Hi everyone, welcome to the AAPMNR Pediatric Rehab Medicine webinar series. We're very excited today to have Dr. Rinaldi speaking about peripheral nerve injuries and rehabilitation management. So before passing it along to him, just a couple of quick things. If you have any questions, you can put it in the Q&A or you can put it in the chat and then we will wait until the end to ask those questions of Dr. Rinaldi. And if you're watching this asynchronously and you have any questions that you wanted to reach out, you can always reach out to AAPMNR and they can pass that along to Dr. Rinaldi as well. So without further ado, I'm going to pass it along. Great. Thanks, Mary. So I'm excited to talk about this with you guys. Peripheral nerve injury is something I've been interested in way back to my limited graduate studies after undergrad, which I took an interest in neural development and nerve regeneration and nerve development was part of that. Really, really an interesting topic that's, I think, segued into one of my major clinical areas of interest, which is PNI plus BPI. Those of you who know me know I do a lot of brachial plexus injury work and have for about 25 years now. So this is an area that I'm really excited about clinically in terms of management of it and even from a research perspective. It's just a fascinating area, particularly when you consider that we're working in pediatrics, we're working with developing organisms. And the, I think, subtleties and some of the secondary complications from peripheral nerve injury in developing organisms is quite interesting and challenging in many ways. So the crux of this talk is not to necessarily go through heavy epidemiology, surgical interventions, things like that with PNI. It's more from the rehab doc's perspective. What are the types of things that we need to be thinking about and how do we approach peripheral nerve injury as clinicians? So it's going to lean more into the rehab side of this as opposed to, I think, heavy duty pathology and epidemiology and data and things like that. So we'll get going with this. Once again, if you guys have questions, please feel free to ask. We should have some time at the end of this to answer questions for you guys. I have no financial disclosures. So the objectives, we're going to describe different degrees of peripheral nerve injury. Some of this is going to be very familiar to you guys. Some of it may not be. We're going to understand the peripheral nerve's response to trauma and how I conceptualize injuries. We're going to understand the basic concepts of neural regeneration following PNI, describe the utility of EMG and the assessment of PNI. Again, this should likely be familiar to you guys. List the four common areas of concern for rehabilitation management of PNI and the four things you need to be thinking about addressing if you have patients with peripheral nerve injuries, and then be able to describe common rehab interventions in acute and subacute PNI. So pretty straightforward. All right. I'm going to start with a little anatomy. Again, a lot of this stuff's going to be familiar to you guys, so I'm not going to dwell too heavily on this. You have the central nervous system, obviously brain and spinal cord, which then segues out into the peripheral nervous system, including cranial nerves, spinal nerves, and then the peripheral nerves heading out to the different systems within the body. You've got your motor efferent division exiting the spinal cord, going out to your end organs, including muscle, obviously. That includes the autonomic nervous system, the efferent system, as well as somatic nervous system. You then have your efferent sensory division going back to the central nervous system, and sympathetic divisions and parasympathetic divisions. Again, very, very basic anatomy for you guys. Nothing too crazy here yet. Oops. Back up a slide. There we go. Nerves are, again, pretty straightforward organs, when you think about it. You have your nerve. Now, within the nerve, you've got your individual fascicles with your axons. You have the endoneurium around axons. You have the peroneurium around the individual fascicles, and then the epineurium around the nerve itself. When you think about nerve conduction, we always think about the nodes of Ranvier and myelination. Obviously, the nodes are involved in saltatory conduction, which is something we learned way, way back in undergrad about how the arrangement of the nodes allows for faster conduction down the nerve axon itself. Myelination is important for nerve conduction, as is that internodal distance between the different nodes. That can alter. That does alter with nerve regeneration. You've got your ion channels, obviously, based on sodium, potassium, and chloride. Again, nothing new here. Just kind of a quick review on the importance of some of the structures in the nerve. So pathology, let's get into, I think, more of the meat of the talk here. The pathology, when you think about nerve injuries, there are really a couple different mechanisms. You have traumatic injury, which includes sharp lacerations like knife cuts. You do pediatrics enough, you're going to see enough kids putting their hand through glass windows or glass tables. Blunt lacerations from things such as gunshot wounds or trauma. You have crush injuries, and then stretching and traction injuries, which I think the most common example of that is going to be Erb's palsy or neonatal brachial plexopathies. Klumke's palsy is also a stretch traction injury. We don't see a ton of that in pediatrics, obviously. That's more on the adult side. I can count on one hand, pardon the pun, how many Klumke's cases I've seen, how many lower trunk injuries I've seen in isolation. Ischemic injuries certainly are not uncommon. Most commonly see that with compression injuries, such as compartment syndrome, soft tissue hematomas, and then nerve entrapments. You can also have tourniquet and stricture-based injuries, but the general classifications are going to be traumatic and or ischemic. You can have combinations of these two. What does the nerve do? How do I look at it and classify it in terms of its reaction to injury? I want to know if that's