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Yeah. OK. Yeah. OK. So cervical myelopathy, um Thanks everybody. I've already discussed this very useful reference, text, summary, reference text from BBM J learning. You can get it online at that link or you can get it through um B MJ uh or through your local library, but B MJ if you remember, um and it's a really good summary like Mark Co and Ben Davis who are local East Anglian surgeons, the neurosurgeons from Cambridge who have also together created this remarkable website, which is absolute wealth of resource about every type of possible um uh score scoring system. You could use the only one I'm going to mention here, which is the commonest is Japanese modified Japanese orthopedic Association score for myopathy. Uh We don't use it a great deal here. There are other ones like the neck disability index, but specifically the MJ OA is the one that's most commonly used in myelopathy and it's all on here. And this is an incredible resource that they've set up this academic research. Reg Ben Davis and Mark Cotter, who's a neurosurgeon in Cambridge. Um So, II would suggest you look at that if you want any further information on that. It's all there and there's a really good search item on that. So what is it, what is, what called spondylitic myelopathy? Well, it's in the name really myelopathy, as we all know is to do with a pathology of the spinal cord itself. Um as opposed to radiculopathy, which is a, a pathology of the nerve root at the origin of the spine, which is usually due to compression. Um uh er which causes pain, radiculopathy has to be, by definition has to be something that causes pain. Myelopathy doesn't usually cause pain. It can frankly, it can cause anything. Just like many of the weird and wonderful neurological conditions can uh but there are other specific symptoms which you'll come to and really if you had to say what it is, it is what it says there in that opening bullet point manifestation of long track signs resulting in a decrease in the space available for the spinal cord ie that red bit, which is the neural canal and that is that, that definition of a decrease in the space is su specifically going to be spinal surgical causes ie mechanical causes that require mechanical solution, which really technically only a spinal surgeon orthopedic or neurosurgical could provide frequently as it progresses that in an adult, they will move toward this acquired spastic state. It can be a paraparesis, but of course, it involves your upper limbs, it can be a tetraparesis and if it's particularly bad and left untreated. It can not infrequently lead to a tetraparesis and or or a tetraplegia or a paraplegia. So it's important that this is treated with some urgency once the diagnosis is made. Hence why you'll always see our myelopathies being put on as urgent on our lists and so forth. And it is a pathology that affects the, the function of the spinal cord. But like most things within the spinal cord when it comes to actual pathology and what actually is going wrong with the cord and the various tracks and pathways. It's much harder to know because it's, it's so such a complicated part of the body, but I will try and touch on that as we go along. So here, this is a typical sort of myelopathic type, Mr that you might see in clinic, as you can see plain x rays don't really help. They're relatively unremarkable. But once you get the scan, if you home in on that red circle on that s uh T two image, you can see there's very impressive looking disc prolapse and you can see there's some signal change within the cord associated with that compression, which is there, you can see is corresponding with these um axial images on the side. And that's, that's a fairly typical single level isolated uh C 56 discopathy resulting in uh quite a serious uh compression of the cord. And um in this case, you may even see someone who gets an acute myelopathic picture, acute and chronic, of course, is defined as being within or beyond three months. But the acute myelopathy sometimes they really come in with a very impressive spastic picture. Sometimes they can scarcely walk and they often happen in younger people when a large it like a cold recliner of the neck pops out into the neck. And those are the ones you really do need to identify rapidly and decompress urgently. Um that you should really be doing that as urgently as possible, not see pod time, but you certainly should be doing it first thing in the morning after they've um after the scan has been done and it's been identified what the pathology is. It's almost as urgent really as a cord recliner when you see an acute myelopathic, but they're relatively rare. Um moving on the most. This is a little bit more chronic. You can tell. Can you see my cursor Ben on the screen where I wiggle it? Yeah, great. So you can see here that there it's lost its high signal, meaning this is more of a longstanding desiccated type disc prolapse less acute. But again, you can see the effect it's having with this corresponding signal change within the cord, I'll come onto that more of that later um corresponding signal change within the cord, which is thought to be secondary to that compression, which in turn is causing some sort of injury or insult to the cord. I never been 100% clear on what that is, but I have my own hypothesis, which I'll also share with you later. The commonest treatment for this as things stand is what you see on the right. Which of course is the gold standard, anterior cervical decompression infusion. This is a slightly older implant which you used to use from synthes some time ago, which are quite light uh called the zero P. And um and this is a sort of stand alone type implant cos it avoids that plate over the front of the neck, which sometimes is thought to involve um a little bit more postoperative dysphagia than these types of implants. But I think that's open to debate personally. Um If you want to stop me at any time and ask any questions, please do. Um So um this is taken um directly, I think from that B MJ article. It's a nice little summary of this, of the epidemiology. I've got a summary slide to come after this which really boils this down, but the key messages are about one in 100,000 pe um of people who have uh degenerate DCM is degenerative myelopathy. Um end up having surgery. The prevalence of that is likely to be much, much higher. Obviously, it goes up in prevalence, particularly high as you get older. And a lot of the time you do see in the younger age group, evidence of compression uh, of the cord indentation of the fecal sac with or without signal change, myomalacia, uh, within the cord, um, uh, and compression of the cord, which is all asymptomatic. They don't necessarily have to have, um, any symptoms, um, uh, myelopathic symptoms of a motor neuro signs associated with that signs or symptoms. Of course, and those are the ones where you do need to keep a close eye on them. Um, so a large proportion of them do remain undiagnosed even in the older age group, as you can see from that final bullet point. Um The sort of brief summary of that is it comes originally from the Cockburn paper in 98. Whereas symptomatically, it's about 10 and 100,000, but it goes up on average across all age groups, but it goes up a lot as you get older, particularly above beyond 50 years of age. And again, about 100,000 require surgery. The most of course, because it's an age related phenomenon as Andy described earlier about the way in which the cervical spine changes with age, the commonest is in the eight in the eighth decade. What I didn't know is it is slightly commoner in males. Um And the there is, there are a few papers, this is probably the most useful where if you do have cervical myelopathy and the reverse is true. There is about 15, I was told originally, 20% I couldn't find a paper that supported that. But say between 15 and 20% of patients can have associated lumbar or lumbar stenotic patients can have associated um upper motor neurone signs. So it's always worth looking out for that, particularly if there's a slightly odd appearance to their examination. When you're assessing a lumbar stenotic, they look a bit ataxic. You can just ask them if they've got some upper limb hand and finger symptoms and that often leads you on to diagnosing that you need to scan the rest of their spine. So do look out for that. There is an association as you probably would expect. Given it's pretty much the same pathological process, age related process going on in both areas, top and bottom of the most mobile parts of the spine, which of course is the most vulnerable in the cervical and lumbar spine. Um differential. Well, I mean, I've put a, a few