Thank you very much. As has been already stated, this is an intense course, but it really should be a lot of fun. I think one of the best parts of these courses is it's a fundamentals course and then you get to go reinforce it in the laboratory. You get to pick the cadavers apart in ways that you obviously don't get to do in the clinic. It's a really good resource, so I encourage you to make the best use of the lab that you can. What we're going to do today with the first course is start at the top as we make our way down to the bottom and reviewing the fundamentals. Basically, we're going to start with occipital-cervical fusion, which is really practiced less and less nowadays. How many people have done OCC1C through fusion? Just a smattering. Fair to say it's not a real common procedure. When I went through training, we didn't have the TNF inhibitors and we saw rheumatoid patients much, much more frequently. This was very, very common. This is a weekly event on many occasions. But it's a little bit more rare, but nonetheless a very important technique, and especially with some of the newer screw techniques that have been developed. I'd like to today review a little bit of the biomechanics and anatomy, indications for fusion, look a little bit at some of the most common instabilities and pathologies, and then we'll talk a little bit more in depth about techniques. You all are very familiar with the anatomy. The C0C1-2 junction has evolved as we became bipedal animals for the upright position, really facilitating our rotation. It's basically an articulation between the occiput and C2 with an intermediary C1 bushing. The cup-like articulation of the occiput and C1 prevents and tremendously stabilizes translation while permitting rotation. The ligament is complex, is a prime stabilizer, and really consists of two sets of ligaments. The more peripheral ligaments, like the capsules and the lato-occipital membranes, and the deeper, more robust ligament is complex, which essentially bridges the occiput to C2. The alo ligaments you're familiar with, the apical ligament, cruciate ligament, and the very strong tectorial membrane. I would encourage you again in the lab to dissect these out once you've done your screw techniques. Recall that the occipital C1-C2 junction have very unique and very important biomechanical responsibilities. Principally at C1-C2, that's where you get 50% almost of your cervical rotation left and right. But a lot of people forget that the occipital C1 is probably the greatest contributor for flexion extension, especially capital flexion extension. The reason you need to keep this in mind is when you're about to commit a patient to an occiput to C2 or C3 fusion, you're going to be losing a significant amount of these movements and they're not really happy with it. You really need to take that seriously and inform the patient about the limitations that they're going to have. So, OC instability we see in a variety of pathologies. Trauma is obviously classic. The erosive synovitis of rheumatoid arthritis is probably one of the more common ones. But we'll also see it in congenital insufficiencies like the hypoplastic DENS and the ossoedontoidians. And more infrequently with tumor or iatrogenic with transconvular skull base approaches. So, in trauma, just to kind of go through a little bit of trauma. You're familiar with many of the types of OC trauma. Condylar fractures, AO dislocations, high-grade atlas fractures, transverse ligament disruption, high-grade odontoid fractures, and hangman's fractures. The condylar fractures have been classified into three types. The common unit type 1, which is basically a compression fracture, relatively stable. Extension of the basilar skull fracture, again, quite relatively stable like most basilar skull fractures. And the type 3, which is a little bit higher energy and tends to have an avulsion injury. And with the avulsed alo ligaments preventing apposition of the bone, it tends to remain relatively unstable. So, for most type 1 and type 2 fractures, these can be treated relatively conservatively with bracing. The displaced type 1s and type 2s indicate more ligamentous disruption. And most of the type 3s, and something a little bit more formal like a halo or a collar. And certainly the type 3 fractures with instability require consideration of an OC fusion. So, AO dislocations are another fairly dramatic, but fortunately rare, type of an OC injury that we will occasionally see. You'll definitely see it in your career. Estimated 1% overall of cervical trauma, but it's significantly morbid. Up to 8% of all fatalities have some degree of O8 dislocation. More common in children probably due to ligamentous laxity. There's a propensity with pedestrian versus motor vehicle accidents, owing to the tremendous amount of energy imparted. And the pathology, the fatal pathology, tends to involve brainstem injury, as you might expect. Surprisingly, 20% are asymptomatic. And with better EMS service and awareness, we're starting to see these folks come in to the ED who are awake and alert and still neurologically preservable. The ligamentous disruption is profound, principally involving the very strong and important tectorial membrane, as well as the halo ligaments. So, Trinellis years ago classified these based on what it looked like when they showed up and got x-rays, with the displacement being anterior, longitudinal, or posterior. And it's probably somewhat misleading because the head, as you've seen in other traumas, will undergo significant multiple and complex excursions, not just necessarily anterior, longitudinal, or posterior. Nonetheless, it's a convenient way to think