going to be a reversible lesion or an irreversible lesion. That's kind of number one. Reversible lesions are those that are just that. They're reversible. You can have recovery to some extent. Within that category, you've got ischemic-induced conduction block, which is the common neuropraxic type of injury, which I think we're all familiar with. You have compression of the nerve or minimal traction on the nerve. You can have ischemic effect, which affects axonoplasmic transport and creates abnormal ion channel function. Subsequently, what you get is a lack of saltatory or non-saltatory conduction down that axon. This is temporary and reversible. Very simple neuropraxic injuries are resolved within minutes to hours. Common type of thing is when you're sitting cross-legged and your foot falls asleep. That's a simple neuropraxic injury. We do see this in the OR as well for shoulder positioning. I've seen a number of kids come out of the operating room and they've had a weak extremity secondary to neuropraxia due to positioning in the OR. It's not that uncommon. You can also have prolonged pressure on the nerve, inducing true conduction block with focal demyelination. This is a longer-standing compression type of injury. We see this in minor crush injuries, heavier traction-based injuries, where you actually have myelin sheath degeneration. With that degeneration, you have a conduction block at that point in the nerve, and of course it takes that process of remyelination occurring for that nerve to start conducting fully again. This can last for days to weeks. This is, in fact, the most common type of neonatal plexopathy that we see accounting for probably 70% of neonatal plexopathies are this, stronger, more pronounced neuropraxic type of injury. Now, there's no damage to the epineurium, endoneurium, perineurium, or the axon of these injuries. It's purely a myelin issue. Non-reversible injuries are those where you actually now have some damage to the structures around the nerve. It's affecting the axon, myelin, endoneurium, the perineurium, and the epineurium to varying degrees. You actually have damage to the supporting structures, not just the myelin. These are secondary to crush injuries, traction injuries, laceration injuries. Examples include gunshot wounds, knife lacerations, more severe neonatal plexus traction injuries, and so on. With non-reversible injuries, there typically is an element of valerian degeneration. This is secondary to axonal injury that's typically part of these injuries. With valerian degeneration, as most of you will remember, you have degeneration of the axon and myelin distal to the site of the injury, including disintegration of the cytoskeleton and axoplasm distal to that injury site. What happens typically is the intact Schwann cells and macrophages will begin clearing that myelin debris within about three to four days post-injury. That clearance is complete after about 14 days. Interestingly, you can have nerve conduction still intact distal to that injury site for about the first three to five days. Once that clearance has occurred, you're going to lose conduction. Common mistake that's made is doing an EMG immediately post-injury for nerve conduction study immediately post-injury looking for nerve conduction across the site or distal to the site. You're going to see it. You're going to see it. Again, I think one of the common principles for EMG, at least that I learned when I was learning EMG, is the longer you wait, the better the result. Same thing with these. We want to wait a few days post-injury before we do a nerve conduction study. We do like to classify things. I think common in medicine is classification. We like to classify things. For some reason, our animals like classification, like things tucked in neat little nutshells. The two most common classification systems you're going to see in peripheral nerve injury are the SEDEN classification or the Sunderland classification. They're very similar to each other. They're both based upon the affected structures within the nerve itself, and basically it breaks down. SEDEN classification is more of a descriptor, including neuropraxia, axonotmatic, and neurotimatic injuries. Sunderland is more of a scale score that takes into account the degree of axonotmatic injury. As such, basically they break down as follows. Neuropraxia, as I mentioned before, is simply a conduction block where the affected structure is just the myelin. Second level of injury, Sunderland II and SEDEN classification axonotmatic injury is where the axon is now damaged, but you've got intact endoderm. Axonotmatic or Sunderland classification III is where the axon and the endoderm are now damaged, but you've got intact perineurium. Sunderland IV, axonotmatic, is where you have damage beyond that. You've got axon and endoderm and now perineurium damaged, but the epineurium is intact. And then, of course, neurotimatic injuries or Sunderland classification V is where the entire nerve is completely transected, so the entire structure is now damaged and transected. These are the most severe types of injuries, obviously, and if you do brachial plexus work, you certainly have seen many of those cases where a complete nerve transection has occurred. So you've got the damaged nerve. We've classified it. What happens with regeneration? Well, regeneration begins almost immediately following the injury, and interestingly, multiple levels are involved. It's not just at the site of injury, distal. So it affects the distal axon. The proximal axon undergoes changes, as does the neuron cell body, and, of course, the end organ undergoes changes too, right? Cascade of events, and this is rather interesting, includes increased synthesis of cell surface adhesion molecules almost immediately by the Schwann cells. The Schwann cells also begin producing neurotrophic factors, and the Schwann cells will begin to divide and increase their pool of de-differentiated daughter cells. So they're going to expand their pool of Schwann cells to begin the regenerative process, and with this comes up-regulation and expression of nerve growth factor. So you've got things in play almost immediately beginning to set the stage for