Hello, welcome to the advanced neck pain management session. We really want to thank Academy for having us this year. The staff has worked tirelessly to try to transition this assembly to a virtual one and it's taken a lot of work. There's definitely changes now that this meeting is actually virtual but there's obviously some perks so we hope that you as an audience are enjoying this in the comfort of your own home and as presenters we can worry a little bit less about not fitting into our conference where as much after six months of pandemic lifestyle. I really need to take this opportunity to thank all the speakers for being here today. We certainly had to shift many things with the changes but despite this now being a pre-recorded format we are still going to try to make this as interactive as possible. Our presentations are case-based and we hope you're going to think along with us in your seats. Here is a list and order of our topics and we hope that after the next 60 minutes you'll feel a lot more comfortable when you see cases of infection in the cervical spine and cervical disc herniations along with knowing a little bit more about what to do when you see a case of developmentally narrow cervical spine cancer or cord lesions. So without further ado let me spend the next 12 minutes talking about cervical spine infections. I have no relevant disclosures. This first case I actually took from one of my primary care sports colleagues. So one afternoon in her clinic she was asked to call her 54 year old male patient and his worried wife. Like a lot of our patients he's been having off and on neck and back pain for a while but this was really different. So about a week ago he developed excruciating neck pain and now he can barely move his neck or turn his head. The wife was getting really worried because he's also been developing a fever and in the last few days he felt just really off. His whole body ached and since he came home from work two days ago he hasn't really been able to eat or drink or even make it all the way to the bathroom. And my colleague also knew this was really different from the patient's baseline as she was his primary care physician. He's overall a very healthy gentleman except for a remote history of splenectomy when he was 19 after a bad bout of mono. Of course things like this never happen on Tuesdays at 830. It always happens at like 430 on a Friday. And so my colleague in talking to the family eventually just suggested perhaps they should just go to the emergency room and get an expedited workup. He made it to the emergency room. He was febrile with a fever as high as 104. They sent off labs. His white count was very elevated. The rest of the labs weren't actually that bad. He was a little bit dehydrated. There was maybe a very mildly elevated lactic acid. Everyone was thinking infection at this point and his blood was sent off for cultures. There's nothing that makes me have a component leak as fast as being presented a pathology slide. So luckily someone else told us that this is showing some gram positive diplococci growth. You know this with a history of splenectomy. I'm not sure if you guys are thinking of it but at least infectious disease was definitely thinking this could be strep pneumo. And what do we see on his imaging? If you're interested in reviewing some of the things you should be looking at for when you're looking for infection in the cervical spine, some of our presenters are also involved in a cervical spine imaging interpretation session that's also going on in this year's annual assembly. But let me point out a few features here on just the static images. So I have on the left side of the screen the Sagittal T2 and on the right the Sagittal T1. And you can see that at the C6 and 7 discs, so if you kind of count it down from C2, C3, C4, C5, C6, C7, there's a little bit of a T2 hyper intensity around that disc. And there's rather more than expected diffuse T1 hypo intensity changes. That could still be consistent with a MODEC type 1 change. But what's even more concerning is that if you were able to scroll through the images you would see that there's rather indistinct cortical margins around that C6, 7 disc space. So when you're thinking about ruling out infection on imaging, you should add some magic sauce to your MRI. And that magic sauce is obviously gadolinium. So here you can see our post contrast images. And then so on the left now you have a Sagittal and on the right you have the corresponding Axial. And you can see, wow, there's diffuse enhancement around that C6, 7 disc, around the surrounding bone marrow. You can see there's thickening and some enhancement in the prevertebral space as well as in the ventral epidural space. So there are still two good things about this. So one is, you know, despite the amount of enhancement, the enhancement in the soft tissue is rather uniform. So this is evidence of phlegm and not an abscess or something which tends to be rim enhancing. And the other good thing is if you were able to scroll up and down you would actually see that overall this patient still had patent spinal canal and neuroforamen. And that's a good thing because that did correlate well with the fact that he was still neurologically intact throughout all this. And he did really great. So after they started brought antibiotics in the ED, he was already rapidly improving. Because he didn't have any neurological changes or evidence of instability, he was managed non-operatively. Soon he was discharged after a pipeline was placed for six weeks of IV antibiotics. By the time my colleague actually saw this patient back, he had finished his antibiotics and his pain was pretty much gone, just mostly stiffness. And he was quite a happy man. The second case I want to touch upon is a little bit different. It actually involved eventually surgical intervention. And I just want to use this as a juxtaposition to tell you when surgery will be needed. So this was a 67-year-old male with chronic neck pain with radicular features going down both arms. This isn't the first time he's had neck pain. He actually just developed acute exacerbation of what felt like his normal pain after starting to work out for the first time. He knew a pain management physician and returned for a C7 T1 interlaminar epidural sero-injection. Initially he felt like he may have had some relief, but each day afterwards he felt worse and worse. And at day 10, he was having so much more symptoms that it was decided that a repeat MRI cervical spine was needed. In this imaging, you can actually see some of the common findings of infection a little bit better than the first case. So if you just counted down your segments, you will notice that at C5-6, you can find again that T2 hyper-intense and T1 hypo-intense findings. In this one, you can see a lot better that there has been significant loss of disc height, and in fact, complete erosion of the cortical margins at some point. Of course, if you add in a little bit gadolinium, you can see there's very significant enhancement around that disc space, around the surrounding bone marrow. There's significant hyper-intensity in front of the vertebral column, as well as all around the epidural space. And when you look at the axial cut, this is starting to get really concerning. He had significant spinal canal stenosis before, and the fact that there's so much inflammation around the epidural space all around the canal, even though we didn't see myelomalacia on imaging, it's concerning for a possible spinal cord involvement. This patient was actually referred initially to ID, who got him into urgently the spine clinic, asking if there's a role for bone biopsy. By the time my surgical colleagues saw the patient, the patient was developing some worsening hand discarity and was kind of having an off-gait on his tandem gait. There was also some mention