here from this little screenshot but to be frank, it's as long as you like, you can add transverse myelitis, glim Barret and all the other multitude of things to that. Um particularly bearing in mind the multiple sclerosis which is not uncommon can present as many neurologists keep reminding me as quite literally anything. So, um th so basically, if you cannot find a compressive cause for the cervical myelopathy that fits both the level and the pathology with your um symptoms and clinical findings, then you should have a low threshold. This slide is there to remind you have a low threshold for sending these patients um to the neurology clinic. And I think it's fair to say many of it, many of us do have a low threshold for that before committing them to surgery and the risks that that entails. Um Here's a little reminder of this slide that often makes trainees and to be frank with these consultants heads um on the back of the neck and on end, especially when you get this slide in a vi. Um but I think it's worth just reminding yourself particularly of the gray areas which can tend to get affected um in some pathologies that we will come to shortly, which is often a progression of myelopathy. But I thought I'd cover it at this stage to do with the incomplete cord injuries because this is a sort of progression of preexisting radiological myelopathy. They don't necessarily have to have symptoms as in a tight mechanical compression within the neck. And of course, the elderly person falls over in Sainsbury's or something or sitting in the car gets a whiplash and suddenly they've got this horrible sort of incomplete cord injury presentation. And if you scan them, you often see this preexisting type, probably preexisting type stenosis associated with this quite diffuse acute sort of my myomalacia change with in the cord corresponding to the level of the compression and the different areas where you can get compression on the cord. This is a sort of representation here of the neural canal. And of course, you've got the disc with the um osteophytes depending on the chronicity of the disc prolapse. And how long it's been outside the native disc space, which creates local information and calcification leading to what some people call a disc bar. Perhaps. We don't 100% know perhaps but even more chronic change associated with that. But there is a genetic predominance in um Pacific rim populations. I understand with um ossification there, o PLL ossification of the posterior longitudinal ligament, the young convertible joints, we discovered all of this in our previous um slide show, we did the anatomy and examination of the spinal spine can also become degenerative and lead to osteophytic changes, also impinging from the front into the back towards the cord. And then of course, there's the actual apo apophyseal joints or the facet joints and then on the yellow ligament down here, which of course gives the name away for the ligamentum flavin which can thicken with age. So you've got the usual sort of battery of insults that the cord can have from a compressive point of view that can result in these symptoms as you do in other parts of the spine, particularly in the lumbar spine. There's some more recent data trying to look at interrupting the in these uh slightly unusual um uh blood brain on the other side of the central nervous system, a blood brain barrier inflammatory cascade which occurs um um in the spinal cord as it gets compressed and the, the, the obviously it starts with the compression that leads to a hypoxia or ischemic type event, which in turn leads to some cell death. Be that the lid denys or the glial cells or indeed the, the, the axons themselves and the uh nerve cells. And then of course, there's an involvement to do with the actual blood vessels as part of the inflammatory cascade. And there's an attempt that's going on at the moment. Um I can't remember, sorry, I can't remember the name of the stuff, but they're trying to disrupt that cascade and reduce the neuroinflammation. Um And my failings is leaning on that at the moment and then if you let the inflammatory cycle reoccur this is where we thought you, you start to see this demyelination or whatever this signal changes within the cord that represents that high signal, which is often what it's called by radiologists when they report that myelomalacia change in the cord. Um In my opinion, it probably is demyelinate c a certain amount of demyelination because of the li li ligo death, glial cell death, which in turn then leads to um neurological dysfunction. So as I said, just briefly touching on the types of incomplete spinal cord lesion, right? So quickly, I know Ben's online. I'm sorry, Ben, I'm gonna t pick on you. What does the top one show? There's three types. Hello. Hi. Sorry. Central cord syndrome. Yeah, it is. And that is the, that is the commonest we see associated with a preexisting compressive myelopathy, particularly in the elderly age group. It doesn't always have to be the elderly. They have a big disc. You sometimes get in the younger age groups. Right. Moving on to someone else. Not BEN, the one below that. So, it's affecting which part of the cord, isn't it? So you've got the sulcus. So that's the front of the cord. So what do we call this? If that's a central cord syndrome? What would that? There we go is that me who put that forward? Has someone else got control of my slide show? What's going on here? Ok. Well, there we are. It's all in there. And then you've got the Browner card, the only time I've ever seen browner card is slightly unusual cord injuries associated with the cervical fracture. Uh and it's quite impressive. It's exactly how it looks. And just as it says there, look at the central cord, they do have a good prognosis, they do recover. Um And frequently they are also associated in the neck when you get it there with a Horners as well. You should look out for that. Um If you do get ever see that clinically, possibly even in the exam, the anterior because it's a vascular event is clearly gonna be poor, good. And this is, and this is sort of just to help you out, you can see here the, the, the stc sacral thoracic, you can see how they're arranged and how, when you get either a central or anterior, how these will get affected and how preferentially they do tend to get more weakness in the upper limbs than they do in the lower limbs. It's to do with the way in which you can see here in the, in the um descending motor paths just here. You can see how this is slightly more midline than the sacral. So you get a predominance of a more of a motor effect in the upper limbs than you do in the lower limbs which just become, they don't lose any power, but they become very spastic in the central cord type syndrome. So, these pathways do have a role in slightly helping to understand how the anatomy relates to the pathology in the central cord syndrome. I hope that makes sense. Um Right pathophysiology, moving on a bit more. Roughly speaking, you get the disc degeneration, which of course is the loss of the proto glycans which hold in all that hydro hydrophilic water as it becomes desiccated, proglycinin break down, you get a loss of disc height and loss of the collagen content, which can causes the disc to stiffen. This is the same in the lumbar spine to be frank. And then you've got an alteration in the biomechanics which in turn affects the facets and uniquely circling there, those unconvertible joints as well as a thickening of the flavin, which was originally described by those two chaps buckles and thickens. And then in turn, uh you get the osteophytes and you get the loss of alignment and subluxation that we'll look at a bit later. And you can see just down there how um there's some compression on the cord. Um The other factors that are important in terms of, of determining the severity of the myelopathy is particularly what is the remaining ap diameter of the spinal canal. And this becomes particularly important, the further up the cord you go particularly in the axial as opposed to the subaxial region, I come to that a bit later. But there is this thing as you all know, called the posterior Atlanto dens of all the paddy. And if that's less than 10 millimeters, that's regarded as critically stenotic, and you can simply because of its proximity to the brain stem and the fact that it's higher up in the cord, it's going to affect far more and the quicker you can get on and decompress those patients, the better they do they should be particularly urgent cases. You also have this thing listed here called the dynamic cord compression. That's sometimes where it's not so much here. You see this signal change within the cord, but you don't see any obvious clear