here's another paper from 2016. And if you'll look at C in particular, see the narrowing of the nerve there with a constriction. And you can see on the right there where it's narrowed. And they're able to release that and have a much better outcome, release the epineurium. So there is a surgical indication here for patients who don't get better. You can see E in the top right there, the narrowing, and then right below there, they've released it and the nerve is perfusing much better. Here's another paper from last year showing that hourglass-like vesicular nerve constriction in the top on ultrasound, which I must say is very difficult to get a good longitudinal picture like that on ultrasound. Gross anatomy below that, and then the microscopic anatomy below that. So we're just about ready to finish up here. Will you see Parsonage-Turner syndrome? Well, not if you don't look for it and not if you don't know what to look for. Now, I can't see the chat box at this time, but does anybody see anything funny in that picture? You really have to know what to look for. If I told you to look for a mountain lion, would anyone see anything funny in that picture? I'm looking, oh, yeah, there he is. And now it becomes a little more obvious, doesn't it? And they're out there, trust me, a year or two ago, someone, a solo hiker got killed by one on Mount Hood, very close to where I live. So, but you know, once you're looking for a specific thing, you're much more likely to find it. And so quickly, this is a great paper from 2015 on incidents of Parsonage-Turner in a primary care setting. In a patient of nearly 15,000 patients, they had an annualized incident rate of one per thousand, which is about a half to a third as much as myocardial infarctions. And compare that with TIA, it's much more common compared to a really good stroke study on incidents of TIA from Mayo and Olmstead County. So it's much, much more common than we realize, and medical and surgical treatment are possible. So summary and objectives here, I appreciate your time, and there's a lot to say, I've had to cut this down. But think of Parsonage-Turner syndrome early and often with subacute onset neck, shoulder, arm pain. And remember, you know, not everyone took, you know, general anatomy in medical school or is so specialized in musculoskeletal as you. And you know, as it is in the low back or hip, neck for patients is not necessarily the same as what we mean right above the clavicle for many patients is the neck. Examine the infraspinatus and scapular wing, it really doesn't take much time. And then treat, have a low threshold to treat with this very short steroid course. And, you know, try and start within 30 days of the onset of symptoms. You know, logically, the earlier, the better. And I have treated patients after 30 days at their request, but I really, you know, wonder if there's gonna be any effect. You know, advise patients, inform them, outcome is for significant recovery in three years, it may be incomplete. Get into specialized shoulder PT with a PT who's interested in this. And you can communicate with the PT or a physiatrist. And this will be very helpful. So don't over-localize to the brachial plexus. The attack can be anywhere along the peripheral neuron pathways. This is really a brachial plexopathy. And in patients without significant improvement may benefit. This is only done, as far as I know, at the hospital special surgery in the United States at this time, but it may be more common. Surgical release of vocal nerve constriction. My address is, email address is just my name at OHSU. Feel free to email me. And I was hoping I could tell you guys at the end of the talk that I was headed to that mountain where they're still skiing for the next three days, but I tried to get a lift ticket yesterday at two o'clock and they sold out in five minutes. So I'll be in my windowless office working on my Grand Rounds talk. What mountain is that? That's Mount Hood. Mount Hood, okay. Yeah, yeah. Well, I'm sorry you couldn't get a lift ticket, but I'm glad you were here with us today. So thank you very much for that discussion. That was very helpful. This is something that I think we come across, but certainly I've never had, I've never been exposed to this level of detail on before. So I appreciate that. Going back to this kind of, you know, picking up on your comment about looking at the outcomes of the Dutch study and your experiences there, I think is interesting. Kind of highlighted concept in health economics called moral hazard, this tendency to over-utilize low or no cost assets. A RAND insurance trial. If anybody hasn't read about the RAND health insurance experiment with Bob Brook, go take a look at that. It kind of taught us most of what we know about health economics. But yeah, with the Dutch, that was an interesting example of how countries often have to choose between high sensitivity and high specificity for some of their social safety nets. And then of course, in the news, you hear about the false positives and false negatives. That's an interesting kind of side note to that conversation and then kind of also illustrates the importance of looking at the definitions of the paper, right? How did they define recovery? And I think too often we look at a journal article and look at, you know, read the abstract and say, oh, well only this number recovered or wow, a whopping this number recovered. And we don't look at the definitions of those things. So that's a valid point, I think. Yeah. But thank you very much. This is fantastic. I'm gonna leave this up both because it's a beautiful picture and because your email is right there on the screen. I'm not seeing any questions right this minute, but if anybody has any, please feel free to send them through. But they can email you directly at that email address if they have questions. Yeah, yeah. Many of our participants are now watching on the videos later in the day just because of, you know, ramping up clinical responsibilities. And so we're finding that some of these questions are coming, you know, as people are getting to watch these videos. So you may get a trickling of questions later in the day, later in the week, even later in the year as some people are still deployed to ICUs and whatnot. Oh, that's fine. I'm really interested in this. And I feel like it's a area that's under-recognized and we can really help patients. So I'm actually working with an emergency medicine physician who was sent to me and didn't get the diagnosis. It occurred around the birth of her baby about nine months ago. And we're thinking about starting a patient advocacy group for this. Oh, wow. Yeah, yeah. That's really, that's really interesting. But thank you so much. This has been phenomenal. Like I said, certainly more information than I've ever seen about Parkinson's disorder, but this is something that I often come across in terms of patient has a history of this or it's on the differential. So I appreciate very much you're willing to spend time with us today and explain this to us. Okay, thanks. Thank you very much. It was great and the AAP is terrific. So I'm happy to participate. Thank you. So for all of our participants today, again, these videos are available on the website there, physiatry.org slash webinars. You can reach out to him directly at his email address there on the screen, or you can track any of us down on Twitter. We have a few more minutes till the next lecture starts. Thank you everybody for joining us today. And we are excited for our next lecture. Thank you again for joining us. Thanks. Thanks. Thanks, Sterling. Thanks everybody. Yep. Thanks Candace.

Parsonage-Turner syndrome

brachial neuritis

neurologic amyotrophy

shoulder and arm pain

muscle weakness

muscle atrophy

infraspinatus examination

scapular winging

steroid treatment