Hi, I'm Gautamal Hotra, and I'm going to be, well, first of all, I have nothing to disclose. I'm happy to take on what my residents think are the yucky topics from your CNCT exam study outline, and those are the topics that I'm going to be covering. What I realized as a resident is that we typically look at the patient and equipment as if they were black boxes. We do something to it, and then something happens. Instead of teaching the topics of neurophysiology, volume conduction theory, and instrumentation separately, I've merged them in the same way as when I'm teaching one of you in the lab on the fly while we have a patient. Compared to when I give this talk to physicians, today I'll focus on instrumentation and the physiology, which are relevant to your exam. Try to focus more on what I'm saying and reference the slides later when you review later. So let's start generally with, what is electrodiagnosis? The human body's electrical discharges can be captured with equipment. When disease alters the architecture and physiology of nerves and muscles, observable changes in the discharges can be useful for establishing a diagnosis, monitoring disease progression, and assessing therapeutic interventions. Yes, these tests offer the diagnostic benefit of addressing the neuromuscular differential, but numerous studies also reveal that abnormal EDX affects prognosis and response to treatments. So what exactly are nerve conduction studies? Shocks are delivered to the body for nerve conduction testing after the nerve is stimulated with this exogenous current, pickup electrodes elsewhere on the body display the electrical activity generated by nerves or muscles. The picture on the screen is called the evoked response. The x-axis measures time and the y-axis measures voltage. Since my focus will be on sensory studies, what are sensory nerve conduction studies? Again, a nerve is stimulated. Electrodes pick up the evoked response, which is called a snap or a sensory nerve action potential. The snap is the electrical signal summation of discharges by the sensory neurons depolarizing membranes. This slide is so packed with deeper backstory, and what I'm going to do is take each component of this and unpack it for you. So we use the word nerve. What the heck is a nerve? If we look at the nervous system as being the central and peripheral systems, then everything that's not spinal cord or brain is peripheral. Incoming signals from the periphery are afferent, and those transmitted outward from the CNS are efferent. A bundle of nerve fibers conveying impulses between different parts of the body are called roots, nerves, or rami, depending on where they are in the body. So if you slice a nerve, you'll see that it has a skin or epineurium. Inside are bundles or fascicles surrounded by connective tissue called perineurium, and the bundled axons are themselves surrounded by a matrix called endoneurium. As you learned in high school biology, neurons are cells serving as the structural and functional units of the nervous system sending messages from one part of the body to another. By now, you should know the parts of a neuron, including the dendrite, cell body, axon, and terminal. Structurally speaking, we deal with multipolar neurons where input from many branches integrate at the cell body, and pseudounipolar neurons with their two fused processes. And these are functioning both in the foreground or the background. They give diverse info from the skin, afferent stuff like pain from the periphery to the central nervous system, and the constant feedback from our internal organs, which is collectively the autonomic nervous system. Everything else is efferent or motor. Between upper and lower, it's the lower motor neurons that are relevant to nerve conductions. The alpha motor neurons' cell bodies reside in the anterior horn, and the term motor unit refers to the anterior horn cell, its axonal projection, and all of its associated terminals, junctions, and muscle fibers. So aside from sensory versus motor, neurons can be classified by size and correlated to function. Some neuropathies exclusively affect large or small fibers while others affect both. The large sensory motor fibers are myelinated, and the small ones tend to be sensory or autonomic. Know that electrodiagnosis assesses the largest fibers. Classification by size is mentioned on your test, and a second efferent-only size classification exists just to confuse us. And now we've covered a good portion of neurophysiology for your exam, and now we know what we mean when we say nerve, and it is stimulated by an externally delivered impulse. There's so much to unpack in there, so let me show you. So this is what the setup for stimulation ultimately looks like for trainees who have never seen this, but what you don't see is that I abrasively first swab the hand to improve contact and decrease impedance, then I stuck the electrodes that are self-adhering, or I use tape, then I put some conducting gel down, and then after I dip my stimulator wand in the gel, I put it on the patient where the nerve is. So the stimulator is a device that delivers current to the body using electrodes called cathode and anode. This is what the stimulator wand looks like, and basically it's a battery where charges flow from the cathode to the anode. Those are the poles, and that's what polarity is referring to. What follows is my whole lecture on physics condensed into three slides, so pay attention. Current is basically any flow of charges, so if something has a charge and it's moving, it's current. What is charge? Well, it's a fundamental phenomenon of the universe consisting of positives or negatives, opposites attract, and like charges will repel. The ease of flow of charges depends on a few things. Think of a pump pushing water molecules through a pipe. The pump is voltage, and the water molecules are like charges. The flow will depend on how hard the pump is pushing and the cross-sectional area of the pipe. Similarly, the higher the voltage or push, the more current. The more cross-sectional area means less resistance, which means more flow or current, and that's your Ohm's law, which is V equals IR. All of this is on your test outline, by the way. I'm not just doing this because I'm just a nerd. I am a nerd. So actually, voltage is just a comparison of the amount of charge in one place versus another. It's called electrical potential. So an analogy to height might help when we talk about electrical potential. So when we say six feet tall versus three feet tall, we're actually comparing to the ground as a zero point. Just like heights or gravitational potential, voltages or electrical potential are comparing to the earth or ground being zero charge. The green ground electrode serves as this zero and, contrary to popular opinion, has nothing to do with safety issues. Unless you're an engineer, you probably faked your way through physics and didn't really understand capacitors. A battery attached to two metal plates separated by a non-conducting material will store charge. Essentially, the positives from the battery will build up on the one plate until their repelling force equals the push from the battery. The insulator's dipoles will align to and repel the opposite plate's positive charges to flow down the wire. So although no current went across the dielectric, you just propagated a current. This is called a capacitive current, and we'll come back to this. So you can see how the cell membrane's hydrophilic heads look like the plates of a capacitor separated by the hydrophobic interior, but the membrane ain't this simple on your test. So let's go through a whole semester of cell physiology in one slide. The membrane is an asymmetrical phospholipid fluid bilayer with embedded proteins moving around or attached to the cytoskeleton. The membrane serves as a barrier while the proteins create gradients by selecting what gets in or out. Note the negatively charged intracellular macromolecules stuck inside, and they're attracting positive counter ions and water to come in. So if allowed to, water would rush in until the cell bursts. To counter this, Mother Nature created the sodium-potassium pump, which sends an extra sodium out so that water will follow. And this creates a charge difference, or