How do I do it? I should know. OK, there you go. OK, so this is what we're going to talk about in this talk. I'm not going to talk about the history of nerve repair. We're going to talk about the anatomy of peripheral nerve degeneration. We're going to talk about nerve degeneration and regeneration, techniques for direct repair and grafting, factors affecting outcome, and the cheats that people can use to ask questions about these things. There is one piece of history you deserve to know. And you'll know that this doesn't matter, because I haven't put this key thing at the bottom of this slide. You're going to see YMKT written at the bottom of slides. YMKT stands for You Must Know This. So it's not at the bottom of this slide. You don't have to know this. But this is interesting, and it's important as a part of the story. This is the first demonstration that peripheral nerve repairs work. Bilateral vagotomies in a dog kills the dog. Unilateral vagotomy followed by repair, and then the other vagotomy six weeks later, the dog lives. And so this is what establishes in modern medicine that you can repair nerves. So it would be good to dogs. Let's talk about peripheral nerve anatomy. The anatomy of a peripheral nerve shown on this trichrome type stain is very simple. There's an epineurium. That's this here. Then there's a perineurium. That's this part here. So I mismarked it. Here's epineurium here. It's marked correctly on the slide, but I pointed incorrectly. Then there's this perineurium here separating fascicles. And then there's endoneurium that's around individual groups and neurons. Then there's fascicles and neurons. And in this particular type of slide, the myelin's black. And so not every neuron is myelinated, but many of them are. That makes a big difference in how neurons function. OK. Here's another way to look at a peripheral nerve. Multiple pictures, same concept here. See this? All of these perineurial structures and an epineurium around the nerve. The axons are single nerve fibers. They're much like fine copper wire. Of course, they're different than copper wire because copper wire shares charge across different wires, whereas neurons don't do that. Each individual neuron, 10,000 in a major peripheral nerve, each one of them conducts separately. Some fibers have electrical insulation called the myelin. The fascicles are surrounded by perineurium. Very easy to ask questions about this because it's one of the few things that we all kind of agree about. Here, another picture of the same thing. Now, very high magnification. Look here. This is called myelin. Here's an unmyelinated neuron. Here's a myelinated neuron. This is your brain on drugs. So this is the myelin here. It enables the neuron to conduct fast. And so the things that are most important are conducted with myelinated neurons. OK, and this is another picture of the same thing. I put multiple pictures so that you could just pick one to memorize. Let's talk about the cellular anatomy of the peripheral nerve. There is a cell body. Here's the cell body. The cell body for a motor nerve is in the spinal cord. The cell body for a sensory nerve is not in the spinal cord. And it says it right here. It's important because it's very easy to ask about that. These are segmental. Cell bodies, again, sensory nerve outside the spinal cord. Motor nerve inside the spinal cord. Let's talk about this concept. It's called the motor unit. If you take one neuron out of a human and you ask a motor nerve of can it cell bodies inside the spinal cord, and you ask how many muscle fibers does it innervate, that is called the motor unit. It is important because after a nerve injury, this motor unit grows. I'm sorry, this motor unit grows. A single neuron that makes it through a nerve injury has to innervate more and more of the muscles. And these muscles begin to atrophy within a week of denervation. And so it's very important for you to have this concept of a motor unit. What a neuron, a single neuron, is responsible for. If all your partners but two or three quit, you have to take all that extra call. Maybe not. I do. OK, so the receptors are end organs. You have to know what neurons do. So yeah, we know that neurons innervate muscle fibers. But do we know that neurons also innervate these sensory fibers? Here's a cartoon of every sensory fiber that they can test you for. You must know this. You see, it says it at the bottom of every slide. You don't have to even think about it. And then this is testable. I think one question in 15 years that I've looked through. The only one of these you can see is the Piscinian corpuscle with your naked eye. So just know that. OK. Sensory phenomena. People talk about this stuff. You don't have to know this. But these are words that are useful, like dysesthesia. What does it mean? Hyperalgesia. Hyperpathia. That's a word that no one uses. Lightning pains and causalgia. This is a term that is becoming more and more used in our literature and other literature. And so I just listed these so that you know what is meant with these words. Sensory examination. What are we looking for? What are we testing? What specific types of nerve fibers are we testing? Well, light touch, two-point discrimination, and vibration sense, these are large fibers. Small