Hello, everyone. My name is David Chang and I'm coming to you from Los Angeles. I'm happy to represent the Medical Education Committee as well as the Digital Learning Committee to present this month's National Grand Rounds. In previous years, annual assembly, spine imaging, workshops and lectures have always been really popular and really well attended. And so this is why we thought that we would invite our feature speaker today to give us a lecture on spine imaging interpretation. It is my honor and privilege to introduce Dr. Zach McCormick from University of Utah. Dr. McCormick is a vice chair, is a vice chair and associate professor of PM&R. He also has multiple other positions at the university, including chief of division of spine and musculoskeletal medicine, director of clinical spine research, and finally, director of the interventional spine and MSK Medicine Fellowship. Outside of the university, he's also very engaged and involved in multiple medical societies, including the Spine Intervention Society, where he is on the board of directors. He's also the chair of the standards division. Dr. McCormick is very busy and he's also active with the North American Spine Society, as well as American Academy of Pain Medicine. We're going to spend the next hour or so learning from Dr. McCormick and I'll be helping to moderate some questions towards the end. Thank you so much and please help me welcome Dr. McCormick. Dr. Chen, thank you so much for the warm introduction and wonderful to see so many people joining the grand rounds. Thanks for being here and hope to make this as valuable as possible. The goal here is I'll work my way through the slides I have prepared, but I'm more than happy, of course, to answer questions and we can ping-pong things back and forth. I'll do what I can to impart knowledge that I have, but I think we learn a ton from each other too. Let me just bring my slides up and all right. As Dr. Chen mentioned, I think this session was really inspired by some of the workshops that we put on during the annual meeting in prior years that seemed to be well received. I'm going to cover a little bit of information that if you happen to attend one of those workshops, some of it might look a little bit familiar, but lots of new information and a different framework. Just briefly, these are my disclosures. We're talking about imaging here. These are not directly relevant, but just to be transparent and keep these in mind. I definitely need to acknowledge a number of colleagues. Vanille Shaw, who is a neuroradiologist at UCSF, Tim Moss, who's emeritus from Mayo, one of my colleagues here at the University of Utah, Megan Mills, and then Aaron Conger, who's a physiatrist and part of our faculty here at the University of Utah. I have borrowed or slightly adapted slides that they shared with me. Big thanks to them. One thing I will say is as much as I've learned about radiology, none of us certainly know as much as a neuroradiologist. I have learned a ton from neuroradiology and MSK radiology colleagues. I think always a fantastic resource to tap into if you have the opportunity on a case-by-case basis in your institution or practice or otherwise at meetings. This is what I'll plan to cover. We'll use the framework of the American College of Radiology criteria for imaging of low back pain. There are seven variants of low back pain, and we'll work our way systematically through those. For each one of them, we'll talk a little bit about when you might select a given imaging modality, why, what circumstances would lead you to one versus another or in combination. I will share with you all examples of pathology for my own patients. Then again, as I mentioned, some slides that were shared with me from colleagues, a little bit on interventional planning. It's really tough to cover all this in the time allocated. I have a little bit less on interventional planning, but if there are specific questions, again, more than happy to dig in at the end during the Q&A session. We'll jump in. As I mentioned, this is the reference. Many of you, this may be familiar, but you can read the full paper. It's worth doing. Specifically, the 2021 update to the ACR appropriateness criteria for low back pain imaging. I should also mention that we are not going to cover cervical and thoracic today. It's just too much to do in our session. The general topic of radiology is already broad enough, so I am limiting the lumbar spine. Red flags. This comes right from the ACR paper and criteria. Just to make sure we're working with the same definitions. When the ACR and their guidelines, when they talk about red flags, this is specifically what they mean. These categories, and you all can see my mouse, just to confirm. Perfect. Things that might indicate suspicion of cancer infection, spinal fracture, cauda equina, or other neurologic compromise. These are what we mean when we say red flags, but I think this audience is well familiar. What's variant one? Variant one is acute low back pain with or without radiculopathy, no red flags, and then no prior management. How do we think about spinal imaging for these patients? Well, you can see it right here. The reality is that you don't usually obtain it. The majority of these folks with acute back pain, with or without radicular symptoms, but acute back pain without red flags and no prior guided care by a physician or physical therapist, et cetera, there isn't really a need to image that. Again, I think very familiar probably to this audience, but it's quite normal to have a variety of structural, quote unquote, abnormalities or degenerative changes that are asymptomatic. I'll show you a slide here next that quantifies that a little bit. The other reality is, and I'm sure that many of you, I'm not sure what the mix is of folks that are in independent practice versus in training, but if you tried to get authorization for an MRI for someone with acute back pain and no red flags, it gets denied. It follows that payer policy really doesn't allow it anyway, but really this is an area where we don't just immediately image. These are a couple of papers. There are many more, but a couple of nice papers to know of are the Bowdoin and Jensen studies where both of these author groups looked at asymptomatic individuals and then simply tallied the prevalence of various, quote unquote, degenerative changes, just protrusions or just degeneration, just bulges, high intensity zones, variety of things that you can see these in folks that have no back pain whatsoever. I'm preaching to the choir here to the physiatry community, but obviously we're matching symptoms with what we see on imaging, not just paying attention to imaging alone. But these studies do a nice job of helping us, I think, counsel our patients on what's normal and what's not. There have been some studies where more and more radiology groups actually reporting some of these data side-by-side on MRI reports so that a patient, they see degenerative disease and that's a scary thing. But interestingly, there have been randomized studies where this normative data is published or is side-by-side with an MRI report and it actually leads to less healthcare utilization, fewer interventions, less healthcare costs, et cetera, if you publish these normative data side-by-side with MRI reports. So just helpful for, I think, primary care and our colleagues in internal medicine also to see some of this information and that seems to bear out in studies where that's done compared to when it's not. So variant two, similar thing here. So a patient presents with subacute or chronic low back pain, again, with or without radiculopathy, but no red flags and no prior management. So same individual, essentially, except that perhaps they've had pain for six weeks or three months or longer. But if there's no red flags and really there's no conservative care that's been tried, there isn't an indication for imaging. So it's the same