that maybe he was developing urinary urgency, which may or may not be real or new, and given all this, he was eventually taken to a semi-urgent C5-6 anterior cervical discectomy and C6 partial corpectomy. When they opened him up, they did find a little pocket of pus, and from that, they were able to grow penicillin-susceptible strep minus, staph capitis, and P. acnes. Of course, ID was involved this entire time, and there was some back and forth, but because he now has hardware in a previously infected space, it was decided that he is going to continue lifelong suppressive antibiotic therapy. So what are the take-home points from this portion of our session? Well, one is we do still need to maintain an index of suspicion for infection. This is especially true if the patient presents with fever or tenderness of palpation, or if they develop acute worsening of their symptoms, or new onset neurological changes. Of course, if this is a patient with prior immunosuppression, whether they were on dialysis or injection drug users, or they had a recent invasive epidural spinal procedure, then our suspicions are higher. If you are suspecting infection, the workup is needed. If the patient is doing overall well, this can still be done as an outpatient. So, you know, for me, we order ESR, CRP, and the CBC on their way out, and we generally are able to get patients into expedited imaging in the next one to two days. If the patient is starting to have already systemic signs of infection, then definitely consider sending them to the ER. And, you know, as physiatrists, we shouldn't have to manage these patients by ourselves. We're very used to working in a multidisciplinary setting. Definitely get your ID colleagues involved. We here get surgery involved very early. Surgery really is indicated if there's a need for surgical decompression or stabilization, if there's concerns about instability. Short of that, a lot of times our surgeons try at least first to do a trial of non-operative management, and it's actually our IR colleagues who would go in and do a bone biopsy or whatnot to get the organisms for the ID team so they can help to establish the treatment plan. Here are some of the works cited that is included in this presentation, especially number five. The Frank article was really helpful if you guys are interested in a good read. And if you guys have any questions or concerns, you know, feel free to email me at any time, and I will try to find the answers for you. So that is the end of my portion of the presentation. I'm going to hand it off to Dr. Steros to talk a little bit more about cervical disc herniations. All right. Well, thank you. The title of this portion of the talk is not all the same. Hard versus soft cervical disc herniations. And as Patricia mentioned, my name is Eric Steros. I'm here at Vanderbilt University Medical Center. So there are no pertinent financial disclosures for this talk. To start, I wanted to define a few terms that were taken primarily from the updated disc nomenclature review by Farden et al. I will be using terms hard and soft disc for the sake of simplicity, all the while knowing that they are not the preferred terms. So hard disc are displaced disc portions that have undergone calcifications or ossification. Soft disc herniations are defined as herniations of predominantly nucleus pulposus and blood or non-bony disc fragments. These tend to occur in younger patients and are typically more acute. A disc osteophyte complex is defined as an intervertebral disc displacement, whether bulge protrusion or extrusion associated with calcific ridges or ossification. So the primary objective of this portion of the talk is to answer the following question. Do hard cervical disc herniations respond to epidural steroid injections? This question or rather a more simplistic belief that hard discs equal surgery and soft discs equal epidural was brought up in a multidisciplinary spine clinic. This patient is a 36 year old male with acute onset left arm pain and a c6 distribution. He had a normal neuro exam and he had pain that persisted despite conservative care. An MRI was ordered and he was referred to PM&R for a cervical epidural. So without any additional information and assuming that this is a disc herniation, do we think this patient is more likely to have a soft or a hard disc? The acute onset in a younger patient makes us think or lean more towards a soft disc herniation, but let's take a look at the MRI. So here is his MRI with the midline t2 sagittal image on the left side of the screen and the left parasagittal image on the right. For the purpose of this talk, let's focus in on the disc herniation at the c5-6 level where he is most symptomatic clinically. So here we can see that the herniation is uniformly dark or low signal on t2 weighted MRIs with mild canal stenosis and no myelomalacia at this level. The axial t2 image on the right side of the screen corresponds with the line depicted in his sagittal image through the c5 disc space. So on the patient's right on the axial image we can see a fairly normal appearing foramen as evidenced by his hyper intense signal there and plenty of room for a nerve to traverse that foramen. On the patient's left side we can see a uniformly dark matter that was described on the ultimate radiographic report of a disc osteophyte complex with severe foraminal stenosis. So now what do we think? So many of us may have seen mild multi-level degenerative changes, reactive end plate changes, and potentially a few of you even noticed some uncle vertebral hypertrophy and now may be leaning more towards a hard cervical disc despite his younger age and more acute presentation. So now the question is can we determine the difference between hard and soft disc material on MRI alone when both are low signal intense or dark on MRI? So this study titled the value of MR imaging in differentiating between hard and soft cervical disc disease a comparison with intraoperative findings looked to answer that exact question. So this was a retrospective review of pre-op MRIs of 41 patients with cervical disc herniations who went on who underwent surgery and intraoperatively were categorized as hard soft or both. Three independent physicians who are not part of these patients care reviewed the MRIs on two separate occasions and asked to determine the presence or absence of hard disc herniations. The intra observer agreement was not great and the agreement between the three physicians was fair to moderate with a kappa of 0.4. The sensitivity was good but the specificity was low due to the overestimation of hard discs on MRI. So ultimately, we can conclude based on this particular study that MRI alone is not a very efficient diagnostic test in distinguishing between hard and soft disc in the cervical spine. Many of you may have been thinking, well, what about CT scans? As we know that CTs are much better at determining the presence of ossified soft tissue structures. So this is an example of a patient I saw with a C3-4 disc herniation who also had a CT scan for another reason. So when you look primarily on the far right side of our screen at his axial CT image, we see that his neuroforamen are widely patent without any osseous structures in his foramen. This is another patient that I saw for other reasons, but they also had a C3-4 disc herniation, although this is on the right side on that axial image. This CT scan, again, focusing on the axial image on the right side of the screen, we can clearly see an ossified disc material in the right C3-4 neuroforamen, and looking back at his herniated disc on the MRI, we notice that the disc material here is similarly hypo-intense or dark when compared to the previous patient's cervical MRI. So for our next leading question, should we obtain CT scans on each patient undergoing epidural steroid injections, as this would certainly