Hello and welcome to the advanced back pain management session. We hope you're all well and safe and enjoying this virtual conference in the comfort of your own home. So I don't know about you guys but every year I go to AAPMR for two things. The first thing is I got a stock up on my free supply of pens for the year and the second is I try to find sessions that can help me review concepts that I definitely should review but never have time to. And so we the presenters very much kept this in mind this year as we were designing our session. We wanted to choose lumbar spine topics that are rare enough that you might need to review but still common enough that you'd be able to apply what you review today in your daily practice. And so this were the four concepts that we came up with and you can see the presenters who will be talking about them. In order to make this as interactive as possible despite the pre-recorded format we're going to try to keep our presentations very case-based. So I hope you will put on your thinking cap and work through these cases with us and I would do my best to keep my big head in this rather narrow window which is easier said than done when you apparently move your head as much as I do when I talk. And let's get started. So the topic I'm going to be talking about are disc herniations. And you're like wait Patricia I thought we were going to discuss some more exotic topics. Why are we talking about disc herniations? Well I see disc herniations day in and day out. Well you probably see some types of disc herniations in your daily practice but you might not see some other types of disc herniations. And I just want to take my 14 minutes or so to kind of review the terminology of how we can describe how discs herniate and where they herniate. And you'll find that depending on how the disc and where the disc has herniated may actually influence its natural history. I have no relevant disclosures. So one morning I opened the door to my exam room and found no one sitting there and I was like confused. Looked around and someone was laying on her side in a fetal position on my exam table. She noticed me and started to tell me she was having the worst pain of her life. Turned out she's a 34 year old, pretty healthy. She's not very active at baseline but on the weekends she goes and do her regular hikes and Pilates classes. But about a week and a half ago she started to experience something very different than her normal off and on back pain. She felt like her entire right leg is now on fire. Where was her, who is she having her symptoms? Going all the way down the lateral thigh to the lateral leg and the top of her foot. I was concerned. Was she having any neurological changes? Well not really. She doesn't really truly feel numb. She still thinks she's strong and there's no bowel and bladder changes. Luckily when I did a neurological exam everything seemed intact. However by this time the patient has tried anti-inflammatories, she's on muscle relaxant, she was started on gabapentin and her primary care doctor even gave her some tramadol and she was obviously still in a lot of discomfort lying there on my exam bed. So we decided to get imaging and this is what we see. On the left side of the screen you see a sagittal T1 and then on the right side of the screen you see a sagittal axial T2. So you can see that on my slides I actually have the scap lines in yellow. So the axial cut is through the L5 S1 disc and sagittally we are almost at midline. You can see that at L5 S1 disc there's been loss of height. There's actually end plate changes that you can witness. When you look at the axial cut there is already a noticeable disc protrusion and it's maybe touching the traversing right S1 nerve but it's definitely not impinging it. I don't know what you guys are thinking. She was describing kind of right buttock, right lateral thigh, lateral leg and dorsum of the foot pain and frankly I tend to think a little bit more L5 but you can really never be sure. So let's check how the L5 neurofibroma is looking. I'm going to start to move the image a little bit more laterally, sagittally and so you can see huh okay. I'm starting to see something that's a little bit interesting to me. I don't know if you guys see that. There's definitely something there and based on my axial cut on the scap line that's not really quite where the L5 nerve should be. Let's keep on going. Okay. Okay well that I think definitely is a right L5 exiting nerve. I don't know what the other thing was. So let me start to actually change my axial cut. Let's go a little bit more superiorly. What do we see here? Huh something is starting to come into view. What is that object? It's definitely not the L5 nerve. Uh-huh. There it is again a little bit more clearly. What are we looking at? Well it turned out that after some back and forth and comparing everything on T1 and T2 it's a very dark structure almost devoid of signals and we actually even correlated this to the patient's CT that she got for other medical reasons. It eventually thought that this was going to be disc material. So um give me one second here while I answer the slide. So what's going on here? The disc material seems to be not contiguous anymore with the parent disc. What is that called? Perhaps this sequestration? You remember that this is a different phenomenon than say a disc protrusion or extrusion. So let me just review those terms a little bit better. On the left we have a picture of disc protrusion. So the distance that the disc material has exited the parent disc is smaller than the base from which it has exited from. And you can compare that to the right which is a disc extrusion and the distance that the material has exited from that parent disc is actually greater than the base from where it has exited from. And you remember that disc sequestration which you can see better examples here there's basically it's a kind of an extrusion that has now entirely lost contact with the parent disc. So here you can see that better on the sagittal T2 and axial T2. Sometimes the sequestration can get so large like in this case or if we just kind of change the axial right here you can actually see it's entirely obliterated the spinal canal. And when we're starting to talk about disc herniations it's important to really standardize our terminology. So something that I would really recommend you to review if this is something that you haven't looked into for a while is the