thing, trial of conservative care first before beginning to obtain imaging. So that then brings us to variant three where things get more interesting. So now this is, again, subacute or chronic pain, again, with or without radiculopathy or radicular-type symptoms. But in this case, there has been a trial of conservative care and despite that, symptoms are still high-level or progressing. And there, it makes sense to potentially plan for an intervention, whether it's injection-based, something that a PMR-based spinal interventionalist or pain specialist might perform, or surgery. And in this case, so usually the go-to kind of our bread and butter is lumbar spine MRI without contrast. There are a variety of other modalities, and we'll talk through these that may be appropriate, but certainly lumbar MRI without contrast would be the go-to. And this is really to understand, is there an actionable pain generator? And if so, how might we plan safe and appropriate intervention and effective intervention? So when might you consider radiographs as well? Certainly, if there's evidence of of any instability on the MRI, if there's a spondylolisthesis or rotational instability, flexion-extension films are very helpful. And we'll talk a little bit more about specific scenarios where flexx films are useful. MRI adding contrast, adding contrast or potentially a SPECT scan or SPECT-CT, this is where maybe there's some suspicion of malignancy or infection, adding IV or using a SPECT scan can be helpful in these situations. And then occasionally we'll have to order an MRI when maybe we would, excuse me, a CT scan, when perhaps we would actually like an MRI, but there is a non-compatible implanted device that prevents us from obtaining MRI. In those cases, we can get a CAT scan without contrast. If we need to see the neural structures, then a CT myelogram would be the imaging modality of choice, again, if an MRI can't be obtained. And we'll get into more case-specific scenarios. So let's just walk through some examples. So again, starting to look at common or less common actionable pain generators. Obviously, this is a very common scenario. I think we all, if you do spine care or pain management, you see this all the time. So discogenic radicular pain. So this is, we'll just scroll through. So slowly we see a cut through the L4-5 disc here. These are T2-weighted sagittal image, axial on the right, sagittal on the left. As we scroll down to that L4-5 disc, you get a sense that there's kind of a broad-based bulge with some abutment of the transiting S1 nerve right there in the subarticular zone. And as we scroll our way in the sagittal slices, I'll scroll back for a second, get a sense that, you know, perhaps this is, it's actually a protrusion in that sagittal slice. We're getting a little bit of more than just a bulge. So I'd probably call that a broad-based disbulge with a superimposed protrusion abutting the transiting S1 nerve on the right. So that would be a pretty common scenario that I think we all encounter on a regular basis. Here's another one. So this is a full disc extrusion. This is the L4-5 disc. And, you know, as we start to think about interventional planning, so, you know, what do we expect to happen with a subarticular zone, a central disc protrusion or extrusion versus subarticular zone versus foraminal or far lateral? You know, what do we expect to happen symptomatically for that patient? So, you know, this is showing you axial slices on, this is T2, and then this is a T1 with FATSAT. So getting a sense that this particular extrusion is in that subarticular zone or maybe paracentral. And that's probably going to affect the transiting nerve root, right? So at L4-5 would be the L5 nerve root. So you get a sense that that's probably the, you know, the presentation that we would expect L5 distribution of radicular pain symptoms, and that's going to guide our interventional planning. And here's another one. So this is an L4-L5 disc protrusion or probably extrusion that is in the foraminal zone. So we expect that is going to affect the exiting nerve root. So that would be the L4 nerve in this case, as opposed to if there was, again, a subarticular zone extrusion that would affect the L5, the transiting nerve root. So here we see L4 radicular referral pattern. So just, you know, epidemiology, disc herniations, symptomatic disc herniations are most common at L4-L5, and then L5-S1. Typically, the most common herniation is going to be posterior lateral. So in that subarticular zone, perhaps foraminal, but more common to be subarticular. So that's going to, more commonly going to affect the transiting nerve root. So again, if the extrusion's at L4-L5, that's going to affect the L5 nerve root rather than the exiting L4 nerve root. So like I mentioned, you know, where does that bring us in terms of, you know, planning for a treatment? If this patient has theoretically, you know, failed more conservative care or non-interventional care. If we've got, for example, a patient with a large right subarticular zone L4, L3-L4 disc extrusion with an L4 radicular pain syndrome, where do we place the medicine? You know, do you take a, in the literature, there are papers that describe a pre-ganglionic approach, and what they're referring to is essentially a retro-discal approach at the level of the herniation. So in this case, that would be, you know, retro-discal or an infernal approach at L3-L4. Or what about taking a supra-neural approach at the one level lower? So at the L4-L5 foramen, it's essentially coating that nerve, the nerve that's affected from a subarticular zone extrusion. Do you inject at that level? And, or do you do both? Do you do a two-level transforaminal injection? And I think if we pulled the audience, I think we'd get a whole variety, I imagine, of answers, because the reality is there really isn't great data to tell us what we should or shouldn't be doing. There is, this is a systematic review that's a handful of years old now, but where these authors took a look at all the data that's been published on whether to perform that retro-discal injection at the level of the herniation, or take that supra-neural approach one level below to really target the transiting nerve root. And this author group, in this review, when they aggregated the data, they did see that the retro-discal approach actually was associated with greater, with improved short-term outcomes. I think we could probably pick apart the individual studies and their flaws, and that would take a long time, but, you know, so maybe somewhat of a grain of salt here, but at least this is what this systematic review showed. Separately, this is, you know, and this is retrospective work, so these are not, you know, super high quality, prospectively collected data, these types of studies. But the second one that I have down here, this group, Ricky Singh and colleagues at HS, at Columbia and Cornell, they take a look specifically at two-level transfemoral injections. So this isn't, they didn't stratify folks by retro-discal versus supra-neural or one versus two level. They specifically look at, you know, consecutive patients who had two-level transfemoral injections, and what they did find was when they stratified out outcomes with those patients, that those who had a subarticular zone or paracentral disc herniation or disc disruption had the best outcomes. So again, grain of salt, this is retrospective data, but if you're considering a two-level injection, it seems like the right scenario would be those patients with a subarticular zone or paracentral herniation. So the thought there being that, you know, perhaps there isn't quite adequate spread to the area of the herniation if you're taking a retro-discal approach, and perhaps you're not getting ideal spread either from that subarticular, excuse me, the sub-particular or the kind of the classic supra-neural approach to a transfemoral injection. So, you know, this