Age-related spinal changes can be relatively benign – but they also can result in spinal cord dysfunction. Orthopedic surgeon Kevin Hwang, MD, describes symptoms that should raise suspicion of degenerative cervical myelopathy; presents the latest research on predicting disease progression; and offers an update on surgical techniques, explaining why laminoplasty might be a better option than you think. Also: Hear which medication shows promise for better outcomes.
All right. If everyone wants to take a seat, I think we'll be ready to get started. Um I saw it there. He is. Um Do you need anything else? And then are you gonna stand behind? I think so. Yeah, no problem. If you, I came here earlier, then I saw you out there. I just, I don't think I would be that, that we have been person and she gave like a great e she like came out brown kid. All right. Um So just um as we get started um one announcement, so the Mount Zion Health Fund um they had awards for residents and um Doctor Sarah Stroud was one of the four recipients of that for providing excellent care at Mount Zion. So um Sarah is at home on maternity leave but congrats to Sarah on great achievement. And then uh for today we have uh uh one of our faculty members, um Doctor Kevin Wang, um and he's going to speak to us about degenerative cervical myelopathy and for an introduction, turn it over to Doctor Tate. So this is gonna be short and sweet Kevin. We are so happy to have you. Um Kevin started one year ago, uh and he is our main person at uh Marine General Hospital and is spearheading our spine service at Marin Health and in combination with U CS F health, he is a co-director of the spine service over at Marin General and um is building up a practice of mental invasive surgery, which is his passion and his research passion as well. He's going to be talking to us about degenerative cervical myelopathy, the state of the art and um look forward to learning some stuff from you. All right. Thanks for the nice introduction, Drew and Bobby. I'm very excited to be here. It's been a few years since I've been up at the podium as a chief presiding grand around. So I'm very happy to be here. It's uh I think the 10 year anniversary of me showing up here at UC as a, as a medical student, as a visiting medical student a long time ago, sitting sitting in the back and trying to uh avoid eye conduct. Um OK. Uh So today we're gonna talk about a clinical interest of mine, degenerative cervical myelopathy. I'm gonna review a little bit about where we've been and where we're going and its treatment. Um I have no relevant disclosures. Uh We'll start with a little bit of an introduction of the pathology. We'll talk about diagnosis and treatment and the evidence underpinning that and then we'll review modern management options and talk about future directions as well. Degenerative cervical myelopathy arises from age related multifactorial structural changes that are seen in the cervical spine that can lead to static or dynamic spinal cord compression. Uh It's the number one cause of spinal cord dysfunction in adults worldwide. The structural changes can arise from a variety of things that can include disc degeneration, osteophyte formation, uh ligamentum flam facet hypertrophy, e ossification and then changes to dynamic motion such as oses all contributing to a common endpoint of compression upon the spinal cord, which drives path of biologic changes within in the spinal cord itself. Neuro inflammation, cytokine release alterations in vascular architecture and neuronal apoptosis. With the end result of neuro neurologic dysfunction. Uh the germ myelopathy has a major impact in quality of life scores for patients. Uh Research done here at U CS F has shown that, you know, on global function testing, uh patients with moderate or severe myelopathy have diminished physical and mental function scores equivalent to other severe disease states, you know, diabetes, heart disease, cancer, and hip and knee arthritis. Um epidemiology incident estimates vary quite widely looking at hospital admissions. Uh and coding, it seems to be somewhere in the range of 2 to 8 patients per 100,000 each year. Peak incidents tends to happen somewhere between 5070 is seen more commonly in men than in women. It seems that myelopathy is likely under diagnosed in the general population when they do cross sectional studies. Looking at the incidence of asymptomatic spinal cord compression in large populations, we tend to derive a number somewhere between 20 40% in patients older than 60 will have some degree of asymptomatic spinal cord compression. And when these patients are followed over time, they tend to progress to symptomatology somewhere in the rate of half to 1.5% uh within each cohort, which would predict an incident significantly higher 10 or 20 times higher than what we actually see. Uh So a as a way of review, I'm sure you're all familiar. A common clinical presentation of myelopathy involves loss of manual dexterity in the hands. Patients say they feel clumsy or they have some weakness in the hands can present with sensory change or with pain. Often in non dermatomal distributions involving primarily the upper extremities as symptoms. As disease progresses. Patients can start to have similar complaints in the lower extremities as well. Uh There may or there may not be any component of neck complaints at all that tends to be highly variable between individuals. But gait instability on steadiness is a very common symptom or signs. Patients will present with impaired gate difficulty with tandem gate in the office. They may have sensory loss or weakness and non dermato nonm myoma distributions and reflex exams often show hyperreflexia, brisk reflexes or reflexes with spread and pathologic reflex is most commonly seen being babinski or an inverted radio, sorry hoffman's or an inverted radiole atypical presentations. Uh atypical findings are seen kind of widely throughout the literature and case series. Uh patients with intrinsic hand wasting with uh complaints of primary tremors or fasciculations or even headaches and tinnitus. Ok. Common imaging findings. The MRI is the diagnostic study of choice. Uh It allows excellent visualization of the neurologic structures of the CS F space of contributing an atomic structures to cord compression allows for uh excellent visualization of the cord