compression. Now, under those circumstances, the options are you get a plain X X ray hang on. It's probably me there. You got a plain X ray to look to see if there's movement across here. There is a slight slip at that level that C 45 or whether you can arrange something called a dynamic MRI scan, it can be done here. It's difficult. They don't like doing it. It uses up a bit more MRI time, but I have seen one case here where you could indeed. And I'm sorry, I couldn't drag out this, the pictures of that, but you could see clearly in neutral, there was no compression, but when they extended, the cord was being compressed and it corresponded to the signal change. It's extraordinary. Actually, the normal canal is there, the spinal cord takes up that much. So, anything less than 13 millimeters you can see will start to cause some form of stenosis. And some people have what we call a constitutionally narrow canal. Again, that occurs in lumbar just as much as it does in the cervical spine. And that can obviously predispose them to myelopathy at a younger age. This is what I've just discussed with you in terms of the paddy. I don't think I need to say anything more. I showed this slide last time as well to do with the anatomy of the um of the axial spine. Very good. Here's a little bit more pathology how different parts of the cord are affected, whether you're in flexion or an extension ultimately, the whole thing is the same as you can see here with the contusion on the cord. And then there's degenerative changes will result in, in, in, in with the abnormal movement or lack of movement, other structures um degenerating in an accelerated fashion. As you can see here, this slide was taken from the B MJ Cotter review, which is really a much better illustration of the previous slide. You can see the loss of vertebral body height, the loss of disc height. You can see how the the alignment is also slightly lost with some slips here, resulting in some compression, both on the posterior and anterior columns. And you can also see how you can get uh ossification of the ligamentum flavum as well as ossification down here of the O PLL. Some of that is illustrated in the MRI here. Um The final thing is we often say plain x rays of the neck aren't always that helpful, particularly in trauma. That is true. But in when assessing for myelopathy, I think they have a role particularly here when you're looking for a lateral dynamic view of the of the cervical spine and looking to see whether there is a slip or some movement. And I think that's important to establish. So if you see a slip associated on the MRI scan at the same level with some compression, then often getting some dynamic views can be helpful when you're deciding whether or not you need and we'll come to that later, whether you need to address the compression either anteriorly or posteriorly or indeed, both. And that is a possibility but not as common as it sometimes is for trauma. So, yes, I was gonna mention this. This isn't often spoken about, but I have heard it come up previously in a viva, but I'm a bit old now since I've done the exam. But if you, I'm sorry, that picture is quite small. But if you hone in on that, there are different types of um myomalacia change within the cord, there's currently three types. There used to be two. The first type is this more acute fuzzy diffuse change, which is what that's meant to represent down here, which you often see perhaps after a central core type syndrome insult, you see that very fuzzy whiteness in the cord associated with the compression, the type twos or the type threes. This is more long standing as you might get in the higher bit up there. You see this discrete white area within the cord and sometimes it's in one particular part just like it is here, either on the left or the right hand side of the cord itself. And you can see it on the axial and it's usually quite a discrete area and that often takes time to develop and is often indicative of some longstanding insult of the cord that is sort of finally resulted in in just the a complete white out of that particular part of the court. I usually take that to be significant Axonal death I think is what it is. I've never seen a paper that's ever told me exactly what that is, which is why the radiologists stick to just using signal change characteristics. They don't use pathological terms, which is very reasonable and safe. Um, so what symptoms do these patients get? Well, the main ones are the ones that are listed here. See, they tend to start off by having some tingling and numbness usually in the tips of the fingers and the thumb. And then it progresses in this retrograde fashion to involve the fingers and the rest of the hand. It's frequently involved, both some numbness and some paresthesia. And as things progress and you know, the hands become more numb, of course, it becomes, you can become much more clumsy with what you do. So they lose upper limb, fine motor tasks, manual dexterity. And it's always ask, worth asking a person, you know, do you have trouble putting a key in the door? I often ask them about picking up small pieces of change or buttoning a shirt are good questions to ask, to try and nail that down. Um Then um as the posterior columns are affected to do with balance, they get do get balance problems. And the classic, this classic Ataxic gait simply really because the legs are becoming more spastic and they're much harder to control and balance with particularly on uneven ground. Um, the other symptoms they'd get is they can, if, as they move the neck, they can get these shooting sensations throughout their body, twitching and jerking of their limbs, bladder and bowel disturbance can occur, but that's usually very late. And that's a real sort of red flag that this person's cord is seriously decompensating if you get bladder and bowel disturbance associated c cervical myelopathy. And of course, you must scan the rest of the spine because you must ensure there isn't anything else going on below, particularly in the caudal sac that might account for that. Um And a again, as I said earlier, pain is not a common finding. This is just to remind you of the, of the main features of where you, you, you can establish the different levels. It's always worth having a reminder of that. And I think this is pretty accurate, actually, quite light where they've got the, the finger dermatomes and often take most of that um radial forearm to C six with C five covering. Again, that sort of lateral border of the elbow T two tends to occur as you approach the axilla with C eight going half way up the ulnar border of the forearm. Um pretty much as you can see um uh on this picture, but I think C eight is a little bit higher. In my opinion, it can overlap, there is some variability of that. Um, and the, the T three and T two, dermaton won't occur in that area. So, what are the signs? Well, we've already been through the Ataxic gate, but then you can test their balance with Romberg's. Um, which of course is getting them to stand. There's a little picture of that in a minute, um, and closing their eyes, taking out one of the three things that helps control your balance and seeing if they're still able to stand because you need at least two. So if you've still got your vestibular apparatus, but you're affected your posterior columns and you get rid rid of your visual input. There's a risk you could fall. You must be wary when you're doing that with a patient, have them standing near the couch. Um You can accentuate it with variations and ask them to put their hands out in front and there's other things you can do. Um There's a tandem gate um where you can test their balance, where you ask them to walk heel to toe as often drink drivers are made to do by the police. I understand both here and the estate. The hermit classically is the picture shows is where a patient flexes their neck forward. You can ask them to extend as well, but classically, it was a neck flexion and you get these electric type shots extending down their arms or indeed down their torso or even their legs. That is often a relatively late sign and I use that as quite concerning feature Hoffmann's. This is a picture of it. Here is the way I do it. Holding the middle finger, you flick that distal P IP and you look for movement, a sudden chronic jerking movement in the index or the thumb of the hand. You just need to prax it, prax it, practice it if, if you're in. No, no, come and practice it on me. I've got a Hoffman signs, 5% of patients without cervical myelopathy do have it. Or maybe I've got a congenitally tight cord. I don't know, I don't want an MRI scan. Most spinal surgeons don't, it'll just terrify me. Probably um