about this entity. The diagnosis can be somewhat problematic, so you have to have a high index of suspicion. The mechanism of injury is important here. And again, I've alluded to children and pedestrian motor vehicle accidents. Plane films, and this is kind of more of a historic value because nobody gets plane films and makes a diagnosis like this of plane films anymore. But there's a whole, very rich literature looking at relationships on plane films of the basion to the C1 and C2 structures. The sensitivity is not that great. Surprisingly, the soft tissue swelling here is actually quite sensitive, and that's been shown. Greg Przybylski published a paper like that a few years ago looking at the soft tissue swelling and how telling that is for OA dislocation. Sensitivity is somewhat less sensitive, depending on technique, and the MRI about the sensitive as a CT. The nice part about MRI, as you all are very aware, is you can actually see the ligamentous disruption, not infrequently. And this is a representative of an OA dislocation with a condyle on the CT scan. And on the MRI, you can see this nice big hematoma up here again, which is a very characteristic of this injury. You can actually see some of the disruption of the ligamentous structures. This is funny. You've probably all studied these and you've probably been quizzed on them, but nobody really uses these anymore, which is kind of fortuitous because of the significant variation in your ability to measure on plane films. But back when that's all you had, this is what you did. You measured plane films and you measured key indicators, such as the distance from the base down to the tip of the odontoid and this powers ratio. Again, this is very key when you're looking at kids with vascular vagination, things like that. Surprisingly, this measurement of Harris turns out to be the most sensitive, as reported in the 90s. And again, it's how anteriorly or posteriorly displaced the tip of the DENS is from this ideal line versus the back of the C2. And actually, it's quite telling for OA dislocation. But again, in the modern era, you will get a CT and an MRI. How do you manage these, folks, once you make the diagnosis appropriately, carefully? I underscore that. Obviously, you have to follow protocol for the ABCs because invariably, they've got additional trauma. But if you don't address this issue, they will all progress neurologically to obviously an extremely morbid end. Is traction indicated? Probably manually. And I'll show you a case where just finger traction increased the dislocation by over a centimeter. Is a halo indicated? As many of you know, the halos are not really that stable except for gross flexion extension. There's a lot of up and down with movement of the shoulders or even respirations, and almost 30% will deteriorate. You really need to operate on these folks and take control and stabilize these folks once you make the diagnosis. That's with a little manual traction here. So, what do we do? Well, the preferred technique nowadays, we're going to go a little bit more in depth with this, is an occiput to C2 fusion with something rigid, something that's not going to allow translation, anterior-posterior translation of the skull relative to the C1-C2 complex. Plus or minus a halo, and it kind of depends on the particular technique that you use and how rigid this is. If you are somewhat concerned about the rigidity of your construct or the purchase of the bone or the quality of the bone, you can always supplement that rigidity requirement with an external halo. This is a case, this was a 30-something year old gal who was out on her bike and got run over by a car, was dragged under the car for a bit, and came in, was stabilized, and came in and was still neurologically intact. She was intubated in the field, and there was a question about soft tissue swelling anteriorly, which prompted the CT, and you see sort of an empty C0-C1 condyle here. And after gentle reduction, you see this is what was done, that was the diagnosis was made, an attempt at rigid stabilization was made. This is a, as we'll go into in a minute, a Steinman pin with some wires and a C1-C2 transarticular screw. Well, the transarticular screw very nicely takes care of the C1-C2 instability, but you've got occiput to semi-rigid wiring construct here. And you see this has re-dislocated with this much space posteriorly, and this is another shot showing that a very simple flexion of the head is still allowing significant dislocation of the occiput relative to C1. That's because it's a wiring construct. Wiring constructs are not rigid enough. Well, she ended up with post-op hydrocephalus and cerebellar infarction, had to be revised with a screw rod type of a construct, which is significantly stiffer that you see here, which was able to maintain reduction. This is another case. A 45 year old was hit by a car, came in with an absent gag reflex because of brain stem trauma and bilateral six nerve palsies. Remember, the sixth rhythm is the longest intracranial course down along the clavis, and a longitudinal stretch injury will cause disruption or even avulsion of the sixth nerves, and they'll come in with crossed eyes, very characteristic in telling that there's something going on at the occipital cervical junction. And as you see, very minimal finger retraction allowed for a scary degree of dislocation. There's an empty ring on the CT scan and an avulsion fracture of the condyle characteristic, as you see here, and pre-dental hematoma with tectorial membrane disruption on MRI. Pretty characteristic of this devastating injury. So, he underwent rigid fixation with a plate and transarticular