aid in differentiating soft discs from those with more osseous components? So this is a population-based cohort study of over 12 million individuals under the age of 19 from South Korea, where 1.2 of them, or 1.2 million of them, were exposed to low-dose ionizing radiation for diagnostic reasons. Among the individuals who underwent CT scans in particular, the overall cancer incidence was 54% greater in those exposed than those who were not exposed. The overall cancer incidence was 54% greater in those who underwent CT scans than those who did not. So the initial patient case that I presented wasn't in this same demographic as these two reviews, but I'd argue that 36 is still fairly young, and at least worth discussing the risks of CT versus potential added benefits at this point in his care. So now that brings us back to our original question. Now that we know it can be challenging to determine if a hard, sorry, a cervical disc is hard or soft on MRI, and that CT scans are not completely benign, does it matter if we are able to determine if a disc is at least in part ossified, do we still immediately think surgical referral, or do hard cervical disc herniations respond to epidurals? So let's back up and look at the prevalence data. So in a population-based study from Rochester, Minnesota, looking at cervical radiculopathy, soft disc herniations were determined to be the etiology in 21.9% of cases as determined by radiology or surgery. Hard discs or a combination of both were the most common to be implicated, and were present in nearly 70% of the time. This is intuitive in the sense when we contrast this to the lumbar spine, where the cervical disc has much less nucleus pulposus and disc, and has less force that can cause, or less force going through the disc that causes acute disc herniations when comparing to the lumbar spine. So finally, let's take a look at the effectiveness of cervical epidural steroids in treating cervical radicular pain. So this is a recent systematic review by Conger et al., specifically evaluating the effectiveness of transferaminal epidurals for radicular pain. The outcomes are broken down by etiology in the following table. So here we can see on the left side of the screen that the studies were broken down into radicular pain from disc herniations, spondylosis, or heterogeneous in etiology. The second column of this chart defines success after the injection with the success rate on the far right side. Overall, of the nine studies, the majority had greater than 50% of their patients respond favorably to cervical epidurals, which sum up to 70%, which is significantly higher than the prevalence of soft disc herniations that we saw in that Rochester study. So this data implies that, yes, hard or disc osteophyte complexes can respond favorably to epidural steroid injections. So in summary, it is difficult to determine the components of a cervical disc herniation based on MRI alone. CT scans may differentiate, but are not entirely benign. There's no clear evidence to suggest superiority of management when comparing hard or soft disc herniations. And the positive response rate in cervical epidural steroid injections is greater than the prevalence of soft disc, which does imply that hard cervical disc herniations do respond to epidurals. These are a few of the references that I cited throughout this study. And next up, I believe, is Dr. Yang. All right, thanks, Eric. My name's Eric. I'm also at Vanderbilt here. And I'll be talking about cervical spine and cases of cancer and other miscellaneous findings. I have no relevant financial disclosures. So my outline is I'm going to first start with a case example, then talk about overview of spine tumors, and then finish up with more cases and take-home points. Just so you know, this is two of my three daughters in front of a cervical spine of a giraffe, which also has seven vertebrae, just like humans. Fun fact. So really, when I was making this PowerPoint, I wanted to know, in a busy clinic setting, what kinds of things should raise some type of concern about malignancy as the cause of neck pain? Again, cancer is causing neck pain is pretty rare, but I also wanted to point attention to what are the most common types of cancers that you may encounter if you do encounter a mass or a malignancy on imaging. So this was a case that I saw about two, three years ago. It was a 65-year-old gentleman who came in with four months of pain along the right medial scapular border. He was recently retired. He picked up a couple activities, such as pickleball and golf. He tried some ibuprofen without any relief, and there really wasn't anything that made his pain worse. He just mentioned that movement in general made his pain better. I referred him on to physical therapy to work on some of the scapular rotators, as well as the shoulder area. And he came back after four sessions, and this time he was having radiating symptoms down the back of his right arm. And as a result, I ordered a cervical spine MRI thinking I may see something related to maybe C7 radicular pain pattern. So here is the MRI. On the left side right here is a T2-weighted sagittal MRI, and here is an axial cut. And really what I'm trying to point attention to is along the right side, along the apex of the lung, you see this mass right here. And the mass was noted to also infiltrate the second and third ribs. And as a result of these findings, we obtained a CT scan of the chest with contrast. And so on the CT scan right here, you can see along the right lung apex, there is a mass right here. You can see some infiltration along the second rib right here. So as a result of these findings, the patient was referred to oncology, eventually had a CT-guided biopsy, which came back as squamous cell carcinoma. He underwent chemo and radiation, eventual surgical resection, and he was lucky to achieve full resection with negative lymph nodes. Just as a side note, pancostumers, which are really defined by this location on the apex of the lung, tend to be squamous cell carcinomas with relatively good outcomes with surgical resection and chemo and radiation. The other thing that, you know, subsequently went back and saw was that he was a smoker for about 20 years. However, he had quit for a few years before he had seen me. So it really wasn't as relevant when I was taking the history, but something that definitely can be seen, especially with pancostumers. So really, when you look at the literature, most of it focuses on back pain and not as much neck pain, which I'll explain here a little bit later. But this was an interesting study done by Deo when he looked at 1,900 patients who came into a walk-in clinic with a primary chief complaint of back pain. Out of those 1,900 or so patients, 13 of them were eventually diagnosed with cancer as a cause of back pain. And again, you can see here, it's relatively low, but about 0.66% of the time as a cause of back pain. Again, in a primary care clinic and causing back pain, not neck pain. What they also saw was that most of these cases could have been uncovered by a x-ray, CBC, and ESR. X-ray looking for any bony erosion, CBCs looking for anemia, and ESRs for any inflammatory process that might be going on. When you think about presentations based on practice, I found this very interesting. If you're in a tertiary care center, your incidence and prevalence of seeing something like this is higher than possibly even a secondary type of center. This was an interesting study done by Slitman that did a chart review of multiple private practice clinics as well as academic spine centers. And there was a higher incidence of spinaeoplasia seen in academic spine centers where it's more multidisciplinary. So just something to think about, again, depending on the practice location. In terms of patient characteristics, again, this was going back to the Dayo study