is not definitive data, and I think you're going to find a variety of practices out there. I can tell you anecdotally, not data-driven, but my personal practice is if someone has a very large extrusion or protrusion, and is it particularly in the subarticular or central zone, that's usually what will push me to choose a two-level transfemoral approach as opposed to just targeting, you know, a single level. Now that said, the thing you can do is you could authorize, you could ask for authorization for two levels, but if you are happy with your spread when you inject contrast at a single level, you can just elect to not include the second level, depending on if the contrast seems to be getting to where you need it to be. So, you know, moving on to other pathologies, this is, so I think, you know, this is also very common, so synovial facet joint cysts, and, you know, we're seeing it here in the subarticular zone. So, you know, what are these? They're essentially outpouches of the, or outpouchings of the facet joint capsule, and they tend to occur when there's excessive motion in those joints. So if someone has relative dynamic instability, this may be an indication that it's there. So we may see facet joint gapping. We may also see the formation of a facet joint cyst, a synovial cyst, as, you know, evidence that there's a bit more motion than the joint is happy with that can lead to accumulation of a cyst. So these can be aspirated and or ruptured, and that is a, you know, reasonable thing to attempt if it means potentially avoiding a surgery for the patient. So here's an example, just some images of facet joint access. You can see an arthrogram there, you know, we're filling the facet capsule. In the oblique view, this is over to, it's not quite, it's not an AP view, but closer to the AP view, you know, you're seeing the facet fill. See if I can get my cursor back here. Facet fill, and in this case, I don't have the side-by-side MRI images, but that's actually the cyst filling right there. So then in the next image, we're filling in even more so, even more so, and then we get rupture, and we've got epidural spill. So there's contrast now that's filling the epidural space, and that's where we can, you know, stop the, stop the procedure. Many people will add a little bit of steroid at that point in hopes of perhaps shrinking that cyst or preventing reaccumulation of the cyst, and then, you know, potentially compressing transiting nerve roots again. So I'd actually clarify, you know, the situation where you're attempting aspiration rupture is really where you have neural compression, right? So if there's just back pain without any radicular symptomatology, it's not really an indication, it's not an indication to rupture the cyst. It's really if that cyst is, you know, compressing a transiting or exiting nerve root. And this is, just to take a step back here, so, you know, before you're thinking about potentially rupturing a synovial cyst, definitely important to distinguish that cyst from a Tarlov cyst, and I'll, you know, I'll show an image. That's a, that's a, you know, a cyst of the meninges, meninges cysts, or perineural cysts, and then discal cysts. So the disc can actually form a cyst, and these are two situations where you don't really want to aspirate or try to rupture those. That potentially leads to possibly an infection or worsening pain. So just things to make sure you're distinguishing synovial set joint cysts from Tarlov and discal cysts. The other thing to keep in mind is what's going to happen if you pressurize that cyst and it doesn't rupture, and that's a possibility that you have to be aware of. So it's going to depend on the anatomy in each individual, but if you have a large cyst and it's already creating some, let's say, moderate central canal stenosis, I'd be very careful about pressurizing that. So you may choose not to, you may choose to simply attempt aspiration, but not pressure, pressurization and rupture. In theory, you could create worsening, you know, compromise of the neural elements. So something to be, you know, mindful of if you're considering a facet cyst rupture procedure. You know, there's, there is data on this, outcome literature, and it's not high quality, but from, you know, what has been published, it seems like about half the time you can successfully rupture the cysts and then there is no, you know, subsequent need for a decompression and or fusion surgery. So certainly something that, you know, pending some of those caveats that I mentioned, a reasonable thing to try a cyst rupture. Many folks, myself included, often, you know, you might consider doing an epidural, a nerve root block before rupturing the cyst just so that that area is anesthetized. If you've already gotten neural compression and then you pressurize the cyst and you're compressing a transiting or exiting nerve unit and more so, that can really hurt. So performing an epidural block beforehand is one way of, you know, providing some anesthesia for the rupture procedure. This is an example of a discal cyst. So again, this is not a synovial facet joint cyst. You can tell, I mean, from this axial cut, you know, it is not originating off of the facet capsule. You see that it does appear to be originating from anterior structures. And this is a discal cyst. They're most common at the L4-L5 level. They're way less common than Tarlov cysts and synovial facet cysts. Historically, folks have aspirated these, or especially interventional radiology or neurology, we have aspirated these cysts, and that can be done. The risk is dysgitis. So just with any discal access procedure, you worry about creating a dysgitis, osteomyelitis. So these are actually, I would have shown here, there's some case reports from colleagues who simply have performed an epidural injection, and then the cysts, that which reduced radicular symptoms from neural compression, and the cyst spontaneously resolved over a period of months. So they don't have to be drained. And just something to keep in mind that if you are accessing that cyst and it's discal, there is a real risk of dysgitis. And so finally, the third one that's very common, and we all, these present themselves all the time, mostly asymptomatically, are perineural or Tarlov cysts. And again, these are spinal meningeal cysts. These really, you don't want to poke them. So you can find literature, especially in the neurosurgical literature of draining these and then potentially applying like fiber and glues to try to get them from, to prevent them from reforming. I can tell you, you know, from sort of interviewing many colleagues in neurosurgery, my colleagues really do not like touching these. And they find that it often creates worse pain, worse problems. It doesn't work well. It does reaccumulate, and often just basically creates more problems. And so most neurosurgeons that I've spoken to really don't like operating on these. They might consider decompressing around it if it's causing neural compression in a foramen, for example, but really not draining it. So these are, these are, and I think, you know, from my standpoint, I really never attempt aspirating or rupturing these, like not, not a great idea. So moving on to spondylolisthesis, you know, another phenomenon, obviously, you know, this is a potential structural issue that may warrant intervention, whether it's surgical or, you know, interventional in our realm. So I think this group is very familiar with what it is, and essentially, you know, slipping of one vertebral body over the next. There's debate out there, and there really is no consensus, but somewhere between a two to four millimeter translation between flexion and extension, that is considered a dynamic instability as far as, you know, in the AP dimension or the sagittal plane, a translation, that's dynamic instability. The thing to not forget to do is also measure angulation. So if there's angulation, again, there's, there's