Farden classification. So in 2014 he led a multidisciplinary group to standardize again the disc terminology. This is the Farden 2.0 and I took this graphic from his paper. So you see here that in the horizontal plane this is how they decided to divide up the location of the disc extrusion protrusion or migration. So we have the central canal zone. We have kind of a sub-particular zone which is also called the facet zone. And then we have the foraminal zone and then eventually the extra foraminal zone. So there's actually a very interesting paper by Daigigi and his group. It came out in 2014 and it followed ten hundred patients, consecutive patients with extruded lumbar disc herniation. And what they were really trying to do is get a better understanding of where does a disc usually herniate. So like the Farden paper he divided into kind of this the central and paracentral disc herniations. And you can see that if it's a small disc herniation it might not impact the spinal canal too much but if it's very large it can really cause spinal canal stenosis. There's also facet or sub-particular or lateral recess stenosis that can be caused by this type of disc herniation. And as you can imagine this can cause a lot of impingement on the traversing nerve root. And then there's of course foraminal and even extra foraminal herniations and this can impact the exiting nerve root. So you can also describe what's happening to the disc in the vertical plane. In the Daigigi paper they really just referred to this as being rostral or caudal so whether it went up or down. But in the Farden classification you can see on the left graphic here that they even divide it up further and if you're interested you can read the Farden book paper itself. When Daigigi's team looked at it he found that most lumbar disc herniations tended to be caudal. So more than 70% of these disc herniations tended to be caudal. And it is much more likely to be either central or paracentral. So you can see here that whether it is rostral or caudal it was more likely to be in the center and in fact more than 90% all disc herniations tended to happen in these two zones in the horizontal plane. What's more interesting too is that they found there were no significant associations between gender BMI or the level of herniation with a migration pattern in the horizontal plane. So what are the natural history of these discs if this patient chose to do absolutely nothing at all? Well it so happens that how the disc herniates has a little bit of impact. So this is a paper from Meng and colleagues back in the 1990s. He followed 48 patients who had lumbar disc herniations for up to 40 months and actually performed a second imaging and you will see that many of these patients actually had a decrease in size of these discs during that time frame. So group 3 there is the group of the patients who had more than 75% decrease in size of their discs and 31 of these 48 patients were in that category. He subsequently kind of delved a little bit deeper and tried to see which type of disc tended to resort more and what he found out was that the larger the disc herniation, so if the disc was actually larger than 50% of the spinal canal, they tended to actually resort the most. So 13 out of 15 of those patients had more than 75% decrease in the size of their disc herniations. So here's an example of one of my patients. He's had prior work done at L5-S1 and a little bit scoliosis so I just want you to also count with me up so L5, L4, L3, L2. The axial cut on the right is an L1-2 disc space and you will see here there's a disc extrusion into the foraminal zone and if I took you near the cut, there it is. It's actually extending into the foramen on the sagittal cut, really filling entire that neuroforamen. He was lost to follow-up. 11 months later he came back. He's like, actually my right back, buttock, and kind of thigh pain went away and now I'm having new and different left leg pain. So we got another MRI just to look for that source. Again here is his L5-S1 hardware. If you look, we are now back at the L1-2 space but nothing's there. This disc actually has resorbed. There's nothing anymore at that neuroforamen. So what's that mean if there's radiographic changes in the disc? Well to answer this question, Komori and colleagues looked at 77 patients with lumbar disc herniation and radiculopathy. On the first column there you see that they had the radiologist kind of subjectively grade if there's been any changes in the size of the disc and on the next two columns they rated if the patient had excellent work and good progress, which meant they had reduction in the amount of pain and improvement in any neurological signs, where they had no improvement at all, which they termed poor. And you see the far majority of people during the follow-up, which is 150 days, actually had improvement in their clinical course. And even the patient who had absolutely no change on imaging, 13 of those 28 actually had improvement, while only 15 out of those 28 continue to have poor outcome. And so they actually summarized that larger and migrated herniations tended to decrease in size more. I found some other studies, a very small Korean one, which showed that if they're sequestrated, like our patient here, they did very well, maybe even a little bit better than the extruded discs. And the changes in these disc herniations are usually observable after six months. But the important thing that they note, and which I want to emphasize here too, is that symptoms can improve without decrease in size of discs. So what happened to our patient? Well, she tried to do everything possible without intervention first. After a few days, we tried to start physical therapy, she had chiropractic, she tried acupuncture. When gabapentin wasn't enough, we actually added some BOLTA, but she was just having a very hard time. We eventually did do a transpiramidal epidural steroid injection. And if you guys have any, you know, wanted to review just what are the non-operative and operative treatments for lumbar disc herniations, especially with radiculopathy, I actually highly recommend the NASS evidence-based clinical guidelines. I know the one for low back pain was just updated this year and that's actually endorsed by AAPMR. They have a fantastic one on disc herniations with radiculopathy. So she did actually very well currently after the L5-S1 transpiramidal epidural steroid injection and we're hoping that she will