looking at back pain specifically. But 94% of those patients reported spontaneous onset of symptoms. Just something I took away is if I see a patient, they report, you know, 5 to 10 years of neck pain, unlikely may be a malignancy that's the cause. In terms of the other characteristics, history of cancer, that was seen about 55% of those patients. I highlight it because I do still think it's very important to think about when you're going through a thought process when you're evaluating patients. In terms of characteristics, symptom duration greater than a month, often aching, again, in the back pain, patient aggravated by standing. And night pain, interestingly, was seen in less than 50% of the population that was eventually diagnosed with back pain. Again, what I took away from this is that just because they do not have night pain does not mean they don't have malignancy as a potential cause, but still a very important question to ask. When you break down spine tumors in the spine, I'm really breaking down by primary spine tumors, which are relatively uncommon. Again, in the grand scheme of things, they're rare in terms of total tumors, about 0.4%. In terms of primary central nervous system tumors, again, still pretty rare, about 2 to 4%. But the majority of these primary spine tumors are benign, and they present with symptoms of neural compression, as opposed to METs, which are going to be by far and away the most common type of tumor seen in the spine, is going to also present mostly with axial pain as opposed to neural compression symptoms. So I'm going to first go over metastatic tumors because, again, this is really going to be the most common type of tumor that you're going to see in the spine if you do come across one. So spinal METs comprises about 90% of masses encountered on spinal imaging. Majority of them are found to be within the bone, and about 20% of them are going to invade the spinal canal and cause cord compression. Again, why we don't see that as much in the cervical spine, thoracic is going to be the most common location for spinal METs, followed by the lumbar, and then lastly, the cervical spine. Patricia did a great job talking about infection in the spine. In terms of spinal METs, it spares the intervertebral disc, and the main reason is because most of the cancer spread hematogenously through Batson's plexus, and knowing that the disc is relatively avascular. When you look at Batson's plexus, it's a venous drainage for the spinal cord and the vertebral bodies, but also it is the drainage for other organs, especially the genitourinary organs, breast, thyroid, and so a majority of cancers that metastasize to the spine is through Batson's plexus as opposed to direct tumor extension. So I wanted to really, if I was going to take away one mnemonic from this, it's BLT pickle. So these are going to be the most common primary sites that are going to metastasize to the bone, especially the spine. Breast, lung, and prostate are going to make up about 50% of the spinal METs that you're going to see, and you have renal, GI, and thyroid. Someone else mentioned BLT with a kosher pickle, so kidney for renal, so that'll cover a majority of the cancers that are going to metastasize to the spine itself. Other things to think about, which I'll go over in further detail, are going to be other primary tumors such as multiple myeloma, and then again, spinal infection is something else to think about. My spine surgeon colleagues did mention that it can often be difficult to biopsy in the cervical spine, so they often think about getting a CT chest, abdomen, and pelvis to look for primary causes of cancer elsewhere, which may be easier to biopsy as opposed to directly biopsying somewhere in the spine. So we're going to switch gears and talk about primary spine tumors, and so Dr. Smoot did a great job previously discussing this in the past. We primarily talk about these tumors based on anatomic classification, so in really relation to the spinal cord and the dura. So the three different types that we have are extradural, which is going to be here on the far right, which is going to be tumors that arise outside of the dura and outside of the spinal cord. These are going to be by far and away, again, the more common primary spine tumors that you're going to encounter. The second most common are intradural, extramedullary, essentially what this means is within the dura outside the spinal cord. And the rarest of the primary spine tumors are going to be intramedullary tumors, again making about 5% of tumors seen that are primary in the spine. So starting again with the most common, we have benign and malignant neoplasms in the spine. Again, most of us have seen a hemangioma. These are going to be the most common benign neoplasm that we come across. In terms of malignant neoplasms, METs again are going to be the most common extradural spine tumor. But if we're strictly talking about primary spine tumors here, multiple myeloma are going to be the most common primary spine tumor you're going to see in general. Again, you don't want to necessarily always go to neoplasm first. Most of these extradural masses are not neoplastic, so making sure you rule out other causes such as infection, hematoma, disc herniations, and osteophytes. So brief word about multiple myeloma, again, the most common primary neoplasm of the bone that we're going to see. It's caused by neoplastic proliferation of plasma cells, which happen to be abundant in the spine, especially in the hematopoietic marrow. And so in about 50% of cases of multiple myeloma, you will see involvement of the axial skeleton. And what you're essentially looking for in x-rays are these punched out lesions. And that can occur because there's increase in osteoclastic activity leading to bone resorption. In terms of MRI, it really depends on what stage they have multiple myeloma. But in general, you may see a diffuse pattern similar to other marrow proliferative disorders. And so what you're essentially looking for is, here on the right side, you're seeing a T1 sagittal MRI, and you can just see just a diffuse marrow replacement. It all looks the same shade in terms of the color compared to the spinal cord itself and the canal and the disc. So really, if you see just a diffuse marrow replacement, you can look at this on T1, and it'll look really homogenous in signal. And really, the main takeaway from this in terms of multiple myeloma is, really, if someone presents with a compression fracture that is unexplained, it should raise some level of concern. Usually, the initial workup involves an x-ray, SPEP, UPEP, which are relatively easy to get. But again if patient comes in with no known risk factors for a fracture and you see this maybe just raise some concern about potentially getting more imaging and some more blood and urine samples. And then moving on to other primary spine tumors, intradural extramedullary. Again these are tumors that are within the dura but outside the spinal cord itself. Majority of these are benign. Again majority of them are going to be either meningiomas or nerve sheath tumors such as schwannomas or neurofibromas. And then lastly the rarest of the primary spine tumors and that is a good thing because majority of these happen to be malignant and majority of these are gliomas of which they are either an astrocytoma or appendymomas. Appendymomas commonly occur in the age of 30 to 40 most common and this is the most common intramedullary spine tumor. And again these are mostly malignant and that is mostly because again glial cells happen to be more prominent in the brain but not as much in the spinal cord itself. Hence the reason why we don't see as much intramedullary spine tumors. So I want to run through a few brief cases and just sort of walking through how we think about things. Again a lot of these are going to be mostly in the lumbar