voltage, across the resting membrane. So that was the whole semester of cell physiology in one slide. So that's the resting membrane potential. Of the three ways current can flow in a neuron, the fastest one is if ions just flow longitudinally, intracellularly, from one end to the other, like in a wire. Another way is capacitive current, like I showed you with the capacitor, with charges collecting on one side of the membrane and repelling the positives away. That movement is flow of charges or current. So capacitive and longitudinal current don't require anything to be moving through the membrane, but when we also can move ions through channels, and that's how you can get a transmembrane current. So we said resting membrane potential depends on the sodium-potassium pump, but when voltage-gated ion channels open, that's when we get this all-or-nothing, self-sustaining, rapid, highly efficient way of relaying information when stimulated. This is the action potential. And the phases are based on when a channel opens or closes. Although simultaneously initiated, the sodium channels open and close quicker while the potassiums are delayed. So they're stimulated to open at the same time. It's just sodium gets there quicker and potassium gets there a little later. And so action potentials can propagate down an unmyelinated neuron by little patches of channels opening and then stimulating the adjacent membrane like a game of pass the parcel. A myelinated cell, however, has Schwann cells segmentally wrapped around the neuron with spaces in between where the channels can allow influx of ions and depolarize. Once inside, the sodiums immediately float intracellularly to the next exposed patch and depolarize it. These large myelinated nerves are the ones we are testing on nerve conduction studies. And I just don't agree with calling it saltatory conduction. Wee, I'm jumping from node to node. I propose we say something like natatory because the ions are swimming from node to node. And so unmyelinated conduction is like walking in a pool, which is slow, while myelinated is like swimming underwater, popping up for air, swimming again. Maybe that helps. So now we've explained a lot of the neurophys informing your test questions. But we started by wanting to explain how current from the stimulator gets into and stimulates the neuron. Now that you understand capacitive current, you can understand this. I'm going to show you with my own drawings that look like they've been drawn by a four-year-old, but please bear with me. So note the cathode and anode on the skin and below is the membrane's bilater. I don't know if I can point. Does this show if I'm pointing? Nope, it doesn't, okay. Well, so let's say you press the stimulator button and positives are delivered from the anode and they make the outside of the membrane very positive. The intracellular positives are repelled and want to move adjacently where their presence repel the extracellular positives under the cathode, which also attracts them. So it's a capacitive current and that's how neural stimulation occurs without any flow of ions through the membrane. So now you've seen it and you can forget it if you want, but at least someone's explained it to you. So let's continue to unpack our definitions. What are electrodes? Well, we've mostly revealed what's inside the patient now. It's time to look at what's really inside the black box of the equipment as it relates to your exam. Electrodes are any metal that conducts electricity. They are the interface between machine and human making all direct contact and you have two types of electrodes, surface electrodes that attach to the skin and needle electrodes which go through the skin. You see different shapes and types and there's advantages to each. You have to learn the names of the electrodes. We already talked about the stimulators cathode and anode. For pickup electrodes, you have different naming conventions where E stands for electrode, G for grid, which refers to the old tube technology, and then active reference and ground. So they're all synonymous, just don't get them confused. So the problem with surface electrodes is that you've got this giant resistor called skin making it hard to pick up these microvolts snaps. Abrasively swabbing the skin to remove oil, sweat, dirt, dead skin cells, makeup, lotion, this can all help decrease impedance. We talked about resistance. In electrodiagnosis, we actually use the word impedance because we're dealing with varying voltages. Otherwise, they're essentially synonyms. So if you understand what resistance is, you're kind of good with, just call it impedance from now. Gel also helps with conduction of the current being detected by the pickup electrodes. And if you wipe the gel on your black pants instead of a towel when it dries, you get to explain to your wife why you have all this white powder on your pants. So when you press the button on the stimulator wand, current flows from the cathode the way I showed you in that four-year-old diagram, and it spreads throughout the body via paths of least resistance, like the skin and the interstitial fluid. That chunk of current actually gets picked up by the electrodes immediately, and it gets displayed on the screen, and that is called stimulation artifact, the shock traveling throughout the body. When you press the stimulator button, the computer treats that as T equals zero, stores it, and then whatever happens afterward has a time associated with it. So we've talked about nerves, stimulation, and electrodes. So next is what pickup really means. Volume conduction theory is just the physics of how electricity behaves in a three-dimensional volume. And since we're using current, and many of our patients are three-dimensional, you'll probably be tested on this. So I simplify this for you in one slide now. So I like that volume conduction explains the pickup electrode, which is attached to the skin and basically works like a microphone. It's picking up the traveling wave of depolarization through the skin, and you start to see a waveform. As it propagates away, the displayed waveform changes. This is mind-blowing if you haven't thought about it before, that we can explain what we see on the screen, and that's what volume conduction theory is, super simplified. So we've addressed nerves, stimulation, pickup electrodes. What remains is clarifying one of the bigger misconceptions my residents have. Remember how we said the axon generates an action potential? Well, a nerve is going to be a collection of all of those action potentials. It's a histogram. If we counted all of the axons in a cat's sural nerve under a microscope and plotted based on their diameters, larger ones have larger amplitudes and conduct faster. So you can use a computer to model how a summated waveform would look. And when you add them all up, it looks like a snap. So the main point here is the snap is a histogram. So we've discussed pickup electrodes, and now we can move on to the next component in the equipment, which is the differential amplifier. So if the purpose of the electrode is to pick up the tiny voltages, the purpose of the differential amplifier is to reveal the differences between what's being picked up and then amplifying them. So breaking down the word differential amplifier helps. Amplifier just means making something bigger. Since looking at tiny microvolt discharges, we need equipment to magnify them for us to work with them. The factor which we multiply them by is called gain. This can be calculated by dividing the amplifier's output signal by its input signal. And I have an example here for you to calculate later. I'm going to skip that. So differential means comparing or subtracting out. You know, there's all this electrical noise everywhere on your body, and that can obscure the signal of interest. We use the second electrode on the body as a quote, unquote, reference of this baseline noise. So we can improve the signal by subtracting out this noise. Specifically, E1 and E2 are plugged into two different amplifiers that are identical, except that the second one inverts the signal. Their outputs are then summated. So if both of them were seeing the same exact thing at the same exact time, that is probably considered noise, and the