continue to improve. So my take home from my portion of the talk is that not all disc herniations are the same. We should really standardize how we talk about them and for that I recommend your review in the FARDEN 2.0 paper, a great read. If you get anything out of this talk, you remember that disc herniations tend to be rostral and paracentral and the type and location can somewhat influence natural history with larger migrated herniations decreasing in size a little bit more after six months. But the thing is symptoms can improve even without any radiographic changes. So here's my works cited. At the very bottom I've actually put my email because it's hard for you to actually ask questions or let me know what you're thinking. Feel free to email me anytime. So from here I'm going to turn the talk over to Dr. Zach McCormick who is definitely a star in the pain and spine field and probably has published the most out of anyone I know in the last year. I recently found out he's also actually a star athlete and he actually still holds the record for high jump in his high school, I think the entire school, even now so many years out. So Dr. McCormick. Thank you for the kind introduction Dr. Zeng and I was unaware of that that statistic or record I guess. So I practice at the University of Utah. I'm the chief of our spine and musculoskeletal rehab service and I'm gonna speak a little bit about arachnoiditis. A few disclosures, none of these are directly relevant to what I'm going to speak about. So this is a patient of mine that I'll use as an example. So this is a real case and I'll walk you through our thought process with what we'll call her CM. So 72 year old woman, you can see her comorbidities there, Parkinson's, obesity, type 2 diabetes, peripheral neuropathy, pretty common stuff. And when I originally met her, she presented with classic neurogenic claudication symptoms and I'll spare you the nitty-gritty details of her early care but essentially you know we did our best to optimize non-operative treatments. Her symptoms progressed, quality of life was tanking. So she ultimately ended up with with a laminectomy without fusion. So she had severe spinal canal stenosis. I won't show those images but the L45 spondylolisthesis, no dynamic instability but severe stenosis. So ultimately the decision from our surgical colleagues was laminectomy without fusion and this resolved her symptoms of neurogenic claudication as one would expect. So after her surgery, within a few days, she began describing new fixed sciatic type pain. So she described it in the posterior buttock and thighs, burning sensation, very intense and and again fixed, not claudicatory in nature. So when I saw her back in the clinic, just the high points of the exam, she continued to have similar Parkinsonian features to her neurologic exam but otherwise no real changes in strength and sensation. Reflexes were symmetrically down the same way they had been prior to her surgery and then she had similar range of motion restrictions again as to prior to surgery. So really nothing had changed objectively on my exam when we saw her back post-surgery. So these are her plain foams. You can see the the AP image and the left hand panel, the flexion foams in the middle panel and then the extension foams in the the right side panel. You can make out that spondylolisthesis at the L4 and L5 level. You can see that it's not really moving, not really appreciably, maybe a millimeter or two. So that really didn't change post-surgically. She's not developed instability. You can appreciate compression fractures at the L2 and L3 levels and I'll just I'll mention that those are those are remote, that's unchanged compared to pre-surgical imaging. And then clearly has you know general spondylosis, disc height loss. She has some bridging osteophytes at the anterior end plates up high in the thoracic spine. She has facet arthropathy. Again all of these features were consistent with with her pre-operative imaging. So then we'll move on to her MRI. So these are these are T2 weighted images. You'll see in the in the left panel we have the sagittal imaging. In the right hand panel we have axial images. The scout line is shown in the left panel and sagittal with that white line. So that's the level that you're seeing at the axial cut. And at this level just I would just draw your eye to the central canal. So look at the right panel, look at the central canal and you can make out those darker structures, those punctate kind of ovals. Those are obviously the coticline or the nerve roots. And then the brighter signal is the CSF around it. So at this point at this level we're looking at what 5 4 3 2 1 kind of L1 lower L1 spinal level. You can really make out those nerve roots just fine. They seem to be floating in the cerebrospinal fluid. Nothing that looks particularly remarkable. So as we go down a cut maybe you see some migration of those spinal nerve roots of the coticline and the central canal. A bit off to the patient's right and posteriorly but nothing nothing super remarkable yet. And then things change. So as now we're getting down to the L3 vertebral body level and you can see again those those punctate dots are now seeming to cluster. So you see kind of two different areas where the roots almost seem to be migrating to and separating themselves. And we're losing a bit of the ability to distinguish one nerve root from the next. And then in the next cut, one, you know, a level lower, or rather at the three, four disc space, again, attract, you know, attract your attention to the central canal and the right-hand panel. And now we're really seeing two focal areas where those nerve roots seem to be clustering or adhering, one group more anteriorly, one more posteriorly in the central canal. Same thing here at the next level down. And then we almost lose a bit of the ability to see the nerve roots at this next level, which is more or less at the level of the L4, L5 disc space. So we do see some, you know, evidence of nerve roots there kind of posteriorly and centrally in the central canal, but we've really lost most of them. And ultimately they seem to be adhering themselves essentially to the dura radially away from midline. And that continues here. So almost an absence of the ability to appreciate spinal nerve roots, except for a few there posteriorly in the central canal. Same thing here as we move down. And then we see a re-emergence of some of these nerve roots, but