spine with a few cervical spine mixed in. But this is a patient who came in with axial back pain worse with ambulation. In the clinic you get the MRI and you can see here there's just bony destruction again telling you that it's more extradural. Eventual diagnosis was prostate mets. This was a second case 25 year old female came in with a mid-back and bilateral hand weakness and looking at this imaging you can see an extensive mass here within the spinal cord itself here on the sagittal view as well as the axial cuts as well. And this was eventually diagnosed as a pendymoma. More common case that you may come across this is a 46 year old female comes in with mid-back pain. And what you're really looking for is looking at the signal intensity on T2 and T1. The eventual diagnosis was a vertebral hemangioma. And what you're really looking for is an increased signal intensity that is seen on T2 and T1 and that occurs because of the high fat content and as well as the high water content. This is opposite of what you may see with mets or even infection where we often see a greater T2 signal intensity as opposed to T1 signal intensity. And lastly this was a patient that I actually personally saw a year ago. 41 year old female who came in with right arm pain and numbness to the thumb. I thought maybe it was a C6 radicular pain pattern. I obtained the MRI and maybe a little bit difficult to see but you can see a little bit of hyper intensity within the cord itself up here near C2 area. And eventually the eventual diagnosis was multiple sclerosis. So again really coming back to what should I know what should raise some red flags as I evaluate a patient and there may be some concern for malignancy. Again think about BLT pickle, breast, lung, and prostate again comprise about 50% of those malignancies. So just again even thinking about hey is there a cancer history at all. Second thing, night pain is not going to be seen frequently but still an important question to ask. And then the most common primary tumor that you're going to come across is multiple myeloma. If someone has an unexplained fracture just think about multiple myeloma as a potential diagnosis. So some take-home lessons, spinal meds are going to be the most common primary tumor that you're going to come across in the spine. Understand that we classify primary tumors based on anatomic location. I don't think it's necessary that you you know memorize all the different types of tumors but know that we at least classify them based on where it's located. Extradural spine tumors are going to be the most common primary tumor, multiple myeloma being the most common. And lastly vertebral hemangiomas are the most common benign tumor. Think about signal hyperintensity T1 and T2 often being pretty similar in intensity. Here's a brief summary of citations. I want to acknowledge DJ and Matt for helping out with some of the slides and going over that with me. And so I'm happy to take any questions feel free to reach out. Here's my Twitter and going off that I'm going to hand it off to Dr. Nagpal. Thanks Aaron, thanks everybody. The next section here we're going to talk about is what to watch out for for interventionalists when you have a developmentally or congenitally narrowed spine. I'm a division chief and associate professor of pain medicine at UT Health San Antonio. I don't have any relevant disclosures to this talk but I have several committee memberships and consultations that are unrelated. So what we're going to talk about here is to describe radiologic findings for congenital spine and explain how that may alter your decision-making when it comes to interventional pain procedures. I think it's also important for us to note that we're talking about the cervical spine today but the prevalence of cervical canal stenosis due to congenital changes is significantly different than lumbar. Though most of us assume that if you have congenital spine stenosis it is probably occurring throughout the entire spine. But most of the studies that have been done on this have kind of demonstrated that cervical canal stenosis prevalence can range from anywhere from two and a half percent to somewhere in the range of almost as high as eight percent which is difficult to believe but nevertheless studies of athletes have shown as high as 7.6 percent. And so without knowing ahead of time the normal cervical spine dimensions then we can't really know what there is what are the abnormal. And so the normative spine cervical spine dimensions have been postulated and changed over the years but the work that most people kind of refer to is is Dr. Ulrich's work and from 2014. And in that what we just demonstrate is that the normal cervical spine canal ratio differs from level to level and if we look at C7 you would expect about 15 millimeters at C even at higher levels maybe a little more. The classic the classic ratio or calculation that's always been done over the course of many years is the torque Pavlov ratio also called sometimes just the torque ratio or just the Pavlov ratio. And in that we there's an estimate of the ratio from the spinal canal to the entirety of the of the excuse me the spinal cord to the entirety of the spinal canal and that ratio being under 0.8 has been consistent with consideration for canal stenosis in the cervical spine at C3 and C5 specifically. However that is based upon going way back on the data radiographic findings some people would argue CT findings but maybe not on MRI findings which is something that we deal with quite a bit more as interventionalists though some of my colleagues have spoken about the great utility of CT scans we more often than not are working from MRIs when we're offering interventions to our procedures. And so a more updated attempt to create what would be a better way to detect if somebody has congenital cervical stenosis using MRI was approached and developed and is now sort of widely used by neuroradiologists specifically and that's the spinal cord occupation ratio or the SCOR or the score a score greater than 70% which is look it's essentially similar to the torque Pavlov ratio but we're do but this is very much validated in magnetic resonance imaging and that is an effective criterion and what we find in there in their data is that it not only is the score of greater than 70% or equal to 70% effective at diagnosing congenital spinal stenosis in the cervical spine it was also compared to the torque Pavlov ratio and simply the spinal canal diameter both at C3 and C5 which are the classic levels at which we look at this. The other thing that's interesting is it's better let me not use the word better it's able to predict future ominous findings such as myelopathy and future weakness and neck disability index scores that are worsening. So the nice thing about this particular diagnostic tool is that it gives us some idea about the potential for a consequence later. This cartoon demonstrates something that we we all and I think let me go back just a bit here I'm so sorry okay so one of my slides appears to be missing but in brief I just want to mention I was gonna you know what I was gonna blame the Academy this is pre-recorded it's not their fault it's my fault the slide wasn't missing I just skipped over it here it is for everybody to see. The facts about congenital cervical stenosis are that it tends to be when we think about congenital cervical stenosis we're talking about idiopathic disease when somebody says that to you we're talking about idiopathic disease that's congenital in nature but we there is all this is also seen in achondroplasia so that's something to mention. The fact the basis upon which we can identify congenital canal stenosis is classically described as shortened or thickened pedicles or shortened and thickened pedicles which decreases the sagittal diameter of the canal. This causes the lamina