Our next speaker is Dr. Wilson. He is a graduate of the University of Nebraska School of Medicine and completed his residency in neurosurgery at the University of Michigan, as well as a fellowship in peripheral nerve surgery at the Mayo Clinic in Rochester. He is currently in practice at Stanford University, where he is clinical assistant professor of neurosurgery and co-director of the Center for Peripheral Nerve Surgery. His research focuses on ways to improve data-driven decision-making intraoperatively during peripheral nerve surgeries. He is very well-published, with over 75 articles in peer-reviewed literature and numerous book chapters. He actually spoke at our breakfast session last year and just got such rave reviews we wanted to invite him back again to talk about peripheral nerve, and in particular, how to get the most out of the testing that you'll get in the clinic. Thank you. Dr. Wilson. Well, good morning, everyone. So we're going to talk today about peripheral nerve diseases and some of the testing that you can get that can aid in diagnosis of a variety of different peripheral nerve pathologies, but I'm going to try to put it in the context of spine pathologies as well, because I think for probably the majority of people in the room, peripheral nerve disease is probably a very small portion of what you see, but thinking through spine versus peripheral nerve versus central etiologies is an important skill to have in thinking about that on the exam and the diagnostic testing that you can get. So that's going to be the goals for today. So I don't have any disclosures for this talk. So when we talk about testing for peripheral nerve disease, what I really mean by that is the physical examination and the history. That's probably the most important component of all of the testing that we get, particularly relevant for peripheral nerve disease. Now there's going to be some ancillary testing that we'll go through as well, but I think if we really get a lot out of talking about how we can hone in our physical exam and clinical history-taking skills, then we'll get a lot out of what we're talking about today. So the history and the physical are really the keys to the evaluation for the peripheral nerve patient, and electrodiagnostics and imaging really should be thought of as extensions of that rather than replacements. I think a lot of time we use our ancillary testing like EMG, MRI as a crutch when we're not doing a great peripheral nerve exam. And really, we need to think about using this as our primary means of making diagnoses. So at the end of the day, once we've taken a good history and physical, really the goals are to think about putting this into a category. So is this a mononeuropathy? Is this a plexopathy? Is it a radiculopathy? Or is this a myelopathy? Or I guess I should add maybe even other central nervous system pathologies to that list or musculoskeletal pathologies. Second, can we localize the lesion? Third, can we determine the severity of the lesion? Fourth, can we try to determine what's the likely cause or the likely diagnosis of the pathology that we're dealing with? And finally, can we put that all together to ultimately develop an appropriate diagnostic and or treatment plan? So understanding how to do a good peripheral nerve exam and take a good history for that matter really requires having a thorough knowledge of the peripheral nervous system. And so that involves thinking about sensory distributions of various peripheral nerves as they compare to the dermatomal distributions of nerve roots. And it also requires an understanding of what nerves innervate what muscles. And even more detailed than that, where those branches to each of the given muscles occur so that you can try to figure out where along the pathway a lesion or an injury might be. So as we think about the peripheral nerve history, and again relevant for spinal disease as well, there are a variety of things that we should try to elicit from patients as we take a good history. So what are the symptoms exactly? Is there pain? Are there sensory symptoms like paresthesias? Is there weakness? And what's the nature of the pain if it's present? Is it sharp, dull, electric, burning? Does it radiate to any particular distribution? All of these are going to be clues to what the source of the pain is because patients will use certain buzzwords when there is nerve type pain. They'll give you a clue as to what the distribution is if you really focus in on where the pain might be radiating to. And then finally, what is the distribution of those symptoms? Do the pain and sensory symptoms have a very discrete, defined border, or is it hazy? And what I mean by that is can the patient take one finger and draw you a line around where those symptoms are, or do they do kind of one of these? It's a little bit here and a little bit there. And that'll tell you a lot, and we'll come back to what that really means in a second. What is the chronology of the symptoms? So if there is pain, sensory, and weakness, what order did those symptoms come on in? Did they all come at the same time? Did one follow another? Again, that'll tell you a lot about what the diagnosis might be. Are there aggravating or alleviating factors? Was there a particular inciting event? Can the patient really pinpoint there was something that this was related to after which all of my symptoms started? For the purposes of treatment and diagnosis, whether the symptoms are improving, worsening, or staying the same is a really important feature. It's going to tell you a lot about how aggressive you need to be in working this up and managing it. Are there any nighttime symptoms? Have the patients had similar symptoms previously? Maybe the patient actually has had somebody else give them a diagnosis, and you can kind of hone in on these being similar symptoms to what they were diagnosed with previously. Are there any constitutional symptoms or skin findings? And then, have there been any interventions that have been tried, whether they've been successful or not? And then last, is there any family history of any peripheral nerve problems? This may clue you in on things like neurocutaneous disorders that may be the underlying issue in what they're presenting with. Are there any other medical issues that might be contributing to their overall pattern of symptoms? And then finally, is there any occupational hazards, like repetitive movements, maybe toxic exposures? Could be a wide variety of occupational issues that can contribute to peripheral nerve pathologies. So how do we put this then together? So what we should really do is use what we've garnered in the history in order to then perform a focused neurovascular exam. And I'd emphasize that this really is two different parts. There is a neurologic assessment, but a vascular assessment is also a very important component of the exam when it's done well. So if we've taken a good history, we really ought to be able to be pretty organized in the way that we do the exam. So we can think in terms of spinal nerve roots and peripheral nerves, and really always be asking ourselves, what muscles, reflexes, sensory distributions do I need to really localize this lesion? And again, we're clued in on that based on the history. So going through this a little bit step by step. So the first component, again, and I think often overlooked, is the vascular component of this exam. And this can really aid us in diagnosis. So for example, thoracic outlet syndrome, there is oftentimes prominent vascular features to that diagnosis. So we should be thinking about doing that exam. The vascular exam can definitely affect our surgical planning. So particularly