hyperreflexia, of course, is in keeping with the spasticity. And um and then of course, you get the extensor response, which is the Babinski Ski, which you can see here. Strictly speaking. I think Babinski described that in Children which disappears after six months of birth, they stop being neonates because of the myelination of the spinal cord tracts. Now, what I think is interesting is I think this reappears later in life because of the demyelination of the same posterior column tracts. So I think it's the reverse of what occurs as a child in the normal healthy chord. When you get that whiteness within the chord, that signal change. That's just one of my sort of off the cuff theories. The increased tone goes with the spasticity, finger escape. Again, I think is a relatively late sign. That's not one for the exam necessarily. And there's another one where you can do like a La Hermes type test of getting to bend their neck. And then you can also see if the Hoffmann's appears as they flex and extend their neck. That's known as dynamic Hoffmann's. That's another way of picking up a more subtle compression. But again, I don't think that's one you need to mention the exam, you get the uh the finger escape, you get them to hold out their hands in front of them. If they're particularly myelopathic, what you'll find is they'll get this ulnar drift with a little finger, sometimes the ring finger just gently floating away from the other fingers laterally and sort of f you know, uh where they like you would spread your fingers out with the interossei. This just naturally happens in people who've got particularly myelopathic axial or proximal subaxial cord. Um Here's, yeah, here's the Romberg's that I mentioned earlier. Those are the three things you need. And if you knock out one of those cerebellar being also the poster, if you knock out one of those, you must, the other two must work. So if you close their eyes, this is a good way of testing your posterior tracts as well as your middle ear. Any questions about that so far good. Um Just a little reminder of this is where the primary roots are for the deep tendon reflexes in the upper limbs. Um uh And I think that and the lower limbs, actually, I've added them on there. That's just a little uh reminder, remember triceps is C seven, biceps C six. And remember when you do triceps, it's nice. If they've got no shoulder problems, you must ask to do that pillar type movement with a 90 degree abducted shoulder with a hand, pace for pace, relaxed and facing towards the ground. And you gently tap that distal tricipital tendon to see if you can get a sort of movement of the hand as the reflex occurs. It's a really good way of doing it if you want to try and reinforce an upper limb reflex, the only way I know you can do it is asking them to clench their teeth. Whereas in the lower limbs, you'd get them to clench their hands as you as probably all of you should know differential when you're examining, of course, is you must test for a peripheral compressive neuropathy most commonly carpal tunnel syndrome, which clearly tends to occur in manual workers, particularly in their fourth or more decade and also in women. Um uh slightly more commonly than men. So the natural history of this, there's some papers that have been going on for a very long time, um tends to be quite poor if you don't get on and decompress their independence and their mobility will deteriorate. And uh you know, quite some time ago, it was determined in 2000 there that surgery is better whilst their symptoms such as pain and tingling and numbness may persist. As Sampath discovered their functional status improves as in their fine motor control in their upper limbs and be able to sort of feed themselves, walk, dress themselves, perhaps do a bit of shopping for themselves. And of course, that has even these small changes, as we so frequently see in spinal surgery across most pathologies, if you're able to make a small change in terms of their independence and reduce their care needs, particularly important cord injuries, their, the costs and their care needs and the implications of their care needs. Plummets. It's amazing how even a small change can make a massive difference in terms of cost and effort and requirement. So it's very important uh when you're at the sharp end, as we all are as surgeons to be able to identify quickly when there's a problem and get on and operate because the clock is ticking their neurological status at the time of the surgery is the status you would expect them to maintain. After the surgery, I will come on. There are papers showing that up to 60% do get some improvement. But I still, I'm still cautious and I tend to say to patients particularly the more severe myelopathy that the best I'm hoping to achieve is that their neurological picture remains the same. And even after a technically excellent decompression, that isn't always the case. Um This has a use sometimes in studies or if you're trying to objectify how bad functionally they are. I ran wax is the classic, which is originally actually for um I understand for uh rheumatoid patients who are getting compression as little as little bit slides later on about that. But NIC is the one I like most simply because you've got the two extremes of uh you know, completely immobile lost all independent motor function in terms of being able to walk and then someone who's got scarcely got any difficulties at all. And the rest of it is to whether or not they can have a job, whether or not they can still perform their AD L LS or whether they can't perform the AD LS and they can just about walk with the assistance. I think that's quite a simple little score scoring system. I don't think you need to know the scoring system for the exam will correct me if I'm wrong. But you should be aware there are classification systems. Uh The reference for which is below. Um Yes, I mentioned this earlier. I think this is probably the most universally used male pa score. Um We, I have to admit we're not frightfully good at this hospital collecting outcome scores for various reasons. I don't need to go into here, but essentially it's made up of upper limb and lower limb motor and sensory, as you can see, uh mainly in the upper limb with sensory. And then obviously, there's the ability of your bladder and bowel function, um which can obviously have a significant impact. So it's quite good functional assessment and the p you get more points, the, the better you are and you are regarded as severe by definition, if you're 11 or less. Uh Certainly again, if you knew, knew about the modified Japanese orthopedic association score for cervical myelopathy as an outcome, that would probably be all you needed to know. Um uh Yes, we've done the natural history already. Um This is another slide about it when NIC also looked at this in non surgical and surgical patients in terms of their improvement. And again, you can see really this is a surgical pathology one where you really need to consider operating unless there are extremely good reasons. Um why er not to um because of the, the almost inevitable deterioration in the functional status of the patient. Um So, if we now consider whether we need to do anterior or posterior or both, again, this really depends on the pathology. And if you cast your mind back to those lovely detailed graphic pictures of the cord in a degenerative degenerative spine, all of those colors, you can clearly see some of the pathology might be coming from the ligamentum flavum or the posterior column, um or uh a facetal or apophyseal joint hypertrophy with um osteophytes or indeed unconvertible or anterior could be calcification of, of the um of the posterior longitudinal ligament which is ossification. O PLL as well as um disc bars and disc prolapses. So where the compression is frontal back matters, it depends on how many levels you have compression. The more levels generally speaking, you should be thinking about posterior rather an anterior approach cos you will lose um the uh the motion segments within the anterior neck as when if you are gonna operate anteriorly, either the corpectomy or an anti cycle decompression infusion, I have mentioned it, but you can use disc replacements in myelopathy as well as well. That is not unreasonable to do that. The movement that you, you keep with myelopathy um with a disc replacement doesn't seem to um I impair its recovery, which is what you would expect because we do often operate from the back with a simple laminectomy and they do still do quite well. I don't know why we weren't ad advocating using disc replacements previously, but they are now able to use them. Um Of course, if there is instability, then you do need to think