So, like the previous talk, what I'll do is cover very targeted topics in the categories of spine as well as hip. And as orthopedists, you're very good at looking MRI and correlating symptoms with imaging findings. Spine MRI is a huge challenge for radiologists, and there are a couple of reasons for that. First of all, in people who do not have any symptoms, there are oftentimes positive findings, as Jessica mentioned earlier. And therefore, in the setting of an individual who does have symptoms and multiple imaging findings, how do you decide which is the most important one, which is the pain generator? Well, radiologists tend not to have much information about symptoms, and therefore, you've seen over and over again our reports that are these laundry lists of findings and very unfocused conclusions. And so, what I'm gonna do at the beginning is really discuss this diagnosis of pain generator based on two important things. One, the value of symptom MRI correlation, and also sometimes very subtle signs of inflammation on the MR images. And then I'll briefly address the segmental instability. So starting off with symptom MRI correlation. So first of all, we have a T1-weighted image and then a T2-weighted image. The CSF is low in signal intensity, the bone marrow FAD is bright, so this is a T1. And the discs, you'll notice, all have the same signal intensity. And on this T2-weighted image, the CSF is bright, and then here is a normal disc, nucleus propulsus, high in signal intensity, very watery. And here is a disc that is degenerated. So is that the cause of symptoms? Well probably not, disc degeneration being so common. So this individual has an S1 radiculopathy and an obvious extrusion at the L5-S1 level. And its location can be characterized best on the axial images. So I was wondering why I couldn't see anything. That's better. And so it's become a little bit more distal, there's this disc extrusion that's displacing and causing mechanical impingement on the left S1 nerve root. And clearly there is a symptom imaging correlation that even a radiologist can see as being quite obvious. And that might be addressed with a targeted left S1 nerve root block. Here is somebody with left arm pain, well there's no stenosis involving the canal. And as we come over to the left side, starting to see this very focal disc osteophyte complex. And the sagittal images are very valuable, I think, in the cervical spine as well as the lumbar spine. And so you'll notice on a sagittal image here that the foramen is clear. There's a nerve surrounded by high signal fat and veins here, here. And then at this level, the offending lesion, the one that's most likely corresponding to the left arm pain, characterized by the loss of the fat and the visualization of the nerve in the foramen. And that can be addressed with another nerve root block. Now this is a person who came in for an injection with us, actually a physician at MGH complaining of right L4 symptoms, anterior thigh over the knee. And so, right-sided symptoms. So just follow this right L4 nerve. And so there's a very small intraforaminal disc extrusion that's displacing and causing mechanical impingement on that right L4 nerve. And it's this kind of small but important finding that you are much more likely to identify than the radiologist. Because this is an example of an important but small extrusion that was missed prospectively. And why is that? You have the advantage of knowing the clinical symptoms. Okay, signs of inflammation. This is a skier who had a radiculopathy and a disc extrusion to explain it. But what I want to really point out is what happened seven years later. So this is a comparison of the T1-weighted images. And at the L4-5 level, the disc space is increased in its degree of narrowing. And T1-weighted images are okay for fractures, but there is some subtle bone marrow edema that's much better seen on the T2-weighted and fat-suppressed T2-weighted images. And then there is this small area of fat at the L5-S1 level as well. So bone marrow edema is a clear indication of inflammation. And it's very likely that the low back symptoms developed seven years after the herniation are the result of this disc degeneration at L4-5. And these fat-suppressed images are important to look at. They are more sensitive in the demonstration of bone marrow edema that may explain symptoms and also allow for the differentiation between discogenic bone marrow edema and discogenic fatty marrow transformation. So the L4-5 level has the marrow edema. But here at L5-S1, notice this area of high signal intensity that is low in signal on the T1. So this is the MODIC-2, and this is the MODIC-1, the much more likely pain generator. MODIC-2 always start off as MODIC-1. So here's a golfer with intermittent low back pain. And this is the typical classical T1 and T2-weighted images. And the facet joints all look normal. Now when you look at the fat-suppressed T2, you are going to be much more sensitive in the demonstration of this bone marrow edema at this level of mild facet arthropathy. And then this capsular edema showing enhancement after contrast. And so it's this enhancement that is the correlate to inflammation along with the bone marrow edema. These axial images show some focal cartilage loss on the left. And on both sides, there's this peripheral enhancement indicating inflammation at the L4-5 level and no enhancement whatsoever at L5-S1. So we normally don't give contrast. This person got it because of a history of carcinoma. And the point is, it can be very difficult to identify prospectively on MRI. The contrast in this particular case demonstrated the edema and inflammation at L4-5. Here's a person with L5 radiculopathy. There's an extrusion at L4-5. And you look at this and you think to yourself, well, that's a pretty good-sized disc extrusion with caudal migration. It's not as big as you think, however, because here, some of that is accounted for by the surrounding granulation tissue or inflamed tissue, which is showing enhancement post-contrast. So