for traumatic injuries, if we detect that there might be a vascular injury, that's going to be something that we're going to be well aware of before we go in and do an operation in that area and tread into a difficult vascular situation. So we may want to have our vascular surgery colleagues available. Or something as simple as, can I use a tourniquet during the operation? If there's vascular compromise, that may be something that you don't want to do. And then finally, the vascular exam may also inform you as far as what the surgical options are. So when we're thinking about things like a free muscle transfer for reconstruction after a nerve injury, we've got to have a good vascular supply to be able to plug that muscle into. And so understanding the vascular injuries that can be associated with nerve injuries is really important. So again, palpating, inspecting color, inspecting temperature, these are all kind of our basic maneuvers for doing the vascular exam. But we also might want to think about provocative maneuvers. So putting patients into positions of stress where it may compress the vasculature. So good examples are moving the arm through range of motion and palpating the pulses when there is stress onto the thoracic outlet, for example, where the vascular exam at baseline may be normal. But with provocative maneuvers, they may have drop out of those pulses. And that can clue you in as to where this may localize to. So once we've finished the vascular exam, there are several important components to then performing a good neurologic examination. And the first really is inspection. So one thing you'll notice is that this patient has their shirt off. I think that's a really important component to doing a good peripheral nerve exam is you really want to be able to see what you're examining. So you want to be able to see is there a flicker of muscle movement, for example. Or maybe something like atrophy. So there's a lot of atrophy here in the infraspinatus muscle. And that immediately clues you in on to what might be going on. Or are there signs of external trauma that may immediately put you into examining nerves and structures that are going to be localized here in the arm as opposed to up high in the brachial plexus. So use all of the external clues that you have to hone in what you're going to examine. Palpation can be an important part. So if you palpate nerves that you think might be involved in the disease process, you can sometimes pick up things like enlarged nerves. You can pick up masses. And palpating the mass can tell you a lot. Is it a mobile mass? Is it a firm mass? Is it very fixed? These are immediately going to help you to classify what this is likely to be. And again, give you a clue as far as how you should work this up additionally. And then for particular nerves, so the ulnar nerve, for example, if you're thinking this might be an ulnar neuropathy and you're considering an operation, you want to palpate that nerve through range of motion to see if there's subluxation. How does the nerve move over the top of the medial epicondyle? Because it may completely change what surgery you're going to offer this patient. So the classic neurologic exam, I think, is the motor exam. So that's what people really focus on. And most people, I think, probably do a pretty good general neurologic motor examination. But I'd argue that there really is an often overlooked but equally important component to the motor exam. And that's really the range of motion. And passive range of motion, in particular, is the part, I think, that we are not as good at remembering to do a good job of. And so things like orthopedic injuries or contractures, these things can be picked up by doing passive range of motion and can be mimickers of neurologic injuries in a way that we want to always be able to be thinking, could there be an orthopedic component to what we're seeing rather than a neurologic component? So once we've done passive range of motion, then we move on to our organized motor examination. And this is where I think we can really be organized about how we approach this. This is where we're really going to try to hone in and sort of cone in on what the diagnosis might be. And so I use an exam sheet like this. This is actually something that I picked up at the Mayo Clinic where it divides out all of the muscles. This is a brachial plexus exam sheet. But it divides out all the muscles of the upper extremity into their peripheral nerve innervation and their nerve root innervation. And it gives you a very organized way at performing the examination and thinking about, is this nerve root problem, is this peripheral nerve problem, and it keeps it really organized. So as part of the motor examination, sometimes you can pick up on very characteristic postures that are quickly going to give you an answer. So this is a patient who has a finger drop without a wrist drop. That's characteristic of a posterior interosseous nerve problem. So there are these buzzwords, if you see them in the literature, where there are characteristic exam findings or characteristic postures that might immediately show you, oh, that's probably what nerves involve. So this is an example of a patient that can't make the OK sign here on the left. They're doing more of a duck bill. And that's what's characteristic of an anterior interosseous nerve problem. So if you pick up on these kind of characteristic postures, you can really quickly have some information about what nerve is probably involved. The sensory examination. So this is where I think, if you do this, the most important thing to try to get out of this is, is there a fuzzy border versus a very discreet, sharp border where things turn from normal to abnormal? And I'll freely admit that I definitely do not do as good of a job of the sensory exam as a neurologist would, where they would test multiple modalities. They test vibration and pain and temperature. And I'll freely admit that I don't do that on a routine basis. But I think even as something as very rudimentary as doing a gross sensory exam, you can oftentimes very quickly pick up whether or not this is a very discreet border, like this border for the lateral femoric cutaneous nerve, where the patient can literally draw one finger around where the symptoms are. This is in the radicular patterns, where it tends to be much more fuzzy. The patient will kind of wave their hand over the top of what's abnormal. Provocative maneuvers. So depending on what you think the diagnosis might be, you may want to use a set of provocative maneuvers to try to bring out the exam findings. So these are all carpal tunnel provocative maneuvers. So this is the Tonell's test at the wrist. This is the Durkin compression test, and this is Phalen and reverse Phalens. Using your provocative maneuvers to try to really bring out their symptoms can clue you in as well onto the diagnosis, first of all, and then second, to the severity of the diagnosis. The Tonell's test can be used in a variety of locations. So this is a Tonell at the knee for the perineal nerve. But we also want to think about provocative maneuvers in the context of spine pathology. So if we're really trying to differentiate between peripheral nerve etiologies and spine pathologies, maybe we also want to use our spine provocative maneuvers, like Sperling's maneuver or the straight leg raise test. Reflexes. These are also going to help us clue in to whether or not we're dealing with a peripheral problem versus a central problem. So in addition to our traditional muscle stretch reflexes like the biceps reflex, we also want to do our upper motor neuron reflexes. So things like Babinski, test for