about instrumentation, either with an ACDF, as I said, or Corpectomy or indeed posterior lateral mass screws. I will mention that. And then if there is a kyphosis or loss of alignment, it is good if you can try and incorporate into your approach, usually anteriorly, if it's kyphotic to try and improve that alignment, posterior will not do that. Uh anterior approach is much better at doing that as I'm sure you can imagine, particularly if you're putting in cages, which can be slightly higher and larger and it placed in the right way can help improve the kyphosis. So here, um these are the questions that you need to ask yourself. Age is important. Of course, there's comorbidities and the stability problems and that I like this, This MRI here. That's a classic picture of that type two signal change which I mentioned earlier in the MRI scan. Some might even say that could be a disin distended syrinx, which of the two, it is, it would be hard to say, but that if you had type two, that's what it would look like. So this is a summary of whether you would be going anterior posterior if they still maintain their normal cervical aosis, if they tend to have com compression over many levels and the posterior is the way to go. The options which I have mentioned anteriorly at least is ACDF Corpectomy or disc replacement, intervertebral disc replacement. Um And this also obviously depends whether you want to be motion preserving or fusion. And that of course, with the motion preserving as Mister Cooke mentioned in his talk is to do with reducing this risk of adjacent segment degeneration, accelerated adjacent seven generation, which we quote at 2.5% per year, which if it's a young patient you can see, can accumulate very quickly, 25% over 10 years, 50% over 20 et cetera. Um And then posteriorly whatever happens, you must ensure that you do satisfactorily decompress the cord and there are a number of different ways of doing that. Um This is quite interesting in terms of, of, of um of uh the benefit, the improvement you get and function. And this is a paper from uh slightly unusual online journal called plus one. What I hadn't appreciated is actual fact, Michael Failings is the editor of this. He does tend to put a lot of his papers on this site, but this is actually not a bad paper and it does provide, it's about a 60 per up to 60% of patients do get some improvement um from their my myopathic compression with a timely decompression. And that can, that's almost regardless of the degree of compression, which I thought was very interesting. So there could be a sort of Muric four and they'd do as well as a Muric three uh in terms of the 60% figure, which I found quite interesting. So I personally, you can mention that there is the possibility of getting improvement, but this has not be something you would guarantee as I think what you should say in Aviva. But if you get pressed on it, you could mention um there has been some papers that have shown you do get a significant proportion of patients that do improve. So there is the key in red phrase operation prevents progression. Um And the, and there's a little bit about the pathophysiology at the top there um To help you with that. Um Sorry, I don't, yes, surgical in the most predictable. I'm not sure what that slide is doing there, but that's just to emphasize that surgery is particularly important. So, anterior procedures, this is a list of them. Um um and the posterior laminectomy decompression. I took these photographs out of the bass leaflets you've got front and back there, including the disc, disc replacements, which I haven't mentioned in that list. And remember if you're doing an anterior approach, you must remember about the risks which we discussed in the previous lecture last week, particularly there. That little pink purple thing going out the side, which is the recurrent laryngeal nerve on the left side, it tends to be more protected because it doesn't lie quite so deep. Um quite so it doesn't lie quite so lateral on the left because it's, it's very closely aligned to the trachea as it does on the other side where it can be more vulnerable to a neuropraxia or traction injury, resulting in the things that you see below including swallowing issues as well as voice problems. Um Again, this is the evidence for some of the specific surgical procedures um to do with stenosis and they're all very good at supporting that we should decompress promptly. Um uh with um with these procedures offering a satisfactory outcomes. Um posterior approach, this is the set up we use here, which is like AC flex, which really allows a lot of movement. The patient's head is in this, in a prone position clamped here across the equator by these 23 pins in what's called a mayfield head clamp that attaches to here. This is an excellent little set up. And once the head's clamped in here, you can move it quite freely on this device which gives you almost about five degrees range of movement. And the patient is lying on a monetary or with his head and shoulders, overhanging into this space here with the patient's face facing to the floor. The risks of course, depending on where they are, but the great occipital nerve higher up and the vertebral artery is always at risk particularly in the axial spine. The room complications is would, would be as you'd expect including dural tear and C CSF leaks. But these tend to heal quite quickly in the posterior spine because they tend to be a lot more low pressure than they are in the lumbar spine. So, um but still addressing these and putting a drain in, um keep um you can sit the patient up. It does, in my opinion, unlike the lumbar spine, in my opinion, helps the juror heal a bit quicker, which is usually within maximum 48 72 hours. Um Again, this is evidence to support the posterior laminectomy and laminoplasty. We will briefly mention that in a second can also be used and has just a good as good outcomes as anterior surgery in treating the my myelopathy, not necessarily the sach alignment issues like kyphosis. Uh As I said, if you've got kyphosis, you'll be thinking about an anterior approach. So things that mean that the outcomes might not be as good are things I think most of you will know age, which in turn can lead to poor vascular etiology where the blood supply, particularly from the anterior spinal artery isn't as good. If they've had a lot of symptoms for many months, more se segments are affected. And if there is more signal change within the core, this myomalacia change, of course, if there's loss of alignment, that can also be um cause further issues. This is just a little summary of the different types of laminoplasty. Essentially, this is a um this is an option where you can increase the diameter of the neural canal and offer a decompression to the posterior neural canal. But what you're doing is you're not removing the lamina and you're putting these um various types of in interposition grafts and there is even sort of pros small prosthesis you can use to try and increase this diameter. Sometimes you can just, you can still um break them and remove them or split them through the top and then like here, I think that's called French door. Um, and make more room for the cord and they in the right hands, they tend to work quite well, but they're very fiddly and I think you need to do what you're comfortable with. I have to say this tends to be something that is more used um by neurosurgeons than uh orthopedic surgeons. This, in my opinion would not be something you'd use for a compressive myelopathy. Because if anything that's decreasing the diameter of the cord, as you can imagine, this is a technique I really like, which I inherited from the Great Bob Crawford who used to work here, of course, and set up the really set up the spinal unit in knowledge. Um and this is a Shiras paper, it's quite old now, over 20 years, this is a very neat little procedure where you can decompress where you can see here and here in his original paper, pictures, you can decompress that by sparing the lamina and the versa in between. And this is the important bit there is there soft tissue attachments. And what you do is you split down the middle between the two different parts of the spinus process. Keep all the tissue attached to that split them apart and then you can literally expose the lamina like that. And it really does work really nicely. Does it reduce the risk of postoperative kyphosis and damage to the posterior cervical extensor muscles in my opinion, I think it does shash, certainly think it thought it did and had evidence, not great evidence to support that. But I would agree with him. So sparing of the nuchal ligament and the cervicalis muscles I think is definitely a