debate here, but somewhere between 10 to 15 degrees, depending on what you read, between flexion and extension, angulation at a given segment, that's considered dynamic instability as well. So yeah, just, just keep that in mind that we're not, you don't want to just measure the translation, but also the angulation changes on flexion extension views. So I alluded to this earlier, but I think there's really, keep in mind three different scenarios that would be considered, the word dynamic instability can be diagnosed. So one is that, you know, you see a spondylolisthesis on, you know, a CAT scan or MRI, you know, on static imaging, and then there, you do pick up translation or angulation when you obtain flexion extension views. So, you know, clearly that can happen. And that's why we get flexion extension views. You can also pick up where there is no spondy on static imaging, MRI, or non-weight bearing imaging, right, a CT scan or MRI. But when you do weight bearing views, then there is, there is, you do pick up on angulation or translation. And then of course, that may be the case as well with adding FlexX. The other thing that I think that if you look for it, you'll find it, is that you may see that you obtain flexion extension views. And, you know, it's when you read the report, radiologist says it's a fixed spondylolisthesis, but your MRI, and so you see it, right? Let's just say there's like three, four millimeters of translation on your FlexX films, but it doesn't move. So it's, it's consistently three to four millimeters on flexion and extension, but you have an MRI and then that MRI shows there's no spondy. So essentially good alignment. Well, that tells you that the patient is, is when they're weight bearing, they are moving. And if, if they're not actually, there isn't a change between flexion and extension, they're probably splinting. They're probably not really fully allowing themselves to flex and extend fully because there is a reduction of that spondylolisthesis when they're relaxed and in supine position MRI. So that is, that is a diagnosis of instability. So you can look for that. Modic changes. So, you know, this has become, this has really come into the forefront recently because there are, you know, now there are technologies and means of potentially treating pain associated with Modic type one and type two. And I won't spend a huge amount of time on, I think many are familiar with what Modic changes are, but you know, Modic one, these are, this is consistent with edema. So edema, you know, in the end plate and in the bone marrow. So it's going to look bright on T2, dark on, darker on T1, and going to look bright on STIR or other fluid sensitive sequences. Modic two is going to look relatively bright on both T1 and T2. These are fatty infiltrative changes. So fat's going to look, you know, relatively bright, not dark, certainly on both T1 and T2. And then a Modic three changes is a sclerotic or fibrotic infiltrate. And that's going to look dark on both T1 and T2. And, you know, there's some thought that these changes may progress from a type one to a type two to a type three, but patients can absolutely stall out in one phase. It's not necessarily the case that they ultimately will end up with Modic three changes. Someone could have Modic one changes for years, and that could be true with Modic two. And then of course, it's common to see mixtures of Modic one, Modic two, or Modic two and Modic three together. So, you know, what do we know about, you know, prevalence and, you know, what is the association between Modic and low back pain? So historically, I think everyone is very familiar with the phenomenon of quote unquote, discogenic pain. And, you know, we really thought about high intensity zones, annular fissures, provocation discography, potentially, you know, telling you whether there's a painful fissure. And, you know, we look at, this is a systematic review and then a meta-analysis or aggregate data that was, you know, published a number of years ago now, but looking at asymptomatic and symptomatic individuals and trying to kind of put some numbers to prevalence rates of these phenomena in symptomatic and asymptomatic patients. So certainly annular fissures are about twice as common in folks with symptomatic low back pain than folks without, but you can see them in the asymptomatic population and perhaps about 10%. Modic changes, similar numbers where all comers with Modic of any type about twice as common to see Modic changes of any type, one, two, or three in folks with low back pain who have, you know, symptoms compared to the asymptomatic population. And then Modic 1, it's even a little more so. So more than twice as common to have, you know, Modic 1 changes in the symptomatic low back pain population. So this is just, you know, this is association data. This isn't causation, but a little bit more data. Interestingly, if we look at the association between Modic changes and then positive provocation discography, so, you know, functional tests, obviously of pain at a given discovered T-rule, you know, motion segment, there is four times the likelihood that someone with positive provocation discography has Modic change, right? Or the other way around. If they have Modic change, there are four times more likely to have positive provocation discography at that level. And then if we specifically look at type 1 Modic, so that kind of inflammatory edematous type Modic change, an individual with that Modic change at a given motion segment is six times more likely to have positive provocation discography. And there are associations with the size of end plate defects in association with Modic change. So larger defects are, you know, associated with greater low back pain related disability. Still associations here, not necessarily, you know, it doesn't tell us about causation, but, you know, information from the epidemiologic literature. A little more on the phenotype here. So like I alluded to, I think everyone is familiar with the concept of discogenic pain. And this is probably a definition that we need to change. So we probably should be alluding to discover T-rule pain. And there is likely a spectrum where on one side there is perhaps pure annular pain, you know, mediated through nociception through the center vertebral nerve. On the other end of that spectrum is pure vertebrogenic or vertebral end plate pain, which that pain is going to be mediated through nociception through the basal vertebral nerve. And then there's going to be some mixture of folks who have a combination of both. So there's, you know, there's been some work and, you know, we were involved with some of this work to try to help define, you know, what is this phenotype of more dominant vertebrogenic pain as opposed to annular sinus vertebral mediated pain. And, you know, this is a much longer conversation, but the very short story is, if we look at robust responders to basal vertebral nerve ablation and assume that they have dominant vertebrogenic pain, and that is an assumption, right? But we use that as our definition of, you know, probable dominant vertebrogenic pain. And then we look at all the factors, clinical, physical exam, radiographic indices, et cetera, looked at dozens and dozens of factors. And these are the things that come out. So they have chronic axial back pain. Well, that's clearly the case, right? That's no surprise there. Generally, they're gonna, if they have dominant vertebrogenic pain, they don't have all the other stuff that we would expect to cause pain. Stenosis, radicular pathology, scoliosis, instability. You know, someone could have vertebrogenic pain and have these other pathologies, but they're gonna have mixed pain, right? Not dominant vertebrogenic pain, likely. This pain is gonna be midline predominant, and you may notice gluteal referral. And that doesn't really help you distinguish from annular or clinical discogenic pain. But