broncho itself. Here are examples of different types of myopathic findings commonly seen in patients. And then here we can see a common chord changes that are seen as well both on T two and T one signals. So I'll stop here and give a little summary, cervical myelopathy, common disorder of the spinal cord, frequently underdiagnosed symptoms present as clumsiness in the hands, sensory change in the hands, pain or weakness and balance difficulties. I'd like to move on to talk a little bit about the natural history of this disorder. So, um the literature surrounding the natural history of myelopathy goes back into the early to mid 19 fifties. This paper is likely the most cited about it. This is Clark and Robinson's paper describing 100 and 12 cases of myelopathy and this is the origin from whence we talk about myelopathy presenting in this stair step type manner. Um So here, this is the first time when they talk about this stepwise decline. And the authors suggest that over long periods of time, about 75% of patients will experience a stepwise decline in their overall symptomatology. Uh And that 75 will have percent will have progressive worsening with only 25% of people uh experiencing an arrest in progression or static symptoms. Um Even from the beginning, this concept was fairly widely debated. Um Lees and Turner published this paper in 1963 a few years after Clark and Robin said that that argued that the course of disease was generally benign and nonprogressive. And in this chart that they published um that they highlight symptomatic periods as these dark black lines. Uh and the open wide space represents periods of static symptomatology. Uh And Nick himself also argued that, you know, the course of cervical myelopathy tends to be nonprogressive and relatively benign. Despite leaving patients at times with permanent symptomatology, this debate went on for many years um with quite a bit of heterogeneous literature coming together to try and help us determine what's going to happen with patients once they start to present with symptoms. And the most recent or the most widely cited recent work is this 2013 meta analysis. Um And the takeaway for many of us was that patients have a risk of symptomatic deterioration once they present with myopathic symptoms of somewhere between 25 and 62% which from my perspective, quite a wide range uh over a three to a 6.5 year period and that patients initially treated non operatively, uh have a risk somewhere between four and 40% of progressing to surgery over the same time period. Authors attributed this high variability to significant variations in the definition of neurologic decline which was often left up to the treating provider and also indications for surgical intervention. And the work itself is littered with, with contradiction On the same group that state of year that there was very little progression to uh symptomatic deterioration also measured quantitatively, patients abilities to perform their own. Ad LS and noted that over a 10 year period, more than half of patients would go on to have difficulty with basic daily tasks. So this has been investigated further on uh trying to standardize our assessments of neurologic progression. And the group from Toronto used a wide range, not just JO A which is traditionally used, but dash scores, grip strength measures, measures of and function and balance uh in a more quantitative way and found that up to 57% of patients had quantitative worsening of their overall myelopathic symptoms over a period of only 2.5 years. Uh The the figure on the right side shows these measures as they tested and and uh the associated analytics. And the figure on the right shows assessed survival, survival being defined as no progression of neurologic symptoms over a 60 month period. Many efforts have been made to try and synthesize this into data that could be used by our patients when trying to counsel them on the risk of neurologic progression from myelopathic symptoms. Uh This is again a publication from the group in Toronto where they put together progression free survival scores based on uh available literature and patient severity, severity of symptoms on presentation. And so the blue spectrum and the blue dotted lines represents the probability of neurologic of disease free survival from neurologic symptoms for patients are present with only mild or minimal overall symptoms. And that was defined as jo a score greater than 14. And the red line below that represents uh disease free progression uh in patients that presented with moderate or severe disease. And they postulated that initial presenting severity of myelopathy was the number one predictor of later progression. And that patients with mild symptoms would progress only at a rate somewhere between 10 and 15%. But that patients with moderate or severe disease progress at a rate closer to 50% in the near term. Ok. So trying to bring this all together again, myelopathy, common disorder of the spinal cord, frequently underdiagnosed symptoms of clumsiness in the hands of the feet. And evidence on natural history is quite heterogeneous, but symptoms seem somewhere between steadily deteriorating and generally stable over long time spans. But individual prognostication still very challenging. Ok. So I I included this slide because I wanted to talk about it, not because it makes a lot of sense in the context of the presentation, but we're gonna do it anyway. So, depending on who and what you read. Cervical spine surgery in the United States started almost 100 years ago with, you know, the first, uh, traditional case being performed in New York around 1925 by this gentleman Charles Ellsberg who looks to me alarmingly like Joe Patterson, um, and I needed ac 5 to 7 posterior laminectomy for a for a disc excision and no comments on how the patients did. Uh in the years that followed, there was a proliferation of posteriorly based surgery to treat uh de gene of spinal pathology and this is what it looked like back then. Uh This is Clark and Robinson, their surgical colleagues for this and it would be a long laminectomy. It would be uh intentional opening of the dura isolation of the individual nerve roots to section the denticle ligaments which attach the spinal cord to the anterior and the posterior roots into the dural edge. And this was done in part because there was some concern