So, one of the highlights of this course every year has been the addition of a musculoskeletal radiologist. There'll be three sessions today, short sessions, and this year we welcome Dr. Joseph Yu from The Ohio State University, and you'll see that these are meant to be very clinically relevant reviews of radiology. Thanks, Dr. Wu. Thank you, Bruce and Chris, for the invitation. Good morning, everyone. In following these excellent lectures that we've had this morning, what I'm going to do over the next 15 minutes, maybe a little longer since we finished a little early, we're going to cover some of the imaging findings that are important in the shoulder, and we're going to emphasize some of these topics that are listed in the slide. One of the most important questions that I get asked is, when you do an MRI in 2019, which is the best type of MRI? Is it a 1.5 conventional MRI? Is it a 3T MRI, or is it an MR arthrography? And by the literature in 2019, an MRA and a 3T MRI are now considered nearly equivalent, but in my opinion, MRA still has certain advantages in being able to distend the joint, and obviously, it optimizes the capsule labral demarcation and imbibition of detachments and tears. But one of the unique features of an MR arthrogram is the abducted external rotation view. And as Dr. Bishop indicated, it's important in identifying the anterior band of the IGH. The way we do this, we position the arm over the head in an abducted external rotation view. We put the coil in the axilla, and we draw a prescription grid along the long axis of the humerus. And with that position, as we already heard, we see the anterior band of the inferior glenohumeral ligament very beautifully, and it puts tension on the anterior inferior labrum, really allowing interrogation of the integrity of that piece of the labrum. The anterior side of the shoulder is on this direction with this view, so this is the anterior capsule, and this is the undersurface of the rotator cuff. Most normal labral morphology is going to be triangular. However, the rounded morphology can be seen in about 30% of normal labra, and is most commonly seen in the posterior labrum. The second thing that we typically see on MRIs is the undercutting of cartilage, demarcating the labrum and the glenoid bone. So typically, these are going to be intermediate in signal intensity, and the way that you identify intermediate versus high is that you just need to find an area that's going to show high intensity, which is typically the fluid, so you can always make that direct comparison between the undercutting and the fluid in the joint. Now we've heard a little bit about the normal variance, and this is important testable material because it really can interplay on a lot of different things that mimic pathology. So we're going to talk about the superior labral, excuse me, the sublabral recess and the foramen and the buffer complex, but all of these occur between the 11 and 3 o'clock positions, so this is really the target site that we're going to be concentrating on for the next couple minutes. The sublabral recess or the sublabral sulcus is nothing more than a cleft located between a normal superior labrum and the superior portion of the glenoid rim, and it's very common. We see it in about three-fourths of people. Now typically, it's thin and smooth, but it may extend to the sublabral foramen. Typically it can extend quite a bit, and it can kind of overlap with some of the morphology of slap lesions, so what makes this not a slap? Well, we want to look for very smooth margins, and we want to see integrity of the periosteal labral complex above the labrum, and then certainly it should not include the biceps anchor. The sublabral foramen is seen in about 11 to 15% of MR arthrographies studies. It represents focal detachment at the one to three o'clock position, so typically you can see it right from above the level of the supraglenoid tubercle and extends above the level of the equator. The high signal intensity parallels the glenoid in both the coronal and axial plane. Now the mnemonic for fluid-sensitive sequences, it doesn't matter where you're looking at a gradient sequence or a proton density with a high TE or T2-weighted sequence, all of that different types of nomenclature, if the water is white, then it's fluid-sensitive, and that's helpful for all of the studies that we're going to be reviewing today. I included a lot of questions in the talk, and really the handout is much more comprehensive than the 15 minutes that I have, so in order to follow through with the questions, I demarcated them by number, so make sure that if you're writing down any notes, that you put in the appropriate questions. So in this patient, 42-year-old with rotator cuff symptoms, we see the very abnormal rotator cuff. I just want to point out this finding here. So this is a normal sublabral foramen. Notice the detachment of the anterior labrum from the anterior glenoid rim. You want to find the location of the coracoid process because this abnormality is always going to be located above the level of the equator, so when you look at that, make sure that you find the coracoid process. Now the Beaufort complex is seen in about 1.5% of patients. The key finding is this absence of the anterior labrum, so here's the superior labrum. We're starting to see the middle glenohumeral ligament here. There's no anterior labrum here. There's no anterior labrum here, and we see a cord-like middle glenohumeral ligament extending to the subscapularis. This is a 21-year-old triacathlete with clicking, so we're just, again, looking at the level of the coracoid process, or we're above the level of the equator, so we're up here, and we see absence of the anterior labrum and a very large middle glenohumeral ligament. The sagittal nicely shows the very thickened middle glenohumeral ligament, so this is a normal Beaufort complex. In question four, it's a trick question. Is this a Beaufort complex? I think it's quite clear that the subscapularis is abnormal here. It's intermediate in signal intensity on the proton density sequence and hyper-intense on T2, but the key observation here is that the biceps tendon is not in the intertubercular groove, and there's an intra-articular