screws with a structural graft that you see interposed here and then was wired to the plate. I believe he was put in a halo after that, and this was a number of years ago, but still worked out pretty well. And let's talk a little bit about another indication for stabilization in this area, the rheumatoid patient. Now, this presents a different set of challenges, not only the instability and the need to stabilize the junction, but what you're working with now is compromised. As you know, these folks, either due to the medications that they're on and or the primary disease, have very poor bone stock. Many of them are females with smaller anatomy, and as we'll look at specifically, the squamoid, the occiput, doesn't really hold much. So, it makes it a little bit more of a challenge. Remember, this is a instability on the basis of erosion of the joint structures, destruction of the condyles, with progressive vasovagination of C1 on C2, with C1, I'm sorry, C0 on C1, with C1, C2 not infrequently subluxing forward. By definition, vasovagination involves more than a third of the joint ends, both the foramen and magna. So, the important numbers with C1-C2 subluxation in kids, you have a little bit more leeway, up to 5 millimeters in less than age 8, 3 or 4 millimeters in adults. This is the atlanto-dental interval anteriorly. When a lot of this is destroyed in rheumatoid arthritis, you really can't measure it very reliably, and the posterior atlanto-dental interval is probably more reliable. There's been some indication that it has prognostic value, and really below 14, you're in danger for the patient injuring their brainstem and suffering sudden death. So, this is a patient with dynamic instability with rheumatoid arthritis, and the careful, awake, dynamic views certainly are feasible and can be very helpful in determining active instability. I'll also tell you whether it's going to reduce and whether you need preoperatively to put them in traction to gain reduction. This is a 71-year-old lady who for 20 years had rheumatoid and comes in with increasing neck pain, and really is getting myelopathic at this point. You see her PADI is about 13 millimeters, and the MRI is very telling, revealing the brainstem compression, and undergoes plate rod fixation, occiput C1-C2. It's a rigid construct, involves rigid purchase of the occiput screws that you see here. We actually went down to C3 to fortify and add to the stability of this C1-C2 trans-articular screw that you see here. So, I'm going to drop back a little bit and develop a little bit of the background for what we use today. People have been playing around with these techniques for years, like in the 20s, they'd use fibula, period nickel of halo fame, sort of capitalized on the halo and the risser cast by doing a lot of onlay grafting, or even leaving them in traction for six weeks after onlay grafting. Obviously, high rates of failure due to non-union and significant complications of immobility. We've learned our lesson. Believe it or not, people used to do this. That led to grafting wire, and Henry Bowman, years ago, and unfortunately he just died a couple years ago. Henry Bowman was a giant in spine surgery, orthopedist, and he developed a whole series of variations on this technique where he passed wires either through the spinous processes and then he used them to lash down corticancellous grafts harvested from the iliac crest. And he extended this concept to the occiput as you see here. And this has been varied tremendously. There's a Japanese group that developed a bender so that you could contour these grafts and all kinds of really kind of interesting things. But you tie it together with a neat bow and it tends to work reasonably well. But again, as I talked about earlier in this talk, wiring techniques are not stable. The wire parallelograms and the wire allows rotation within the wire and it's not a fully rigid technique. So people use augment with polymethylmethacrylate. Put a big horseshoe of glue around these things and it's just really, as you can see, it was pretty awful. You live in a good age. This is kind of what it looks like on x-ray. They do work. So Eduardo Luque, if you're not familiar with his work, you will be, he did a lot of work especially with paralytic scoliosis in the 80s and basically developed the concept of sublaminar wiring to a rigid member that you contour in the contour you want the spine to come to. Well, people extended that concept in the occipital cervical region, as you see here with a sort of threaded Steinman pin. I guess the sophomore Danek back in the day had sort of this neural contoured rod that people would bend into a loop as you see here. And that led to some dedicated structures as you see with this Lansford loop. Then again, using Bowman's principle would be lashed with wires to the occiput and upper cervical spine for stabilization. The problem with this is passing a monofilament wire potentially violates the canal. So this has led to use of cables or twisted wires or even heavy suture back in the day when we were using wiring. How does it work? Just a couple of years ago, this group did a systematic analysis of the OC fusion literature. And some of the, as you might imagine, as I've alluded to, some of the conclusions, even though it was a heterogeneous population, they were able to make some conclusions. And what they found with the overall outcomes regardless of pathology, favored rigidity. And as you again would imagine, the wires failed more than the screw rod constructs. As you see here, up to 45%. So forget the wires, we've evolved and we've moved on to plates and screws and other fun technologies. But it's