that that tethering of the spinal cord itself could contribute to, to compression. Uh but also that in order to reach anterior pathology at the time, the spinal cord would need to be uh moved over to the side. And this allows for some motion of the spinal cord. And there's as I was preparing this talk. There was an alarming number of case studies talking about uh osteophyte excision, central disc herniation, excision being done around the spinal cord. It's not not something that we commonly do at this point. Um But thankfully, we moved forward. So in 1955 Clark and Robinson described what most of us think of as a modern A CD F approach. And at the same time, independently, Ralph Cloward described his procedure with the, with the dowel and the field rapidly moved away from opening the dura to access and pulling the spinal cord aside to access the disc towards anteriorly based procedures. And patients benefited from this. Uh It wasn't until this was around the same time. So this was like 1958 when Cloward described uh his technique. And then in the 19 sixties, there is a development of lateral approaches to the spine which I don't know if anyone here in the room ever ever did. You know, re retro carotid approaches, direct lateral approaches to the cervical spine, which has subsequently fallen out of favor. Uh the diagram in the bottom, right. This is Hirabayashi paper from 1977 of what is now considered a modern laminoplasty, laminoplasty first developed or first described in Japan in the early 19 seventies, went through a long series of iterative improvements before we settled on what we we still do today for the most part, not with suture anchors or now now with now with some hardware. I didn't come to the United States until the early 19 eighties and it wasn't until, you know, chart of the millennium around the two thousands that Atul Goal and Jurgen Harms described what we think of as model, modern segmental instrumentation on the and go described a segmental screw placement, but they didn't have pedal screws and rods, Multiaxial screws at that time. So he had to place them through a plate which takes quite a bit of skill. And then here we have uh Jurgen Harms Pedicle screw and rod instrumentation, which is what we do today look, should look like what you're used to seeing today. I'd hope. Ok. It becomes a little relevant as we move on. All right. So uh there is a single prospective randomized control trial comparing operative and non operative treatment of degenerative cervical myelopathy. It was a study of at its maximum 30 patients, 32 patients in each group. It was performed in the Czech Republic and patients started enrolling in 1993. And this group led by uh Canada showed that patients were included if they had MRI evidence of cord compression, no other confounding neurologic diagnosis like a LS or multiple sclerosis and an mjo, a score of greater than 12, which would place them into this mild or moderate disease category. They were randomized by coin toss to operative or conservative treatment and no details of what that treatment actually entailed were included. So, that's what they did for them. Uh The initial cohort 48 patients, 24 in each group uh showed no difference over 24 months in JO A scores. And so this is the non operative group here highlighted in blue and the operative group here in green. Uh And they published later on 10 year follow up. Uh By that time, the groups had expanded to 32 the severity of disease had alleviated with a total average jo A score. The group of 15 and they again concluded between the blue non operative and the operative groups that there were no differences in jo a score outcomes and patient better outcomes. But they also concluded that both groups sustained fairly significant uh worsening of their ability to perform their AD LS. And the final conclusion was that surgery didn't make, uh did not induce any improvement in patient symptoms. You know, the literature wouldn't stay there, but it would be more than 10 years before another perspective trial was published, there were two that were sponsored by the A O. At the same time, these are the results from the CS MN A study which was focused on patients in North America. And this work, this project enrolled 278 patients from 12 North American sites. U CS F was one of them and they reported 87% follow up at 12 months. Uh In this, in this work, the way they presented it, they divided patients into those who received anterior and posterior surgery for analytics. About two thirds of the overall group underwent an anterior fusion. About 30% underwent a posterior fusion and 5% of patients received a laminoplasty. And they tracked a variety of uh reported outcomes. Joanind I score neck pain, as well as SF 36 global function pain and mental health. And they noted significant improvements uh from baseline across both surgical types that were not significantly different from one another. And that is improvements in in all of these individual measures that met MC ID. Uh They reported a 12% complication rate in the anterior group and an 18% complication rate, the posterior group. Um but you know, these were all American patients, all American surgeons. And so the process was done at the same time on an international basis. And so the second trial results of which were published in 2016, uh focused on an international cohort and enrolled 480 patients from 16 international sites, about two thirds of which were either in Europe or Asia. And they presented their data comparing uh other spondylotic degenerative forms of myelopathy. Comparing to OPLLOPL patients comprise just under 30% of this overall cohort. And in this group, approximately 60% of patients underwent an anterior procedure, 20% underwent a posterior fusion and the remaining 20 had a laminoplasty done. And again, across the same measures this time two year outcomes. Mjoannd I and SF 36 they showed significant improvements from baseline kind of at odds with our original randomized control trial from the Czech Republic. And this is, this is the latest, this is the latest prospective study that we have. This is from Zha Gola at the Leahy Clinic. It was published during my time in Boston again. U CS F was an enrolling site for it. There's a prospective randomized trial comparing patients to ventral or dorsal surgery and the treatment of multilevel degenerative myelopathy. 