of the cervical canal to laterally be directed and we'll look at that in a bit in some imaging in some axial images. The other thing that's quite common quite important to note is that this this is something that people get diagnosed within the third or fourth decade of life. We don't see this typically being something that they see in spite of the fact that's congenital when they're in their teen years or earlier than that and degenerative congenital degenerative cervical stenosis is not usually something we think of in third or fourth decade it's more along the lines of people in their sixth or seventh decade of life and that's backed up by data as well. Okay so we'll catch back up now great so this is a cartoon demonstrating the cervical spine in an axial view in an oblique view and if we look at the size of the pedicle in the cervical spine it's small. It's not the size of the pedicle in the lumbar spine which we're very used to looking at. It's a very small structure. The lamina also oriented obliquely due to the pedicle separating the vertebral body from the lamina directly and that's very important because if we look at this axial view we note that that lamina points out at a oblique trajectory but in congenital stenosis because the pedicle is shortened and thickened it flares out laterally as I mentioned and that's this cartoon should be able to demonstrate why that might happen and it pulls the lamina towards the cord and so what happens there is that you wind up getting compression of the intrathecal canal from all three zones posteriorly and both lateral zones which leads to what's classically been called the trefoil appearance or triangular appearance of the canal. So this is a case of a patient that I had in my clinic who was in her late 20s actually presenting with bilateral cervical radicular pain that was not very ambiguous. I couldn't tell which distribution it was in which is a normal finding in San Antonio. I'm not sure if that's true in the rest of the country but in San Antonio a lot of the times people don't show up and say it shoots straight down my arm into my thumb and then have a concomitant disc herniation that looks right at the same level. That doesn't always happen to me. So but she also interestingly had a bit of a scissoring gait. She was complaining of falls and she had a positive Hoffman sign on both of her fingers and had complained of mild urinary incontinence and retention both and so and she also had a positive Laramide sign and so on my imaging I acquired I noted that certainly if we look at those levels C3 through C5 we see both posteriorly and anteriorly on a lateral that at those levels that there is compression of the cervical canal and while we maybe and if you look at the T1 and the T2 here we don't we don't necessarily detect that there's a change that's going to be consistent with myelopathy like we don't see myelomalacia but the cord is being compressed in both directions and that is indicative of a congenital disease state. Now could it be also due to degenerative change? Yes but one of the things that to note is it's multiple levels right we have a young patient young female and the fact that it's coming from anterior and posterior strongly indicates degenerative change. I'm sorry strongly indicates congenital change. This is a different patient but to kind of bring the same point home and here's where I have T2 and T1 you see at multiple levels especially in that C3 to C5 distribution you're seeing both anterior and posterior compression in the scalloped distribution and you see it at the disc level so sometimes this gets this is another one of my patients and sometimes this may be misconstrued as pure as degenerative because of the fact that's happening at the levels of the disc and one of my colleagues spoke earlier about the difference between a soft disc herniation and a harder at disc herniation that may come with a disc osteophyte complex which occurs at the level of the discs but we don't expect the lamina to be pushing anteriorly in those situations. You could have facet arthrosis that may cause a little bit of posterior change but not to this degree. The other thing to note is that the posterior elements in the T1 you can see them much more clearly and you can see them defined especially as we get down towards C6 and C7 as they kind of come they don't they don't have the classic appearance of that you would see in a normal cervical image because the lamina are getting cut right through and you're seeing them right through a lateral view because they're not oblique and because of that you see sort of the cortex and the medullary bone of the lamina which is a giveaway for a giveaway for congenital stenosis. Now this is a axial cut of that of that MRI of the first patient actually and the canal in the canal we only have seven millimeters approximately of space at C6 which is again consistent with not enough space. We also see that there is slight triangular shape to the canal due to the lamina being pulled anteriorly which will then lead to compression posteriorly. Here we have a CT scan of a different patient of mine who presented similarly and what there's a bone window and then a traditional CT scan view here and what we want to look at here is well it's tough to say in this lateral view that there's come that there's degenerative changes that are compressing the canal but what we can see is that as we approach C6 and C7 counting from the bottom we see typoplastic posterior elements and that and they look different because they're rudimentary in nature and that is seen in congenital stenosis sometimes in on CT scans but if we go to our axial cut we have the same problem where the spot the canal is narrowed and the lamina are pulled anteriorly and they're not as horizontally aligned and so this is about an eight millimeter canal. So why does this matter? Well this is a cartoon of a transforaminal epidural steroid injection of the cervical spine which some of us do commonly and if our superior articular process is in direct relationship to the lamina if the lamina is pulled anteriorly and caused to be go from its usual oblique appearance to a lateral appearance that could compress the canal itself and you may not have room for a needle to get into that area, and you may wind up getting a paresthesia, not because you're doing the procedure incorrectly, but because the nerve might be displaced due to the congenital canal stenosis. So it's crucial for us to review our imaging, the sagittal views, and the axial views when we're performing these procedures. The same is true when we do interlaminar injections. The needle on the left in this cartoon is approaching for an interlaminar epidural steroid injection, and the needle towards the bottom and a little bit to the right is approaching for transforaminal. Now that interlaminar space will also be compromised as we saw those axial views. There's the cord to canal, not just the torque Pavlov ratio, but the score, the spinal canal occupancy ratio will be decreased when there's less room in the epidural space, and this puts you at risk of potentially unintentionally having a cord injury during your procedure. I think most of us who do interlaminar cervical epidural steroid injections tend to stick to C71 for a variety of reasons that I could explain it to anybody anytime we want to have that conversation, but it's outside the scope of this talk. But you're most safe at that level, but you really need congenital stenosis want to look at that level. It does affect all levels of the cervical spine. C3 through C5 are the worst affected most commonly, but we do want to look at this and make sure that there is room in the epidural space. That diminished size of the posterior epidural unsafe may make interlaminaries unsafe. If you have a smaller foramen because those thickened and shortened pedicles pulled