important to know where a lot of this stuff comes from. The failures sort of prompt development of new technologies. So a few years back, Peter Grove, back in the 90s, developed this Y-plate. It really was kind of groundbreaking for the time. But again, as you can imagine, you're really pivoting on this one post and the stability is somewhat limited. But it also requires an art degree to be able to bend this in three planes adequately to properly fit the anatomy. It's kind of fiddly and kind of technical. But this started an explosion of plate screw occipital-cervical fixation techniques. This is our friend, the wiring with the Steinman pins and look your rods. A lot of folks then went to using the keel and supporting it with a structure such as this or even with plates as you see now, ushering in the modern era of fixation. When you look at it biomechanically, the plate screw systems are much more rigid as you would expect from the wiring systems. And actually the plate rod systems were performed the best, which is why that's still the workhorse for what we use today in occipital-cervical fixation. Okay, what are the danger zones? And again, I would encourage you, if you don't do a lot of these or if you have any questions, tear these down on your cadavers and really check out this anatomy in full view. Sometimes it's the only chance you get to look at the anatomy that thoroughly. But there are some landmarks that are important when you're thinking about putting one of these constructs into the occipital bone. Certainly the squamous, you know, is the least stout in some folks. It's as thin as two millimeters. Your superior nuchal line reflects roughly the position of the transverse sulcus. You may want to stay out of that. Also, this is where your extensor musculature attaches. And if you want to avoid having your patients have hardware eroding through their thin scalp, you definitely want to ensure that your fixation, your occipital fixation, is below your superior nuchal line. This has been studied. Robert, years ago, did a cadaveric study of posterior fossil morphometry. Clearly, the wheelhouse of fixation here is this thick occipital midline, which can be as high as 14 millimeters in his series, but I've definitely put in 14 millimeters, millimeter screws in the midline keel. And the squamous is almost worthless. It's important to remember, because remember a lot of those wiring techniques, the wires just pull right through this stuff, especially in older osteopenic patients. And as we know from our biomechanics, that the bone thickness correlates directly with pull-out strength. So this has led to the evolution of the modular systems. Everything's gone modular from the pelvis to the occiput, which is a good thing. You can build on the ends of your other constructs. You can use hooks if necessary, certainly across lengths, wires, but importantly for our region here, the screw techniques. Trying to take advantage of that thick midline keel, many of the plates have developed this sort of midline design with additional wings if necessary. And attachment structures with multiple degrees of freedom. And there are literally 10, I wouldn't say hundreds, but tens of these types of designs available. But these are some of the more popular ones. The plate designs necessitate lateral placement. As I said, this is the thickest area of bone. So these, you can get them to work, but they lose favor. And again, bringing it above the superior nuchal line as is depicted here in this model is not a great idea. You have to bend these plate rod systems and not infrequently the bending will cause stress risers. And I've had more of these or seen more of these break right at this bend to try and contour than anything. And I think for that reason, they've started to go by the wayside if they haven't already. This is the workhorse, these plates that take care of, that take advantage of the midline keel for purchase. Pretty much standard and you'll get a chance to do this with several different vendors in the lab. It's the drill trap, the drill tap screw routine or procedure is the same for trauma, just like a long bone as it is for occipital fixation. I like to use a pre-op CT measurement, just it makes it stupid simple, which is good for me. A lot of the systems have either an angled or a universal type of a driver, drill, tab. These universal drivers are kind of nice. You'd be surprised, especially on big people where a lot of the soft tissue anatomy gets in the way and the angles can't be appropriately maintained. And then the screws are inserted. You like to put three in the keel if you can and attach the rods. Now this is a bent rod and as I said, this portion of the connection has been made easy with four degrees of freedom for the connection. You want to get about 105 degrees on the standard adult. If you can get the hard pallet approximate, approximately even with the floor, they will be totally functional and your risk for adjacent segment degeneration will be decreased and they'll love you. If you're significantly off of this, even five to 10 degrees, it tends to challenge the rest of the spine just to be able to keep your head up along the horizon. The problem of the fracture here has been attacked by some of the vendors by providing pre-vent rods or even a kind of a cool hinge mechanism. I actually prefer this just because it's so much easier to approximate your preoperative angle or having the attachment pre-vent, although that puts the stress riser on the screw plate interface. Here's a case, kind of an interesting case of a young gal, 23, six months of episodic hand and left foot paresthesias, neck pain, really starting