output will be ideally canceled. So this is how the differential amplifier works. As a thought experiment, what if one amplifier didn't invert the signal? And then you'd get basically a giant version of it, right? So if you understand that, then you understand differential amplifiers. Unfortunately, I've added this slide on common mode rejection ratio because it comes up on our exam annually. And basically, the common mode is all the stuff that's common to both amplifiers. And how good an amplifier is at removing that is called common mode rejection ratio. And the answer is 10,000 to 1 on our test every year. But I found this from the 2013 SAE. And even though this question is about EMG, it's asking about what happens when you forget to plug in the reference. And you know that you will have too much noise, and the screen will be unusable. So how close should the electrodes be to each other? Well, ideally, we want to cancel out as much noise as possible without canceling out the snap. When experimentally trying this, progressively separating the electrodes increases the amplitude up to 4 centimeters. After that, the amplitude stops increasing, and only noise increases. This is why the optimal separation in the upper limbs for snaps is found to be 4 centimeters. Amplitude is reduced as you get closer, smaller separations, as more similar information is being eliminated by the differential amplifiers. We can also algebraically calculate this in the lower limb, and you get away with 3.2 centimeters, which is what you find the bar electrode distance to be. So I'm going to skip these questions. Next are filters. So let's keep it simple. Filters remove stuff, and we want to remove noise, the undesired stuff. Low-cut filters remove low frequencies. High-cut filters remove high frequencies. Everything that's in between is called your bandwidth. And if you remove too many frequencies, then it affects the waveform. So let me explain how we know that in very easy-to-understand terms. Can you see how algebraically, if I add up all of these sine waves, I'll get the top as a resultant? Well, this concept can be applied to biological signals, too. Maybe it's a little bit of an imagination stretch, but you can see how adding them up might result in that top waveform. So the digital filters are either removing high-frequency stuff or low-frequency components of the waveform. As you can see, low-frequency components will affect things like duration, whereas high-frequency stuff is affecting onset. Removing lows leave you with relatively more highs, and you're going to be getting more phases, just like those high-frequency. Maybe your peak comes in a little earlier. And if you have more low-frequency stuff, you have a bigger amplitude. So if you can just qualitatively, conceptually see that, then this next slide doesn't become so difficult. And this is where all the test questions come from. So basically, if you increase the low-frequency filter, which means you're removing more low frequencies, that's going to take out amplitude. That's going to bring your peak latency earlier, because now there's more high frequencies contributing. It'll shorten your negative spike duration, and you'll have more phases, because it looks more like the high frequencies. One point of confusion is that raising and lowering is referring to the cutoff frequency, not how much you're removing. So it's actually not synonymous with lowering and raising the amount of filtration. So it doesn't mean that if you're lowering a certain filter that you're not filtering as much. And it doesn't mean that if you're raising a filter, you're filtering more. It's just whether it leaves you with less or more bandwidth. So I'm not going to go over this in detail. You have to sit and think about this, because this is on your test. And so it's worth doing. And I also have another reference for you later. So lowering the cutoff frequency on a high-frequency filter doesn't really affect amplitude so much, but they do affect your onset latency. So if you remove high frequencies, your onset latency will be further away. So these are Dimitri's recommended filter settings, but no universal settings have actually been enforced as far as I know. So sound would be the next thing. It's important, but because you're techs, you're not performing needle EMG. During needle EMG, sometimes we can hear things that we can't see. I used to go into this computer stuff in depth. And for this, I'm just going to say this. The computer takes an analog signal, and then depending on how strong of a calculation it does, it can affect resolution. These days, computers are really powerful, and it's not practically affecting us in the lab anymore like it was back in the day when computers were first being used. This is pretty obvious with photos, where you can see the increasing pixelation and resolution. Analog versus digital continues to be a controversy in the recording industry. But the good thing about having a computer is that it stores the waveform, and then we can perform calculations such as averaging. So let's say you have this waveform on top that just looks like garbage. It could be that the snap is buried in a sea of noise. So you can acquire another waveform and add them algebraically at every point, and then divide by two to get the average. After enough of these averages, the snap will reveal itself as the noise cancels out. This is a powerful technique for low-amplitude snaps muddied by noise. Automation is the computer's attempt to figure out where cursors go, but you can't always trust it. So always check and consistently place the markers where they actually belong. Displays have simplified as the technology has improved. Remember those old cathode ray tube computer monitors? They're basically just photo electrons being shot on a fluorescent screen and moving across the screen really fast. And that's how oscilloscopes worked. And we're using the digital version of oscilloscopes now. So that's where I think you get the word sweep because the oscilloscope had to sweep back and forth on the x-axis. So when we use the word sensitivity or display sensitivity, we're talking about how big something is on the screen, measured in microvolts per centimeter or microvolts per division or millivolts per division. And it really isn't as important for sensory as for motor studies because the more you magnify, the earlier you can move your onset. It gets confused with gain because when you turn that gain knob, you're actually changing display sensitivity on the screen in addition to changing the gain stage of the amplifier. So now in order to explain what happens in the machine, I had my former resident draw this and I put together this animation that I'm kind of proud of for you. So the stimulator delivers current to the nerve and the action potential propagates to the hand. The three electrodes pick up the activity and feed it into a differential amplifier which amplifies the differences between the different electrodes. The resultant signal is then filtered and converted into computer ones and zeros so it can be stored, manipulated, and measured. This can then be heard through a speaker and the evoked response can then be viewed on a display. Thank you, thank you very much. Now that we've defined everything here, let's get to some technique issues. When stimulating, we keep increasing the number of amps and then maybe how long the current is delivered, that's duration. The terminology for stimulations are functional terms based on the evoked waveform. If there's only a stimulus artifact, it's considered a sub-threshold stimulation. But once we start to see a little blip, that's threshold. And then it's sub-maximal stimulation until it stops changing which is when we call it maximal. Then we crank it up and add 20% more juice and this is supra-maximal stimulation which ensures the entire nerve is stimulated. For your reference, here are the steps I go through when performing nerve conduction studies. Once obtained, we look at the amplitude which reflects the number of axons and how synchronously they've been stimulated. This tends to correlate with clinical symptoms and can be measured as base to peak or peak to peak. We also look at onset latency which is how long it takes for