I think the point here is that a lot of folks that we labeled as discogenic in the past are probably discovered vertebral and maybe vertebrogenic dominant pain. What we found in regression analyses as well is that these folks have pain that they report, they self-report as worse with activity and not worse with lumbar extension. So, you know, reminiscent of facetogenic type pain with posterior column loading in lumbar extension positions. You know, interestingly, we looked at numerous MRI factors, end plate, the defect size, the volume emotic change, the height emotic change, whether there were high intensity zones or not, whether there were disc bulges or not. Gosh, what else? Whether there were any element of stenosis, but lacking radicular symptom presentation. So we looked at numerous factors, and if you're interested, you can take a look at these papers for more detail. The only thing we found to be predictive was actually a lack of facet joint fluid. So remember, these patients did all have type 1 or type 2 MODIC, but if they had type 1 or type 2 MODIC, it was a lacking facet joint fluid in an MRI that predicted they would have a robust response to basal vertebral nerve ablation, again, sort of our best proxy, at least for now, for diagnosing true, quote, unquote, true dominant vertebrogenic pain. And so facet joint fluid, as I mentioned earlier, if there is gapping, or if there is at least two millimeters of fluid in a facet joint, that is an indication that there's probably some segmental instability, some relative dynamic instability. And then, of course, that's gonna be a more complicated picture than just vertebrogenic pain. So this is just a schematic kind of giving you a sense of the two different nociceptive pathways. So annular pain is gonna be, again, mediated predominantly through the sine vertebral nerve directly. The basal vertebral nerve is gonna mediate pain through the end plate. That ultimately does join back up with sine vertebral nerve, which joins up with the nerve root, and then obviously back up through sensory pathways up to the brain. But this nerve can be disrupted, and this is a therapy that a lot of folks are becoming more and more interested in because it theoretically is helpful for this subpopulation, this very specific phenotype of low back pain. So you can get a sense, this is electrode placement at the stem of the basal vertebral nerve to interrupt it. And we now have five-year data on outcomes. This is just showing you a meta-analysis. Aggregate data from a variety of studies, seeing forest plots here, six-month data, 12-month data, and then data out to five years, looking at improvement in pain scores, at least 50% pain reduction. There's a, you know, responder rate is somewhere around 65% at six months, 12 months, but it does seem to be durable out to five years. And then similar stuff with ODI, if we use a 15-point improvement in ODI as a robust threshold of improvement. Okay, so moving on to the next variant of low back pain. So this is low back pain with suspected cauda quina syndrome. And I don't need to spend a lot of time because I think folks are very aware that you need to image this, and it's frankly a surgical emergency. So some interesting facts though about cauda quina syndrome. The most common symptom and kind of the earliest symptom of cauda quina is actually urinary retention, in addition to back pain, obviously. But this is actually, it's actually urinary retention first, and then that potentially leads to overflow incontinence, right? But the lower motor neuron issue, right? So, you know, you're affecting, you have kind of hypotonic bladder and you're gonna retain because the trucer is not contracting, as opposed to spastic bladder with an upper motor neuron injury where you've got, you know, bladder's not filling before it just empties prematurely. But so urinary retention, most common symptoms. So that's something to ask about if you're thinking, does this individual have true cauda quina? Is it, is it not? Retention is one before there's even, you know, true incontinence, whether it's urinary or fecal. And I think folks are familiar with, you know, saddle anesthesia and obviously weakness or paralysis. You know, there's no question there, what's going on, but, you know, urinary retention's a good one to keep on your radar. So most commonly, this is due to a very large central L4-L5 or L5-S1 disc herniations. And it's actually much less common for it to be due to, you know, cancer, infection, to hemorrhage, other processes, more, you know, pathologic processes. Usually it's a very large disc herniation that does this. And then again, I think this audience knows it well, that the prognosis of neural recovery is far greater if the individual decompressed within 48 hours or faster. So, you know, surgical emergency. All right, moving on to variant number five. So this is folks with low back pain and a history of prior lumbar surgery, whether or not they have, you know, current radicular symptoms or not. And so, you know, this is certainly, we're gonna image these folks, presuming that they're, you know, worsening or symptoms are persisting despite, you know, various conservative care interventions. So what's helpful? Well, you know, radiographs and CAT scans are very helpful for taking a look at spinal hardware, assessing for, you know, malpositioning or misalignment, fractures of screws or hardware or loosening of screws. CT spec scan is actually probably the best modality for looking for hardware loosening. I actually don't have an image of that, but SPECT is a nice sensitive test to get a sense if there is some hardware loosening that isn't evident on a CAT scan or plain radiographs. CT with myelography, potentially, if we need to see the neural elements, this is gonna be useful if there's metal artifact from implanted hardware. And then an MRI with and without contrast is potentially helpful to distinguish new disc herniation, especially in patients that have been recently operated on within six months or so, new disc herniation versus granulation tissue and scar from, you know, just resulting from the prior microdiscectomy, for example. You can also get a good sense of if there's evidence of arachnoiditis, if you add contrast to the MRI study and then infection as well. So here's an example. You know, this is a contrast enhanced MRI study showing you what it looks like if you've got new disc herniation versus granulation tissue. So granulation tissue contains new vessels, new vascularization. It's gonna enhance when you add gadolinium, whereas herniated disc material is avascular, and so it's not gonna enhance. So that's what can help you distinguish one from the other, and that potentially influences, you know, treatments, whether what a surgeon may or may not decide to do, if depending on one scenario versus the next. This is a good example of harbor loosening. So if you see a lucency or a halo around a screw, this is indicative of screw loosening. So generally, more than two millimeters is considered clinically meaningful loosening. If you're not sure, again, this is where a CT spec scan can definitely be helpful. So CT spec is gonna show you the technetium-99 agent, it gets taken up by osteoblasts. So it's gonna enhance, it's gonna light up in areas where there's a lot of osteoblast activity laying down new bone. And that's gonna be the case where the bone is kind of trying to heal and heal and reheal itself, where a screw is continuing to move and kind of carve out bone, and then the body is trying to fill it back in. So you'll see that enhancement on CT spec. Example here are fractured screws. Here's an image series of adjacent segment disease or degeneration. So you get the sense that there's fusion here from, I believe this individual is fused from L3 all the way down to sacrum. And there is some stenosis and likely facet arthropathy that's been developing at the adjacent segment. So those