clonus, or Hofmann's sign. And as we finish up the exam, what we really want to think about is, now can we put this into a category? So when we're thinking about peripheral problems as opposed to spinal cord or brain, then we're going to try to put this into a category of a peripheral neuropathy versus a radiculopathy. And there can be a few clues on your exam and your history that should help you kind of lump it into one of those categories. So peripheral neuropathies tend to have a very discrete sensory distribution. These are the ones where the patient can take one finger, draw it around the border. Muscle atrophy is also oftentimes, in more severe peripheral neuropathies, a prominent component. Usually, any given muscle is innervated by one peripheral nerve. And so if the nerve is densely affected, that usually will lead to atrophy of that muscle. When you compare that to radiculopathies, they often have a very fuzzy sensory distribution. So this is the hand-waving that patients will do. They'll give you a general sense of the distribution, but not necessarily be able to draw a discrete border. And most muscles are innervated by multiple nerve roots. And so unless multiple nerve roots are affected, usually muscle atrophy is not a prominent finding on the exam until late in the course of the disease, or if there's multiple nerve roots that are densely affected. So if you think about using those findings to differentiate between the two, it will quickly help you try to put it into one of the two categories, because then you can really hone in on what additional diagnostic steps do I need to do to firm up my diagnosis. And so ultimately, what we want to do is use our understanding of the peripheral nerve innervation, realizing that each peripheral nerve usually receives contributions from more than one spinal nerve root, and each spinal nerve root usually contributes to more than one peripheral nerve. So we've got to figure out how the pattern of weakness or sensation overlaps to put that into one category, one nerve or one nerve root, if we can, and then ultimately use that pattern of motor loss to differentiate. So let's do a few examples of how that might work out. So the first case, there's a 54-year-old right-handed female. She presents complaining of pain and paresthesias in her right hand, particularly in the first three digits of the hand. Occasionally there's pain that radiates from her hand towards her shoulder. It's been progressing over the last year. She has frequent nighttime awakening, and shaking her hand out seems to relieve those symptoms. She's had clumsiness of that hand over the same time course, and she works as a transcriptionist, and she's noted that she has progressive difficulty with typing with that hand, and no significant past medical history. So let's break this down just sort of one at a time. So if we think about the pattern that she described, digits 1 through 3 of her hand. So when we think about the sensory dermatomes for the nerve roots, they're variable. But most people would say that the thumb is C6. The second digit is probably usually C6, maybe C7. It's variably drawn. Usually the middle finger is always C7. But let's say that instead maybe her complaint was that it's the first two digits. Now we're not really sure where this is going to fall into. So could this be a C6 distribution problem? Could this be carpal tunnel? So let's look at how they compare. So for the distribution of C6, the distribution goes along the first and second digits and all the way up the arm about to the elbow for C6, as opposed to for the median nerve where it's the first three and a half digits and ends at the palm. So when we compare them, C6 stretches all the way up to the elbow. So even though they have somewhat overlapping distributions in the hand, one of the findings that may help us tease these two apart is, does the patient have symptoms that are proximal to the wrist crease? If so, we should immediately not be thinking that this is the median nerve that's involved. Carpal tunnel should not extend beyond the wrist crease. So this is, again, an example. This is the carpal tunnel distribution, again, showing that it stops at the wrist. Well, what if the sensory is somewhat fuzzy? What about our motor exam? Can we use our motor exam to try to tell the difference between C6 and median nerve? So the way we can think about this is, what muscles are C6 innervated but not median and vice versa? What muscles are median innervated but not C6? So the biceps is a good example. It is C6 innervated and musculocutaneous innervated as the nerve. So if we're thinking that this is going to be a C6 radiculopathy, we might think that the biceps is involved, as opposed to median nerve innervated muscles, which are not C6. So the abductor pollicis brevis and the opponent's pollicis in the hand are median muscles that are innervated by C8 and T1. So if we had a median nerve problem, we'd expect these to be weak but not the biceps. If we had a C6 problem, we'd expect the biceps to be weak but not these muscles. So we can use the patterns to try to tease this out. We can then also use our provocative maneuvers. So in a C6 radiculopathy, we would not expect any of the carpal tunnel maneuvers to be positive. So Tonell's sign, Dirken compression, Phalen, reverse Phalen. and then we can try to tease out the opposite. So is Sperling's maneuver positive, which might make us think that this is coming from the neck? So in this patient, she had decreased sensation in the first three digits, and on detailed testing, actually the radial half of digit four, she had no abnormal sensation beyond the wrist crease. Her biceps was normal. Abductor pollicis brevis and opponent's pollicis were affected. And all of the provocative maneuvers for carpal tunnel syndrome were positive with a negative Sperling. So when we put that together, we should be thinking this is carpal tunnel syndrome, median neuropathy at the wrist. So let's take a very similar, sorry, so how might you support your diagnosis? And I'm going to come back to this. So this is where we might use our ancillary tests. So how could we really try to add some legs to the stool for diagnosis to show, yes, this is carpal tunnel? Well, we could get an EMG. That may be helpful. Or we could get an ultrasound. We could ultrasound the median nerve at the wrist and see if there's enlargement of that nerve. And I'll come back to how we can use these tests. But let's take a very similar patient. So now we've got a 40-year-old right-handed man who presents with pain radiating from the neck to the first and second digit of the hand. So reasonably similar sensory distribution. Symptoms began a year ago without any inciting event and have been progressive. Does not feel as strong in the right arm as he used to. No nighttime awakening, no trauma history, no significant past medical history. So again, a relatively similar sensory pattern as we saw before. The first two digits are involved. So in this case, though, the sensation is grossly normal. The biceps are affected. The brachioradialis, which is another C6 innervated muscle, but innervated by the radial nerve, is also affected. And all of the median innervated muscles are normal. In this case, all of the provocative maneuvers for the carpal tunnel are negative. But there's a positive spurling radiating to this first and second digit as they described. So in this way, we've now taken a fairly similar initial complaint, radiation of pain into digits one and two, and we've teased out that this is probably not carpal tunnel, but is in fact probably a C6 radiculopathy. So that's our suspected diagnosis in this case. So if we wanted to add