the fastest nerves to conduct. Some prefer reporting peak latency because it's easier to see. Finally, we can calculate conduction velocity by dividing the distance by the latency. Unfortunately, this is highly prone to measurement error. The terms orthodromic and antidromic stimulation just mean that we can obtain these waveforms by stimulating and picking up in the same or opposite direction as it physiologically conducts. The main differences are that antidromic tends to be larger amplitudes but also comes with more motor artifact. Performing nerve conduction studies is deceptively simple but obtaining reliable results is something else again. So let's go through some pitfalls and solutions. So first, why not just crank up the stimulator all the way up? So this is actually a sea map but imagine throwing a pebble in a pond and you get a ripple. If you throw a giant rock in there, you have a huger one. So if I give a giant stimulation at one point, then it's effectively stimulating a bigger footprint. So I've shortened the distance from my pickup electrode to where I'm stimulating and that can artificially reduce your onset latency. The second problem with too much current, if you crank it all the way up, is stimulus artifact. So when the current from the stimulator moves instantly, extends throughout the body to create this, then it can really throw off your study by obscuring the onset latency and base to peak amplitude. So this is literally one of my studies where I could not get rid of the stimulus artifact and it's obscuring my onset. And so I've put together a list of things you can do, basically a lot of cleaning, make sure you've got gel and then there's this another thing you'll see some physicians doing, it's called anodal rotation. So with the palm stimulations, it's especially helpful. Once you've found the peak of the snap, you keep the cathode where it is and then you just start moving the anode like you're using a compass. And what this does is it changes those isopotential electrical lines you saw when you were doing physics and that adjusts the stimulus artifact. Another issue with cranking it up too much is inadvertent stimulation of nearby nerves. See how close they are, the median and the ulnar at the elbow. So this results in misinterpretable wave changes in the waveform morphology. So look for, if you suddenly see an initial positive deflection on your motor studies, maybe that's what's happening. So this is typical and I still do this sometimes. The machine just switches the cathode and anode polarity between studies and I forgot and so really this distance of X is based on where the cathode was but you happen to not switch the cathode and anode. So now you've added this extra three centimeters. Since you haven't factored that into your calculation, the velocity will seem to be slower. So each time you do a study, look at where the cathode is and make sure it's in the right place. Let's see, I think I'm going to again skip questions. They're here for you if you need. Recall that the snap is a histogram, remember? With fast and slow fibers. Well, if they were all conducting at exactly the same speed, you'd have this really thin, really high amplitude waveform but since that's not the case, it's spread out a little. That's called temporal dispersion and for that reason, your amplitude will be lower. I stole this slide when I literally took a picture from Dr. Bromberg's lecture a couple years ago at AANM. You may hear this whole runner's analogy where you have people who can run a seven minute mile and those who can run a six minute mile and there's a bunch of people that are somewhere in between. After one mile, the difference in time between the fastest and slowest will be about a minute but if they run 10 miles, you're gonna see a huge difference between the fastest and the slowest ones getting there. Point is, over a short limb distance, there'll be less temporal dispersion in your snap than there will be over a longer distance. So your snap amplitude will be lower just by the fact that you're stimulating further away and that's due to temporal dispersion. So snaps have up-going and down-going components or negative and positive peaks. Well, because they're temporally dispersed, the up and down can overlap and that can cause cancellation. So not only do you have temporal dispersion, you have phase cancellation. So the more that things are dispersed, the more out of phase and cancel each other out, the further you go up from where you're picking up, the lower the amplitude will get and this is a normal finding in snaps and you just have to keep that in mind and be careful calling significance when amplitudes drop. The confusion occurs when you see abnormal temporal dispersion and what that is is it's trying to show that you could have a certain amount of demyelination where the runners are running through a swamp and so there's more of a difference between the fastest and the slowest. So that would be abnormal temporal dispersion. And so if that's the case, meaning that temporal dispersion and phase cancellation decrease amplitude with distance, then you should never see a larger amplitude with proximal stimulation. If you do, then consider one of these three reasons and my residents used to call this Mulhother's rule because I would just ask them this over and over again. So anytime I would see a bigger amplitude proximally, I'd make them check for submaximal distal stem, overstem proximally or to explain how it could be an anomalous innervation. Okay, I think. Finally, if you have a cold limb, the ion channels are going to be both slower to open, resulting in a prolonged latency and slower conduction velocity. They'll also be slower to close, allowing more ions to enter the axon for a longer period of time. This results in longer durations and larger snap amplitudes. So when you see a crappy test by someone who spent five minutes with the patient and large amplitude snaps that were delayed to its load conduction velocities and they labeled it diffuse sensory demyelinating neuropathy throw that study out, they just had cold limbs. Can I make that easier? Can you make any of this easier, please? So when people are cold, everything goes up except for velocity. That is easier. So the latency number will go up because it's prolonged. The amplitude number will go up, but then it's slower. So the conduction velocity will be lower. And the duration will go up. That's it. All right, well, I think I took too much time, but thank you. I hope I made that a little more. I have a online YouTube longer version of this. It takes two hours to actually explain. So I'll try and share that link with the coordinators. Thank you. Okay. Well, the topic that Dr. Malhotra went over is a very complex topic, and I thought you explained that very well. So, I think we're all more familiar with upper limbs, and so I'm going to go through this a little bit faster and hit some of the things that I think of are a little bit more testable. I don't have any financial disclosures. I'd love to have some, actually. So, the first thing is the carpal tunnel. We spend a lot of our time, obviously, evaluating this in the electrodiagnostic laboratory, and the one thing that we think about are what the contents of the carpal tunnel are. And so, here you can see a diagram with flexor pollicis longus here. You see the little, let me get my little pointer here. So, flexor pollicis longus, the slips of flexor detorum profundus and flexor detorum superficialis, and the median nerve. One thing that's important to realize is the flexor carpi radialis is not in the carpal tunnel, and the ulnar artery and ulnar vein are not on there either. One interesting thing, and I know the focus of this is an ultrasound, but this is a cool thing when you do do ultrasound, is you'll notice the floor of Guion's canal is the roof of the carpal tunnel, which is an interesting thing. If you look at your hand, we all know those three digits are most affected by carpal tunnel syndrome, and clinically, when you're bringing the patients back, you'll sometimes find the fingertips are affected, but not the entire distribution of the median nerve, and that's not unusual. The other thing that's important and sometimes testable is that the skin over