nerve regeneration. Macrophages also increase at the site of injury, as I mentioned previously, and the macrophages will up-regulate interleukin 1. This subsequently induces more transcription of nerve growth factor and actually triggers Schwann cell proliferation. So you get into this cycle of Schwann cell proliferation, macrophages come in, macrophages are going to trigger that Schwann cell proliferation. Both are going to lead to increased nerve growth factor transcription. Interestingly, the nerve cell body also becomes involved and will begin expressing growth-associated factors such as GAP43 almost immediately, and then that's associated with up-regulation of genes that are associated with axonal regeneration. So again, there's this cascade of events that occurs almost immediately following injury, leading to nerve regeneration, setting the stage for regeneration. So the proximal nerve stump, the ending, you'll actually begin to see axonal sprouting, or these regenerative units, almost immediately. This occurs within days of the injury. And they'll have growth cones at the tip of each regenerating axon, and then there's a guided interaction with the distal stump. So the distal remaining portion of that transected nerve or damaged nerve will actually target, in a way, these growth cones. So it is a guided regeneration, which is quite fascinating. We do know that operatively, if you take a transected nerve and you do grafting on that nerve, the sooner you do the grafting of that nerve, the more accurate you're going to get that motor mapping to occur, and the more accurately you can get those nerves to connect back to the distal segments. So again, we sort of take advantage of this guided interaction, this sort of targeted regeneration, if we can. As you all know, rate of axonal regeneration is about a millimeter per day of average growth. It occurs a little bit faster in younger patients and in proximal lesions, and it occurs slower in surgically repaired lesions. Affecting successive nerve regeneration include end-organ changes, so muscle fiber atrophy. You got to have an end-organ to re-innervate if you want full nerve regeneration to occur. We see neuromas develop at the injury site, and of course, scar tissue and neuromas can prohibit axonal regeneration and axonal targeting of that distal segment. And then we can have axonal misdirection and pathfinding areas, so you have abnormal re-innervation occurring. I think the most common thing we see in that most common example is synkinesis. And if you do brachial plexus work, you've undoubtedly seen co-contraction phenomenon in our brachial plexus injury population, where the kids will go, when they go to move the joint, say bend the elbow, not only does the bicep contract, but the tricep contracts as well. We tend to see that in the axilla, when the kids go to abduct the shoulder, the muscles of abduction contract, but the peris and latissimus also contract, so you don't get that decoupling of the agonist-antagonist across the joint, you actually get a coupling of contraction. Some people think that that is secondary to aberrant re-innervation and sort of these axonal misdirections. I don't know that that's necessarily true. I think there are some, I think, some misconceptions with that. The biggest reason is because we can put Botox in this type of co-contraction and see changes almost immediately post-injection. If it were aberrant re-innervation, I don't think we'd be seeing changes in Botox almost immediately. So it's an interesting phenomenon. This young man, one of my former brachial plexus injury patients, you can see some co-contraction as he begins to abduct the shoulders about 90 degrees. As he begins to go a little bit higher, you can see muscles contracting around the scapula. He had a very common type of co-contraction phenomenon that we see in brachial plexus. Again, is it misdirected or misguided reinnervation? Nobody really knows at this point. So we do think about these types of things, though, in regeneration. We do think about these things and what's going on and try to take advantage of them. So the assessment, what do we do when we get called to see a peripheral nerve injury? What are the types of things we need to be thinking about? The assessment's actually pretty straightforward, I think, as most of you guys would know. First thing we want to know is the level of injury. Is this a root-level injury? What's causing the weakness in the upper extremities? Is it a root-level injury, root-level problem? Is it a proximal peripheral nerve? Is it a cord? Is it a division? Is it a terminal branch of a peripheral nerve? Exactly where is the issue at hand? You can generally tease that out through strength testing, through sensory testing, and understanding peripheral nerve anatomy. You can generally figure out the level of injury. I think that's something that struck me back in medical school, the beauty of neuroanatomy, neurologic examinations. It truly is an examination where you can pinpoint the level of lesion pretty accurately, whether you're looking at a cord-level lesion, peripheral nerve-based lesion, brain-associated lesion. You can usually tease it out based upon the symptoms you're seeing in the physical exam findings. We do the same thing here. You're going to test sensation, proprioception, vibratory sensation, tactile sensation, including pressure, stereognosis if needed. We check range of motion. I want to know what my passive range of motion is like. I want to know what my active range of motion is like because I need to know what that joint is going to look like that I'm trying to affect function on following regeneration, following rehab, and then of course strength testing as I mentioned. So full physical examination trying to pinpoint the level of lesion and what that extremity looks like. The role of EMG. Obviously EMG plays a role in this. Again this is not news to you guys. We do the two-part study including the nerve conduction and the EMG portion, the needle portion. Nerve conduction assesses axonal and myelin integrity. Again nothing new to you all. And then EMG, the needle portion, assesses stability of the muscle membrane and nerve innervation. You can