the lamina anteriorly, you may make a transforaminal difficult to perform, though I would argue maybe not unsafe. So the difference here is that it may make an interlaminar unsafe because you may get a cord injury. So long as you're performing under the appropriate guidelines using SIS guidelines to perform your transforaminals, it may not be unsafe. It may just be that you can't accurately or correctly perform the procedure, and you may want to try to go to a different level. And there, that's the last point here is to consider a different level if access is unsafe or unobtainable when you pre-review your imaging. And these are some of my references. And lastly, I want to pass it along to the esteemed Dr. Smoot, who will finish this off. Thank you, sir. Thanks, Amik, and thanks to everybody else for your wonderful presentations. I get to anchor it up here with a discussion of what to watch out for in the cervical spinal cord. My patient is a patient that presents to your clinic with myelopathy, and that's that. So what are you going to do with a patient with myelopathy? And we're going to go through that in a broad view at the beginning, and then focus in on the most common cause of myelopathy that we see in our clinics. These are my disclosures. None of them are closely tied to the things we're talking about here today, but they're listed here for you to make that determination, not me. So when you have a patient with myelopathy in your clinic, if you don't already have imaging, the first thing you're going to do is image them, typically MRI or some other form of advanced imaging if that's not available. And certain types of myelopathy or certain progressions, you're probably, you might not even image, you might send that patient to the ER with a phone call to your friendly emergency room doctor, and at my institution, a phone call to the spine fellow on call to alert them of who's coming into the ER and why. But a lot of times myelopathy will present in clinic where you're concerned, you're going to work it up, but it's not an emergency. And when you do that, different things might show up. So when tumors show up, we heard a talk about that earlier from Aaron, and tumors show up If you're going to try to characterize a tumor, you generally are going to want contrast. You may not know that when you order the MRI, but in a patient with a history of cancer, probably a good idea to go ahead and get the contrast with the MRI that you order it because tumors are going to enhance with contrast, and that's going to help with characterization of the tumor. You know, it'll assist the people that figure these things out about where to look for primaries and so on and so forth. Here's an example of an ependymoma. You can see on the right side of the screen, the contrast enhancement with gadolinium. Some patients that seem myelopathic turn out to not have myelopathy at all. And so something like multiple sclerosis can present in a similar fashion, but these lesions do not enhance with contrast. So while they're bright on T2, like you saw on the previous with the tumor, the post contrast images do not enhance. Here again, you're going to refer the patient out for appropriate care. Next on the list, vascular malformations can present with myelopathy. These are characterized by flow voids. The flow voids are seen both in T2 and T1 images within the spinal cord, and that's due to voids created by the rapid movement of blood that create these dark voids on the MR that are described as flow voids. Any of these cases, you're working them up. You see these things. You're going to refer the patient out for appropriate care from the specialists at your institution that are really specialized in dealing with these disorders. You may see the person back ultimately to help with the rehabilitation course, but you're not going to be the primary provider. However, the last group on this list, the patients with degenerative compression of the spinal cord, this is kind of your bread and butter. And patients with myelopathy are more likely going to have this than other things. There is the congenital group that you just heard about, but that's not nearly as common as the degenerative cervical myelopathy group. And in fact, when you look at patients that have surgery of the cervical spine and the reasons for it, degenerative cervical myelopathy really ranks extremely high when you compare it to things like tumors, subdural hematoma, aneurysms, and even traumatic spinal cord injury. This is very late breaking data that I got from the recent NAS annual scientific meeting. So we're going to spend the rest of this time talking about degenerative cervical myelopathy, not just because it's the most common, but because new guidelines have come out that actually are quite useful for us. And I want to review those guidelines so that everybody that attends here today comes away from this talk with an idea of those guidelines and how you might apply them to patients you see in your practice. With the guidelines, there's really two things that factor in. One is the clinical. Is the patient clinically myelopathic or not? Some patients can have compression of the spinal cord and not be myelopathic. And the second thing is what do you see in the spinal cord itself? Is there myelomalacia of the cord and how does that factor into the thought process? So we're going to talk about each of these two key considerations and how to categorize them in your mind and in your approach to your patients. So let's start off with the radiologic part. The radiologists have classified myelomalacia into three types. Type 0 means there's compression of the cord but no signal change. Type 1 is displayed by the left-sided image here, and that's where there is a hyperintensity on T2 within the cord, but the margins are ill-defined and it's usually not super bright. In milder versions of this, sometimes you're trying to convince yourself whether or not you can see myelomalacia or not. Type 2 are the ones where you know for sure there's myelomalacia. There's a bright signal within the cord. It's usually highly bright and it's fairly well-defined. All right, so type 0, type 1, and type 2. This is useful. In fact, this may be the limit of most people's knowledge here because we've been taught over the past decade or more that these appearances are important because they're prognostic. Type 0 and type 1 patients, well, let me back up a little bit. From 10,000-foot point of view, you see a patient with cervical degenerative myelopathy and you refer them to the surgeon. They're going to ask you, okay, what can I expect here, doctor? I'm having a little bit of trouble walking or I have some clumsiness with my hands. Is that going to get better? And generally, our response has been to tell them, well, I hope so, but that may not happen. The goal here with surgery is to prevent further deterioration. And that's important because, and then you explain to them what deterioration means. But you don't really promise any improvements because that's not expected. However, we've learned that these type 1 lesions are more likely to show improvement after decompression than the type 2. And so there is a subgroup of patients here where some improvement in the presenting myelopathic features is expected with surgical treatment of the myelopathy. And that's helpful, especially as a rehab doctor, to be able to deliver that story. However, you have to be a little concerned because you don't want to undermine your surgeon colleagues and overpromise. You know, a patient who has a decompression for cervical degenerative myelopathy who's expecting a great recovery because of some false story you gave them might, you know, be upset with your surgeon colleague when they come out with lack of any progression and the expected outcome, but don't return to normal. And so you don't want to give