the thenar eminence is innervated by the median nerve, but not distal to the carpal tunnel, so people will have a preserved sensation over the thenar eminence in classic carpal tunnel syndrome. A couple of other things to keep in mind when you're planning out these studies. It is very rare to have carpal tunnel syndrome, particularly mild carpal tunnel syndrome, without pain. So whenever I'm evaluating people, I'll often kind of just be a little bit more suspicious, be a little bit more open-minded when they don't have pain. The exception to that can be people at the extremes of age, older adults, and that sort of thing. A lot of times, a question that I'll ask people is if they're shaking their hand out at night, nocturnal acroparasthesias, and then you can also ask a functional history of them. A lot of times, people have difficulty buttoning or fine motor skills or dropping things, and I'm sure a lot of you, if you're thinking about the exam or are experienced with this, you kind of know it when you see it, and I think a lot of being a really good technologist is kind of hearing enough of these stories to know when something is off and when you need to be a little bit more deliberate about things. So one example from a session we did this morning is at the Mayo Clinic. The technologists are the ones who often pick up Lambert-Eaton syndrome, because somebody comes in for a particular complaint, you find all the motor conductions are down, and you end up having them exercise and watch the conduction go up. And so I think carpal tunnel, because it's so common, really the question is when you've got a story that's a little bit different. This is the grading of carpal tunnel syndrome, and this gets really important because there's a lot of work on fraud and abuse, and if you understand this grading scale, it allows you to be more thoughtful in terms of the number of nerve conductions that you do. For mild carpal tunnel syndrome, you're going to have just the prolonged sensory latency. Or another way of saying it is the myelin of the sensory fibers is affected. For moderate carpal tunnel, we start to see the motor latency prolong, and we start to see the sensory amplitude decrease. And then for severe carpal tunnel syndrome, you start to lose the median CMAP, or you have a spontaneous activity on EMG. Now, one nuance to this is Gotham was showing us the motor conduction to the palm, and so when somebody has a low amplitude of their median study, you don't know whether that's conduction block or axon loss that's driving that. And that's where doing a study of the recurrent branch of the median nerve, like Dr. Molotra was demonstrating, can be helpful in terms of sussing out is this axon loss, which would be more in the spirit of severe carpal tunnel, or is it conduction block, which in my mind would be a little bit more of a moderate picture. And so we know that if you do those routine sensory nerve conductions, about 15% of the time you're going to miss somebody with carpal tunnel. And that's where we have these comparison studies that come on where we can compare the transcarpal, where you're doing the mixed nerve studies. One kind of nuance about this is I think you showed a slide of the fiber types, correct? So these mixed nerve studies test the 1A or the A-alpha fibers. Those are your largest, most metabolically sensitive fibers. And so some people would say that this is the most sensitive test for carpal tunnel, and since you're comparing the median and the ulnar nerve, it's going to be a more precise study. You can do the comparison sensory study to digit 4 and digit 5, and the numbers that I have up here are some potential cutoff values for each of these studies. The problem with any one of these studies is that if you do a little bit of a measurement error, it's going to potentially really throw things off, because that's really the key to the whole test. And so that's where we had the combined sensory index, and then CSI Miami came out, so they decided to rename it the Robinson Index. And about 1.0 milliseconds, if you add up the differences of these conductions, and it's less than 1 millisecond, boy, you're pretty confident that carpal tunnel is off the table. And then the motor comparison study is another option that you can do. I don't have it here, but you can just put a recording electrode over the second lumbrical and stimulate the median nerve, record the second lumbrical, stimulate the ulnar nerve, record from one of the inner ossei, and if the motor is more than 0.4 milliseconds compared to the ulnar, that is sensitive. And one pro tip is that when I'm doing my routine nerve conduction sensory and motor, if I notice a little bit of a bigger split between the motor median and the motor ulnar, that might make me decide to do a motor comparison. And if I see more of a split on the sensory, that might make me think to do a transcarpal or a Robinson Index. And then I'm going to follow up on what Dr. Malotra was talking about. And so he was talking about the anatomy. And I think that's exactly right. When you see that large proximal conduction, you know it's either an anatomical variant or some sort of error. But when you have carpal tunnel superimposed on that, there's three things that you're going to see. You're going to see that increased proximal amplitude that you would see even if there wasn't pathology. And then you'll see a very high conduction velocity. The way I think about this is you've got a traffic jam. And because there's a Martin Gruber anastomosis, the fibers can go around the traffic jam. And so it appears to the machine when you do the math that the conduction velocity is really high because you have less time. And then you have a positive deflection on proximal stimulation because you're going to have things firing that are at a distance from where you're recording electrode is. The next one will be the ulnar nerve. And here you can see the anatomy of the ulnar nerve. And one of the things that I tend to think about is that carpal tunnel syndrome, to me, it tends to most commonly be one pathology. You've got a nerve. It's tight in the canal. It's not moving as well. And you end up with carpal tunnel syndrome. Many of us think that ulnar neuropathy can be some different things. And so in history, you'll sometimes hear that somebody had the ulnar neuropathy start right away after they had a surgery. Or they'll have hypermobility where the nerve will be snapping. Or they'll have the entrapment in the fibroosseous tunnel. And the anatomy is also more complex where you have the humeral ulnar arcade. You have that retro epicondylar groove. And then finally, you have the arcade of struthers. And so anywhere along that elbow, there's several sites where you can be entrapped. And some people really get excited about doing inching studies or using ultrasound to figure out right where the entrapment is. I always find that no matter where I tell them it is, the surgeon will just release the whole thing. So I don't get too excited about that. But not to say that's right or wrong. Medical findings. And so one of the things that's important to suss out on these patients is that the ulnar nerve only innervates to about the wrist crease. And so if somebody's having numbness up in the forearm, sometimes that will happen in ulnar neuropathy. But anatomically, it really shouldn't be a dominant thing. You should really see symptoms limited to the hand. Here you can see the dorsal ulnar cutaneous nerve. And so I'm really interested when I'm setting up a nerve conduction for a patient with a suspected ulnar neuropathy, what's that distribution? Is it just the palm, which makes me think more of a Guillain's Canal lesion? Is it the dorsum of the hand and the palm, which makes me think elbow, the most common? Or is it going up the medial aspect of the forearm, in which case I want to be expanding my differential and checking a medial intubrical cutaneous to make sure there's not a more extensive pathology coming on? The other thing that I think is helpful clinically is that when you have mononeuropathies, the lesions tend to be very well defined. And so if somebody has median or ulnar neuropathy, you'll be able to sense the difference between these two fingers. But if somebody has a