again, kind of clumping or clustering together where we really don't get a good sense of individual nerve root structures. Okay. So then we'll move on to T1 weighted FATSAT post-contrast images. So these are, these ultimately are useful and we'll talk more about that. So this is, it's not, it's not incredibly apparent in these images, but I'll do my best to describe it. If we again, look at the left panel, and this is the sagittal image, right-hand panel is the axial cut with the scout line shown in that linear, the white line on the left-hand panel. So again, just draw your eye over to the right-hand panel, central canal. And as I scroll down, what you'll notice is there are some subtle, but sort of enhancing areas within the canal. And again, just as a reminder, so T1 imaging within the central canal, that bright rim is epidural FAT. The dark stuff is going to be cerebrospinal fluid. So fluid should show up as dark on T1 imaging. And then we see, if you look carefully at that, at the posterior aspect of the spinal canal, just anterior to that bright epidural FAT, you see sort of a brighter patch. And that's a little bit of enhancement with contrast around nerve roots that are clustering close to the dura. So that, that fits with, and I'll talk more about this, but that fits with arachnoiditis inflammatory process. We see, we see contrast gadolinium based enhancement with this process. And then again, you can see within, within the dura, posteriorly and slightly paramedian to the patient's left, a little bit of enhancement around those nerve roots that are clustering towards the dura. Same thing here in this cut. So, so this is adhesive arachnoiditis and you know, ultimately what you'll find if you, if you review the literature on this is there just isn't much written. There are really, we have case reports. We have some expert opinion. We don't have certainly large cohort studies to inform us about the epidemiology of this phenomenon. It is likely rare. I can tell you anecdotally it comes up every so often in my practice, not commonly, but that's anecdote, not data. You know, risk factors that have been described infection, trauma, especially spine surgery. So spine surgery being a potential inciting factor for adhesive arachnoiditis, otherwise tumors and intrathecal injections. So blood bleeding heme is thought to perhaps be a factor that could incite the process of adhesive arachnoiditis. There's debate around certain contrast media or preservatives within separate steroid preparations. Really no hard data on this, but these are, these have all been proposed by let's just call it medical experts. Um, so the pathophysiology, like I, um, alluded to, it's really, that should say, uh, not procession, but process. This is an inflammatory process that leads to fibrosis and then adhesions of the PIA. And it's, it's very, it's healing is challenging because this, the PIA is, uh, and the arachnoid, excuse me, the arachnoid is a vascular, and then you have cerebral spinal fluid right there. That's washing away macrophages or other cells that might be involved in scavenging fibrotic tissue or aiding with the healing process. Um, so challenging, um, it will typically present as radicular pain, particularly if, uh, in the lumbosacral region, um, rather than a thoracic, for example, and often maybe in a sciatic distribution, um, it is associated potentially with bladder dysfunction, um, and it can progress to paralysis. And that's described in a number of cases that you can find if you search the literature. Um, I alluded to some of the imaging findings. So, so MRI, um, with, uh, with contrast is truly the best way that we have right now to make this diagnosis or rather to support the diagnosis with imaging. Um, and what's shown here, one through five, generally, this is thought to be the progression of imaging findings associated with adhesive arachnoiditis. So arachnoid cysts followed by clumping, thickening of the nerve roots, and then displacement radially or towards the dura away from the line that as, as we saw in our patient, um, and potentially it could progress to, uh, again, if at higher levels, um, above the, uh, the conus, obviously spinal cord swelling, um, T2 signal hyperintensity in, uh, in the cord itself, um, associated with spinal cord compression, um, essentially with arachnoid webs or separations. Um, and it is also possible to see syrinx formation. So how about our patients CM? Um, well, I'll be honest. So as I mentioned, there really isn't good, high quality data. Um, you know, no one has really studied this in a rigorous fashion because it is fairly rare. So ultimately we have case reports, excuse me, my light went off. There we are. So, uh, um, this is my approach to management based on what I extrapolate from what seems reasonable, um, based on similar conditions, whether it's a radicular pain, um, other neuropathic pain conditions, um, uh, not actually structural pain based on impingement per se, um, but kind of fibrotic tissue that, um, uh, you know, maybe tacking down nerves. So, um, with, with this patient, we started with, um, with physical therapy, heavy focus on nerve glides. We also tried a bit of pool therapy for her. Um, she had been on Cymbalta previously, um, and had been on a lower stable dose. We tried increasing the Cymbalta, you know, obviously has some, some, uh, uh, properties that are helpful for neuropathic pain. Um, separately, we did touch base with neurology to optimize her cinema just in case this might've helped. Um, you know, ultimately I can't say that it made much of a difference. Um, a number of weeks later, hadn't really improved much. Um, we tried a steroid burst. We put her on gabapentin, up titrated that, um, we gave her PRN tramadol because at this point she was quite miserable. Um, and we increased the frequency of her PT and really tried to optimize that mechanical approach. Uh, we did order a new MG just to get a sense of whether or not something new was going on. We found no new objective changes on the MG. So still evidence of the same, um, sensory peripheral polyneuropathy, no evidence of a new radiculopathy. And then, um, we did, um, at that point proceed to epidural injections. So, um, you can see, um, you know, transforaminal injections here, um, at the L3 L4 level, um, excuse me, the L4 L5 level. So at the level of her list thesis, um, just of note, uh, you can tell that the needle on the patient's left side, obviously needs to be further