also assess nerve regeneration using EMG by looking for nascent motor units. I found this to be really really handy and it's about the only time I really use EMG in peripheral nerve recovery assessment and in brachial plexus injuries. I used to do EMG a lot in my neonatal plexopathies, a lot less so these days. The only time I use it and I found it to be really handy is if I have a kid who I think should be continuing to regenerate, say six months old, and that child has plateaued in their recovery way before I think they should be plateauing in their recovery. The EMG can be fairly handy at that point to see whether or not you've got ongoing reinnervation by looking for these nascent motor units. So it's a nice way to assess and it's a nice way to track ongoing recovery if you've got an injury that you're not quite sure what's going on. So I found it useful in that regard for my BPI population. And then obviously nerves reach developmental maturation by five years of age. I'm not going to say that'll show up on any future examinations, but it's a fun fact to know. There are some caveats. In nerve trauma with axonal loss, it can take up to three weeks for evidence of denervation to appear on EMG. So positive sharp waves, fibs, things like that, it may take a few weeks before you see those. As I mentioned earlier, it can take three to five days for evidence of distal axonal loss or degeneration to show up on nerve conduction studies. So we don't want to jump in too quickly with EMG or nerve conduction study for a couple of reasons. Normative values for nerve conduction studies in EMG vary by age. Again, as you all are aware, as I just mentioned, nerves don't reach really physiologic maturation until about five years of age. So we do use normative data tables for kids less than five for these things. And then you got to have access to nerves you want to stimulate and muscles you want to put a needle in. That can be tricky. If you've got a kid up in the trauma unit who has, say, compartment syndrome and they're asking about whether or not the nerve has been damaged, yeah, sometimes you can do needle EMG, sometimes you can do nerve conduction studies, sometimes you can't, sometimes you just have to wait to do these things. So you really have to base it on the patient. And the old caveat, the longer you wait to test, the fuller the picture is very, very true with peripheral nerve. Okay, so that kind of gets through some of the basics of injury, of regeneration, ways to think about those two things, classification systems, and then assessment. So let's get into the real crux of the talk, which is rehab management and how we want to think about these things if we get consulted into the trauma unit to assess for peripheral nerve injury and to begin help managing that patient, how you want to assess the patients on the outpatient side who are coming to see you post-operatively, and so on. So, you know, the old adage for us, I think, in physiatry is, you know, we can assist in the diagnosis and conservative acute management of these injuries regardless of the cause. We can manage these folks longitudinally, and that's true of any condition we see, right? You can have anything walk into your office or your outpatient clinic. You may have never heard of the diagnosis before, but we can assist in that, you know? We've got a toolkit we can use to assess the degree of injury or impairment. We know what to do with those. Same thing holds for this. We want to focus on function. That's always the crux, and as you guys know, function is the ability to perform tasks necessary for daily living, leisure activities, vocational pursuits, and social interaction. So, that always becomes our function. Even in these types of injuries, we think about function, particularly in regards to incomplete regeneration, incomplete re-innervation, which, again, sort of the example I think we know well in pediatrics is brachial plexus injuries. Many of those kids don't get full re-innervation or regeneration are left with pretty significant impairments and disabilities. Okay, we can't fix that, but we can change function, and there are things we can do to affect function. So, we always think functionally as physiatrists. There are four areas and major roadblocks to functional recovery that we need to overcome with peripheral nerve injuries, including neuropathic pain, weakness, and distal muscle atrophy, joint contractures, and then sensory changes. And really, I've always kind of looked at this as that, you know, nerve regeneration won't matter if we don't think about these things and we don't have functional recovery. And these can all be addressed, and these can all be minimized in terms of their impact on recovery of early intervention. It's always harder to come from behind the aid ball than to be in front of it. So, pain management, we'll talk about that first. And again, I think this is going to be pretty common knowledge for most of you guys. So, you've got a kid who's had a peripheral nerve injury. They've perhaps had some trauma to the extremity, and they're having pain complaints. Well, obviously, we need to differentiate what's the generator of that pain. Is it soft tissue injury? Is it post-operative pain? Is it trauma-related otherwise? Or is it neuropathic? Is it secondary to the nerve? Well, neuropathic pain is the characteristic presentation, burning, crushing, electrical, shooting along the nerve distribution. Kids will many times have dysesthesia, hypersensitive skin. The types of common things that you think about with neuropathic pain holds true for peripheral nerve injuries as well. And we know the causes of this. You know, there are changes in the primary afferent nerve at the site of injury. We have sodium channel expression being increased. There's increased membrane excitability, decreased depolarization thresholds, and sensitization as well. I think the common mistake that's made with neuropathic pain is that opioids and NSAIDs generally aren't going to be a benefit to this. I can't tell you how many kids I've seen in clinic who've come in with peripheral nerve injuries, and they're on opioids, or they have neuropathic pain for other reasons, and they're on