radiculopathy, it'll be a more vague sort of complaint because of all the overlap that occurs. And then we run into the same issue that we had with median. When you think somebody has an ulnar nerve issue, but that routine recording to ADM is normal, what are some steps that you can do? And one of the first things I like to do is a recording from the first dorsal neurosis. And so sometimes the FDI recording will show conduction block or demyelination at the elbow where the ADM did not. And so I think that's a nice step. Dorsal ulnar cutaneous can be helpful. Obviously, if that's absent, that's suggestive of an ulnar neuropathy. Medial intubrical cutaneous, if that's normal, that's more suggestive of an ulnar neuropathy. And that's, I think, the big parts there. So we are caught up. I am Betty Mitchell, I am a technologist at Lubbock Spine Institute in Lubbock, Texas. I'm just going to touch on some of the troubleshooting topics that some of the techs can face in real life and it's going to be some questions on some of the tests as well. They've kind of been touched on a little bit already. I'm just going to do it very basic. Some of it's going to seem what would seem entry-level, but I've talked to techs today that have only been a tech for a couple of months all the way up to 40 years. So I know there's a big span here today and a lot of those haven't taken their exam yet. So a lot of this can come natural as you work. It's just going to be second nature to come up with some of these troubleshooting things and know what you need to look for and know what you need to change. And then some of it, you're in a hard test, your patient's irritated, you're in a time limit and some of it you just seem so basic that it's just something you forget to check but could ultimately be why you're not getting the response you need or just not able to come up with a good waveform itself and help come up with the correct diagnosis. There we go. I have a different PowerPoint and they were having trouble telling me how to change these slides. Okay. There we go. So the first topic, again, has already been talked about a little bit, cold extremities. So temperatures below 31 degrees can slow the opening and the closing of the sodium channels which is going to prolong the depolarization and slow the conduction. So this can be slowed up to 2 meters per second per degree Celsius. This can be, it can cause increased distal motor latency, increased F wave latency, decreased sensory motor conduction velocity and can result in current flow and increased amplitudes. It can cause false diagnosis of demyelinating peripheral neuropathies, peripheral mononeuropathy or sensory neuropathies. You can fix this by heat lamps, warming blankets. We do procedures in our office as well. So we have warming blankets. This usually helps. Heating pads. Of course you want to be careful to put a barrier between the heating pad and the patient depending on how long it takes to warm their limb. And depending on their problems, why their limb is cold, is it cold in your room, do they have circulation issues, they have issues, sometimes CRPS, different other health issues can cause this as well. So usually pretty easy to warm. Sometimes I find it usually takes about 5 minutes or so. Sometimes it can take about 20 minutes. You want that limb to be warm for a little while before going on with testing. Age is another factor. A bunch of studies show that it can start, you can start seeing age changes at the age of 40 years, usually a little bit more prominent in patients over the age of 60. This is due to nerve fiber decrease in that number and a reduction in the nerve diameter. This can cause increased distal motor latency, increased F-wave latency, and decreased sensory and motor amplitudes. There's reference ranges for your area that you can apply. And usually we have a really good Cadwell rep. We use Cadwell. So they came in and fixed all of that for us. And so it's just a real easy click to do to apply all these age reference values. Electrode placement, I know that's been talked about a little bit today. You want to make sure that that recording electrode is over the muscle of the belly and that the reference is corresponding tendon or a nearby bone. And again, been talked about a little bit, most 3 centimeters apart. New studies are showing 4 centimeters apart. So anywhere in that 3 to 4 centimeters, of course, the bar electrodes are going to be set for you already. The electrodes can become dislodged due to patient movement or a strong muscle contraction due to the stimulation. Always check the contact integrity before the stimulation is done to reduce the number of times you're going to stimulate that patient. Pressure on the electrodes during the stimulation decreases the distance between the electrode and the nerve, reduces the volume of tissue fluids between the skin and the nerve, which can cause an increase in amplitude of the sensory response. So sometimes it just kind of feels like just a reaction to hold that electrode in place, but you don't want to put too much pressure on that electrode and stem. It can cause falsely increased amplitudes and increased latency. If a motor response has an initial positive deflection, you can move that recording electrode a little bit more over the belly of that muscle and then just make sure that the skin is free from oils or lotions. Perspiration can cause that also. Sometimes patients get really nervous, they'll start perspiring and that can cause your electrodes to move as well. In some cases, you might need to shave the skin and you can consider using a light abrasive skin prep gel as well. These different nerve anomalies can pop up, can make sure or cause interpretation to be difficult on that. So the RCA, the connection between the ulnar nerve and the median nerve in the palm, the Martin Gruber, the crossover of the median to the ulnar, most commonly found in that forearm there, and then the ADPN comes off the superficial perineal nerve. Can cause misdiagnosis or an under or overdiagnosed severity of a mononeuropathy. Always be mindful of the possible anomalies that these things just don't seem right, if something's just not adding up, and then just be studied up on that anatomy and the limb that you're testing and be aware that that can be an issue. The inadequate skin preparation, too much of a good thing can be a bad thing. While conductivity gel can be the difference in a response and no response, it can also be the difference in an erroneous response and an accurate response. So this can be referred to as a gel bridge, and again, patient perspiration can be a cause of this. Too much gel can cause your stimulator to slip out of place, and of course that can be important, you want that stimulator to stay in place whenever, especially whenever you're doing the repetitive stims, you want to be sure that that stimulator stays where you started to get that baseline. These can cause stimulus artifact, little or no response, and again, cause stimulator slip during stimulation. You can use a gauze to wipe that excessive gel or the perspiration, and then place the ground electrode between the site of the stimulation and the recording electrode. Pain in the patient, this one is usually the biggest hurdle to get over, the patient's hurting and then you're stimulating them, and that just can cause just an uncomfortable situation, which again, can cause you to overlook some of these troubleshooting things that can seem very basic. It can cause the false decrease amplitudes, the inability to complete the test, and interfere with electrode contact. The EMG portion of it, the needle part can cause harm if the patient jerks, it can mimic insertional activity due to muscle contraction, can cloud the reading due to inability to relax, and can inhibit the reading upon contraction of the muscle because they're unable to do so. I always start with a really slow stimulation, work my way up. I usually have a long conversation at the beginning and ask if there's any questions. I start up a conversation whenever I'm testing, that kind of helps just kind of take their mind off of it. Through the EMG portion of it, of course, encourage proper breathing, ask the patient to count down between needle sticks helps. Some want to hear