100 and 63 patients were randomized. 63 getting a ventral surgery and 100 receiving a dorsal approach. And uh the specifics of each surgery was left up to the treating surgeon, but the patients either received from the front some combination uh or one or the other of an anterior cervical discectomy infusion or a cervical corpectomy and posteriorly either a laminectomy infusion or, or a laminoplasty. Um And, and I like how they presented this day. It's an interesting way of looking at it. Primary outcome for the study was sf 36 physical function component scores and change against baseline is shown here uh in the graph, uh the right of the left of the screen um with patients initial states outlined as the solid line climbing to, to the peak and changes being represented by the histogram bars, the vertical bars um for each of the individual patients from the study and absolute changes uh are shown here on, on the right side between dorsal and ventral surgery uh over the same time period showing improvements in sf 36 physical component scores. Um There's an interesting note that was made in the study, you know, not every surgeon, uh 24 out of the 24 enrolling surgeons, only eight, regularly performed laminoplasty and they were encouraged to do so if they felt that it would be appropriate for patients. Uh and they noted uh the, but they noted uh improved physical component scores at one in two years in patients that had undergone laminoplasty as opposed to laminectomy infusion. Mm, complication rates between the procedures differed quite significantly. Almost 50% for anterior procedures though they included dysphagia as a as a complication, 30% for dorsal fusion and 11% of the lamin plaster. So we're gonna keep going back to the slide. We're gonna keep adding to it. Uh myelopathy comma disorder, the spinal cord symptoms of clumsiness, balance, difficulty, natural history is quite heterogeneous, but probably trends towards symptomatic worsening of the long time spans. And surgery can improve neuro both neurologic and and global function outcome scores in in patients with neurologic symptoms. So that kind of brings us to this discussion of, of what modern management of degenerative myelopathy looks like. Um This is a diagram that I borrowed from from Donnelly at all that was published for Family Practitioners Journal of the American family practice. And it provides a nice outline for how we think about diagnosing and treating myopathy, looking at the residents. So one. So of course, all of this starts with a patient history and a physical exam. And patients that report neurologic symptoms, potentially suspicious of myelopathy should kind of be divided into this cohort where they seem to be relatively high probability or relatively low probability in patients where there's a real concern for these types of symptoms. Uh they should have some type of of imaging screening. Uh X plane X rays can show general spinal lytic changes that increase or decrease the suspicion of disease, but they certainly would miss any soft tissue. So really the study of choice would be an MRI and uh patients with concerning MRI. Findings should be referred to a spine surgeon for evaluation and patients without compression, visualized on MRI should be referred to a neurologist. And among those patients that do have spondylotic myelopathy or we do have symptoms of myelopathy. Uh treatment has generally been divided based on jo a scores and uh patients with moderate severe symptoms are generally recommended surgical intervention based on the data that I just reviewed and patients with mild symptoms or patients seen as asymptomatic with risk factors and the risk factor that has the most support in the literature right now seems to be ridiculed, get a discussion and uh there's some equi pause on what appropriate treatment is in that situation. So there are talk about surgical intervention, talk about structured rehabilitation and patient education is a large component to this as far as symptom surveillance. And a large proportion of these patients will have actually uh isolated cord compression without any symptoms of myelopathy. And for those patients, the general recommendation is is education and clinical follow well. So you know, when I, when I look at this chart, I see a lot of a lot of structure and I see some data that supports it, but I also see quite a bit of room for for further improvement, kind of them, the more set in stone, you know, this has been set in stone by guidelines here uh from the A O from CS RS from Japanese orthopedic Association, basically all tier their treatments in a very similar manner. And it raises a number of questions about how we can improve this type of care. What other data we can gather to try and guide our treatments really around? What do we do for this mild myelopathy pathway? How can we predict how symptoms might change for patients? And what do we do about educating patients who have asymptomatic or compression? And what kind of expectations can they have for the future and also what surgery is best for them? So that kind of brings us to this idea of future directions areas for further improvement. How can we better predict natural history for ourselves or our patients uh what really constitutes optimal non operative treatment. And is there is there any role for medical treatment and what can be done to improve our surgical outcomes and decrease morbidity? So there is a quite a bit of, of literature around this. Um probably enough to fill its own grand rounds talk. So I'm going to run through some of this without filling the screen with charts. So, factors that have already been identified as potentially related to symptom progression, symptom severity at onset, other neurologic symptoms from uh the cord around the same level. SSCP and mep changes have uh been shown to have some prognostic value but haven't made their way into widespread clinical practice. And there's a few MRI findings that have the potential to contribute. This is not widely borne out. But the things that seem to be most reproducible are cross sectional area of the cord measured quantitative and compression ratio. So that is a to P dimension compared with uh media to lateral dimension in the spinal cord at any given level. A me notably on here absent is the presence of T two hyperintensity, which I think