opioids, or they're trying NSAIDs. Doc has given them codeine, stuff like that. And of course, it doesn't help, right? So, it really behooves us to understand what the pain generator is before we know how to treat it. The neuropathic pain in PNI will present with your typical types of things. You know, the way I've always approached this is pharmacologic treatment is not a bad thing. Gabapentin is typically my first line choice. It's not very expensive. It's generally pretty well tolerated in terms of the side effect profile, particularly if you begin lower dosing. Pregabalin is much more expensive. Do I like Lyrica better than Gabapentin, or do I like Pregabalin better than Gabapentin? Yeah, I do. I think it works a little bit better with a little bit less side effect profile, perhaps, but it, again, is more expensive. So, I always try Gabapentin first. Other medications include the tricyclic antidepressants, things like tramadol, topical lidocaine patches can be of benefit, topical capsaicin cream. I've utilized that in patients before to apply over those areas of dysesthesia, and those things can sometimes help. And then there's some literature suggesting botulinum toxin injections can help. I've never done that for neuropathic pain, but there is some literature supporting that. Some people do do that. Don't even ask me how to use that for this. I don't know. It's not something I do. Non-pharmacologic interventions can include TENS units. There's questionable evidence that that helps with neuropathic pain. The nice thing about it, though, is it's a non-pharmacologic intervention. It's pretty cheap. The kids can use it as much as they want. It doesn't interfere with other things you may be wanting to do with that nerve. TENS units, it's worth a try, potentially. Again, I think there's some conflicting data, and you may not get the benefit you want, but it's one of those things that really, I think, truly is no harm, no foul. Typical approaches to neuropathic pain that you do with other types of neuropathies and painful nerve conditions. We want to promote strength and muscle preservation. We're controlling pain. You can't really work the extremity until you control pain. It can be hard to do. Once we've got pain under a little bit better control, we can start doing things. This is the next step, promotion of strength and muscle preservation. That includes passive muscle stretching and mechanical loading, as well as progressive strengthening activities. Interestingly, when you passively stretch a muscle, there are things occurring at that muscle, including upregulation of signaling pathways, leading to gene expression that will help with sarcomere growth. You get increased production of actin and myosin. We do know that muscle loading leads to increased cross-sectional area in the muscle. We want to begin muscle stretching as soon as possible and as soon as tolerated. We want to begin mechanically loading that muscle for various reasons. Progressive strengthening activity, once you get some activation in the muscle occurring, we want to take advantage of that. We want to begin progressive strengthening activities. Again, understanding that if we can load that muscle, we're going to be better off in the end. As reinnervation occurs, we get going with our anti-gravity plane progression, working on strengthening that muscle the best we can with gravity eliminated. Then we can go against gravity and begin adding resistance. Closed kinetic chain activities then play a role. Then we progress to open chain activity. We go closed chain to open chain for the simple reason that closed chain is much easier to control. It takes a little bit less motor coordination to do that, so you can really isolate muscles very easily with closed chain strengthening activities. Then we go to open chain strengthening, where you're actually bringing more muscles into play. It's on a less stable platform. It takes a little bit more coordination to do, so closed kinetic chain progressing to open kinetic chain. Then concentric versus eccentric. Concentric contractions, as you guys know, are a little bit more energy-sparing than eccentric, a little bit easier on muscle eccentric strengthening activity. Passive muscle stretching, we're going to begin loading that muscle very early. Then we're going to begin with active strengthening once that muscle starts firing. Don't wait for that muscle to fire. We want to be stretching that muscle. We want to be loading it as we can. Things such as NMES, neuromuscular electrical stimulation, certainly can be employed. There is some evidence suggesting that NMES can lead to increased innervation in motor units following nerve transection repair. There's actually some really interesting research out there now about utilization of electrical stimulation of the nerve in the OR immediately following nerve grafting. Some pretty compelling evidence showing that that leads to better outcomes if you do short interventions in the OR the day of grafting. Really, really interesting stuff. I've always been a big fan of electrical stimulation to nerves in nerve injury. I think there was some early debate when I started my practice 20, 30 years ago with people a little bit hesitant to utilize it, but you can. There's some really, really good basic evidence that electrical stimulations and electrical gradients actually are beneficial for nerve regeneration. Functional electrical stimulation, we all know about, we all utilize that. You can utilize it in these injuries as well if you've got multiple nerves involved, if you've got lesions at the plexus level involved, whether it's lumbosacral plexus or brachial plexus, you can certainly employ functional e-stim in these patients as well. You get these patterned movements, these patterned functional movements going. There's no harm utilizing FES. Typical FES setup for the lower extremity. Again, this should be very familiar to you guys. Above and beyond pain management, strength and management, we want to work on contractures. We want to prevent contractures because your active range of motion is only as good as your passive range of motion. I think that's an important thing to remember. You've got to have the