advanced. Just make sure that we're on the same page from a technical standpoint, but you can see good, uh, you know, foraminal and epidural flow on the patient's right side below the pedicle of L4. And, uh, ultimately that was helpful, but for about a day. So we said, okay, why don't we try something different? Um, you know, she had been decompressed, didn't have a lot of, um, interlaminar space, um, up in the lumbar spine. So we try to call epidural injection with particulate steroid, hoping that that might have more robust and durable effect. Unfortunately, similar effect, she felt great for a very short period of time, symptoms came roaring back. So ultimately, um, after an ongoing discussion, we did perform a spinal cord simulation trial, um, which was, uh, successful. Um, she reported significant pain reduction. Um, our recollection is around 80% relief reduction of her, um, the neuropathic time, pain symptoms in her legs, um, associated with functional benefit, sleeping better, and just generally improved quality of life during the trial period. So she did go on to have implantation, um, and at least up until now has been happy, um, with, uh, with the result. So, um, here is a list of just the key points related to adhesive arachnoiditis. And, um, I'll ultimately be happy to take questions, which we'll save for later. Thank you very much. And I will pass the virtual microphone over to Dr. Popescu. Hello. Uh, I'm, uh, Adrian Popescu. I was asked to present on, uh, developmental narrow spine. I work, uh, in the Penn Spine Center at the University of Penn. Um, very happy to be here, uh, with you guys today. And we're gonna, uh, try a, uh, a slightly different approach where we, where we, um, will, uh, basically, uh, learn or review some of the information that we already know. And we continue with, uh, uh, some, uh, interesting, uh, cases. Um, what is the clinical significance of the developmental narrow, uh, uh, spinal canal? It can definitely contribute to the clinical symptoms and any, uh, normal degenerative changes or other pathological processes can lead to earlier clinical symptomatology in patients with congenital canal narrowing. It does influence surgical and procedural decision-making. Um, and we all have to keep in mind that, uh, uh, the developmental central canal narrowing, um, uh, has, you know, it's, it's, it's present in about 15% of spinal stenosis patients, uh, most typical with short, thick pedicles with a reduced anterior-posterior diameter of the spinal canal. So, let's, uh, go, uh, and find out what is significant with narrowing of spinal stenosis. And we find out that in the literature, a cross-sectional area, uh, at which the intrathecal pressure increases is 77 square millimeters. Uh, most common canal compromise is the L4 level followed by L3, L5, and L1. And the normal, uh, anterior-posterior dimension of the thecal sac in the mid-lumbar region is 12 to 14 millimeters. Uh, and you can see the white, uh, uh, line, uh, that shows the AP dimension of the spinal canal in an ex vivo lumbar vertebrae, um, specimen. Uh, less than 10 millimeters of this, uh, AP diameter is clear anatomic evidence of stenosis, but the correlation with clinical symptoms is, uh, somewhat poor. Um, uh, moreover, the cross-sectional area of the thecal sac, uh, can be directly measured on, uh, CT, uh, myelogram or MRI, um, with, uh, above 130 millimeter square millimeters is considered normal. Uh, about between 100 and 130 early stenosis and less than 100 is commonly quoted threshold for anatomic stenosis. Um, why do we need to differentiate the, uh, developmental central canal narrowing from clinically significant spinal stenosis? Um, we have to understand that, uh, this is, uh, useful in, um, uh, not, uh, sending patients for surgical intervention early on. Uh, it can contribute to the clinical symptoms of spinal stenosis and also can reduce the space. A retrospective study, uh, of, uh, Dr. Yarvik showed that, uh, for patients with moderate to severe central canal narrowing, um, about, uh, 7% of asymptomatic, uh, younger patients younger than 45, uh, they have developmental narrow spine, 11% of those 55 to 65, and 21% of subjects older than 65 year old. So it's pretty, uh, uh, impressive that a significant proportion of asymptomatic individuals have at least moderate to severe central canal narrowing. Moreover, uh, the movement, we always take, uh, x-rays for our patients, uh, flexion extension x-rays, and that will reduce the area of the dural sac by 16%, while assuming axial load, uh, can reduce the area by 20% up to 19%. Um, so how do we assess for, uh, congenital central canal narrowing? And one way to do it is to look at the short pedicles and more objective way to do to use it is a torque ratio, which is the, uh, uh, basically a ratio between the, uh, anterior posterior, um, uh, canal diameter, uh, and the anterior posterior, uh, diameter of the vertebral body. And, uh, torque ratio less than 0.5 is considered spinal stenosis with, uh, um, for two standard deviation below the mean at, uh, 0.38 for at L4 vertebral body and 0.37 at L5. And the homework for all of us would be to understand what, uh, disorder can increase this denominator, what disorder can increase the AP diameter of the vertebral body. Um, how do we grade central canal stenosis? Um, there was a radiologist, North American, um, neuroradiology society that, uh, got together, um, a bunch of, uh, experts and they said, okay, we have 27, um, criteria of getting, um, grading, uh, uh, central canal stenosis and we probably need less. Um, uh, and they found out that, uh, probably five parameters are key in reporting, uh, central canal stenosis. And, uh, uh, they decided that have two central components compromised as a central zone. And you see the long arrow on the left side image, you see the, uh, relationship between the fluid and the quadricoina. You have the small arrow, um, the left side image, and also you see the, uh, arrowheads showing the, uh, ligamentum flavum enfolding, um, as a compromise of the, of the spinal canal. On the, uh, lateral, uh, component, uh, you, we should look for, uh, nerve root compression, the lateral recess. Um, uh, Dr. Zhang already, uh, put, uh, the, uh, that would help us understand that better, the zones of the spinal canal. Uh, and the foraminal stenosis, which we include the nerve root impeachment and compromise of the foraminal zone, and that's on the right hand side picture, we have the long, uh, arrows