somebody unexpected outcome expectations either or unlikely outcome. So this has been looked at a lot more over the past 20 years. And unfortunately, the picture has gotten fuzzier, just like the type 1 appearance. Relative measurements of these through more advanced imaging techniques have produced disparate results. Some studies showing that the fuzzy borders do predict more likelihood of reversal of some of the myelopathic features and symptoms, whereas other studies have shown the opposite, that the fuzziness actually is a worse predictor and that patients with type 2 and the more defined lesions recover more than patients without. So the picture from MR actually has gotten more complicated and confusing about being able to predict who's getting going to get better and who's not. Now, fortunately, more advanced MR techniques are coming online and things like diffusion tensor imaging has been shown to perform better than the old T2 ratings. But these aren't things you're going to see in your clinic. You don't pull up an MRI and see the quantitative diffuser tensor imaging results that has to be produced through an algorithmic evaluation of the scan and it's produced numerically. So this isn't something that you're going to interpret in your clinic as of today. And then some other advanced MR imaging techniques are showing early promise as well. So we may get better at determining whose myelopathy is going to reverse to some extent with decompression. But I would say as of today, we're not there. So really, at this point, the radiographic myelomalacia issue isn't that helpful in determining what you're going to do with your patient in the clinic. But the clinical side of things, which is where we shine, right? That's where physiatrists are really, really at it above everybody else, is what helps determine the treatment algorithm. And let's talk about that in specific detail. This algorithm, it derives from a consensus study done through AO Spine, which is a spine surgeon organization. But to their credit, they reached out to non-surgeon providers of spine care as well as patient representatives and other folks to get really a comprehensive view of this problem to learn what it is that patients with myelopathy want when they're getting treatment and to make sure that their algorithmic approach is based on best evidence and on what patients really want to get from their care when they have degenerative cervical myelopathy. You can read that document here. A better version of it was published just this year in Nature Reviews. The graphics are better and it's an easier read. So I'd actually recommend you read this instead. And this is the algorithm for what you do with a patient that comes to your clinic with degenerative cervical myelopathy. And while this looks complicated, believe me, it's not. I don't like complicated algorithms. Really the only part of the algorithm you need to worry about is this part right here. And let's zoom in on that so that we can discuss what it means. And in this part of the algorithm, there's only two things you have to figure out about your patient. All right? The top part of the algorithm I cut off is about the patient, you know, comes to the clinic, they have imaging, they have canal stenosis, and that's about it. The bottom part is all the clinical part. Okay? So the first clinical fact that you need to figure out is the patient myelopathic or not. Okay? If they're not myelopathic, they go over to the right side of the chart and down that group. If they are myelopathic, if they have symptoms of myelopathy or signs of myelopathy, then they go over to the left side of the chart. Okay? So, question one, pretty simple, myelopathic or not. If they're not myelopathic, but they have radiculopathy, then you have a discussion with them about surgery. It's been shown that patients with radiculopathy who have degenerative cervical stenosis are more than twice as likely than patients without radiculopathy to proceed to surgery or to proceed to myelopathic features. And so the patients that present with radiculopathy are higher risk and more likely to convert to myelopathy. So having that discussion with them, not just around their current symptoms, but potential future state, causes some of them to determine, you know, I just want to get this taken care of and have surgery. Now, it's not required that they have the surgery, but that discussion happens. Patients that don't have radiculopathy, that don't have myelopathy, you treat them conservatively. You don't send them to the surgeon for prophylactic surgery just because their canal is narrow. Okay? That's question one. Question two is the patients that move over to the left side of this graph because they are myelopathic, your job is to determine is their myelopathy mild or is it worse than mild? That's it. If they're mild, you treat them just like the patients with radiculopathy. If they're worse than mild, you send them to the surgeon. And what do I mean by worse than mild? Well, there's three categories. There's mild, moderate, and severe, and that's determined by the modified Japanese orthopedic association scale, which is a highly validated scale for cervical myelopathy. It's been used for years and years. Every study you read of cervical myelopathy will have this scale in it if it's worth its salt and this scale is very useful in terms of contextualizing a lot of things around cervical myelopathy. It's also useful in this context because here are the scores that determine if you're mild, moderate, and severe, and if a patient scores in the mild group, you can treat them conservatively if they want to be treated conservatively or you can send them to surgery if they prefer that option as well. It's a shared decision-making process. And just to give you an example, you know, what is a mild myelopathy based on this scale? It's a score between 15 and 17 and higher is more favorable score, lower is a worse score. And a scale of 15 comes in these four categories through motor dysfunction in the upper extremity being somebody who's able to button a shirt but with some difficulty. So they've got a little bit of bi-motor issues in the upper limb. Motor dysfunction in the lower extremity is that they have a mild lack of stability but they're able to walk smooth in the clinic and unassisted. But if you challenge them with tandem or other things, you see some instability. In terms of their sensory dysfunction, they have some mild sensory loss. And then in terms of sphincter dysfunction, they have normally functioning bladder. So, you know, that's a pretty common presentation of a cervical degenerative myelopathy who you might consider for surgery. But according to the surgeons and their own algorithm, they don't necessarily have to have surgery. They can be monitored and they can be treated conservatively. They can elect for surgery but it's not required in this instance. Patient that's worse than this, that scores at a 14 or lower, then you should send to the surgeon for surgical evaluation. So my take home is really this, look at this algorithm, understand there's really only two important questions you have to figure out. And then if a patient is myelopathic, it takes very little time to compute this scale and determine, you know, is it recommended that they see a surgeon and have surgery or do they have the option of being monitored and treated conservatively. And my references are provided throughout the talk for anybody who wants to look into this in more detail. Thank you and here's my contact information if you have questions for me. Questions for all the other authors can be sent in as well and we'll be happy to help in any way we can.

spinal pathologies

bony destruction

axial back pain

hand weakness

mid-back pain

arm pain

red flag symptoms

spinal metastases

myelopathy

clinical assessment

surgical intervention