factor. And that really is. That's, I think that's a good way, a good way of offering a non fusion decompression in a multilevel uh myelopathic. This is of course, a picture of an anterior cervical decompression and fusion going through the front of the neck. You can see how all the tissues have been pushed out of the way. And this thing is here to remind you that you should be using magnification um with the microscope um views here and good illumination to be able to see down into both of the foraminal lateral recess areas um which can often become quite impinged. Here's an X ray of a slightly older anterior cycle decompression, effusion cos they've used a plate and you can see that there's a nice little dosis there. It's got that cage has got a good height to it, probably restoring the same height to what they originally had. And what you often do perioperatively and postoperatively is you look at the distance between the lateral masses particularly here because those are the two lateral that corresponds to that, that lateral mass is connected by a pedicle to that, that lateral mass should not look any more open than it does the lateral mass above and the lateral mass below. And in my opinion, it doesn't. So I think that's a very encouraging sign that that's a nice implant that's been put in for the right height and the right design you can use, of course, lateral mass screws. Here are the landmarks for the mare screw. You should try and go out at an angle at least 15. I often use 20 degrees that is to avoid the transverse foramen where the vertebral artery is. Remember if you damage the vertebral artery frequently, there is a dominance. Apparently, it's an 80% of people. It's the left one. Um So one of the vertebral arteries can be sacrificed, but you, you really shouldn't damage the vertebral arteries if you can possibly help it because they are one of the most major and significant um blood supplies to the brain via the basilar artery in the circle of Willis. I've got a picture of that later on to underline that point. And that's the, that is the, um that's the axial landmark and that's the sach landmark just on the inside of the lateral mass. Once you split it in two, you can see that point there which you should begin as a bur and should try and avoid the drill, sliding off. These, the lateral masses are delicate. They need to be gently drilled and gently tapped. You need to take your mind when you take your time when you're doing it. Uh And that's just a reminder that the pedicle and the pedicle really. I don't know if you can see my cursor is this bit here. There are a few people in the world that do instrument pedicles in the cervical spine. But as you can imagine if you do, you get these screw heads that come out right to the side and it's, they're actually quite hard to use and get rods into. And it's a very specialist technique because of the proximity of the virt archery. But usually you go medial to it, the screw goes medial to it. Uh but it, it's a very specialist technique and I think um vast majority of occasions the lateral masses are fine. You can use the flat part of a mcdonald's probe to try and determine what the Sagittal angle should be for the lateral mass compared to the 20 degrees of um angulation from the midline which the previous slide showed. And if you put it into the lateral mass, you can actually see what the angle is and where the screw should go. Here's an example of a multilevel foraminal compression, which we decided to instrument in this case, although I must say the anterior discs all look pretty good. And here this is another, yes, this was um this is a Morath though here you can see he's got compression right at the top of his neck. C 2334, he's had previous fusion in the past with a, a bone block that's actually now in itself contributing to some compression. Further compression, probably somewhere around C 45, C 56 is fused. And then at C 67, you can see there's a lot more compression at the front and this is all probably long standing and has been present for a very long time. That's what his original MRI looked like about 10 years before that one. before he had his surgery, I think it was way way back before he then had his surgery and his um corpectomy with an iliac crest graft that resulted in this picture. And here you should be thinking posterior surgery. It's multilevel, it's uh there's a long and you're gonna go right to the top and to decompress that you really need to think about instrumentation possibly from C two, possibly as far as the thoracic spine cos the C seven lateral masses tend to be too small to instrument. Here's another example um of, I think it's the similar one I mentioned before and you can see here how tight he was uh on those actual images. Um And again, this is, yeah, this is a nice example of the diff again, I think the different types of signal change you often see associated um in the MRI scan with the myelopathy. Again, we've seen this slide already where that's the example of the ACDF. Here's the slide about um the disc replacements. Many years ago when I first started out, I was using the synthes version that became de pre synthes, which at the time was called prodi and the prodi c and you can see this person needed a two level decompression. Um And um they do quite well with it. Uh And this particular implant didn't cause he heterotopic ossification. And what's nice about these images is you can see preoperatively there is movement across the bio motion segments, postoperatively, that movement is maintained, which is particularly important. So it shows that these disc replacements do work. I think they do tend to gradually auto fuse. Some of them can last as much as 10 years. They're sort of better what the better, more recent ones. But previously, I don't think they were lasting more than a few years, maybe 2 to 5 years at most, but at least they will help. We hope and data is showing that they do offset this accelerated adjacent segment change where you would expect that segment there to be to generate in an accelerated fashion. You're hoping now you've put this in that rate of acceleration will reduce from the 2.5% per year as originally quoted by Hillebrand. Um I'd now like to just look at a case. Are there any questions about myelopathies, myopathy so far? I feel like I'm sort of jaunting my way through this, but I'm just wondering if I'm missing anything or anybody's not clear, clear on a particularly key issue. This would be a good time to ask. I just got a question, maybe not related directly to myelopathy. But when you're doing an A CD, what when do you decide to use a plate in addition to the cages? Well, that's a good question. Um So you would now would I in the sort of slightly more modern era dare I say it of a act f then um you would try and stick to one of those standalone cages, which doesn't, at a single level, doesn't necessarily need the screws. You know, you saw the those cages with screws in, you know, a lot of these cages, there's a lot of examples of cages where they are just literally a peak implant with a bit of titanium markers in them and you put them in and what we find is in the vast majority of cases, the neck is so prone to fusing. Once you remove that disc and you stop that level moving, it will fuse pretty fast unless they're on industrial doses of steroids, heavy smoker. I mean, it's, I think it was Rod Lange at, you know, the senior neurosurgeon Cambridge once said it and he's doing in the spinal group meeting, you could put a Smartie into it and it would still fuse and it's slightly glib comment, but there is a truth to it in necks there. One area, anterior neck tends to fuse virtually almost whatever you do to it unless of course, there's infection, things like that can change that. So you would tend to just use either a stand alone cage with or without screws. Now, in a trauma situation where you have a cord injury with acute oppression of compression of the cord and they're not complete or they, they, they've actually got some good motor function distal to the level of the cord injury and you wanna get on and decompress that and say they came in during the day, got some scans. I probably wouldn't leave them overnight. Then particularly if you get that most pressing of surgical indications, which is the deteriorating neurological picture. So if I took them to theater to decompress their cord, I would be using iliac bone craft in that case. So I take out either a corpectomy or a disc or whatever it is that's acutely pressing on the cord. And I would put in some bone graft. And in that instance, I would have to supplement. You can't put bone graft on its own a tricortical graft from the iliac crest, I would put in