dislocation, so this can mimic a Beaufort complex, but notice that we're already below the level of the coracoid process. There's a slide in there that demarcates normal variations, the typical findings from labral tears, but suffice it to say that they generally are hyper-intense on fluid-sensitive sequences, and usually they appear irregular in its margins. They usually imbibe fluid, either joint fluid or contrast, and we look at quadrant one for SLAP lesions, and lesions that are in combinations with quadrants three and four or four and five typically will manifest some sort of instability on clinical examination. Now one of the enduring testable materials has always been Bancard and Bancard variants, and Dr. Bishop covered the Hagel lesions, so I actually omitted that from my discussion, but I'll show you some demarcations on how to make that diagnosis, but the key questions you want to ask when talking about the Bancard lesions is, after identifying the torn anterior inferior labrum, you want to interrogate the periosteum. Is it disrupted or is it stripped, and if it's stripped, by how much? You want to see if the glenohumeral ligaments are torn and the cartilage damage as well as the bone. Now the definition of a classic Bancard lesion is an avulsion of the anterior inferior labrum by the anterior band of the IGH associated with disruption of the scapular periosteum. It is the classic soft tissue Bancard lesion, and you want to make that distinction. The reason why it's important to make that distinction is because of the variants and it affects how you may treat patients. So here we see the anterior band of the inferior glenohumeral ligament, and we see hyperintensity from the avulsed labrum. On the ABR view, we see disruption and distraction with fluid imbibing the defect. As you recall, the Hagel lesion is a defect on this side, so you can see the difference between the two. The Perthes lesion, again, it's an avulsion of the anterior band of the inferior glenohumeral ligament on the anterior labrum, but the scapular periosteum is intact. So when you look at it, it looks like you have the detachment of the anterior labrum, and then you can follow the scapular periosteum. In this ABR view, you see distraction of the labrum, but notice that the periosteal surface here is intact. The Perthes lesion can progress into an ALPSA lesion, the anterior labral ligamentous periosteal sleeve avulsion, and when that happens, the anterior labrum can then get sucked into this anterior patella's recess, and when that happens, it can fibrose down and affect the integrity of that structure. So, again, the most important finding here is that the anterior scapular periosteum is intact. When you look at the images, two different patients, you can see that there is tremendous stripping of the anterior scapular periosteum, and in this patient, in the ABR view, we can see that the anterior labrum is no longer present in its typical location, but it's now displaced immediately and associated with this fibrosis adjacent to it. The GLAD lesion, the glenolabral articular disruption, is actually a defect in the cartilage. So when you look at the cartilage, there's going to be a cleft that then burrows its way underneath the labrum, so the labrum integrity should be normal, and the scapular periosteum should also be intact. So it's an associated injury of the cartilage. So when you look at either a T2-weighted or fluid-sensitive sequence or an MRI, what you'll see is nothing more than the defect in the anterior labrum, but the key thing here is that this is a very typical lesion in patients who have forced adduction or subluxation, so this is a manifestation of one of those unstable anterior patients. Now posterior lesions are exactly the same as anterior lesions, just on the posterior side. So let's just kind of go through a couple of them so that you feel familiar with those. So question 12 is an atrial with posterior pain. Let's go through some of our questions. There's the labral tear right here, and we can see that it's a little bit detached. The periosteum is stripped, but still intact, so this is a reverse or posterior Perthes lesion. Question 13 is a 27 with seizure, and here we have a disruption of the labrum. We have disruption of the scapular periosteum. When you look at the anterior margin of the humeral head, you see that there is a trough defect surrounding bone marrow edema, so this patient had a posterior dislocation, so this is a reverse Bankart lesion. Again, 22-year-old Lyman, we see that there is marked detachment of the posterior labrum, but when you follow the posterior scapular periosteum, it's intact, and there's some fibrosis at the base, so this is a pulp solution, so the posterior labral ligament is a periosteal sleeve. Let's talk about the SLAP lesion, because as all of the speakers have already indicated, it's a very testable material, but we're going to concentrate really on questions two through four, or types two through four, because those are the ones that you can really see on MRI. Since then, there has been a whole bunch of other ones that have been described, but for the purposes of the exam, you just really need to know two through four. So let's cover that, because they have unique features that are very interesting. In type one, you just see some fraying at the base, and that's not very interesting, so the tears are really going to be seen in two, three, and four, and they each have demarcating findings that help to differentiate those. So in a type two, you have a clear detachment of the superior labrum that can extend variably into the biceps tendon, and you classify them by their location, and the axial view is frequently a good view to help to identify whether it's purely an anterior lesion, that's type 2A, or a posterior lesion, which is type 2B, or if involved in entire superior labrum, which is a type 2C. Type three is the bucky handle, and a bucky handle is very easy to identify when the images are clear, so here I would prefer the 3T image, and what you'll see is that the retracted portion of that bucket handle is going to be covered by, it's going to show fluid on both sides, so here we're seeing that the fluid is in both sides. This is the