is something that many people assume is related to symptom progression, but it has not been and and there is also literature on what relates to post-operative outcomes because we know some patients uh will recover quite a bit more neurologic function than others. And what clearly differentiates those people has been a topic of much debate over time. Uh Generally symptom severity, symptom duration, cord signal change or atrophy on MRI is related to less post operative improvement as well as the severity of concomitant metabolic or vascular disease. But can we build on that? Are there things that we can build on that? You know, it seems like the next step and this has been in the work flow now for almost 10 years is uh DT I MRI S OK. So diffusion weighted MRI S um have been associated in some studies with both preoperative severity of clinical symptoms as well as post operative recovery. In particular, this fractional uh an isotropy and this has been produced now by, by a few different sites in a few different ways though the manner in which this that is generated is still highly variable and has not been fully standardized. You know, a another area that seems to be further developing every year is looking beyond just radiographic markers of disease towards other potential indicators of natural history and genetic markers are starting to show more promise in helping define the course of disease for individual patients. Uh The most well studied of this of these is uh apo lipo protein E this is a 299 amino acid protein that's involved in uh the regulation of lipid transport in neural tissues. Uh There's three major polymorphisms E two E three and E four and they differ by a single locus or a single amino acid at two different loci and studies in a broad range of mammalian models. And also in humans show that it's a regulator of disease related microglial changes seen in degenerative neurologic diseases. And it's been seen in Alzheimer's and A LS. And it's being studied now in traumatic spinal cord injury and degenerative spinal cord injury among other things. And this E four allele, which is seen globally roughly in about somewhere between 15 and 25% of the population has been associated with a decrease in neurologic recovery after spinal cord injury. So, you know, with regard to non traumatic spinal degenerative spinal cord dysfunction, um it's been associated this apo lipoprotein E four has been associated with decreased improvement in symptoms or decreased recovery and symptoms after surgery, right. And you know, if it is associated with a neurologic recovery and in patients. So this this study out of Berlin, looked at patients with asymptomatic cervical cord compression and looked for symptom progression over time and identified the presence of the E four allele as increasing the risk of developing symptoms of more than 66 fold over the study period. Yeah. Now, this is not the only thing that that's been looked into though it is generally the best to find there's a wide range of potential genetic targets that have been implicated in the progression. Uh and the recovery from degenerative cervical myelopathy and the data underpinning all of this continues to be developed and I think new, new genes and new proteins. I haven't heard of get added every year. Uh An another question that I had brought up before is whether there's any role for medical treatment and medical therapy for the management of, of myopathy and the agent that's had the most interest is Rizo Rizal is an anti convulsive medication. Uh That's been approved by the FDA and the treatment of uh A LS. And it's been shown to have a modest survival benefit in those patients. Um It has multiple mechanisms of action. It primarily works as a noncompetitive pre and post synaptic inhibitor of sodium channels with the end result of decreasing glutamic release from pre synaptic channels, lowering the thought of neuro excitability. Um There was a prospective double blinded randomized control trial. It really is all done in degenerated cervical myelopathy patients. Uh around uh comparing a placebo to a six week per operative course around the time of surgery, two weeks before four weeks after uh they enrolled uh 290 patients with a primary end point of Delta mjo A and final results failed to show significance. Although there was a bit of a trend and curiously, there's a trend towards improvement in post operative pain as well. So nothing conclusive but wait and see on the horizon. And then I think we're gonna get a little bit more towards, you know, my personal interest here and my favorite thing to talk about, which is uh improving, improving surgical outcomes for our patients. And so, you know, in, in the clinic, I tell my patients, there's really four things that we do with surgery to, to treat these types of degenerative changes and it boils down to something pretty similar. We do surgery through the front of the neck or through the back of the neck, anterior or posterior approaches and we do surgery that either preserves motion or takes it away. And so modern treatment options are generally, you know, anterior cervical disc replacement, infusion and laminoplasty or laminectomy infusion. And we'll talk about these separately. So again, one slide for something that really could be a whole talk in and of itself, I'm gonna try and move through this in a timely manner. Optimizations for anterior surgery, in particular, the conversation that's been going on over the last 10 or 15 years has focused on decreasing uh morbidity for patients after surgery. And the primary identified problems being dysphagia, pseudoarthrosis, adjacent segment disease. And to a lesser extent surgical invasiveness for anterior procedures. And you know, changes that have been made, improvements that have made made in practice are application of of steroids for dysphasia. Improving operative techniques, low profile implants or zero profile implants for a CD FS or pseudoarthrosis implant materials have certainly improved the scenario of constant improvement as well as the use of Ortho Ortho biologics or fusion adjuncts. You know, cervical disc arthroplasty really intended to help improve adjacent segment disease. And depending on who you talk to, that may still be an area of debate and hybrid procedures. Something fusion, uh A fusion disc replacement constructs are becoming