a countdown, some don't want to, they just want you to stick the muscle and get it over with. Another troubleshooting thing can be equipment. The wires can become frayed, amplifiers can become old, and where the plug, we just had an issue where our amplifier plugs in, and we kept getting interference and found out that that was one of the big things. So incorrect stimulation parameters can cause misleading results. Always regularly review and adjust the stimulation settings such as pulse duration and intensity to match the specific requirements for the study of the patient's condition. Regularly check your electrode wires for cracks or splits. Regularly check the amplifier plug to ensure they're plugged in all the way to prevent interference. Regularly check expiration dates on gels, electrode packets, and needles. And then just always look to your doctor or a lead technologist if you have any questions or if you need guidance in the study. The old saying, two heads are better than one, it's usually true in our field, most fields, sometimes it takes three or four. We have an EMG session with Dr. Norbury sometimes, and it just helps to kind of get everything, more eyes on your study or more eyes even during the actual study itself. Just call someone in if you can't get anything figured out. Never be afraid to open a book. Actually can comfort the patient if they know that you've taken an interest in why they're there and actually have to open the book and you're trying to figure out what the issues can be. Again, always explaining what you're doing before and after, making continuing education a priority. And these diagnoses can lead a patient to surgery or keep them out of surgery or send them to another doctor, another specialist, or keep them out of that. So our education, our skills, and our knowledge are valuable and they should always be used to the highest potential. Thank you. So, good afternoon, I'm going to be finishing the session today with lower extremity nerve conduction studies. We'll have some interactive questions, so if you can pull out your devices, there will be a little QR code for you to scan. So we'll review the anatomy of the sensory nerves in the lower extremities, as well as the anatomy of routine nerve conduction studies and why people send them to us and to you as the technologist for the nerve conduction studies. We'll look at pearls for each nerve conduction study and we'll have practice questions interspersed. So I wanted to start with just kind of a quick definition of the anatomic man and how we use orientation terminology. I think a lot of the challenge in learning nerve conduction studies is the new terminology that's presented. So as you know, there is a routine manner of describing patient's orientation. So we think of the anatomic man as someone kind of lying down, their front facing towards you. So that's called anterior. And the back is posterior. And then anything kind of going outward, as depicted in these arrows, is lateral. And inward is medial. So good terminology to know is that the sensory innervation of the posterior lateral calf is the serral nerve, which is a branch of the sciatic nerve. And the medial calf is the saphenous nerve, which is a branch of the femoral nerve. And anterior lateral calf is the superficial perineal or fibular nerve, which is the newer terminology. And then the lateral thigh is the lateral femoral cutaneous nerve, which is actually not a branch of the femoral nerve. And then the bottom of the foot is the medial and lateral plantar sensory nerves. So we'll start with our first practice question. So I'll show it to you. And then on the next slide, you'll see the QR code if you want to participate to scan it. So based on the prior picture, your knowledge and experience, what nerve provides sensation to the medial calf of the leg and is a branch of the femoral nerve? So I'm going to go on and you can keep voting as I go on. So the medial calf of the leg and the branch of the femoral nerve is actually the saphenous nerve in that picture and the sural nerve is more the posterior lateral sensation or sensory nerve which is a branch of the sciatic. Thank you. Keep going. Okay, so that's a sample question about some of the neuroanatomy there. So you can see the saphenous nerve which is the medial calf and I'll sometimes add this it's not part of the routine nerve conduction studies if we're interested in a femoral neuropathy or a plexopathy. Now I know we're all familiar with this which is part of our routine lower extremity studies which is the sural sensory nerve conduction study here. You can see that your G1 or E1 or active electrode is placed posterior to the lateral malleolus and then your G2 either this fixed distance it is a bar electrode that's being depicted in the image or 3 to 4 centimeters distal and different centers have different protocols but most do tend to stimulate 14 centimeters proximal. We tend to do these sural studies and they're indicated in polyneuropathies, plexopathies and mononeuropathies particularly sciatic. So some pearls this is probably the most challenging nerve that we do routinely. It is the smallest amplitude response that we're looking for. Many books say that it could be absent in a normal patient over the age of 60. So a few things that we do in our lab to try to find that sural sensory nerve is sometimes we'll use a shorter distance to verify if it's present. It requires a different calculation of the conduction velocity if you're going to be using shorter distances and also find bar electrodes to be very helpful to reduce the impedance that Dr. Mahotra talked about in his initial talk to improve that response. He also mentioned the average button as well which can also really help ensure that you have a good sural response. So he explained it previously so as a review anywhere in any EMG lab even if your room has like the best setup you're going to have some random noise that occurs. And this becomes a challenge when the signal of interest is a very small response like the sural nerve. So you can see in this image that the sural nerve is the random noise is kind of approaching your signal of interest which is the sural nerve sensory amplitude. So when it comes to those situations what you can do is you can use the average button on all of our modern EMG machines. And what happens is the computer just generates the time locked signal and displays it. And this serves to amplify the true response which is called the signal. And so the average button serves to improve your signal to noise ratio. So here's our next practice question. I'm going to go to the one with the QR code. So which of the following statements regarding the sural sensory nerve conduction study is true? So here are your choices. It is a robust and reliable response in patients over the age of 60. The sural sensory response may need to be averaged for reproducibility due to its small amplitude. The sural sensory conduction study is typically normal in a link-dependent diabetic neuropathy or the sural sensory study would be spared in a lumbosacral plexus lesion. Okay, so I think you can keep voting, and that's great. We have the correct response, which is it is a small response and it often will need to be averaged for reproducibility. Great. So next we're going to talk about tibial motor studies. So you can see here the G1 is placed inferior to the navicular bone, G2 4 centimeters distal. For me, a pearl for the tibial motor study is that proximal site of stimulation is pretty tricky. It can be often painful. It's behind the popliteal fossa, and it can drop by more than 50% in some normal patients just based on body habitus or how deep the nerve is. So it's something to consider when you're doing the proximal site on the tibial. It is affected in poly, can be affected in polyneuropathies, lumbosacral adiculopathies, tibial neuropathies such as tarsal tunnel, sciatic, plexus, muscle conditions, and even local foot trauma. Another pearl is the tibial nerve can also be misplaced quite easily, the G1 or the active electrode. So you want to watch for a positive dip when you're stimulating the study and collecting that response. When you see that positive dip, you should move your G1 or active electrode and, oh, sorry, and then