fibers are the pain. They're unmyelinated. You think, oh, pain should be myelinated. You don't want that conducted quickly. There's many reasons for it. But just memorize this if you want to know what different nerve fibers do on a sensory level. All of these fibers, their cell bodies are outside the spinal cord in that dorsal root ganglia. It's a slide a few slides ago. Nerve injury. OK, now we've talked a lot about what neurons do. What nerves do? Well, when nerve injury happens, the fate of the injured nerve depends on the mechanism and severity of the injury, duh. Crush and traction injuries may damage myelination. The important concept to understand here is there's such a thing as a partial injury, and that's what you're waiting around for. Transsected axons undergo this process called valerian degeneration. I'm going to show you what that is so that there's no confusion. Valerian degeneration. The distal cut axon dies. Here it is. It's dead. It's useless. But it guides outsprouting of this. Distal Schwann cells clear the debris. They're like macrophages after this injury. And then the axon proximal prepares for sprouting. I found a picture from a previous talk of this sprouting. This is a cartoon, but I have an actual picture of this stained. And regeneration from this axon sprouting, it occurs randomly. And then the sprouts themselves start to follow nerve growth cues that are in the distal stump. So these terminal sprouts start inside the basal lamina. That's testable, although it's never been tested. It's something that's agreed upon. Look at this. This is the axon sprouting. These are the filopodia. You don't have to know that they're filopodia. Here's the proximal nerve stump. And here's the sprouting. And then after a while, it starts to congeal. And it will go in the direction. If you put a little thing of nerve growth factor on the plate, it'll grow towards it. And so it samples the environment, and it's looking for this. This process is what happens at a millimeter or so a day. And in mice, about four millimeters a day or three millimeters a day. And so that's what's important. OK, moving on. Classifications of nerve injury. Oh, my. There are lots of elements of classification of nerve injury, and you don't have to know all of it. My recommendation for you is pick the simple one, which I'm going to tell you what it is, memorize that. Because classifications of nerve injuries are not meaningful, because you can't use them to classify the nerve injury the moment you see the patient. So although these are relevant for questions, they're not as relevant in life. And so they attempt to determine which injuries will recover from which ones won't. Of course, you need that information the day you see a patient. Sedan is the one I wouldn't memorize. This was written in the 50s. Neuropraxia, axonotmesis, neuronotmesis. One, two, and three. There's another classification called the Sunderland classification. I'm going to show you what the differences are. You have to know that there is classifications. And you have to have some understanding of if it's cut, it's not just going to heal. Am I going too fast? I've been accused of that. All right, good. So this is something you have to know. Sunderland has this classification, and he has five categories. A sixth one was added by McKinnon some years ago. This is the most relevant part of this other classification. The idea that there can be a mixed injury, because most of the injuries we actually see are mixed injuries. What's important is going to heal, partial heal, or maybe heal, probably not going to heal, probably not going to heal. That is to say, if there's interruption of a major part of that nerve, it's not going to just heal on its own. OK, this is a picture of the same thing you're going to see over and over in my talks. I'm going to put many examples of the same thing. Just pick the one that you like. Some people like this picture. This picture is a very bad picture, because, of course, it models a 10,000 neuron nerve as one neuron, which is not right. But it's good for memorizing this classification. And it's important to know, these always make it better. These never make it better. There's murkiness here, but these probably do OK. And the most important factor in predicting how well these do, I'm going to talk about in a second. But it's actually age. Remember, it's age. It's age that makes the biggest difference in what happens with a peripheral nerve. This is the results of nerve injury by classification scheme. It's exactly what we just said. Evaluation of the nerve injured patient requires an understanding of what the nerve does. Variables affecting outcome. Here it is. It's age. The other things are true, but it's age. And so there are many ways to evaluate sensory nerves. There is this two-point discrimination. It's the standard. This is a McKinnon-Dellin two-point discriminator. Light touch sensation is injured on the contralateral uninjured distribution using a 1 to 10 scale. That's a quick tool, but you want to basically look for two-point discriminations. Five, six, seven or less is normal. More than that is abnormal. OK, so you're going to look at a patient. Everyone here knows what you look for for a particular nerve. If you don't, just memorize