to that, how might we do that? Well, now we're thinking this is probably coming from the neck. So we may order a completely different set of diagnostic tests to support that diagnosis. So an MRI of the cervical spine is probably going to be your best diagnostic test. You may also consider an EMG or nerve conduction study to add to your support. So third case. So a 52-year-old female business executive presents with a foot drop. The foot drop began three months ago without any inciting event. It progressed over a month to be a very dense foot drop. She's been wearing an ankle foot orthosis for two months, and over that time has not seen any improvement. There's very mild pain and paresthesias radiating from the knee to the dorsal surface of the foot. No symptoms in the contralateral leg. She does have chronic low back pain that's relieved with over-the-counter pain medications, and no other significant past medical history. So when we think about foot drop, the two leading diagnoses should be L5 radiculopathy versus a perineal neuropathy. So how might we separate those two from each other? Well, you'll see in this case the sensory distributions for L5 coming down the leg onto the dorsum of the foot is very similar to that for the perineal nerve. So again, coming down the lateral aspect of the leg onto the dorsum of the foot. So your sensory distribution in this case is pretty similar. Going to be pretty hard to tell the difference between those two pathologies. So how might we use the motor examination? This is where we can do a good job of trying to tease out the two. And an often forgotten exam maneuver is inversion and eversion. So I think that that is one that we as neurosurgeons oftentimes don't use, as well as maybe we should. Because it can quickly help you try to differentiate between L5 and the perineal nerve. So the L5 nerve root contributes to dorsiflexion and inversion, whereas the perineal nerve contributes to dorsiflexion and eversion. So you could use that pattern to try to differentiate. So let's take, so and then we can also use some provocative maneuvers. So we could try doing a tunnel at the fibular tunnel to see if there is signs and symptoms of perineal compression. We could use a straight leg raise to see maybe is there signs that this is a radiculopathy. So in this case we can put this all together. So this patient again had decreased sensation on the dorsal surface of the foot. Not sure what to make of that. So let's move on to the motor exam. So dorsiflexion was zero. Extensor hallucis longus was zero. Eversion was zero. Inversion and plantar flexion normal. Straight leg raise was negative. And there was a positive tunnel at the fibular tunnel. So if we just ignore even the provocative maneuvers and come back to just the motor examination and we think back to our chart, dorsiflexion weakness with eversion weakness preserved inversion. That's a pattern that's consistent with a perineal neuropathy. So by doing this we can, I think perineal neuropathy in particular is one of the commonly overlooked diagnoses that I think sometimes patients get spine operations for incorrectly when they've really got a perineal neuropathy as opposed to a lumbar radiculopathy. This patient had back pain if you remember in the history. Lots of people have back pain. And I think when they say that as neurosurgeons we oftentimes immediately jump to thinking this is a spine pathology. But if we do a good job with our physical examination, we can avoid unnecessary spine operations for patients and get them the right treatment. So how might you support your diagnosis in this case? Well, an EMG nerve conduction might be helpful. It can aid in firming up the diagnosis of a perineal neuropathy. You might get an ultrasound of that nerve. Again, see if it's enlarged. See if there's any masses at the fibular tunnel that might be contributing. And you might get an MRI of the knee. So again, it's going to put this into a completely different set of diagnostic tests as opposed to if we're thinking should I get an MRI of the lumbar spine. So this brings me to the ancillary tests. So when we're thinking about peripheral nerve pathologies, we have a reasonably limited set of diagnostic tests that we're going to order. So electrodiagnostic testing is probably the mainstay. So EMG and nerve conduction. These, after peripheral nerve injuries in general do not give you the complete picture until about two to three weeks after the nerve injury. And I'll come back to why that's the case. So particularly for nerve injuries, traumatic nerve injuries, you oftentimes do not want to order an electrodiagnostic test until at least this time point, about three weeks after the injury. Acute electrodiagnostics are not as helpful. But these can be used to confirm lesion localization. They can help you detect subclinical changes. So things that we're not picking up on our exam when there's very subtle muscle involvement. And can also be used to follow for nerve recovery before we can clinically detect that nerve recovery is happening. Imaging studies that are available to us. Ultrasound is a good option. Nerves that are at proximal sites to the injury, oftentimes when they're compressed, they become enlarged just proximal to the site of compression. So enlargement of the nerve can help aid in a diagnosis of compression. It can be used to detect masses. Can be useful to detect any aberrant anatomy that might be present or unusual anatomy. And then finally, can also be used as part of a diagnostic injection where we might want to numb up a nerve and see if that improves a patient's symptoms. MRI can also be useful. It has fairly similar uses to ultrasound, but gives a little bit more definition. So oftentimes in my practice, I use ultrasound as a screening modality and then use MRI as a follow-up to that if there's anything that's detected that I may want to see in more detail. X-rays have a pretty limited role in the evaluation of the peripheral nerve patient, but there's a few specific indications. It can be useful to examine fractures that can be associated with nerve injuries. So healing fractures may form large callus. There may be a jagged edge to a healing fracture. There may be irregular healing of the bone after a fracture. And all of these things may clue you in on that the fracture healing or the fracture itself may be what's involved in your nerve injury. And then it can also be used to screen for what surgical hardware might be in place after a fracture that you're going to want to be aware of if you're going to go and operate on that nerve. CT and MR myelography can be useful when we're thinking about nerve root avulsions after traumatic injuries. So we can look for things like pseudomeningoceles that suggest that maybe this nerve root has been pulled out of the spinal cord. So high-resolution MR imaging can be used, or this is a contrast CT myelography. Neither of those are acceptable. I think increasingly people are going to using MR myelography as opposed to CT myelography. But that definitely varies still center to center. And then another additional test specifically for tumors that can be useful in some indications is PET scans. So these can be useful particularly if you're thinking that a mass might be a malignancy. It can be useful in the evaluation of a benign versus a malignant nerve sheath tumor. So this is, I'm going to go through the very basics of EMG and nerve conduction studies. And again, this is the very basics. So if somebody in the audience is really an expert on this topic, I apologize. Because this is not going to be certainly at the degree that say a neurologist very well versed in EMG nerve conduction would give