to go off the rails. And de jure numbness. Remember, you know what de jure numbness is? Remember that? That dizzying pattern of facial numbness? You know, the onion skin? Dizzy numbness up here? Am I talking French? Anyway, the somatotopic organization of the facial nucleus up in the cranial cervical junction is attenuated and the lower portions will start to manifest with sensory changes more peripherally centering on the center of the face. So she comes in, she's got this kind of funny numbness, a little bit worse on the left on her face, which kind of tips you off as well that something's going on in her cranial cervical area. She's got a nocturnal tachycardia and shortness of breath. She has Dwayne's syndrome, which is a congenital abnormality. She's got this long, thin, complex copephile deformity. Copephile deformity, right-sided deafness, probably from the osseous deformity. Congenital strabismus, and as I said, a high-grade copephile. In the examiner, she walks normally. She is hyperreflexic and somewhat myelopathic on her left side. And importantly, her gag and cerebellar testing are normal. So she's got a hypoplastic DENS, as you see. This is the base of C2, and this is an ossicle. C1 looks a little misshapen and asymmetric. And she has an ossoedontoidium, as you see here, is the anterior rim of C1 plus the rim of C1. And then she's got this thing. Any ideas from the crowd what that could be? It's a tumor. No? Do you want to give me a best guess? Pardon me? Pannus. What's a pannus? Excuse me? Your turn to speak up. Overgrowth of the soft tissue from the ligament. What causes a pannus? Instability, but classically, the inflammatory pannus that you see, what causes that? Yeah, more of a synovitis. It's got a lot of giant cells in it. It's more of an inflammatory reaction than anything. Any other guesses what this could be? Is it intradural or extradural? Well, intradural or extradural? Extradural. Yeah, it's got that kind of myelogram appearance of tapered ends to it, doesn't it? Somebody said a cyst. What kind of cyst? Who said that? Yeah. A degenerative cyst from where? It's the bursa, right? I'm sorry? I think the bursa might be what you're looking at there. Yeah, the TLL has a very nice synovial bursa, yeah. And that's probably what it is. As you see here, the MRI, it's filled with hyper-intense fluid, and the thing is acting just like a tumor, and it's a little bit eccentric on her left side, and very nicely explains a lot of her symptoms. But these folks with the clipophiles, especially the high-grade clipophiles, will have adjacent segment degeneration to beat the band, and it's very, very common. So what do you want to do with this? First of all, do you need to do anything with the ossoedontoid hemp? Is that a stable lesion? How many say yes? Stable lesion? One. How many say no? What would you like to do with it? I think it's an operation. Okay, what do you think? They say you're applying O2C2. O2C2? What are you going to do with this? Okay. And once you say your name and the quality of it, you can see if it's minimal to menstruate it, or if it's secular or anything like that. Do they ever go away if you stop the instability? Sure. So now your cyst's less so, but the pannus from rheumatoid arthritis will to a degree. Would you do a transporal? Would you go transporal? That's an option. Could you get this from the side? It's asymmetric to the left side. Yeah, I think it would be a bit of a challenge to get this from the side. We... As you see, she's grossly unstable. So we took your advice, we put in a trach, and we did a transoral fenestration with synovial cyst drainage and resection, and then fixed her down to C5. Just wanted to make sure that we had enough of a lever armed into her, into her congenital clopaphyl fusion. 103 cranial cervical angle. And that's what it looks like down here. Okay. So what's new and what's latest and greatest, you're gonna hear about C1, C2 fixation, but some crazy people, like our own Franklin Mark, have suggested that we actually put screws into the occiput. And indeed, he's done a great initial anatomic work looking at the feasibility of placing screws into the condyle. This is a great paper, 2008, looking at the anatomy and technique. They used computer guidance and sort of a relatively straight ahead forward in technique. And this is a screenshot from slight medialization of the transcondylar screw placement. The concern, obviously, are these structures. You have a very, very narrow bony corridor, which the tolerance for error is extremely low, not only for the hypoglossal nerve and the sensory vein, which, you know, you put the screw in, it's probably gonna stop bleeding, but your jugular bulb is right here. Your vertebral artery is right behind you. And even forward, if you get too exuberant anteriorly, is your carotid. So it's very high priced real estate, but it is one area that's reasonably consistent in terms of dense cortical bone that is an alternative if you've had extensive resection or you have very poor bone stock. People increasingly are thinking about using this. I'm not in with Juan Uribe, who will be here tomorrow, just published 12 patients who underwent transcondylar screw fixation and complications, I should say. There were no neurovascular complications. They felt radiographically, they all fused. And I guess it begs the question, are increasing image guided screw fixation techniques like this the future beyond keel fixation? So with that, I will look forward to seeing you in the lab tomorrow. Thank you very much. Thank you.

occipital-cervical fusion

cranial cervical region

anatomy

biomechanics

fixation methods

stability

complications