T2-weighted post-contrast, T1-weighted images. Here the canal is a normal size. Here there's stenosis and a little bit more distal. We're seeing this caudally migrated disc material with a surrounding enhancement. And this is the explanation why a steroid injection might help. Because it's going to address not the central disc, but the surrounding inflammatory tissue that may be irritating the nerve and causing the radicular symptoms. Okay, so that's issues related to bone marrow edema and inflammation. How about segmental instability? The most important thing to be looking for on radiographs is anterolesthesis. And it is always associated with some important abnormality, either degenerative, facetarthropathy, or isthemic PARS defects. And there are all kinds of different symptoms that might be manifested. Low back pain due to the disc degeneration and the facetarthropathy, foraminal stenosis, radiculopathy, spinal stenosis, claudication, as Jessica mentioned. So I call him a mature athlete, although his girlfriend was very young. And there is only a slight degree of listhesis. But you can see that there's a high degree of stenosis. And that stenosis is clearly identified, characterized here on the axials. And what is the main reason for it? Well, look at the facet degenerative change with the bony remodeling in the anterior translocation of one articulating process compared to the other. And that's the main cause of the degree of stenosis in this particular case. I also want to point out this column of fluid across the facet joint on the right. This is in the supine position, non-weight bearing. But what happens when this guy stands up? This slides forward and the stenosis gets even worse. So look for joint space widening on the supine images, MRI, that then will become, indicate an increased degree of stenosis with load bearing and standing up. This person also has a mild degree of antralisthesis and a normally wide canal. And I think that the PARS defects, especially when the listhesis is minimal, can be very, very difficult to identify by MRI. And if you go back and look at the facet joint and that looks normal, then I think with a greater confidence then you can identify these otherwise very difficult to identify PARS defects. And in the absence of any listhesis, this is the kind of problem that is challenging for the radiologist, just like the small intraforaminal disc extrusions. And so these PARS defects are probably relatively commonly missed by the radiologist. This is the same patient on the CT. And so the CT clearly shows a PARS defect. And I want to point out its communication with the facet articulations above and below. A mild degree of listhesis, a large PARS defect, and communication. And in the procedure room we can take advantage of that and target one facet or the other with the expectation that the contrast will flow into the PARS defect and then in this case both into the 5-1 as well as the L4-5 facet articulations. A brief comment on flexion and extension views. I think that the technologist can have a very difficult time coaching patients on how much flexion and extension, especially when they're guarding and in a higher degree of symptoms. And so what you're looking for is whether or not the patient was able to put in a good effort as in this particular case. And then not just an increase in degree of anterolisthesis with flexion as in this example, but also the development of an angular kyphosis. And so normally with flexion the disc space heights remain similar anterior to posterior, but at L4-5 here there's an asymmetric degree of narrowing anteriorly resulting in this development of an angular kyphosis, not just increased anterolisthesis. I'm gonna make a transition to the hip and I'd like to start off with some bone marrow abnormalities. So here's the classical stress fracture involving the medial femoral neck, typically in a female runner, cortically based with prominent surrounding bone marrow edema. And as obvious as it is on a T2-weighted or stir image, it tends to be very difficult to identify on a T1 if there is very dense surrounding bone marrow edema. Here's a 20-year-old, an avid runner, who develops left hip pain. And the presumption was that she had a labral tear, and therefore this MR arthrogram was done. Now what is the pulse sequence that you're looking at? It's T1-weighted, but it's fat suppressed. And so the bone marrow is dark. And I'm always surprised by the number of studies that I see that come in from the outside that only use fat suppressed T1-weighted images in the setting of an MR arthrogram. And the reason that's a potential problem is because you don't get a good look at the bone marrow. Here's the T1 without fat suppression, and it's still hard to see that focal abnormality because the marrow edema is blending in with the surrounding erythropoietic marrow. It's obvious on the T2-weighted image, here's the stress fracture and the surrounding edema. Now that same individual was on crutches, did fine, four months later goes back to running and develops some right hip pain. And I'm showing this to you because this is a patient who no longer has left-sided hip pain, but still has this large abnormality with surrounding bone marrow edema on the T2-weighted fat suppressed sequence. So the resolution of symptoms can take place long before the resolution of imaging findings. And then here in that same patient is the symptomatic right side now showing a stress fracture in the typical location. This is one of our technologists, and the point of this case is three things. First of all, take a look at these coronal images, T1-weighted, and then here fat suppressed T2. Is this a stress fracture, or is it a stress reaction? The vast majority of radiologists are going to read this as a stress reaction. And in retrospect, this is probably an early developing stress fracture. Now because she worked at MGH, she was able to be cajoled into follow-up imaging. So three months later, her symptoms are nearly gone, and we now see a definite