you. But I think it's the basics that can help you read a report and understand what does that really mean. So understanding the EMG really requires an understanding of the basic structure of a nerve. So at the basic unit of a nerve is an axon. And really a nerve is a bundle of a bundle of axons. So a myelinated axon is the very basic unit that is surrounded by a Schwann cell, which is what forms the myelin. And then that is all ultimately bundled together to form a nerve. So if we think about how a nerve impulse propagates down a nerve, what allows the speed of the propagation of that signal is the myelin. So the signal actually jumps between different nodes of the nerve. And what allows that to happen is the myelin covering. So if the myelin covering is disrupted, then that nerve signal can't have this jumping or saltatory phenomenon. And the speed of the conduction is changed. As opposed to if I disrupt the axon itself, then the signal just can't get down the nerve. The axon is how the signal is actually traveling from point A to point B. And the speed is determined by the myelination. Okay? So if we think about what happens in a nerve injury, if you disrupt an axon as part of the nerve injury, you separate the distal part of the nerve from the cell body of the nerve. And when that happens, you can't clear toxins, the supply of the necessary nutrients that get down to the distal part of the nerve can't occur. And what happens ultimately then is the distal part of the nerve degenerates. So the distal part of the nerve regresses all the way to the point of the muscle. And that's a process called Wallerian degeneration. That process takes about two to three weeks to happen. That's why the full findings of an EMG or nerve conduction study are not present until this process has completed itself. So that's the physiologic basis of the timing of EMG. Now, if we instead leave the axon intact, but we disrupt the myelin sheath, now there is no Wallerian degeneration. You've left the axon. All of the supply chain is still there. You're going to change the conduction properties, but all of the process of axonal loss and changes in the muscle are not going to occur. So let's see how that really sort of works in practice. So for demyelination, again, there's no axonal injury, no Wallerian degeneration, but our conduction velocity is going to change. So let's say we take out this segment of myelination, and we try to send a signal down the nerve. That signal will eventually still get down to the muscle. But it's going to happen in a slower fashion because you've disrupted the myelination and the conduction. So if on a report you see that there is axonal preservation, but there is a decrease in the conduction velocity, we should be thinking about demyelinating conditions. So let's compare that. So now an axonal injury. So now we've cut the axon in some way or injured the axon severe enough that it is permanently impaired. So now we've separated the distal part from the cell body. We're going to get Wallerian degeneration. And now what we're going to see is because that Wallerian degeneration happens, the muscle is now not going to have a normal signal, and it's going to give off abnormal discharges. And we're not going to be able to get that signal to the muscle in a normal way. So if we think about the amplitude, now the amplitude is going to be reduced. And there are going to be signals in the muscle, things like fibrillation potentials that occur because the nerve is now not innervating that muscle anymore. So on a report, if you see something like fibrillation potentials, decreased amplitude, that should clue you in that there's an axonal process going on. So what about a focal conduction block? This is something that people will also describe in some of the reports. So in a focal conduction block, let's say I take out this strip of myelination. And now instead what I do, though, is I send a signal from here to here. Well, the myelination and the axon in that segment are actually normal. You're going to get a normal conduction velocity. Let's say I try to send a signal from here to here. Well, again, that stretch of myelination is normal as well. It's going to be a totally normal signal. But if I try to send a signal from here to here, now I'm going to get a decreased conduction velocity. So they will do things like inching studies, where we progressively try to send a signal inching along the nerve until the point that you actually see a drop-off of the speed of the signal. And that is what will tell you that there is a focal problem. This is what happens in things like compressive disorders, like, say, an ulnar neuropathy at the elbow, where there is a focal point of compression. The distal nerve is normal. The proximal nerve is normal. And there is one short segment that's affected, where there will be a focal conduction block. So that's the basics of EMG nerve conduction and some kind of buzzwords that can clue you in on what you might see on some of the reports. So one other thing that I wanted to mention in the differential before I go through how we put this all together in some of the common peripheral nerve diagnoses is Parsonage-Turner syndrome. I think this is also another thing that's overlooked many times. It's a great mimicker and very under-recognized. So this is an inflammatory or autoimmune neuropathy that usually involves the brachial plexus. But it actually can involve any nerve in the body. So the lower extremity, we usually don't call Parsonage-Turner. But it's the same process. And the classic history for this, and this is why really teasing out the chronology of symptoms is so important. So the classic history for this is acute onset of pain. Oftentimes, it's around the shoulder girdle. It'll last for a few days, so two, three, four days. Night pain is a very prominent symptom in this. And the pain tends to be non-mechanical. The pain then resolves, either goes completely away, or at least is markedly less. And then following that, there's the onset of weakness. So if a patient ever really describes that classic pattern where they say, I really had a lot of pain, the pain just all of a sudden kind of went away after a few days, and then I woke up with weakness, that should clue you in that this might be the diagnosis that we're dealing with. Over 50% of people with this diagnosis have some sort of a priming event, surgery, childbirth, vaccination, trauma, infection. So maybe in the history, they describe, I had a surgery, but I didn't wake up with this problem. So again, a patient who wakes up from, say, a cervical spine operation with profound weakness, well, that's probably the operation itself causing that problem. But it's a completely different picture if that patient, two weeks following a spine surgery, then all of a sudden developed their weakness. Now, we can think about things like epidural hematoma or hematomas, but one of the things we should think about in the differential would be Parsonage-Turner syndrome. Surgery can be a priming event where you can get this delayed weakness, and the classic history is usually present. There is a predilection for certain nerves, so the upper extremity tends to be more involved with this. Another term for this diagnosis is idiopathic brachial plexitis, referring to the fact that it's usually the upper extremity that's involved. And it does have a predilection for a certain set of nerves. So while that is a little bit esoteric, I think it's important to just have heard that at least once so that if you ever hear that pattern, you sort of have that on your differential. But let's go through some more common peripheral nerve pathologies and sort of work