forces have to go somewhere and they tend to go above and or below a fusion segment. So if you've got a patient with a fusion construct, you're gonna look above and below for kind of the greatest yield or likelihood of symptomatic pathology. The discs will wear out faster, the facets will develop arthritis faster, potentially new stenosis, radicular symptoms, facet, joint pain, et cetera. Arachidonitis. So this is an imaging series. These are just T2-weighted images. And if we scroll down, take a look at the central canal and you get a sense that up here, we can see the nerve roots, the punctate ovals here, they distinguish themselves up high. As we scroll down, they seem to kind of begin to adhere to each other. And as we go lower, you can't even make them out. So these are nerve roots that are adhered together. The others are probably adhering to the dural and we don't even really see them. Here, same thing. So it just kind of this blob of nerve roots that are adhered to each other and then can't even really make them out otherwise. So that's characteristic of adhesive arachidonitis. And then if we look, these are not the best examples in all honesty, but you can see enhancement. Gadolinium will enhance. This is an inflammatory condition. And you can see some rim enhancement around nerve roots, the brighter gadolinium lighting up. In this case, again, the roots are really adhering to the dura and they're sort of spreading themselves out away from the central canal, but you're seeing some of that brighter enhancement around the nerve roots that are adhering to the dural sac. So that's adhesive arachidonitis. I mean, I know we're kind of running a little short on time, so I'm actually gonna skip through that slide. Variant six. So this is folks with where we're suspecting the potential for fracture. So the big kind of red flags, low velocity trauma in an elderly individual, known diagnosis of osteoporosis or chronic steroid use. These are things that you're gonna think, I need to make sure I'm ruling out a fracture. So obviously spinal radiographs, but MRI without contrast or a CAT scan, obviously are gonna be helpful for assessing the bony anatomy. The reason that you may add contrast would be if you're concerned about malignancy and the possibility of a fracture in the context of metastatic or primary spinal cancer, spinal malignancy. MRI is very helpful. CT spec somewhat, but less so, but MRI is very helpful in understanding the acuity of a vertebral compression fracture and understanding if someone's perhaps a candidate for a febrile augmentation procedure. And fracture acuity is one, and the other is the potential for non-union. So someone may have had a fracture six months or even a year ago, and if they've got STIR or T2 enhancement on MRI, I mean, that's indicative that there's a fracture cleft and it's not healing. So it's kind of behaving like a non-union fracture or as it should heal and give or take six weeks. So here's a radiograph of a wedge deformity, kind of not a whole lot of deformity, but compression fracture there, it's like five, four, L3. Here's what you might see on MRI. So if it's acute or there's ongoing edema, it's gonna look dark on T1, it's gonna look bright on T2 or STIR. And you're seeing a good example of enhancement there, probably a fracture cleft. This is a decision rule, multi-specialty group that got together and the ACR actually did one too, but this similar findings. Essentially, how do you think about whether someone's an appropriate candidate for vertebral augmentation? So obviously one is imaging, right? So the advanced imaging matters. If there's, in this decision tree, when they talk about advanced imaging being negative or positive, that's really referring to edema or evidence of a fracture cleft. And that's helping you distinguish advanced imaging negative or positive. And then understanding if the patient's symptoms are stable or they're worsening. So in this tree, just for example, if they do not have edema or a fracture cleft on advanced imaging and their symptoms are stable or improved, there just really isn't an indication for vertebral augmentation. So non-surgical management, NSM. If you have three or more of these factors, they're saying maybe, maybe you could consider vertebral augmentation, but it's not like it's a given that's what you should do. So these unfavorable factors, meaning pain may not get better, the patient may not do well, it's worth considering augmenting that fracture level. Progression of height loss. So if there's progressive height loss, even if there's no edema or a fracture cleft on advanced imaging, that may do it. Severe impact on functioning, greater percentage of height loss or a kyphotic deformity that's forming as a result of wedge fracture or the nature of the deformity at the fracture level itself. As you move along, you get a sense of what happens. So essentially, if there's worsening symptoms or if there's positive imaging and it's positive for fracture cleft or edema, it takes less of these factors to say, an augmentation is probably the right thing to do. And if you have positive advanced imaging and worsening symptoms, pretty much it's the right thing to do that that individual will likely do better in the short-term and long-term with vertebral augmentation. So that moves us finally to variant number seven. The last one is suspicion of cancer. And so this is really where we're leaning heavily on MRI with and without contrast as kind of the test of choice and with consideration of other potential imaging modalities depending on other factors that may allow them to have an MRI or not, et cetera, or artifact that we're worried about. Interestingly, all the red flags, and I showed that table earlier, of all the red flags that actually evidence-based increase the probability of identifying cancer on an MRI when there's suspicion of cancer and in the context of low back pain is a prior history of cancer. So that's the big one that if your patient says, yeah, I had breast cancer, it's been in remission, I was treated, and they're presenting with low back pain with that history, you should definitely be suspicious that they may have recurrent cancer. So again, MRI with contrast, really good, our go-to. And then, this is tricky. I think the whole topic of identifying various cancers on imaging is more than an hour lecture in and of itself. But a few little tips that I think are helpful that I've gleaned from radiology colleagues and speaking with them, if you see diffusely increased T1 signal, that is typically benign. So think like very commonly that might be a hemangioma, a typical hemangioma is, there's a lot of fat in that. So if that's gonna look bright on T1, it's the atypical hemangiomas that look darker. And then, you might say, the radiologist says, oh, the atypical hemangioma versus possible malignancy, if there's concern, may consider biopsy or re-imaging in six months, but that's usually benign. If the T1 signal is diffusely decreased, that could either be benign or malignant. So benign reasons might be red marrow conversion with that could occur with, due to drugs or hypoxemia or just with age. There also are, of course, malignant reasons for decreased T1 signal and that's myeloma, infiltrated processes, leukemia, lymphoma. These all can show up as decreased T1 signal. So just to look at some examples, here's a hemangioma. So it looks bright on, this is T2 weighted imaging. Here's T1, no, that's backwards. This is T1, this is T2, and here's STR. So if we go back for a minute, so when T1 is, the lesion is hypo-intense to adjacent muscle or disc, that is typically abnormal. So in this case, it's hyper-intense to the disc on T1. So that's normal, right? And then if we look at T2 or STR, so fluid-sensitive sequences, neoplastic processes are usually hyper-intense to the disc. So we expected that this was malignant, this would be brighter than the disc signal, and it's