passive range if you ever want to have the active range. Let's prevent contractures. Contractures are simple lack of full passive range of motion due to joint, muscle, or soft tissue limitations. Connective tissue limitations. That can be tendon, that can be muscle, and that can be capsular. The trick to contractures, as you guys know, is once you have a contracture, it can be awfully difficult to get that stretched out again. It's easier to prevent these things. The factors that lead to contractures are weakness and inability to achieve active joint movement, so immobilization. The number one cause for joint contractures is immobilization. If we're moving that joint either actively or passively, we're going to prevent contracture. As I just mentioned, the problem with contractures is those are going to inhibit your available active range of movement once motor recovery occurs. If we think about motor recovery and nerve regeneration patterns, we do know that it takes about a year and a half for that nerve to regenerate, reconnect to that muscle, that motor unit to mature, and then the cortex to mature. That entire motor pathway has to mature. That can take up to about a year and a half. We want to be maintaining range of motion as much as possible during that time frame. Again, as you guys know, contractures can inhibit functional positions in the extremities. We need to think about these things functionally as well. If we have a contracture developing, how is that going to affect function ultimately for this patient? What are the planes of motion I want to really prevent contractures in if I really want to try to maximize function? you think about the muscle, there is connective tissue around the muscle, as we all know, paramecium, endomecium, epimecium, very similar to nerves, in fact, you have these different layers of connective tissue around the muscle, and the collagen fibers typically are oriented in parallel to the muscle itself, and that makes sense in tractile tissue, so they're typically in parallel to the muscle fibers themselves, again, another breakdown of the anatomy of the muscle, and the different layers of connective tissue around that muscle, again, the important thing is to understand these connective tissue layers, the collagen fibers in these layers are in parallel to the muscle fiber itself, it's important to know for a couple of reasons, well, if you immobilize soft tissues, what happens? Well, your muscle will shorten if it's immobilized in a shortened position, right? If it's mobilized in a lengthened position, that can actually help with sarcomere gain, that's been demonstrated, so we want to immobilize a joint, we want that joint all the way out at full length when we immobilize it, okay, if we're going to immobilize that for recovery purposes from the original injury, I think that's the most common reason a joint gets mobilized following a peripheral nerve injury, so if at all possible, we want that muscle at length if the surgeons are going to mobilize the joint. Mobilized muscles in shortened positions actually lead to sarcomere loss, so we want sarcomere gain, we don't want sarcomere loss, we want that muscle as healthy as possible, so mobilize it in the lengthened position. Connective tissue, if it's immobilized, it'll lose its intrinsic extensibility and elasticity, and the main reason we see that is because we begin to develop abnormal cross-linking between these collagen fibers, so instead of having nice parallel collagen fibers and parallel muscle, the cross-linking in the fibers become a little bit more disorganized, and you can imagine what that would look like if they're in parallel and how that would help with contractility. If these things are disorganized, they're not going to lengthen quite as easily, so you have loss of that extensibility in connective tissue. You also get connective tissue accumulation, which is never a good thing, so there are reasons we want that muscle lengthened out, there are reasons we want that muscle immobilized for as limited time period as possible. Prevention on the acute care side of contractures obviously includes passive range of motion and stretching, item number one, that makes sense, right? Interestingly, there is some literature suggesting there's questionable benefit about episodic stretching, okay, but it makes sense to us, it's easy to do too, so we have the therapists go up to the unit, they stretch the joints, you know, they'll go up for their 30-minute session, they'll stretch the patient's joints, then they're done. What we do know and what's been demonstrated is that stretching for greater than 30 minutes per day prevents sarcomere loss, so that loading for greater than 30 minutes a day is benefit. Stretching less than 30 minutes a day, there's more question, there's a real benefit of that, so we shoot for that 30-minute per day stretch across that joint. Can we truly obtain that with the therapists going to the floor and stretching or parents stretching a joint for 15 minutes a day? Maybe not, we need to be aware of that concept. Sustained stretching for greater than 50 minutes can help preserve connective tissue chain or prevent connective tissue changes, the abnormal changes we just talked about, so sustained stretching is better than short duration stretching, so we think about that, if we have a joint we really, really want to prevent contractures on, maybe sustained stretching is the way to go, right, so static splinting might be what you really want in conjunction with just passive limb motion, so never forget that sort of static splinting concept. Static splinting at length, what does that do? Well, we know that leads to increased sarcomere production, decreased fibrosis, again, we're actually loading that muscle, right, if we've got a joint, we've got a contraction, we put some general tension on that, across that, across that joint, and we splint them in that slightly tensioned position, that's loading the muscle, so you're going to get benefit with that loading in the muscles we've talked about. Typical applications for schedules for applying static splinting, you know, the common two hours off is very easy to achieve, particularly on the inpatient