through the diagnosis of these, because these are the ones that we're probably much more likely to encounter on a day-to-day basis. And it's important to think about these in the context of working up spine patients, thinking about do they actually have a peripheral ideology for their symptoms. So the first is carpal tunnel syndrome. We went through an example case of that already. But the carpal tunnel is here at the wrist. There is a band of tissue, the flexor retinaculum, that contains or that roofs a tunnel that contains a lot of structures passing through it. So nine tendons and the median nerve all pass through this tight space. So thickening of the flexor retinaculum, enlargement of the median nerve, enlargement of any of these tendons can tighten that space down and lead to compression of the median nerve in that location. So this is where an understanding of the branching pattern for the median nerve is important. So the compression point here is right at the wrist. So any of the muscles for the median nerve that are proximal to the wrist really shouldn't be affected. So even though these are median innervated muscles, pronator teres, flexor carpi radialis, this whole list basically right here, none of those should be affected in a carpal tunnel problem. Whereas the hand intrinsics, of which there are four that are median innervated, which include the abductor pollicis brevis, flexor pollicis brevis, opponent's pollicis, and the first and second lumbricals, those are the muscles that we should really be focusing on if this is a carpal tunnel issue. So again, the sensory distribution for the median nerve stops at the wrist. And it involves the first 3 and 1 half digits of the hand, but does not involve the dorsal surface of the hand. So the dorsal surface of the hand outside of the fingertips is radial innervated. So this really should be a palmar problem. So the history for median nerve pathologies is typically pain and paresthesias in those 3 and 1 half digits. Prominent nighttime symptoms are often present where they'll have to wake up and shake their hand out. The hand can be clumsy, and usually they have some sort of a history of repetitive movements. So for example, typing. The physical examination, if you do a good sensory examination with two-point discrimination, it'll show a decreased sensation in those same radial 3 and 1 half digits. Those four motor, sorry, four muscles will be affected. And then we can use our provocative maneuvers, things like TINAL, Phalen, Reverse Phalen, and the Durkin test to tease this out. So the hand exam, I think this is confusing. It was certainly confusing to me for a very long time, what we actually term each of the movements of the thumb in particular. So, flexion of the thumb is bringing the thumb across the palm in the plane of the palm. Extension is then bringing it back out. Abduction and adduction occur out of the plane of the palm, so perpendicular to the palm. So, if you lay your palm flat and you bring your thumb straight up, that is abduction of the thumb. Adduction is bringing it back to the palm. And then opposition is the thumb over to the little finger. So, when we think about testing for, say, the abductor pollicis brevis, which is weak in carpal tunnel syndrome or can be weak in carpal tunnel syndrome, the maneuver is thumb up perpendicular to the palm, and that's the resisted motion they should be tested for. And opposition, coming across, is really the second motion that's pretty easily tested. And those are the two that can be affected in carpal tunnel syndrome. So, the opponent's pollicis mediates this. The abductor pollicis brevis mediates abduction out of the plane of the palm. Again, our provocative maneuvers, so tapping on the median nerve at the wrist, that's Tenell's. The Durkin compression test really just involves compressing the nerve right there at the carpal tunnel. And then the Phalen and the reverse Phalen's test. And again, I think the way that these exam maneuvers are done incorrectly is just too short of a period of time. You should really hold this for at least 30 seconds before you really declare this to be positive or negative. So how might we support our diagnosis, again, of carpal tunnel? Well, EMG nerve conduction. We can use our physical exam to really suggest that this is the diagnosis. But the EMG will give you a sense of what's the conduction velocity of the median nerve across this segment. This is a focal compression. And so we ought to see a focal conduction block for carpal tunnel syndrome. And we may also see muscle changes if this is severe enough to the point that the axons have been disrupted by this process. We may see that the abductor pollicis brevis or the opponent's pollicis have changes to them, which is also suggestive of carpal tunnel disease. The ultrasound may be helpful. It can support your diagnosis. It can help you avoid surprises like masses in this location, cysts in this location. But it can also be a supportive test. It can show that the nerve is enlarged right at the carpal tunnel. So if we think this is the diagnosis, how do we manage it? Well, we can splint, steroid injection, or surgery. And surgery is carpal tunnel release. And there's a variety of different surgical techniques that you can do that are more invasive versus minimally invasive. But carpal tunnel release, the surgical approach to this, is a very successive surgery. Probably one of the most successful surgeries that we have in all of surgery. More than 90% of people get better after carpal tunnel release if you have the appropriate diagnosis. Cubital tunnel syndrome. So this is the equivalent, but for the ulnar nerve, this happens around the elbow. So this is the anatomy around the elbow. The ulnar nerve comes, wraps around the elbow, passes underneath a very tight ligamentous structure called Osborne's ligament, and then passes along the split between the two heads of the flexor carpi ulnaris underneath Osborne's fascia. And a variety of different structures can be compressive of the nerve. So the arcate of struthers, medial intermuscular septum. You can see all the ones in red basically are the potentially compressive structures. So again, understanding the branching pattern for the ulnar nerve will clue you in on what muscles should be involved and what muscles you should test. So the ulnar nerve is the main innervator of most of the hand intrinsics outside of the four muscles we just talked about for the median nerve. So those are going to be your primary muscles to examine. The sensory distribution is the ulnar one and a half digits. So a split on the fourth digit is very characteristic. Again, this is a peripheral nerve problem. So there's oftentimes a very discrete border. So splitting of the ring finger should clue you in as to the idea that this is maybe an ulnar nerve problem. Now different than the median nerve, the ulnar nerve does innervate the dorsal side of the hand. So both sides of the hand can be affected and should be affected when this is an ulnar nerve problem at the elbow. So the history, pain and paresthesias in those ulnar one and a half digits, hand clumsiness, some sort of a history of pressure on the elbow. So truck drivers oftentimes, if they're resting their arm on the console for prolonged periods during the day, will have an issue with their ulnar nerve. Physical exam, again, the ulnar one and a half digits will have decreased sensation. The hand intrinsics will oftentimes be affected minus the median nerve hand intrinsics. We can use Tenell's sign over the elbow as a provocative maneuver. And then we can look for some very characteristic findings on exam. So the first dorsal interosseous muscle