more prevalent. And uh as always, people will continue to push the limit of decreasing uh morbidity of surgery. And there, there are people doing endoscopic A CD FS. There are people that are doing motion preserving corpectomy to try and help patients uh uh recover from surgery. And then for posterior surgery, the same conversation is happening but with, you know, different, different things in mind. So issues that really come up with posterior surgery, uh high rates of CF palsy, you know, up to 10% in posterior laminectomy infusion patients. Uh neurologic worsening has been reported in the literature. More common after posterior surgery, somewhere between one and 71 and 10% depending on who you read. Mm, wound complications are common. It's an area that has trouble healing, post-operative pain, post operative, prolonged hospitalization, pain management, uh motion preservation, not really a thing that you do if you're fusing someone as well as medical complications, which have shown been shown to be quite a bit higher with posteriorly based approaches as opposed to anterior ones. What, what, what are we doing about these things? What can we try to do about them? There's been a long conversation about the role of prophylactic for am anatomy or C five palsy prevention and the jury is still out on that. And the general recommendations around how we position and tape our patients during surgery and the use of inter operative neuro monitoring shown to help improve outcomes. Um Likewise, neurologic worsening. We talk about intraoperative monitoring. We talk about delicate surgical technique, meticulous surgical technique. These steroids are around the time of surgery. You know, for wound complications, we talk about optimizing our patient selection using prophylactic antibiotics. Um post operative pain, it's being managed through e rash protocols, multimodal pain protocols, pain contracts with patients setting patient expectations. You know, we have laminectomy or laminoplasty as motion preserving options. And we really need to focus on preoperative optimization to help manage our medical comorbidities after surgery. But I would actually suggest that there's another optimization for posterior surgery that's not commonly being used or is in a way that people don't quite realize and that would actually be laminoplasty. All right. So um if the goal is to ameliorate the li the list of morbidities from the left hand column, uh Laminoplasty is already a relatively widely done procedure that actually addresses almost all of these issues. It's probably still being under utilized as a tool in our Armamentarium. Uh And the literature is actually, it's an interesting story. You know, when uh when I was formulating this talk, when I was developing my practice, uh you know, it was a practice that full disclosure, I like to do laminoplasty. I do it for a number of them um where this evidence base wasn't there. And the ideas were being developed, people were starting to ask these types of questions, but it really has been in the last two or three years that a large body of literature has come out. And here, here's, here's an example of reviewer from the yellow journal. Looking at a long list of morbidity and complications associated with a posterior cervical surgery are motions bearing or motion preserving. Uh and and in a synthesis of available literature, they showed for all of these green arrowed complications, significantly decreased rates in patients undergoing a laminoplasty as opposed to a laminectomy infusion. And I I realized I've broken one cardinal rule of powerpoint. This is like a table, no one can read. Uh but on it are wound complications, infections, neurologic injuries. C five palsy paralysis need for revision surgery as well as respiratory renal failure and UTIs rates are all decreased in laminoplasty patients as opposed to laminectomy infusion patients. This is a, this is a curious piece of work that was done by some of my mentors in Boston where they tried to quantify what the rate of underutilization of laminoplasty was. Uh and they looked at a sister hospital uh and reviewed 250 patients with multilevel cervical spon alo myelopathy and reviewed them for radiographic candidacy for Laminoplasty. Uh And they found that o overall um 80% of the patients that eventually underwent laminectomy infusion, met minimum radiographic candidates for laminoplasty. And so the rate of utilization uh could had room to increase. OK. But there are some things that people still say there are some things that people say that that were said to me at some point. Um you know, you can't, you can't use it. And all the laminoplasty is a very selective, you have to be extremely selective and most people won't meet these criteria. And so we'll say things like doesn't work in patients that have facet disease because they have neck pain and you're going to leave it there and you're gonna cause more problems down the line. It worsens their axial neck pain because motion drives drives pain. People will say, you know, laminoplasty causes causes kosis. And so you really can't use it in anybody who, who you're worried about kyphosis in and spine surgeons while I worry about hypos in every single patient. Um And you know, motion can, can worsen spinal cord injury if you have stenosis even after decompression, motion is an irritant and it can worsen your outcomes afterwards. And there, there's actually relatively robust literature at this point that kind of refutes all of these, all of these ideas. All right. So, uh there have been a series of very heterogeneous trials coming out of Japan, uh talking about less invasive posterior cervical spine. And this is a comparison of four different studies comparing in the blue uh procedures that attempted to spare some type of musculature. And so this primarily is referring to uh sp semi spinalis services attachments onto the large uh spinous process of C two or alternatively large muscle attachments from the trapezius and from the spinal rotators onto C seven. And the theory by the authors was that preserving these muscles attachments would decrease axial neck pain afterwards. Ok. And the bars represent delta axial neck pain compared to pre op uh showed that muscle preservation decreases axial neck pain uh across kind of a wide range of individual procedures and techniques. They asked the