along with the small arrows and, um, that will, uh, be the foraminal stenosis. Okay. And this is just an example. This is a part of, uh, uh, our Penn Spine Center library where we have a patient with short pedicles with a torque ratio less than 0.5, actually the torque ratio is less than, uh, three here. Um, and any pathology that, uh, including discernation, facet arthropathy, ligamentum flavum enfolding, uh, likely, uh, become clinically asymptomatic faster. Um, um, and this is just another example where, uh, severe, uh, central stenosis, um, can be worsened by, um, um, uh, small disc herniation, uh, and on a sagittal T-weight MRI images, you can see, uh, on the right hand side, a serpiginous redundant roots or dilated veins that can be seen in the pickle sac. On the axial T-2 images, uh, the CSF will be phased, and when you see no bright CSF signal on T-2 weighted images, uh, only the intermediate to dark gray crowded of the roots is visible, and central canal narrowing is becoming severe. Um, this, uh, uh, Nishi, uh, showed that, uh, uh, central canal area of less than 100 millimeters strongly correlates with neuroclaudicatory pain. Um, Porter and Warr suggested that neuroclaudicatory symptoms actually require either multi-level canal stenosis or central canal narrowing plus foraminal narrowing. And these are some of the conditions that can worsen, uh, or fasten the, uh, clinically, uh, significant, uh, picture of a patient with central stenosis, and this is an extrusion, a rostral, um, superior, um, uh, extrusion of the L3-4, um, disc. Um, here you have, um, another example of central canal space-occupying pathology with, uh, significant facet arthropathy, and you see the arrow, the yellow and red arrow, arrow on the right-hand side, as well as central buckling or infolding of the ligamentum flavum. Um, I would advise of not using the so-called hypertrophy term, uh, really, uh, proposed by, uh, different, uh, um, providers that, uh, support, um, some type of intervention to that area. You can hypertrophy a muscle, not necessarily a ligament. Um, um, antero- or retrolysis also, uh, where you have, uh, grade one anterolysis of L3 or L4 that actually worsens the central canal stenosis. Um, this is a, a very successful, uh, 72-year-old woman, uh, executive, um, in Philadelphia that came with just unilateral leg pain and her symptomatology seemed to be central, severe central canal stenosis and you have an x-ray correlated with an MRI, T2 correlated with a STER image on the right side and you see a step-off at L3-L4 level. Spinal canal at that level is barely visible, the space for the quadriaquina and you can see the white arrow with a white kind of space, I tried to trace that, so probably is less than I would say 50 millimeters and she also has, if you look on the right-hand side, behind the L3-L4, you see a bright dot and that's probably some type of fluid in the, like right behind the ligamentum flavum or a space of arcata. Interestingly enough, below the level, you will see a picture that is similar. This is not arachnoiditis, this is just separation of nerve roots, secondary to severe central stenosis at the level of up. Interesting enough, she never got surgery and she's still doing very well four years later, so there's no such thing as preventive laminectomy. This is another example of a patient with normal spinal canal at the higher L2-L3 level and if you go lower down, you start seeing narrowing of the fecal sac and some, you know, the bright signal, this is the middle picture, which is a sagittal T2 image, is not fat suppressed, so you might say that all the spinal canal might be just fine and the fat can be very deceiving and you see going down at the L5 level, the quadriceps, you see the crowding of the nerves to a trefoil shape, severe stenosis, and if we go at L4-L5 level, same patient does have a right side L4-L5 dejoincy, dejoined arthropathy, epidural hypomatosis with neuroclonic arterial symptoms. This is just another example of the same patient between T2, T1, and the third sagittal image of a lumbar spinal MRI. Okay, we're gonna finish up with a nice case where this is a managing partner attorney in the city with prior L4 left hemi-laminectomy with severe left lower limb radicular pain only, better with biking, does not want to have surgery, as worse with walking and standing. He, in the first step, ideal 5S1, L4-L5, that's the first picture on the left side, minimally for a couple of days you will use dexamethasone and then we change the approach in an S1 TFASI with betamethasone and we chose that to instill steroid along the symptomatic route. Leg pain resolved three years later and then he developed in 2020 this year right leg pain similar to what he had on the left. We perform a right side S1 TFASI and this is just to take home that a normal volume of injectate in congenital severe central stenosis can exceed the previously described anatomical landmarks in patients with congenital spinal stenosis. No surgery was necessary. So take-home points, congenital spinal stenosis can change or accelerate the clinical manifestation of otherwise small disherniations. Cross-sectional area measurement is useful and get in the habit of doing that. Multi-level central stenosis or central stenosis and frontal stenosis can result in clinical symptomatic stenosis. Our spinal interventions can be tailored to the patient's needs giving lower volume of injectate necessary to reach suspected target level and after all we are physiatrists. People with spinal stenosis and developmental spinal stenosis are asymptomatic so there's no need for pre-emptive laminectomy. Thank you. All right, my name is Peter Wu. I'm an assistant professor of PM&R in the department of orthopedic surgery at UC San Francisco and today I'll be presenting on cancer that can affect the spine. I have no disclosures. I'll be starting off with a case of a 73-year-old male. His past medical history is involved with chronic spine pain from Shurman's disease. He's found to have on his chart monoclonal gammopathy of uncertain significance or otherwise called undetermined significance over 10 years prior to his presentation. Also had degenerative lumbar stenosis along with various musculoskeletal pain conditions that have affected him over the course of his life. He was also more recently found to have osteopenia. His chief complaint was actually progressive bilateral low back pain and lateral thigh pain over the last six months. And