the reason for that is to try to be over the motor belly. So here's our next practice question. So you're performing a tibial motor conduction, oh, you know what, I think I have to go back. Okay. The picture didn't show up on the Slido. So you're performing a tibial motor conduction study of the abductor hallucinous muscle and you obtained the tracing shown on this slide. The distal motor latency and the amplitude are within normal limits. So go ahead and just read through these to look at your interpretation of the response. And now I'm going to go ahead and go to the next slide where you can vote. Okay, great, so 100% of people got the answer right. This waveform was obtained with the G1 off the motor end plate, so you need to move the G1 and apply another stimulus to get a better waveform. Very good. And the explanation is for motor nerves, we want our depolarization to happen right underneath our G1 and active electrode, as depicted in the top trace in this explanation. And when you have that positive dip, it means that the depolarization is a traveling wave that's going towards your G1 and active electrode, and not quite where we want it. It can change the markers that we collect, such as the distal motor latency or amplitude when we accept that positive sharp wave. Okay, so next routine study is the fibular motor study. So the G1 or active electrode is on the dorsolateral foot, G2 is distal here. And there's three sites of stimulation, the anterior ankle, below the fibular head, and the lateral popliteal fossa. These nerves can be affected in polyneuropathy, radiculopathy, mononeuropathy, sciatic, plexus, muscle conditions, and foot trauma. So some pearls for this study is, if you're doing your routine fibular motor study off the EDB, and your amplitude at the popliteal fossa is larger with a change in waveform as compared to the distal sites, this could indicate that you're co-stimulating your tibial motor nerve at the popliteal fossa, and you would want to consider reducing your stimulus intensity or repositioning your stimulator lateral in the pop fossa. Another pearl is this anomalous innervation that has been previously mentioned by our other speakers, where if your proximal stimulation site, the fibular head this time, not the pop fossa, has an amplitude that's larger than your distal ankle site, this can indicate kind of the three reasons that Dr. Mahotra mentioned, but one of them is an anomalous innervation called the accessory fibular nerve. So if you go back and you check that you are not sub-max at your ankle or over-stimulating at your fibular head, and you're pretty sure you weren't doing those things, then the next step would be to add another trace, trace four on my computers, and then you're going to add a stimulation behind the lateral malleolus. And you can see here in this cartoon how the peroneal nerve has an accessory branch that is moving behind the lateral malleolus. So once you add that foresight, you see a response, which can add up almost precisely to the ankle form. In our lab, we sometimes do the fibular motor study off the tibialis anterior, and this is a pretty true depiction of how we would set up that study with our G1 and active electrode over the tibialis anterior muscle belly. And the G2 at the ankle, you'll notice that that's quite far away, more than four centimeters from your G1, and that's because of how large the tibialis anterior muscle is. So that's a little exception to that rule of three to four centimeters being optimal. This study can be affected in polyneuropathies, radiculopathies, mononeuropathies, and plexopathies. Okay, so I'm going to go ahead and show you this question here because I don't think the waveform will show when I pull up the Slido. So here's another practice question. You're performing a routine fibular motor conduction study off the tibialis anterior muscle. The patient is presenting with a foot drop. On the affected leg, you see this waveform. Which of the following is your interpretation? So A, it's technical. There was a co-stimulation at the popliteal fossa. B, this is an accessory fibular nerve. Or C, this is a partial motor conduction block of the fibular nerve across the fibular head. So now I'm going to pull up the QR. Okay, great. So 100% of those who answered got it correct. This is a partial motor conduction block of the fibular nerve across the fibular head. So what you can see here is that there's a larger response at the distal fibular head site and a lower response at the pop fossa. So this is not technical. It would have the opposite pattern if it was technical, where the fibular neck amplitude would be lower and the pop fossa would be higher with a different waveform. And this is not an accessory fibular nerve either. That is found on the studies off the EDB, and the distal sites are smaller in amplitude. So C is going to be the best answer for this question. Next, we're going to review other routine studies. These are the F-waves. The F-waves were named for foot, but they can also be performed on median and ulnar nerves as well, so a bit of a misnomer. In these studies, you actually turn your stimulator around, and the anode is directed towards the G1. We use the supermax stimulus intensity, so whatever intensity you use to get the best supermax response distally would be what you use for your F-wave. It's not a true reflex. It's more of a backfiring, as you can see in the bottom picture there that's being depicted. Minimal F-wave latency is probably the most common value that's used by most EMG labs, and you can see it marked in the picture as well. The other thing to note is that each F-wave tends to have a different morphology because there's a different population of anterior horn cells stimulated each time. These are affected in polyneuropathy, especially Guillain-Barre syndrome, radiculopathies, certain mononeuropathies, depending on what you're studying, and then plexopathy. The other late response that we do much less routinely at our EMG lab is called the H-reflex. It was named this for Hoffman. You can see in the picture on the bottom right of the screen the setup for this. So this is only reliably done from this muscle and nerve combination. You can see the G1 and active electrode placed on the soleus or gastrocnemius muscle with the anode pointing towards the G1 in the pop fossa. To differentiate it from an F-wave, it is a true reflex. There's an actual synapse that's occurring. And we actually use sub-max stimulus intensities. So it's a little bit hard to read, but in the tracing on the upper right, you're going to see that your H-waves, which are your second response, they're actually better when you use lower stimulus intensities. The reason for this is you want to selectively stimulate these sensory 1A afferent fibers without the motor fibers, which can cause a collision. These are affected in polyneuropathies, again, very sensitive in early Guillain-Barre syndrome, radiculopathy, sciatics, and plexus lesions. Okay, so now we're going to do a practice question. Which of the following is true regarding the H-reflex? Okay, great. So the majority have it in that the H reflex is an early and sensitive finding in Guillain-Barré syndrome. We'll go through each of the other answer choices. So the H reflex has a different morphology with each stimulation. So actually the morphology is very similar. It will just grow in amplitude as you lower your stimulus intensity. It's actually the F wave that has a different morphology each time. You get a different population of anterior horn cells. The other answer choice, it said the H reflex is recorded using a stimulus intensity of 0.1. And it actually is a very long stimulus duration of 1 millisecond, not 0.1 millisecond. And the H reflex, you use a sub-max stimulus intensity instead of a super-max stimulus intensity. Okay, that's all I have. Thank you for your attention.

nerve conduction studies

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electrodiagnosis

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electrodiagnostic techniques

afferent and efferent pathways

differential amplifiers

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nerve conduction studies

nerve conduction study

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