not, right? So that's good evidence that this is probably hemangioma and not a neoplastic process. Alternatively, here's a, this is a T2 weighted image. Here's T1, quite dark on T1, and quite frankly, darker than the disc. That's concerning, right? So that should lead you to suspect that's malignant. So I think that I more or less sort of ended on time. Hopefully, we definitely make sure we have time for questions. I'll leave you with these key points. And I think folks, I assume, have access to the PowerPoint, happy to share it. But I will leave it at that. And I'm more than happy to field questions. Thank you, Dr. McCormick. That was a very thorough discussion of different lumbar spine pathologies. I've been monitoring the chat, which has been very lively, and I've summarized some of the questions that came in. And I will address them to you. The first one is regarding the subarticular stenosis in the setting of a disc herniation, one versus two level injection. And the question comes in the form of, does it really matter? I mean, if we have enough volume and dose where the medication gets to the epidural space close to the disc pathology, does technique actually matter? The truth is we don't know. And I was always kind of mentioning that when we were looking at those slides, is we just don't really have comparative. Someone at some point needs to do a randomized comparative trial, pragmatic trial, where we take folks with symptomatic refractory pain from a subarticular zone disc extrusion, and they randomize patients to either get that retrodiscal approach, the supra-neural approach, a level below, or a two-level injection, and follow these folks and look and see if it does matter. So we really don't know. And I think you're gonna, if we were to poll everyone, I bet everyone probably has a different style and practice pattern in what they do. I shared mine, and this is just, again, this is not data-driven. It's just sort of my gut and my hunch is I will typically use a two-level approach with a large extrusion or protrusion, where I feel like I'm not gonna get adequate flow around kind of the full girth of that herniation when it's in the subarticular zone or central. So that's what I do, but that's just my personal practice and not necessarily evidence-based. Yeah, I agree. I think that for the patient like that, if they're having primarily reticular symptoms and there's compression of the traversing nerve, I typically go caudal. If there is a huge component of disc pain and the herniation is really, really large and the pain is acute, I tend to be more wary about injecting just at that site. But when you have two-level injections, we're planning for that. As soon as you get some patient feedback that they're not tolerating the procedure, well, I think that that can give you some indication as to how much medication to inject. The second question is regarding facet cysts. I think most of us on this call have had facet cysts causing reticular symptoms. And the question is regarding rupture. And Dr. McCormick, you mentioned injecting contrast. You showed some awesome pictures of injecting the facet and then that extended to the cyst and the cyst gets large and it goes away. The question is how much volume, how much pressure? I mean, invariably when I see patients like this, there's a huge amount of stenosis. So I always worry, just like you mentioned, that if I am not successful in the rupture, that the symptoms may be worse off. And a sub question under that is, are there things on the MRI that can give you some indication as to whether you're going to be successful or not with a rupture? Yeah, great questions. So, yeah, first of all, I would definitely proceed with caution. If there is stenosis, if there is central canal stenosis, because that cyst is the geometry of it, the size of it, and the exact location is such that it's already compressing neural sac or roots, you may choose to not touch that, right? You could aspirate it, but probably not pressurize it. In terms of, I will typically actually fill a 10 cc syringe with contrast, because I've just found anecdotally that these cysts, they can accept a bunch of fluid before they eventually rupture. And as I mentioned, I would definitely encourage folks, if you're going to do it, to block the nerve root that's being affected by being compressed by the cyst before you start pressurizing it. Remind me of the other question. I think I answered part of it. The question is, are there things on the MRI that can give you an idea as to how viscous, perhaps, the solution might be, and whether it's likely to respond to either an aspiration or a rupture? Yeah, that's a great question. So, yeah, a few things. One is you can get a sense of, sometimes you can get a sense of whether that cyst actually communicates with the facet joint capsule. So it may wall off. And then the reality is, if it's walled off, you can access the facet joint and pressurize it, but it's not going to make its way into the cyst. Of course, you can access a cyst through the interlaminar space. You can, in some cases, through the foramen. I don't typically do that. It's usually not the greatest idea, but you can access it through the interlaminar window. And you may choose to do that if it doesn't seem like that cyst is communicating with the facet joint. But I think, in my opinion, kind of the safest and simplest is to access the facet posteriorly if it communicates with the cyst. The other thing, rather than it being, communicating or being walled off, is that you can see loculations. And if the facet cyst is highly loculated, you may not, it's probably less likely that you're going to be able to successfully rupture it because one compartment of it may rupture or may fill, but the others may or may not communicate with that particular compartment of this kind of complex loculated cyst. You can also see sort of more density. So if it's just synovial fluid, right, without any junk in there, it's going to look bright, right, on fluid-sensitive sequences, just like an effusion in a facet joint would look bright on fluid-sensitive sequences, T2 or STIR, et cetera. But if it looks darker or sort of heterogeneous, it may be filled with more dense material that may make it more challenging to aspirate or rupture. But my take on this is if you're doing it safely, if you're not going to create potential decompression or I guess decompensation of a stenosis that's preexisting and you're careful, I personally think it's worth a try if it means preventing decompression surgery, because most of these patients, if they're going to have surgery, they're not just going to have a bony decompression and cyst removal. They're probably going to end up with effusion. If they don't get it right away, then when they are decompressed, they already probably were a little bit dynamically unstable and now the surgeon's removed more bone and they're going to be even more unstable. So they're probably going to end up with effusion at some point down the line. So if you can help that individual prevent surgery altogether, I see that as a win. Yeah, no, I agree. There's a question that just came in regarding the needle size. I see this debated. One is that the facet is really arthritic. You can't use a big needle, but having said that, if you use a larger size needle, like an 18 gauge, you're able to pressurize the facet more. What's your practice? I typically use a 22 gauge spinal needle. And if it's tough to get into the, it can be, right? So if you have a very arthritic facet and you've got spurs that are really kind of covering a lot of the posterior aspect, it's tough to access. One thing is, I mean, definitely look at your axial imaging. You can get a good sense as you scroll through the axial cuts, where could you possibly sneak your way into the posterior aspect of the facet? But if you can't, and you really, I mean, there's like a big, arching osteophyte, essentially it's