symptoms were described to have affected the right and then the left posterior lateral thigh and then ultimately affecting his spine. And they were felt to be fairly constant, moderate to severe, throbbing in his back and stabbing in his thighs that were worse withstanding. He did deny having constituted a spinal stenosis. However, pain disrupted his sleep. He had no prior spines or hip surgeries. And he had already had a course of physical therapy and use of anti-inflammatories that provided only mild relief. His exam findings were really just remarkable for suggestion of axial pain coming from the facet and sacroiliac joints, but otherwise had normal neurological exam. So he presented with an x-ray of his spine. And this x-ray was with flexion and extension. It showed no acute fractures. There are some increased lordosis, but otherwise sort of the findings that you would probably expect to find. There's some anterolisthesis of the spinal cord. There's a little bit of spondylosis. There's a little bit the findings that you would probably expect to find. There's some anterolisthesis of the lowest lumbar segments, slightly reducing with flexion, but otherwise no dynamic instability. Some degenerative end point changes at L2 and 3A. But given the persistence of his pain, despite conservative management, a lumbar MRI was ordered. And here, again, on the left half of the screen is the sagittal view, and the right half is the axial view. And as I scroll from head to toe, you can see that it showed no fractures. There were among multiple degenerative changes. His MRI actually was most remarkable for abnormal signal intensity, involving the S1 and S2 sagittal segments with extension to the sacral ala, bilaterally suggestive of osseous destruction. There was soft tissue extension through the adjacent cortical bone into the sacral central canal with complete effacement of the more caudal fecal sac, and cephalic migration of soft tissue along the ventral epidural space to midbody of L5, also facing the fecal sac with at least moderate central canal stenosis. And there were also smaller lesions found on both the right and the left iliac bones. There was an additional lesion that was noted at T12. These findings were suspicious for osseous metastasis. Given that PET-CT, or positron emission tomography and commuted tomography was pursued, this re-demonstrated a destructive osseous lesion centered at S1 and S2 with cortical erosion, epidural soft tissue extension that also demonstrated hypermetabolism. There was a large destructive mass virtually replacing the S1 sacral column with soft tissue extension filling the sacral foramina. And then also other lesions demonstrating hypermetabolism were found in the right humeral diathesis, left proximal humerus, posterior T12, posterior ilium, ninth rib, and clavicular heads. Taken together, these multifocal hypermetabolic osseous lesions were most suspicious for a hematologic malignancy like multiple myeloma, rather than the initial concern on MRI findings for metastasis, given that there was no evidence for primary malignancy found on PET-CT. With further workup, a CT-guided right iliac bone biopsy and bone marrow aspiration found over 90% of core biopsy cellular elements were atypical plasma cells with prominent central nuclei. Immunofixation electrophoresis showed the presence of an IgG kappa monoclonal band. Flow cytometry showed plasma cells that were kappa light chain restricted, demonstrating aberrant CD56 expression that were consistent with a IgG kappa multiple myeloma. His blood work and urinalysis demonstrated anemia, elevated serum total globulin, gamma globulin, and kappa lambda free light chain ratio, elevated urine protein, but otherwise normal renal function, and normal serum calcium levels. So multiple myeloma accounts for 1.8% of all cancers, second most common hematologic malignancy after lymphoma, with an annual incidence that has remained pretty steady at four to five per 100,000, leading to over several hundred thousand new cases and deaths per year in the U.S. It's slightly more common in men than women and twice as common in African Americans compared to Caucasians, with a median age of diagnosis of 65 to 70 years. Multiple myeloma is a hematologic disorder due to clonal plasma cell proliferation. It's associated with abnormal increase in monoclonal proteins that result in damage to bone and specific end organs. It comprises a collection of cytogenetically distinct disgraces, and with such underlying cytogenetic differences in their types, these determine the progression, the course, responsive therapy, and the prognosis. Almost all patients with multiple myeloma evolve from an asymptomatic premalignant stage, termed monoclonal gammopathy of undetermined significance, which over 50% of patients may have had for over 10 years, before often progressing via an intermediate, also asymptomatic, more advanced stage, but without end organ damage. That's referred to as smoldering multiple myeloma. In terms of presentation, it's affected by the interaction between the myeloma cells and the bone microenvironment, which can lead to osteoclast activation and osteoblast suppression that results in bone loss. And so bone disease is the main cause of morbidity, can result in axial or extra axial bone pain, osteopenia that may lead to pathologic fractures, and 60 to 80% of patients have had bone lesions by the time of their diagnosis. The most common site of fractures occurs in the spine or the long bones. It can be associated with vertebral collapse, compression of spinal cord or nerves, and decreased mobility. Bone resorption can lead to hypercalcemia. In the occupation of bone marrow by plasma cells, can crowd out the other marrow cells and lead to anemia, thrombocytopenia, leukopenia. And due to the excess monoclonal immunoglobulins, this can cause hyperviscosity, leading to neurological derangement, renal tubular damage that leads to renal failure, which along with hypercalcemia can lead to altered mental status and platelet dysfunction. The diagnostic criteria have had recent updates in the last decade with guidance from the National Comprehensive Cancer Network. That's also mirrored by the International Myeloma Working Group. And they've given increasing recognition to biomarkers that can be used to identify patients who are at high risk of progression to active disease within the first two years of diagnosis. And so very appropriate for this type of