fracture line with resolving bone marrow edema. And then 12 months later, complete resolution of any bone marrow abnormalities. So to reinforce the point, early fractures often are in the appearance of a stress reaction. The fracture is going on to develop, even in the absence of symptoms. This is a 45-year-old, and she's obese but wanted to get back into shape and was seeing a trainer who was working her very hard. The T1-weighted coronal images show a smudge in the typical location for a stress fracture, but there is no line. And you would be tempted to conclude that this is a reaction and not a fracture. Now on these axial images, notice that there is dense endosteal bone marrow edema in addition to periosteal bone marrow edema. So in the setting of both endosteal and periosteal bone marrow edema, then it's almost guaranteed that there is some sort of cortically-based abnormality, a fracture that is just not visible on the coronal images. These are the same principles that can be applied to shin splints versus stress fracture as well. And so in a runner who develops anterior tibial pain, and the MRI shows no fracture line, but it does show endosteal as well as periosteal edema, then it's in that setting that I think it's prudent to conclude that, in fact, a stress fracture is present. And this woman went on to internal fixation. Here's a 47-year-old runner, and in Boston, when the ice begins to thaw, everyone gets out and runs and starts developing hip pain, and she was suspected of having a labral tear, and therefore here is another MR arthrogram, T1-weighted, fat-suppressed sequence. Is there a bone marrow abnormality? Here on the T1-weighted image, without fat suppression, there is a bone marrow abnormality in the typical location for a stress fracture, except that here is the T2-weighted pulse sequence, and is there a fracture line? So without a definite fracture line, you cannot conclude, despite the location, that this represents a stress fracture. And this was how this woman presented with her breast cancer. I want to contrast the stress fracture, the fatigue fracture in the medial femoral neck with the insufficiency femoral neck fracture that develops in the elderly osteoporotic, the mature athlete. So here's a T1-weighted image, and notice that it's in a completely different location. It's in a subcapital location, and then here is the fracture line surrounded by the bone marrow edema. So whereas the fatigue fracture in the young female runner is cortically based, the insufficiency fracture in the osteoporotic patient is really trabecular based, and rarely extends into the cortex unless it's left too long. So she was internally fixed and then got back to the mall, and now has developed an insufficiency fracture on the opposite side, classical fracture line, subcapital in location, with dents surrounding bone marrow edema and internal fixation. Now in the femoral head, there are all kinds of etiologies for bone marrow edema. There is the subchondral fracture, which is a form of stress fracture, transient osteoporosis, capital femoral necrosis, and even DJD. Here's an individual that has this T1-weighted and fast-depressed T2-weighted sequence showing a joint effusion, dense marrow edema, and on the T2, we can see this curvilinear serpentine subchondral defect. And oftentimes the question is, does this represent osteonecrosis, or does it represent a fracture? And in this particular case, it represents a subchondral fracture, and here it is in the sagittal plane. And I want to contrast that case of subchondral stress fracture in a modern MRI scan with this MR scan from the mid-1990s. This was a really good scan for the mid-1990s. And it shows T1, it shows T2, it shows a joint effusion, dense marrow edema dissipating distally from the apex of the femoral head, and then this very, very dense bone marrow edema on the T2-weighted pole segments as well. And then these were always diagnosed as transient osteoporosis. Well, we know that transient osteoporosis has the same conservative treatment and the same length of time for improved symptoms as subcapital stress fractures. So this is the patient that we just looked at with this very, very dense bone marrow edema. In my practice, we hardly ever diagnose transient osteoporosis anymore, and it's possible that they all represented in the past these subchondral stress fractures. This is an obvious case of capital femoral necrosis in a person who plays lots of golf and is developing new pain on the left. So typically, bilateral capital femoral necrosis is related to steroids and is asymptomatic until mechanical failure occurs. Here in that same patient are the T1-weighted coronal images demonstrating the bilateral osteonecrotic segment, and it's on the STIR sequence that you can see the joint effusion, all the very dense bone marrow edema, and it corresponds to the development of symptoms on this left side and reflects mechanical collapse and what is going to be an imminent, at least a hemiorthroplasty. Now this is after contrast administration, and what I really want to point out is the enhancement of the viable bone marrow, which is inflamed, and the lack of enhancement in this non-viable necrotic segment. And if you really are having a difficult time differentiating the subchondral fracture from true osteonecrosis, this is the potential value of contrast injection. So here is another individual with bone marrow edema involving the femoral head. Looks like transient osteoporosis, except that the T2-weighted sequence shows this subchondral fracture line, and after contrast administration, notice that there is enhancement on both sides of the line, including in the area where if it were true osteonecrosis, you would expect there to be bone death. So this is a true fracture. It's not the death of bone. So with that then, I think my time is up, and we've come to the end of the session, and I thank you for your attendance.

spine issues

hip issues

MRI interpretation

inflammation

segmental instability

bone marrow abnormalities