side, I'm a big fan of nighttime splinting if I can do it and if the kids will tolerate it, which generally they do, I'm a big fan of nighttime splinting for contracted joints, whether it's a heel cord or an elbow or a shoulder joint, I think it's a great time to use static splinting if the kids can tolerate it overnight, again, most do, it allows for that prolonged treatment time at nighttime, it's just a really, really nice way to do this, so static splinting at length, don't forget that concept if you've got a contraction, apply that when you can. The other thing we need to think about too is when we remove that splint, what's happening here when we place that splint, what's happening around the antagonist muscle, okay, we've talked so much about stretching the contracted muscle, we can't forget the antagonist, we've talked a lot about loading muscles, right, so we can't forget about the antagonist, we need to stretch the antagonist and we need to load those antagonists as well because they're being immobilized also, when we immobilize the joint, we want to immobilize and stretch, you know, those muscles are being immobilized as well, so we can't forget about taking care of the antagonist muscles, we want to prevent shortening, we want to prevent loss of sarcomeres in that muscle as well. So, same concept, static splinting at length, we always want to think about placing those joints in position of function and length to get that load, so positions of function include extension of the fingers at the MCP, PIP and DIP, we want to keep the wrist in a functionally extended position if possible, feet and ankles, you know, you want to splint them neutral to end of the range dorsiflexion if at all possible, trying to preserve functional positioning, so again, don't forget about function when you're splinting something. We want that splint to have full contact with the skin as well, you don't want pressure points appearing, that's going to lead to decreased tolerance and you're risking the skin for breakdown from pressure. Therapists, as many of you know and probably everybody here knows, you can use this thermoregulator Therapists, as many of you know and probably everybody here knows, you can use this thermoresponsive or thermoplastic which they can heat up and remold. I'm a huge fan of those because I think they allow you for changing the position of that joint as you're making gain, so I'm a big fan of thermoplasts to really, really be able to do progressive stretching across the joint and then, of course, you want to do skin checks and teach the parents how to do skin checks whenever they're taking splints off from overnight or during daytime if they're on a two-hour, two-off schedule for their static splint. A couple of examples of some very, very common splints, I think the example here, the nice thing about these examples is it's a functional hand position they've got, the wrist is in functional extension of about 30 to 40 degrees, the thumb is in opposition to the fingers and the fingers are in a nice neutral functional position with extension at all joints. We also, in the subacute period, if you've got contractors that have not responded or contractors that over time are actually getting worse, I'm a big fan of dynamic splinting across joints. What the dynamic splinting does, it allows continuous, it's basically a loaded hinge at the joint, so it's a spring-loaded or tension-loaded hinge at the joint and it allows for continuous stretch torque through those spring mechanisms or tensioning mechanisms. We also do this across the ankles at nighttime with things such as nighttime lively splints where you've got Velcro attached at the forefoot of the footplate and then the straps go all the way up to the top of the posterior calf shell, so you can apply tension across the ankle at nighttime. That's a form of dynamic splinting, so you're providing that continuous torque across the joint. These are really, really good at accommodating for that connective tissue creep, those connective tissue changes that I talked about earlier and have been shown to be effective in reducing subacute and chronic contractures. A number of the companies out there that make dynamic splints have these for multiple joints now, so you can get them for just about every time, so they're very easy to apply and they're out there. There is some evidence suggesting the utilization of neuromuscular e-stim plus dynamic splinting in a combined approach can be beneficial to reduce contractures. I've done that with patients in the past where we're providing NMES to strengthen muscles and you're doing dynamic splinting between the NMES sessions, so again, it's possible to combine different interventions here to improve function. Then finally, we want to promote sensory motor recovery as well, so we look for restoration of sensory function. We've addressed pain earlier, we want to prevent allodynia, but sensory function is so critical to movement. I think I probably say that way too much to my fellows in my residence in the EPI clinic, but we have to focus on the sensory components of movement as well, not just the motor aspects of movement. We apply sensory cues to stimulate various receptors, including proprioception. Proprioceptors function, they run through the motor nerve. Proprioceptors run along the nerve with the motor nerves, so if you've got motor nerve damage, you're going to have proprioceptive damage. If you've got peripheral nerve damage, you're going to have proprioceptive damage, you can have sensory damage. We provide proprioceptive input, we provide tactile stimulation, we want normalization of sensory processing. It's so important in ultimate function in these patients. We can use contrasting textures as well, things that y'all should be very familiar with. I think the most common example and probably the biggest example that I talk about, this is with brachial plexus injuries again, it's such a nice model. One of the things we think about in BPI is what I call developmental facilitation. Basically, you're affecting the sensory motor pathways. You think about a two-month-old baby is able to get hands to midline, right? Normal activity, hands to midline, normal