this slide. Very easy to know and very easy to test this, because remember, they can only test you on things everyone agrees on. And this is something that everyone agrees on. OK. Sensory evaluation, areas specific for each peripheral nerve I listed here. The median nerve, the pulp. Again, ulnar nerve. So what you have here in this previous slide is what the motor elements for each nerve are. And what you have here is what the sensory elements for each nerve are. OK. Electrodiagnostic testing. Electrophysiologic testing includes nerve conduction studies and electromyography. We have this tendency to call these EMGs, even though it's actually two tests. Nerve conduction study and EMG can help distinguish between neuropraxia, transection of the nerve. And it can also pick up things like diabetic neuropathy and demyelinating disease. Nowhere in the syllabus is this information included. So I actually put this in here just so that you would know what it is they're talking about when they give you an EMG report. Here, look at this. This is the latency from a stimulus to a response. A stimulus that is created as part of the test and a response that is recorded. This is a sensory study. And so the latency matters because it's measuring what proportion of your nerve is myelinated because myelin is speed. And so that's what latency is. Tends to measure the fastest fibers. Amplitude is the number of fibers that are firing. Does everybody kind of see this? It seems really simple. This is very easy to test this stuff. OK, electromyography. This is the part where you're actually testing the motor function of the nerve. Here, the stimulus is created on the nerve. And you measure whether or not there's contraction and how fast it happens. There are these things called insertional activity, fibrillations. People use these words all the time, but yet very few of us actually ever see these. So I've got some pictures of this. This is regeneration. This is what it looks like in their study. Long duration, small amplitude, polyphasics, motor unit potential. So that's this stuff. You see this stuff here, here, here? That's what regeneration looks like in a nerve. So that's what they mean when they use these words. Here is acute denervation. This is what a fibrillation potential is. No stimulation, boom, one. Boom, one. So these are what fibrillation potentials look like. I don't know that you have to understand this, but at the same time, it helped me to know what these pictures looked like. Because many of us don't actually look at the EMG report beyond the interpretation. We're never supposed to admit that stuff, but it's true for a lot of people. So in any case, treatment of peripheral nerve injury. We're gonna briefly talk about this. There are some things everybody agrees upon. Acute, known, sharp, penetrating injuries. These are probably explored. Traction, crushing injuries. These are probably waited on. You should know that the EMG test isn't so helpful initially. You have to actually wait for that. Serial exams with the EMG make them much more sensitive and specific. Primary repairs are usually done within a few weeks. Nobody's gonna say that you have to primarily repair a nerve the day it happens. Published data does not show clear benefits to emergent repairs. Secondary repair delays often necessary to define a zone of injury. Remember, it's not just the nerve that's cut. It's muscle that's cut. It's vessels that are cut. The one true goal is a nerve repair that is appropriately aligned with coaptation of healthy fascicles in a well-vascularized tissue bed under no tension. Under no tension. That's a question that comes up over and over and over again. Under no tension is very important. Because, probably because the nerve repair rips apart as you're in the post-operative recovery area. So, under no tension is probably a very important factor. It doesn't matter how it's done from a literature perspective. So, from the test, it doesn't matter that you were taught to do epineurial repairs, putting the stitches only in the skin around the nerve. The skin of the nerve is the epineurium. Or, if you're going to do individual fascicles, again, this is a grouped fascicular repair, you have to know that there is a difference between these two. They represent different procedures, but you don't have to know which one's better. You probably ought not believe one is better based on the literature. Here, orientation of the epineurial repair, there is a fair amount made in the literature about whether or not these three little things here, these three little fascicles here, they should be aligned. These three with these. You have to look at the end of the nerve and get them aligned. People believe that this is important. So, this, although it's not testable in the sense that it's not a technique, the orientation of a nerve repair, it's important. You have to understand that this is something you're supposed to look at. You can use lots of different factors in this. Some people actually stain neurons in the nerve so that they can see it. But, you can use the vessels, you can use the appearance of the fascicles. You must know that this matters to people. Techniques to decrease the tension in the nerve repair. What you have to understand is it has to