question of whether or not laminoplasty or laminectomy and fusion really worsen or change radiographic outcomes for patients. And you know, over large enough groups, it seems that laminoplasty and laminectomy infusion result in very similar clinical improvements and curiously, very similar amounts of loss of lower doses. We and you know, is neck pain is neck pain a contraindication to performing laminoplasty. You know, when subdividing patients with preoperative neck pain into mild, moderate and severe uh patients with moderate or severe axial neck pain complaints preoperatively are able to achieve similar post operative patient aborted outcomes at six months in a year compared to patients with mild or minimal complaints. And uh you know, as we keep looking, the literature continues to build that laminoplasty may just be a minimally invasive version of a laminectomy infusion for properly selected patients. And this work from neuros spine really compares uh it was three prospective and 58 retrospective studies. Uh trying to compare fusion patients with laminoplasty patients and continuously reported these types of uh improved patient reported outcomes and decreased post operative complications from from laminoplasty. As well as you know, less post operative pain, shorter hospitalization. We kind of jumped into this conversation ourselves. Uh looking at the patient cohort from my fellowship group in my practice at Mass General and showed that patients with similar pathology undergoing similar procedures, had less immediate pain after laminoplasty than laminectomy infusion patients. That their surgeries cost quite a fair bit less than that in the medium. And the long term, the patients took less pain medication were less likely to be taking opiate pain medication at three and six months that their uh hospitalizations were shorter and that they were less likely to be discharged to a rehab facility. Um And so, you know, this conversation kind of all harkens back, I think to, to to this study, uh which really highlights that there is the potential for getting as good if not better clinical outcomes in patients with fewer complications um by doing emotion sparing approach for people. So we're so we're back to this as a closing slide. Uh Myopathy, common disorder of the spinal cord number one worldwide cause of spinal cord dysfunction in adults, frequently underdiagnosed symptoms or dexterity loss, non demato pain, weakness, sensory change, balance, difficulty, the evidence on natural history is heterogeneous, but generally points to either stable or deteriorating symptoms over time. Surgery provides us with the opportunity to improve global pain function as well as neurologic function. And future developments really show quite a bit of promise in identifying individual risk profiles for patients, medical therapy, for neuro protection and providing more effective and less invasive surgical treatments for our patients. Thank you. All right. Thank you, Doctor Wang. Uh That was a great talk and um it's great to have you back here as well. Uh I think we have some time for comments and discussion. Um See Doctor o'neill and doctor lots. Uh Kevin. Great. That was great. Thanks. Um on the algorithm you showed for patients with mild symptoms. Um One of the recommendations was for education. So what specifically do you educate them about? And I'll just preface this a bit by a lot of patients when they hear that they have, you know, spinal stenosis on their eye scan, they freak out. They say I'm gonna get paralyzed and sometimes that is uh that type of thinking is encouraged sometimes by the recommendations they receive. So what, what specifically you tell them about activities, things they have to avoid, you know, what their chance of regression is, et cetera. Yeah, this is um this is a conversation I probably am having every clinic day if not more than once a day. And uh I've always tried to refine it So in, in patients with very mild symptoms or with no symptoms in spinal cord compression, facial on MRI uh education revolves or for most around symptoms of myelopathy. And so I asked them, we talk about it, we kind of go over this and we talk about ways and means of monitoring. You know, I really encourage them to monitor their symptoms over a long time periods. As opposed to day by day or hour by hour, patients get very nervous, their arm falls asleep when they go watch a move, when they sit down, things like that tell them not to worry. Uh Another part of the conversation revolves around the potential for spinal cord injury with trauma. And there is a body of literature around this that estimates that there's an increased rate of uh severe neurologic injury or paralysis with head and neck trauma. Uh and that the odds ratio of developing this in the setting of severe compression is by somewhere between 10 to 50 times greater than the general population, which is a number that does scare patients. But if you look at the probability of a spinal cord injury today to any one in the general population, the numbers probably somewhere in the range of 1 to 7 to 10 million. And so even if you increase those odds by 100 this is still something that is highly improbable. Um I do tell those patients, I do restrict those patients from any activities that preclude them to a high risk of that type of trauma. And that would be things like, not, not a lot of my 70 year old patients are still playing contact football or like skiing, aggressive, aggressively downhill in the trees or racing motorcycles. But tho those are the kind of things that I do preclude patients from. Um And then there is a conversation, uh uh an idea of symptom progression and, and I, I kind of try to summarize this, this concept that many patients over very long periods of time will see symptomatic worsening. But that individual prediction is still extremely challenging. I really rely on them to monitor their symptoms and I offer to bring them back on an annual basis. Just go, go through a physical exam too, the tucker lips. Thank you. I um have a question about diagnosis and the role of quantitative functional imaging looking at different cervical motions during flexion, et ce et cetera. Is that valuable? Um It's interesting and it's valuable, but it's difficult to build into a standardized algorithm because it's hard for us as providers to really have a