developmental sequence at about two to three months. If the infant can't bring the affected extremity up to midline, I want the parents to place it there. I want the child to begin understanding, I want the brain to begin understanding where that arm should be in space, where it should be in function. There are multiple examples of that following brachial plexus injuries where we build in these concepts of developmental positioning and developmental use of that extremity. We can't forget about that. Even in peripheral nerve injuries from acquired trauma in older kids, the same concepts hold. We want to affect proprioception, we want to affect positioning, we want to affect sensory feedback in that extremity if we want to reach ultimate functional gain. Don't forget that part of it. In summary, rehab approaches are based on addressing and facilitating functional recovery through addressing these four major areas or four major aspects of nerve recovery. We've got to address pain, we want to focus on muscle and strength recovery, we want to affect contractures and reduce those as much as possible to allow functional movement patterns and functional range of motion, and then you've got to address sensory recovery to enhance environmental interactions and sensory motor control. A lot to think about with simple injuries, and it gets even more complex in developing organisms such as neonates. It really is a very, very interesting area when you get down to what's really going on and the things we need to think about managing. I think that's all I've got. If you all have any questions, I don't even know what time it is right now. It's about 10 minutes. I can certainly answer questions. I'm certainly happy to answer questions from email. As Megan said, she can certainly forward questions to me and whatnot. Perfect. That was awesome. Thank you so much, Dr. Rinaldi. Great overview. We actually do have a question already. Dr. Wen was wondering, I'm curious about the use of Botox and neuropathic pain in peripheral nerve injury. Have you tried it? I'd be worried about worsening weakness versus slowing nerve recovery, but if it's helpful, could it prevent CRPS? So many questions. I've never tried it. Yeah, I've never tried it for just those reasons. To me, it doesn't make a lot of sense. The last thing I want to do is denervate a muscle. I'm trying to reinnervate, right? It doesn't make sense. That said, I've never really investigated the use of it. I'm not sure how people are doing those injections. I've not really dug deep enough into it to really know, but no, I certainly have not tried it. It doesn't make a lot of sense to me. Okay, great question. I know there's a handful of folks on, so if anyone does have other questions, you can either put them in the chat box or you can put them in the Q&A box here, and we'll kind of wait and see if there's anything. I'll throw a question in while we're waiting too. In terms of use of e-STEM, have you seen many complications like myositis, osteopagans, anything like that in your practice? Okay. I have not. No, I've not seen that. It's a great question. Certainly something to be concerned about, and certainly something to monitor, but I have not seen that. Even in the kids, we've been fairly aggressive with NMES on not seeing it. I've seen it recently. That's why I wrote up, but yeah, in an adolescent with SCI. Yeah, which just brings up an interesting question and put us in a conundrum of, they want to continue it, and what do we do? I was interested to see if you had any thoughts on that. Yeah, no, I've not seen it. I know we use it. Again, my largest population has been BPI, and we use it pretty aggressively in our BPI populations. I have for a couple decades. God, I'm that old. A couple decades now. Sounds horrible. I've been using it for quite a while, and I've not seen that in that population. No. Yeah, which I guess SCI is definitely a different population there, so yeah, it makes sense. Awesome. Okay, it looks like we have a question in the chat box, so Dr. Morton, are there any exclusion criteria populations that you would avoid eSTEM in? I avoid it. Osteopenia, I'm not a huge fan of it because of the risk for fractures. You're putting a pretty strong contraction in place. Now, you can modulate that to some degree, but I'm pretty hesitant if I've got osteopenic bone, recent fractures. I'm not going to be using it. If I've got a recent yield fracture, I'm not going to use it, so I worry about the bone as my primary concern. Other things, there's some talk about not providing electrical currents over things such as pacemakers, over BNS, things like that, so we avoid those areas. If I'm using any type of eSTEM, I avoid those areas where there may be other circuits in proximity to what I'm doing. Those would be the main things I'd be concerned about. I'm not seeing any cutaneous complications or secondary effects, side effects from utilizing it. It's pretty well tolerated otherwise. If you've got contracted joints and you're providing eSTEM into muscles that cross contracted joints or they're contracted, probably want to decrease the intensity of the contraction. Again, you don't really want to cause any damage to the tendon or the muscle. Probably a slightly higher risk of that if you've got a muscle that's contracted, but otherwise, no. Awesome. All right. Well, it looks like that might be... Oh, yeah. I always say that and then someone puts a question in, so I'm just looking, but it looks like that might be the questions that we have for today. It was awesome hearing you talk and we really appreciate it. Dr. Rinaldi, we're lucky that Dr. Rinaldi is going to be back next month to talk a little about wheelchair and seating evaluations as well, so we're really fortunate for that. For those of you who've listened today, you can get your CME credits through AAPMNR website and for folks listening, you can do that as well. Thank you, everyone. Thank you, Dr. Rinaldi, and hope everyone has a good day. Great. Thanks, guys. Take care. Bye.

peripheral nerve injuries

rehabilitation management

neuropathic pain

joint contractures

sensory changes

pain management

muscle stretching

mechanical loading

sensory motor recovery