talk, the diagnostic criteria for monoclonal gammopathies have been revised to include the use of more sensitive imaging modalities, such as whole-body low-dose CT, PET-CT, and whole-body MRI, such that the diagnosis now requires, in addition to clonal proliferation, the evidence of one or more multiple myeloma defining events, which consist of either indications on diagnostic workup of established features of end organ damage related to hypercalcemia, renal failure, anemia, lytic bone lesions felt related to the plasma cell disorder, or specific biomarkers including clonal plasma cytosis, a free light chain ratio greater than 100, or focal lesions on MRI greater than half a centimeter. And these updated criteria represent a paradigm shift since they allow for earlier diagnosis and initiation of therapy before end organ damage occurs. The patient in our case had anemia, bone marrow plasma cytosis greater than 90 percent, and several lytic bone lesions on PET-CT and MRI. And so therefore patients with suspected myeloma should be referred to oncology for further workup that includes serum protein electrophoresis, immunofixation, and fluorescence in situ hybridization of the bone marrow. Such studies will further help to identify and risk stratify given the presence of certain genetic abnormalities is considered high risk myeloma. And other workup can be found that have been associated with aggressive disease are elevated serum LDH and evidence of circulating plasma cells and peripheral blood smear. Given bone disease is one of the most prominent features of myeloma with vertebral bodies accounting for nearly half of bone disease, imaging is an important role in diagnosis and even follow-up. The conventional skeletal survey is no longer indicated for the examination of patients with multiple myeloma given its poor sensitivity and lytic lesions are only detectable with 30 to 50 percent bone destruction. However findings include the classic punched out lesions, endosteal scalloping, osteopenia, and fractures. It's been recommended that bone disease is best detected using cross-sectional imaging given about a quarter of myeloma patients have an unremarkable skeletal survey, and so the use of low dose whole body CT, PET-CT, and MRI. The extent of bone disease is best assessed by this whole body CT or PET-CT which can detect responsive treatment earlier than MRI. And CT findings can include diffuse osteopenia, endosteal scalloping, cortical disruption, and hyper attenuation suggesting bone marrow infiltration. PET-CT has been reported to have high sensitivity and specificity for detecting bone damage and extra medullary involvement. The modality allows for detecting lesions with high cellular metabolic activity and density to facilitate differentiating between metabolically active cells and normal benign cells. MRI is the reference standard for evaluating bone marrow involvement and it allows for identifying distinct marrow infiltration patterns. MRI is also dynamic to assess for extra medullary disease, spinal cord compression, painful complications, and most myeloma lesions are characterized as with MRI images of this patient by circumscribed intermediate to high signal intensity in T2-weighted sequences and corresponding low signal intensity in T1-weighted sequences. For treatment over the last couple of decades, the availability of immunomodulatory drugs and use of autologous stem cell transplantation has led to better treatments and longer survival times. And therapies and their duration are adapted by risk strata and transplant eligibility. Current standard of care for newly diagnosed myeloma include Velcade, a proteasome inhibitor, Revlimid, an immunomodulatory drug, and dexamethasone steroid, followed by possible stem cell transplantation. Higher risk patients might have a regimen that includes daratumumab, which is an anti-CD38 monoclonal antibody added to their regimen. Regimens are modified for patients who are not candidates for a transplant and over the last decade, several other agents have been approved by the FDA and are being explored. A maintenance therapy for standard risk patients includes linalinamide, which is the Revlimid, and for high risk patients is the bortisamide or Velcade. Treatment also further includes managing of the end organ damage, ranging from orthopedic treatments to restore destroyed bone, manage pain, to hematologic measures to normalize blood factors and to recover kidney function. With this type of current treatment, median overall survival nears six years. Younger patients do better with stem cell transplantation, able to improve survival by approximately 12 months. And so the outcome for this patient, he had a FISHT analysis, negative for genetic abnormalities related to myeloma, and also blood work that show normal LDH and albumin levels in myeloma. All of which gave him standard risk disease. He underwent 10 sessions of radiation therapy to the destructive osteous lesions. He was given this VRD cocktail mentioned above to slow progression of disease before considering stem cell transplantation. His orthopedic management included skeletal health optimization with bisphosphonate, calcium, and vitamin D, pain management. And given pain and the weakening of the cortex from a five centimeter lesion, the right humerus, patient was at risk for fracture and he was recommended and did undergo a prophylactic right humerus intramedullary nail placement and subsequent post-surgical PT. His spinal pain unfortunately worsened after completing radiation therapy. Although he never experienced any neurological compromise and he had consultation with spine surgery and recommendations were for lumbosacral reconstruction, including fusion, after two to three months total of chemotherapy. So currently he's continuing conservative care with PT and spinal precautions to preserve body mechanics, independence, and mobility. Here are the key points for my talk and references. And thank you for your attention. And on behalf of all the members of our group, thank you for attending our session and workshop. We hope you got fairly useful information that can influence your practice, hopefully shape your perspective on these disease. And feel free to reach out to us via email and our contacts listed with AAPMNR.

back pain management

lumbar spine

disc herniations

FARDEN classification

arachnoiditis

central canal

developmental narrow spine

spinal stenosis

multiple myeloma

diagnostic criteria