a plate with it. So that's when you tend to see plates now, which have been used in trauma situations where for whatever reason, you've not been able to use an interbody anterior cervical implant like one of the cages I've shown and you need to use some bone graft, then you use a plate to secure that in the front of the neck? Does that make sense? Yeah, thanks. Great. Any other questions? Good. Sorry. I, I've got a quick question um if you don't mind. So uh towards the beginning of your talk, you mentioned that um you know, there's different types of, of, of um of myopathy, there's the rapid onset and there's the slow onset. Yes. And the rapid onset ones, you treat them like AAA quarter of AAA. My. Yeah. Sure. How about the kind of the slower onset or insidious onset ones which develop over months or years? What, what, what, what about the timing of surgery for them? Do you, do you still have to decompress them as soon as you can or can you wait or sit on them? So I might have, I might, I think I did mention it, but I, I've had a lot to discuss and I might have goss over it slightly. Um, sorry, maybe I wasn't listening. No, no, no, no, you were. No, don't worry. II probably my fault. Who am I speaking to? Sorry. Um One of the Yeah. Yeah. Hi. G good question. So, um, so what it is g if you think about it, vast majority are these chronic myops which occur with wear and tear and age and for all the reasons I showed you on those slides with the facet joints, the thickened flavor. I mean, all the rest of it, you know, that picture I showed you where it's all O PLL all impinging on the court. Now, the d that's, that is the vast majority of what you'll see in clinic once you have established that they have a deteriorating functional status, which is due to that specific myelopathic picture, radiological picture, be it over one or two levels or more? Once that's established, you really need to get, get on and operate because remember, the primary goal in those chronic myelopathy is really only to prevent progression. Sure. Now what's interesting is it doesn't always prevent progression, you decompress them and for whatever reason, possibly due to something to do with the internal complex neuro neurophysiological pathology or deterioration of the cord itself, which is what the signal change is. The cord still deteriorates. I occasionally see that you, you decompress and they still get worse. That's one of the, but you can't, you can't predict sometimes who will or won't do that. That's not common, but it can occur. So you need to just get on and decompress to prevent progression. That's the chronics. Now, the the difference is the acute myelopathy are a different kettle of fish. What you often see is you've got this young, you might usually younger person where the disc hasn't yet degenerated in the neck and they've done some, I remember one and personally, uh one case I had this young guy had picked up his motorbike. He had tried to lift the whole thing for some whatever silly reason. And I think he'd strained himself so much in trying to pick up this motorbike that what had happened is effectively a large part of the nucleus pulposus of the fresh youngish disc in his neck had popped out through the back of his neck and his cervical spine and just like a disc prolapse in the lumbar spine that popped into the neural canal will have clearly the cord doesn't have the, the, you know, the, the the maneuverability like a dural sac, you just can't compress on the cord. So these patients become almost immediately myelopathic, some of them almost present with a sort of mild cord injury type picture. They tend to be tetra paretic weakness all over. They can scarcely walk a super spastic. There's usually some events that's preceded it like that, lifting the motorbike and it's often associated, it can be associated with neck pain, not always, but the onset of the symptoms. Here's the Rab Zhan are much more acute. They're suddenly gone from being completely fine to suddenly they can't even eat their dinner or dress themselves, let alone stand up. Does that make sense? But they, but they're still got power in all four extremities. They can't control them very well, but they haven't yet got weakness or wasting to the extent they might get if you left it, they're the ones you crack on and do, in my opinion, got it. Um Is Mr Las still on the call. Thank you very much. No worries. Hi, Lenny. Are you there? Ok. No, he's never mind. I was gonna ask him if that's his experience cos there isn't much data on it, but that's, that's really the difference. II, can I be honest, I, in the exams you sha I think you'd be really harsh to give you the scan of an acute myelopathy that shows this big fresh disc. I've seen it in the anterior part of a canal compressing a cord like that acutely, it's gonna be a chronic myelopathic picture probably over a number of levels and all you'll be doing is just talking about, they want you just to talk about how they present what their signs are and what you do to treat it. You know, you know, where you consider front or back on the rest of it. It's really basic stuff that sort and it's just what they're looking for clearly as you know, is that you've seen one of these patients in the clinic, you've seen them somewhere before on the ward. You've just got a bit of familiarity about it. That's what they like to see that, you know, the language, you, you're not phased by, it's all that exam stuff, to be honest with you, isn't it exam? So let's look at this ca I mean, that's what it boils down to really, it's a driving test exam and you just, you just have to practice. There's no two ways about it. So um this is a pretty impressive looking neck now. Is it Jahan? Uh Yes, it is. Yeah. G sha sorry to pick on you mate because you've been so trying to put your hand up. So I'm on the phone. Yeah, this, this poor unfortunate lady's just come in through, it's five o'clock in the afternoon and you've just taken an x-ray and clearly she's got a bit of weakness and she's not great. She's still smoking, unsteady gait. Just describe to me what you can see in the X ray. I can't access the X ray. I'm relying on you to tell me. Sure. Um, I guess we're looking at both these X rays, aren't we? Not just the, the bigger, bigger one? Yeah. Well, the bigger one, I think it, it's harder to see what's going on on the AP view. But what you can be reassured about on the AP view is there isn't any coronal deformity on that is there. She's not leaning over to one side. She's not, but clearly that and that's the only reason I put it up there is a smaller patient. So there isn't anything to worry about from a coronal alignment. It's, and, and remember, it's just like the lower back, the sagittal alignment is king that is key to everything you do as a surgeon. So, tell me about how you describe what you can see sagittally. So, um uh this shows a lateral uh, c spine x-ray, uh, with, uh, quite a significant, uh, or with severe degenerative changes all the way from, from C 1 to 4567 is what I can see on top of, uh, um, um, C eight. And, uh, that's why I took a second to think about it. And, um, but the most significantly there's a, um, anes of one to 12, 3/4 by, over sort of 30 40% I'd say. Yeah. Yeah. Yeah. Yeah. Um, there is also an aes of 2/3 by about 25 30% as well. Um, and 12345. Yeah. Yeah, a little bit. Maybe not a great deal. I think it's gone the other way if anything on that level. But what do I wanna know? What did I just say about the Sagittal view? Why do we get SASH views because we want to see what's the word I'm looking for the alignment, the alignment. So I want you to say something global about the alignment. What's to that neck? So there's a loss. Well, obviously it's not aligned anymore, but there's a significant Lordotic deformity. There's a lot, there's a, there is not really a deformity. There's a, she has maintained some of all aosis in her subaxial spine. Do you see lower down there starting from C five downwards? She's still got a bit of lordosis. Yeah. C five C 67 and a bit of T one. However, above that, what has the spine done? Has it fallen anteriorly or posteriorly? It's fallen anteriorly. And we call that a, it is, it's a significant sub um yeah, axial kyphotic deformity, not just at C 34, but also um at a little bit at C 45, but she's tried to maintain her lordosis or even compensate at C 23. Can you see that or it's still slipped? And really, this only really occurs when you've got facet joints which are completely knackered by some undergoing underlying um destructive arthritic process. Can you name one for me, which commonly affects necks or used to? Sorry. Could you repeat that? I II A ru destructive autoimmune arthritic process that