covering access, obscuring access. You know, go at the, I tend to go at the superior recess. You can go superior, inferior, but they're essentially, you've got, you know, sort of the bony aspect of the joint, but then you've got some redundant joint capsule, superior and inferior, and you can slip your way into, I tend to go superior for no good reason other than I just fell into that practice pattern. But even, so you're sneaking into the redundancy in the capsule and you can access the joint and you can get a nice arthrogram and potentially use that to rupture a facet cyst, even if that joint is really gnarly and there isn't good access at kind of the bony levels of the joint. Yeah, I mean, in the example that you chose, I think even if you were not able to rupture the cyst, it looks like it was amenable to intraluminopathy or injection approach where you can actually puncture the cyst through a secondary approach because you're able to see the cyst. Oh, and I might've misunderstood. If that was the question, yeah, you can definitely use, you know, you could use an 18-gauge. Just be careful, right? I mean, just be really careful with your procedural planning, but you certainly can, you know, access the interlaminar space. If you use an 18-gauge, you probably only need to aspirate. I don't know that it even makes sense to try to pressurize it with an 18-gauge. You should actually be able to aspirate unless it's a complex cyst. Great, awesome. I have two more questions for you. The next question is regarding vertebrogenic low back pain and discogenic low back pain. I'm sure you get asked this a lot. You know, there were some comments that patients that present in a similar fashion, the axial kind of flexion-based pain, how do you really know that it is vertebrogenic? Some of these patients have gone, I think historically, and we're looking at literature, they get the discography, but that can also pressurize the end plates. What is the role of discography? What is the role of epidural injection for something like this to tease out how much of the component is discogenic versus vertebrogenic before you proceed with an ablation? Yeah, it's a great question. And I think that, you know, the clinical and scientific communities are still trying to properly answer this. So I can give you my take right now. And I think that our knowledge on this is gonna keep advancing rapidly in the coming years. So that's right. Dr. Chang, you just alluded to it, but provocation discography stretches annular fibers, and that's gonna mediate pain through the center of the vertebral nerve and is suggestive of annular base pain, but it does also create end plate deflection, and that's gonna mediate pain, excuse me, through the base of the vertebral nerve. So provocation discography is probably not a great way for us to distinguish vertebrogenic from annular type or so-called discogenic pain. So really, I mean, it's the cluster of patients' historical factors, exam, and then imaging. And at this point, you know, most of these folks probably do have deflection-based pain, you know, maybe some element of pain with coughing, sneezing, you know, the classic sort of discogenic picture that we think of, you know, midline low back pain, some radiation, maybe perhaps in the buttocks, but not like a radicular referral pattern. So the big thing at this point really is, is type one and type two modic change, is suggested that there's at least some component of vertebrogenic pain, but whether there's annular pain and vertebrogenic, we don't really know. There isn't a great way to diagnose this. And frankly, there are huge limitations to, so provocation discography is not a great test for distinguishing these two. It'll distinguish anterior element pain from let's say posterior element or other sources, but not end plate versus disc. There's no good way to block the sinus vertebral nerve without anesthetizing all the other structures in the epidural space. And there's no good way to block the basal vertebral nerve. So to block the basal vertebral nerve, you know, you need to access the pedicle. That's very painful. I mean, just the, you know, this is typically a procedure that's done with, you know, conscious sedation, if not general, so that you have no diagnostic value there. And even if you were able to do it without putting the patient under some level of sedation, it's so vascular that if you inject into the vertebral body, it's just gonna carry away any anesthetic almost immediately. So basically to be determined, but that slide I showed earlier showing the clinical profile of, you know, dominant vertebrogenic pain is the best that we have from the studies that have been done so far with probably the most important, you know, the radiographic marker being type one and type two modic, that we are definitely gonna have better radiographic proxies of vertebrogenic pain in the coming years. There are a lot of smart people working on this right now and on, you know, imaging modalities that are more sensitive to sort of the pathologic process that goes on that we associate with vertebrogenic pain, where there is, you know, some kind of chronic inflammatory process that leads to upregulation of nociceptors on the BVN termini, the density of those termini, and just the sort of the windup that happens at the base of a terminal termini that we believe is associated with vertebrogenic pain. So there will be MRI-based modalities and probably some other ones that are forthcoming and that are, I know, being studied right now. Perfect. You've been so generous with your time. I have one last question, which is regarding compression fractures. You know, outside of clinical information, when we see a fracture and there's a T2 hyperintensity in a STIR sequence, at what point does that signal subside? And what is the role or the indication to get updated MRI, for instance, for someone whose back pain never goes away after an identified fracture? Yeah, great question. So, I mean, we know that bones should heal in about six weeks. So any fracture of any bone, I mean, generally healthy bone should heal in about six weeks. That hyperintensity can persist for, I want to say, give or take three months or so, but the role for updating imaging is really going to be, in a lot of ways, symptom-based. So if that fracture pain is not getting better with conservative measures, well, one, I mean, you're probably getting seroradiographs, right? Because if they're collapsing further, that's problematic. And that potentially leads to deformity, or you may have fragments that create neural compromise, or you've got more problems now. So following simply the just height loss with radiographs, yes. But if you were thinking about augmentation, getting an updated MRI with a patient with more chronic now symptoms is worth doing, because you're going to understand, you're not going to see a fracture cleft on X-ray. So you really need an MRI or a CAT scan to understand, is there non-healing, is there non-union, essentially, of that fracture? And that's where MRI or CAT scan can help with that. So it's going to be symptom-based. If, certainly, if radiographs are stable and the patient is symptomatically, functionally, they're getting better, there's no need for updating advanced imaging. But if that's not the case, then that's a good reason to image with MRI or CAT scan. Great. I think that's a wrap. Thank you, everybody, for tuning in. And thank you, of course, to Dr. McCormick for enlightening us. I certainly learned a few things here. Just as a reminder, this presentation is recorded, and it will be available on the AAPMNR website. And thank you so much, and have a great evening. Hey, Carol, thanks for joining. Bye-bye.

spine imaging

low back pain

imaging modalities

disc herniation

synovial facet cysts

lumbar spine pathologies

facet cysts

compression fractures

vertebrogenic pain

basal vertebral nerve ablation

cauda equina syndrome