is innervated by the ulnar nerve. And there's often a prominent scoop right there when there is significant atrophy. This is the ulnar claw hand. So this patient is attempting to open their fist, but they can't do that because these lumbricals are affected. So the fourth and fifth digits stay clawed, or it's the benediction sign, when they're trying to open their hand. This is fromant sign. So if you have a patient try to grab a piece of paper and keep their thumbs flat, they oftentimes will not be able to do that on the affected side. They will have a bent thumb when they do that because that's mediated by the flexor pollicis longus, which is median innervated, so not affected. They can still pinch the paper, but they have to do it with a bent thumb as opposed to a flat thumb. And this is Wartenberg's sign. This patient is trying to bring his right hand into full adduction of the fingers, but he can't bring the fingers in because those muscles are weak, Wartenberg's sign. So when we put that all together, we can, again, support our diagnosis with EMG or nerve conduction. We can add an ultrasound, and surgery is reasonably effective for this operation, but the key is having the right diagnosis. Fibular tunnel syndrome, so the perineal nerve. So this nerve wraps around the fibular head and, very similar to the upper extremity ones we just talked about, dives into a tunnel in this location. So if we think about what the symptoms for this should be, well, pain and paresthesias in the lateral leg and the dorsum of the foot, oftentimes radiating from the knee. Foot drop, so again, this is where our L5 versus perineal discussion comes in. And they may have a history of knee trauma or habitual leg crossing, where they're putting pressure onto that area of their leg. The sensory will show decreased sensation in that same distribution. Motor, dorsiflexion, and eversion weakness, again, that's the key. The evertors will oftentimes be affected as well. Provocative maneuvers, we can use a TINEL at the fibular neck, and we can palpate for masses. So masses are oftentimes present. They account for a fairly large number of perineal neuropathies, and so palpating the nerve in that location can be helpful. So this is TINELs at the fibular tunnel. This is our chart that we reviewed very briefly earlier. Again, teasing out L5 versus perineal, thinking about eversion and inversion. And then we can add to that diagnosis, again, with our EMG nerve conduction, our ultrasound, and we may want to follow that with an MRI, particularly if there is a mass found on the ultrasound. So behavior modification is usually the first intervention for this, avoiding leg crossing or any pressure on that area of the body. And then if there's no recovery, perineal nerve decompression at the fibular tunnel can be used. Lung parasthetica is the next lower extremity problem, and again, I think this is an important thing to think about for patients that are presenting with what might be a lumbar radiculopathy. So these are the patients that will say, my anterior lateral thigh basically hurts. They may not put it in those words, but that's where they'll describe. And they can take one finger, draw it around this border, and oftentimes this gets confused for, say, an L2 or L3 radiculopathy. And in fact, if we did a good exam, we would find that it's really limited to this anterior lateral distribution of the lateral femoric cutaneous nerve. And importantly, one of the things that you will find is there is no weakness. That is a pure sensory nerve. And so if there is weakness as a component, we should not be thinking that this is marauser parasthetic or lateral femoric cutaneous neuropathy. This is a pure sensory nerve. The tunnel can also be used, just medial to the anterior superior iliac spine. That is where this nerve passes. And oftentimes, we can elicit a history of some sort of compression in that area from either obesity or wearing of tight-fitting belts, something that's putting prolonged pressure on the nerve in that location. So I'm going to go very briefly through a couple of other diagnostic categories, just so we have had sort of a brief review of these. So nerve sheath tumors is the first of those. And benign nerve sheath tumors, the two most common are schwannomas and neurofibromas. When we're dealing with a nerve tumor, one of the things that we should try to elicit is, is there any history that might be consistent with a neurocutaneous disorder? So things like neurofibromatosis type 1, neurofibromatosis type 2, or schwannomatosis. So maybe these patients have cutaneous findings that are going to tell us that this palpable lump is likely to be a nerve sheath tumor, because it's part of a bigger constellation of symptoms. So I think probably the most important thing when we see a patient with a nerve sheath tumor, or what we think might be a nerve sheath tumor, is to really quickly decide, are there concerning features for malignancy? It's going to change completely how we manage this and how we evaluate it. So features that are concerning for malignancy that should immediately raise red flags would be a fixed immobile mass, rapid growth, big masses, so size greater than 5 centimeters. And then this is the one that I think is really the one that, if you hear, should tip you off, spontaneous pain. So benign nerve sheath tumors very rarely are painful without contact, without some sort of pressure. So a patient who comes in and says, yeah, it hurts when I touch it, is a much different story than a patient who comes in saying, it is hurting me all the time and it is severe pain. All the time pain, severe pain, nighttime pain, any of those should really be a really big red flag that you're dealing with something that is not a benign tumor and needs a different evaluation and management. And then neurologic deficits are the other thing. So if on your exam you pick up that there is weakness or a neurologic deficit related to the tumor, that should immediately raise a red flag that this might not be a benign tumor. Benign tumors almost always do not cause a neurologic deficit. So the classic history for the benign tumors would be, I noticed this when somebody pushed on it or when I pushed on it, and it does hurt when I push on it. It radiates to whatever the distribution of that nerve is. It doesn't really hurt any other time. And the neuro exam outside of maybe palpating a mass is normal. So either way, the workup of this mass begins with a thorough history and a physical examination. And then usually the best diagnostic test to follow that up with is an MRI. That will give you some clue as to what nerve it might be involving. And there are some characteristic imaging features that help you put this into a category. So a word about the imaging. So image with contrast. The contrast can be a very important component of imaging for nerve tumors. And image with fat suppression. So if your center is not doing that on a routine basis, it would be good to request that as part of imaging of nerve tumors. And so this is the reason why. So this tumor, if you were sort of just glancing at this imaging, might be fairly easy to miss. So this is a non-contrast T1 without fat suppression. This is the tumor right here. So on a T1 with contrast and fat suppression, now you can see that that tumor really jumps out. Imagine if we hadn't fat suppressed that, though, and it was sitting in that area of fat that is also going to look bright on a non-fat suppressed image. You'll probably see it. But small tumors in particular are going to be much harder to pick up without fat suppression. And this is what it looks like on a T2. So this is T2 with fat suppression. If this