we're seeing less and less rheumatoid arthritis, correct? This is your classic rheumatoid neck. Well, one of the ways, many ways. So if you was working 30 years ago in the NHS, this sort of patient coming to your clinic would have been your bread and butter. I see with problems and she would have had all the neck pain and myelopathy and radiculopathy that you can, you can get your hands on and you can see here she's got, she's got some tetraparesis, she's smoking. So she's not gonna be a great candidate for fusion. She's getting the upper limb symptoms and all manual dexterity. She's getting all those symptoms and signs we spoke about. Yes. So thinking about that, what, what's the first thing you wanna do? I'm on the phone and going ok, well done. G what should we get before I come in tomorrow? Um, well, we, we want to get an MRI scan but we also want to go to Yeah. Yeah. To rule out, you know, do blood tests rule out infection and, and there is a loss of disc, there is a lot of bit of the disc he here and then I would say even there's a loss of height of the vertebra as there are both at C three and C four. But you're right. Yeah, fair enough. Possibly a bit of infection looks rheumatoid to me, but she's got neurological pictures. So we've got to get an Mr. All right. So that's it. We decided to get an Mr I'm on the phone again. We, we decided to get an Mr that, that late afternoon, early evening. What does it show? Um So the summary headline of what it shows uh it shows myelopathy, severe stenosis at C 23 with signal changes uh at that level 23 have another little look uh 23. So that's probably the peg that's three. So is the myelopathy at 23 or is it another place? So, oh, sorry, you can't see my um Can you see my cursor just to the left of that? That's two that's three directly behind there, that disc space? There's a bit of disc but is there any direct compression across there or is it the three? That's right. It's associated with a marked anteriorly, probably grade two, um, and severe compression of the cord. And it, you might, you could say there is some what within the cord, especially on the axial segments, edema within the cord. Yeah, we'll call it signal change. So I don't 100% know what it is. So, just stick to what the radiologist use, signal change. Absolutely. And there it is, look there, well done. That was very impressive. You did? Well, it's not easy. This is not easy. So, what are the options? I'm not going to subject you to any more pain or whatever. So we could put her on a bit of traction, try and realign her, try and get those vertebra back into a better position and once they're in a better position, we can do this. What's this called ghan this operation? Uh poster. Uh Well, it's, it's, it's a fusion uh fusion with, yes, from the occiput to. So what would you call it? Occipito Eral fusion fusion? And those long screws are C two screws because you get really good bone in C two. So that's a good fusion that would work really well. And what we've managed to do is perhaps you could persuade yourself restored a little bit of her lordosis. Now, we're seeing these things less and less and less now because the of the use of biological treatments uh less and less and the restoration of that lordosis came about probably because of that preoperative traction. Right. We, we're running, there's a picture of it. Can you see that? And you can see the C two screws here as well the way they run up into the body of C two through the C two lamina and they're really good screws. But you've gotta be very careful when you're putting them in and the occipital screws are solid as you like. They're very, very solid screws. So it's a very thick bone. This is a little reminder about the vers artery and these are the vers arteries here forming the basilar archery. And you can see how important it is to the blood supply to the circle of Willis. One of the problems of posterior surgery is it tends to be a very vascular area and being a very vascular area. It some what happens is you sometimes get bleeding postoperatively, particularly if you take the drain out too soon or they're on aspirin or they started low molecular weight heparin. And one of the risks once you've done a decompression of having a bleed in the posterior neck, you can see here is what a cord injury do you see how that cord is being compressed by the blood? And these patients can have an initial improvement of their tetraparesis and then suddenly go tetra tetraplegic all of a sudden because of the blood. Despite all your hard work, I always stick a big drain in next posterior neck, stitch it to the skin and le leave it in for a minimum of 48 hours. Um Here's the, th now we've just looked at rheumatoid spine. So you get erosions, sinusitis, bursitis, all the things um we spoke about, but overall which you get with this disease, uh the, the, the panus, the, the destructive panus that you see in rheumatoid, but a lot of that has disappeared around circling down here with biological treatments and the indications again for surgery in these patients. That's the same. Mr as the patient we had operated on before is again, if the paddy is less than 13 millimeters, it's down to 3010 millimeters or less. Do you remember I mentioned that earlier, you should definitely be considering surgery. Uh and you get these subluxations which we can see here um and uh narrowing of the canal and all of that at that level is serious because they tend to have, they tend to do less well because the cord is being compressed. Um So high, these remember these lines I showed you last week, all related to rheumatoid necks. Whereas a further change with the panas as you can get, the peg can migrate up through the foramen and you can use chamberlains and mray lines to assess that. And here's a both I think I showed this picture last week of this very impressive basilar invagination. And you can see here. That's what the MRI scan looks like of the same thing and you can see it's pressing on the brain stem. Um, and it ge generally what we would do for this is you can't really go in there and do anything about that. You can't put them on traction without damaging either the vertebral arteries or some of the really key neurological structures, which you would put the cord under traction, you just tend to fuse these occipital cervical fusions to stop them moving. And that's usually the best you can do. Um This is just a final little slide to say that we are a department like many, many others. You can see the little blue circles, including some abroad are all involved. Now in this Mark Cotter, Ben Davis through the my, my my pa or that's Ben Davis, that's Mark Cotter. Um uh myopathia or a trial to see whether or not just decompressing from the back or decompressing infusion is better for degenerative cervical myelopathy. It's called the Poly Fix trial. And we have been submitting patients. I know I've submitted at least one to this trial. So we don't really know whether we should be fusing on all of these or not. So it's quite helpful to do these sorts of trials. And what's great is that these guys have got a lot of patients involved, manage to get a lot of funding and then from there, they can start funding these trials it's quite an achievement that I'm actually quite impressed with those two at setting up website, which is so helpful for research and providing money as well as such a rich source for patient information. It's very impressive. Maybe that inspires some of you listening today about setting up your own websites to do with various knee or other orthopedic pathologies cos in my book, this sort of website and do have a look at it doesn't really exist. It's one of those that really crosses patient surgeon boundaries and is really clear and beautifully done and completely funded through charitable means, which is all done by trustees. These guys don't have to worry about it at all. Uh It's, it's quite inspiring. Um So this is the final summary slide and this is pretty much what I took straight from that beautiful B MJ summary article, which is my first slide of the talk. And really what you need to know is it's common in the elderly, remind yourself of what the symptoms are, remind yourself of what to look for. Um uh in terms of signs, you must ask them about incontinence and other issues and it's very important. You do a full neurological assessment and you get a scan and s time matters in these patients, the quicker you get on and, and operate generally, the better they'll do, particularly in terms. And that's the key word, functional disability. That's what you're trying to address with this to prevent any further deterioration, I think. I think that's it. Yeah, that's it. Great. Wonderful.