handle component of the tear, this is the actual tear, so again, three different patients with that. It's a very typical finding, so when you see fluid around something that's floating here, that's going to be very characteristic of a type three or a bucket handle. In a type four, the sagittal and coronal plane just shows that there is something abnormal in the biceps anchor, so once you see that, it's going to be a very clear diagnosis. Now we've heard a little bit about compressive neuropathies, so a couple words on when are we going to image the particular findings. So partial compressions can lead to this thing called the pseudohypertrophy of the muscle, the muscle actually gets larger, versus complete, where eventually the muscle gets smaller and atrophied, and then the imaging will also be demarcated by whether it's an acute versus a chronic condition, so acute phase of compressive neuropathies will always manifest as interstitial edema in the muscle, whereas chronic is going to be infiltration with fat, and we've already heard from Dr. Gill the emphasis of the suprascapular nerve and the axillary nerve, so C5 and C6 are important numbers for you to remember because those are enduring testable material. We've already seen where they get entrapped, so under the suprascapular nerve can get impinged underneath the ligament or as it courses behind the scapula into the spinal glenoid notch, so we're going to just look at what those findings are going to be. So in question 22, we just want to make the diagnosis, in this patient we see that there's a superior labral tear and a cystic structure sitting in the suprascapular notch, so in this patient we already know that there's a potential risk for developing suprascapular nerve entrapment, we interrogate the signal intensity of the muscles, we don't see any hyperintensity, we don't see any changes in the morphology, so in this patient it's nothing more than a paralabral cyst with a superior labral tear. Now in contradistinction to this patient, where there is a proximal nerve compression underneath the ligament and the most common cause is going to be a paralabral cyst, in fact the paralabral cyst is going to be most common for all of them, but in some patients where you can have ossification of the scapular ligament, you can get a very, very small perforation of that foramen and that can cause entrapment of the nerve as well, so acutely what you're going to see is hyperintensity of the supraspinatus and infraspinatus and we've already heard that on physical examination you're going to identify weakness in both the supraspinatus and infraspinatus muscles, so abduction and external rotation. When the compression occurs at the level of the spinal glenal notch, then we have a distal nerve compression and the weakness is only going to be an external rotation and hyperintensity is going to be only in the infraspinatus. Here we have a 64-year-old with weakness in the shoulder and this is the money film right here showing the paralabral cyst below the level of the spinal glenoid notch, hyperintensity in the infraspinatus muscle only, so the diagnosis is spinal glenoid notch entrapment. With axillary neuropathy, it matters when the condition is going to be imaged, usually the abnormality is going to be the posterior branch, so the two areas that are going to be affected is the teres minor and the posterior deltoid muscle, so you can see that there's disproportionate atrophy of these muscles compared to the supraspinatus and infraspinatus and another key testable material is that it can be a traction injury from dislocations, but fibrosis overwhelmingly is the reason for most of these from an imaging perspective. Just a couple words on adhesive capsulitis, we've heard that there's that very strong association with diabetes occurring in older patients and then some other less common but equally important associations. In the freezing phase, it's a very, very easy diagnosis, although it may not entirely be correlative in terms of the time. This is the painful period of the injury of the abnormality, so when you look at the fluid on T2-weighted images, it's not going to look like hyper-intense fluid. It looks like kind of dirty water, so to speak, and so it looks like there's too much gray stuff everywhere and the key locations that you're going to look at is the axillary recess and the rotator cuff region with the associated clinical findings. Once you get beyond the acute synovitis, then the symptoms then starts to transition towards terminal range of motion where the pain is most severe, and when we look at the MRI, we start seeing the manifestation of fibrosinoma proliferation, and the key number here is that the capsule and the axillary recess will be thicker than four millimeters. It's never going to be that subtle. Most of the thickness is going to be way past six or seven millimeters. It's not going to be subtle, and then the fibrosinoma proliferation and the rotator cuff interval and the axillary recess is going to be very nicely demarcated on the sagittal sequences, and then the thawing phase, we'll see some resolution of these, but there will always be some persistence of the thickness of the capsule, so our last two cases, we have a 65-year-old with diabetes, so diabetes is the key association, and all we see is that there's a lot of synovitis, especially in those key areas, the rotator cuff and the axillary recess, so this is the freezing phase of adhesive capsulitis. In contradistinction to this last case, question 33, what we see is that we can't even see the fluid in the joint. These are both T2-weighted images. You can see that by the edema elsewhere, and you can't even see that because of all of the synovitis that's inside the joint, so there's an answer key at the back of your handout that shows all these other lesions. If you have any questions related to that, I'll be happy to go over some of the key imaging findings, but I think you should be able to work through them based on the preceding segments of where the questions are consolidated, so thank you very much. I appreciate the invitation. It's great to be here.

shoulder imaging

MRI scans

labral tears

SLAP lesions

compressive neuropathies

adhesive capsulitis