be tension free. A lot of people will mobilize the nerve, transpose the nerve, shorten a forearm or an arm or a leg. This happens often. But, this one is the one you don't wanna choose. You don't wanna just basically say, well, it's short enough if the elbow's flexed like that. Because, if it is short enough and the elbow's flexed like that, that's gonna fall apart. So, okay, good. We're almost done. I wanna talk about autograft nerves. There are a lot of questions that come up in the self-assessment exam about the nerve graft du jour. Here's a vascularized nerve graft. They're really cool. The questions on the test really have a very hard time favoring one nerve graft over another. There are some general rules. But, in general, they're never gonna make you choose a vascularized nerve graft. That's why it's missing the thing at the bottom. I just don't think that it's gonna make a difference. You have to know that autografts on your test are going to be better answers than fake stuff, cadaveric stuff. In general, that's just gonna be true. If you don't know what the right answer is, don't pick the fancy. Autograft nerves, take the sural, take the medial lateral antebrachial cutaneous nerve. I don't know if it's such a good idea to take somebody's PIN. There are things called allografts. Generally, they're processed. They're acellular. They act as scaffolds. Schwann cells are supposed to grow into the allograft because the allograft is dead. So it has no capacity to do anything except to provide highways for neurons to grow through. And the Schwann cells have to grow into it for it to be useful. The outcome is near normal two-point discrimination in selected case series. In my reading of the literature, most of this is industry-related. And so I don't think that these questions come up on your real test as much as they do on the self-assessment exams because people write those questions based on a little bit lower criteria. But you're supposed to know, there's literature that says that 85% of these are effective for major peripheral nerves. 85% strength recovery in a PIN nerve, for example. All right, conduits. Okay, I'm gonna just basically say this twice, right in a row. Use the conduit in the finger on the test. Do not use the conduit outside of the finger on the test. It doesn't matter on the test whether you use the conduit every day of the week and twice on Sunday. On the test, you use it in fingers. It's great for finger defects. It's been shown even in non-industry-sponsored literature to be very effective there. It has been shown to be effective elsewhere, but this is agreed upon. Always less than three centimeter defects on the test. Okay? Are we still okay? All right, conduits continued. Nerve tubes degrade by plasmids and proteases. I don't think they would ever ask you about this. I can't find a question about it. Gap size, again, less than three centimeters, guys. The longer the tube, the more hourglassing of the nerve happens. These are things that I kind of know about. I don't think you really have to know about it, but if they talk about hourglassing, this is what it looks like. And then this is probably the most common thing that happens with a big nerve that doesn't recover. In somebody who's probably older than 40 or so, nerve repairs do this. Variables which affect nerve regeneration, the patient ones, age, age, age, adolescents do better than young adults, do better than adults. The mechanism of injury, comorbid factors, nerve-specific generalizations. Nerves that don't have a lot of different kinds of fibers in them do better than nerves that have one, that have many kinds of fibers in them. So radial, better than median, better than ulnar. Upper trunk does better than lower trunk. Top of the plexus, better than the bottom of the plexus. One coaptation is much, much better than two coaptations. And two nerve coaptations do better than anything under tension. This is sort of my summary of these factors for you. End organ degeneration. I don't think that this is so important, but just know that motor degeneration can happen even if you just lose the Schwann cells. You can actually have neurons that grow through an injury site and still get atrophy. Loss of the ability to re-innervate happens around one and a half to two years. They're not gonna ask you about exactly when. It's different for every nerve, and it's different for every muscle that's innervated. They can say to you this. How long does it take for the end plate to degenerate? The answer is about a week. You're not gonna know that answer. You're not gonna think, oh, it happens so quickly if you have to wait a year and a half before you throw in the towel. But that's a fact. If you stain for the end plate that the nerve is growing onto in the muscle, that's what you'll find. Okay. Things that happen with specificity, there are specificity problems. So the end organ doesn't get the nerve. It reestablishes continuity. That's the right thing. It goes to the wrong receptor. False localization. The guy thinks it's gotten there, but it isn't. And then no connectivity at all, probably the most common thing that happens.

peripheral nerve regeneration

anatomy of peripheral nerves

factors affecting outcome

nerve injuries

nerve repairs

nerve grafting