was all bright because this is fat sitting around it, it's going to be much harder to pick up this mass. This one you probably would find because it's pretty large. But a small mass is going to be hard to pick up sometimes. So fat suppression and contrast are keys to imaging of these tumors. So as we think about nerve sheath tumors, the typical findings are going to be that on the T1 sequences, they are iso to hypo intense compared to skeletal muscle. They're hyper intense on T2. They typically avidly contrast enhance. They've got smooth borders and very little disruption or signal change to the surrounding tissues. Conversely, if we think about what should raise concern for malignancy, it's large size, peripheral enhancement, perilesional edema, and cystic changes within the tumor itself. If any of those are present, it should at least raise some concern that this is going to be a malignancy. Now if you compare the clinical features versus the imaging features, I would say that the clinical features actually are the more telling of the two. So really eliciting that history of spontaneous pain or neurologic deficit is what we really want to focus on when thinking about malignancies. If there is a concern for malignancy, probably the most important thing actually is to get them plugged into a multidisciplinary sarcoma clinic. These are sarcomas. These are aggressive tumors, and they need an appropriate evaluation in that regard. So PET scans can be helpful, biopsies in some circumstances, but really getting them plugged in with the sarcoma clinics is job number one. If there's no concerning features, we can think about managing these conservatively versus resection. And reasons we might consider resection is sometimes patients actually do find that this is bothersome because of frequent contact to the mass. Say it's where their waistband falls or something where they're having frequent pressure on the mass that's causing them pain. Tumors are easier to resect when they're smaller. These lesions, if they are shown to be growing, sometimes we want to consider resecting them while they're easier to take out. And it does reduce or eliminate the need for follow-up. So for some patients, that's a big deal. This is what nerve sheath tumors look like at the time of resection. This is a benign nerve sheath tumor, very well encapsulated. They involve single strands of the tumor, so single fascicles of the tumor when they're a schwannoma. Again, another nerve sheath tumor, the brachial plexus. And these can usually be taken out on block whole with the remainder of the nerve being left behind. So I'm going to skip this, I think, in the interest of time. I'm running out of time. So just to very quickly talk about nerve injuries. So nerve injuries come in a variety of ways. So this is a glass shard in a radial nerve. This is a nerve that was unfortunately plated as part of a humerus fracture repair. This is a neurome in continuity from a stretch injury. And this is a stab wound to the neck with a transection of a spinal accessory nerve. So they come in a variety of flavors. But really, the sort of bottom line of nerve injuries is that from the time of the injury, changes start to occur in the nerve, the neuromuscular junction, and the muscle such that those changes can become irreversible somewhere between 12 to 24 months after the injury. And so really, the principle of nerve repair and recovery is it's a race to establish re-innervation to those muscles before those irreversible changes occur. And so it's really important to get these patients plugged in early because axonal regeneration occurs at approximately one inch per month or one millimeter per day. And so our optimal time window for making decisions about reconstructing nerves is really in kind of the three to six month time window, maybe earlier actually depending on the mechanism of the injury. But early referral to a surgeon who's comfortable with nerve repairs is really job one for these patients so that you can keep all the options on the table and give them the best chance of recovery. So I'm going to skip through a few of this. So this is, I think, one of the important things to consider. So this is the rule of threes. It's a quick and dirty way of thinking about how we manage traumatic nerve injuries. So for sharp, clean lacerations like stab wounds, those usually should be explored and repaired within three days after the injury. For dirty, ragged lacerations, something like an open injury but blunt force trauma, usually those are going to be explored and repaired within three weeks after the injury. And that's because those nerves are going to display a continued evolution of the degree of injury for about three weeks. And you don't want to repair the end of an evolving nerve injury. You want it to declare itself completely and then ultimately repair the nerve. And then for closed injuries, usually that three month time point is kind of our window for making a decision about a nerve repair. So for traumatic nerve injuries, job one is localize the lesion. What nerves are involved? And that's a good neurologic examination and EMG can also be helpful. We want to make sure we're excluding musculoskeletal mimickers, so things like rotator cuff tears that might be masquerading as a nerve injury. Early on in the course of the disease, we want to keep the joint supple. So splinting and or physical therapy, depending on what muscles are weak, is really important so that we don't get the development of contractures while we're waiting for nerve recovery to occur. So if we get contractures or stiff joints, even if we get reinnervation of those muscles, it's not going to be effective. And so early referral for occupational and physical therapy is important. And then we want to do good serial neurologic examinations so that we can try to detect any nerve recovery. Spontaneously recovering nerves will always recover best. And so it's important to pick up even those very subtle early signs on your serial examinations so that we manage these appropriately. So this is an example of how we might manage a nerve injury with a nerve graft repair. So this is a cabled graft repair between two cut ends of a nerve. Nerve transfers are options. And we oftentimes use intraoperative neurophysiologic testing to make decisions about whether a repair should be done at all. This is an example of a nerve transfer where we've taken one little fascicle of an ulnar nerve and transferred it to the biceps branch of the musculocutaneous. So I point this out only to say that this is actually an evolving field within neurosurgery. We're constantly developing new techniques, actually, that have now made reasonable outcomes for these patients possible. And so this, I think, used to be thought of, nerve injuries used to be thought of as just dire circumstances, not really any options. But that's not true anymore. And so getting these patients plugged into the right clinics early is important. I'm going to skip the case. And I think that is the end. So these are a good couple of books. If you are interested at all in reading more about the peripheral nerve examination, they're good supplements. A lot of times, it's good to actually just have this in your clinic. If you're going in to do a complex peripheral nerve exam, just open the book. Follow along so that you're doing those exam maneuvers right. And that's it. So thank you. No questions? You were so thorough. Wonderful. All right. Thank you. Thank you so much, Dr. O'Leary.

neurosurgeon

peripheral nerve surgery

physical examination

history

diagnosis

treatment

electrodiagnostics

carpal tunnel syndrome

cubital tunnel syndrome

nerve injuries