baseline of how much compression and how much change in dynamic motion MRI is, is normal and what constitutes pathologic problems. Uh And, and there's a specific diagnosis within myelopathy of patients that have uh myelopathy likely attributable to dynamic causes, but Hiyama disease likely attributable to dynamic causes, but without static compression. And that's one area where uh flexion and extension MRI S as has been seen to have some utility. But without a wide base of comparison, most of us aren't using that in our regular practice. Now, what I do to assess for dynamic changes, you know, you look for the severity and degree of static change and we traditionally will compare that to uh dynamic films. And you know, there is a little bit of this conceptual leap that has to be made comparing Mr MRI to X ray. Uh But in patients that already have pre-existing moderate or severe compression in a supine position that have osis or other types of pathologic motion. It's not a a great leap of faith to think that that could, could worsen in a dynamic setting. Thank you, question if there's a time, go ahead talking about patient trajectories. And I'm wondering, is there a role for quantitative dexterity testing as a way to have a more people, people have argued that that there is OK that these symptoms are challenging for patients to detect on a more minute level. And so there's been more of a push to push towards a quantitative dexterity and strength testing, especially in the in the upper extremities have been great talk um with the literature sort of supporting laminoplasty. Why do you think we've been slower to adopt it here as compared to like other parts of the world? Well, you know, laminoplasty was originally developed uh in Japan, it's had a wide uptake in Asia, I think just because of location of origin and comfort with, with the procedure in most surgeons in the United States are, are trained as laminectomy infusion surgeons. And so it's a bit of a leap of faith to say, to go from saying as a kind of a fundamental thought that stability is important and controlling motion is important for preserving a later posture to, you know, oh, we're going to decompress it and we're gonna, we're gonna leave it there and trust that things are going to hang on. I also think that the procedure has changed quite a bit in ways that are challenging to communicate in the literature over the last 20 years, I think people who do a lot of these spend a lot of effort in soft tissue management and and reconstructing the muscle, closing individual layers. And we started doing like spinous process tip osteotomies and then repositioning so that they're in kind of a natural position. So there's these nuances in individual surgical technique that aren't always well captured and that portion of the literature then becomes somewhat more difficult to communicate. Um And I think that that's also somewhat impaired uptake. Then Doctor Berman had a question about the role for diffusion weighted MRI and evaluation is that something clinically that's useful uh that shows promise to be useful in the medium term. But the question with diff diffusion weighted MRI is you know exactly what protocols are being used to generate this. Apparently there's quite a bit of variability between individual institutions and uh there are so many different potential uh data points divining signal from noise is not something that's been done in a widely reproducible manner. Yet other thoughts are to Ma, hey Kevin, great job over there. Um Bring me memories of my days in residency, like doing spine surgery. Uh I, I'm kind of intrigued with the genetic predisposition for um cervical diseases. And is that just for development of the, you know, condition? And also does it change prognosis? And are there any ways that it is modifiable moving forward? You know, that, that, that. Yeah. Yeah. No, this is a very interesting and exciting part of spinal, spinal cord injury, either traumatic or degenerative. Um The thought is that this specific protein apo lipoprotein plays a role in neurologic healing and recovery and whether that is after an initial injury or in response to an ongoing process, either Alzheimer's or a LS or degenerative irritation. Uh And so they both is a prognostic component to predicting whether or not symptoms will come on and also how much recovery patients can have after surgery as well has been associated with this. And so, you know, it would be something great honestly to build into practice where you can give a patient based on a series of genetic tests and individual risk profile for symptomatic progression. And also counsel them on symptomatic recovery after surgery, which is something we didn't really go into has a high degree of variability. You know, you know, the residents, you know, have this conversation too. And if it's not, everybody gets full symptom recovery after spinal cord decompression surgery is intended to stop symptom progression, which we know we're very good at. But the actual recovery of neurologic function is highly variable and appears to be associated with some of these underlying genetic factors. Wonder whether the same, you know, the same uh uh phenomena in other nerves. NG would take care of an orthopedic or carpal tunnel syndrome. That would be very interesting to look into. I mean, and it goes to a question. Well, is there anything that we can do about it? Other than no, like I think that gets into very personalized, personalized medicine? Um And whether or not this is a target or you know, gene therapy or things like that is a question that's way down the line for people way smarter than I am. Is this being captured for the backpack gran? Like, you know, is there any way we can pull that data out? Um Do you guys have like, you know, samples in general blood samples, gene? They get a profile and the patients uh yeah, the short answer is we do have blood samples on everybody but you need really huge numbers to know this as in medical utility determine, you know, something like a based on what the genetic risk score. Um Then that's not something we could do it, the numbers, we definitely interesting direction and any other comments, questions were just about right at time. Uh So I think we'll wrap up there, but doctor Wong, thank you again so much and thank you all for being here. Thanks. Thanks everybody the
